BioMedLib Search Engine
[ goto HOMEPAGE ]
Save time; Find better answers!
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Query is expanded
Login
Skip to content
Export Citations
Search Results
RSS
Email
Articles' Details
Start new query
Reset All
Refine your query
(more in Advanced-Search):
Search all of MEDLINE
Focus on the recent 5 years
Focus on the current year
Focus on the last 30 days
More choices ...
Focus on articles with free fulltexts
More choices ...
Do simple 'keyword' search (no query expansion)
[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click
here to
RESET
all values
Click
here to
GO BACK
without resetting any value
Advanced Search
Submit one or more of the following items, and they will be searched along with your query in the search box above.
Any submit button will submit all of the items you have changed.
+
Publication-Date
Published in the last:
30 days
60 days
90 days
6 months
12 months
this year
2 years
3 years
5 years
10 years
Or published in the following date range: From (yyyy/mm/dd - month and day are optional)
to ('to' is optional)
+
Full Text
Retrieve articles with hyperlinks to:
full text (either free or subscription)
free full text
subscription full text
no full text link
+
Sort-Order
Sort the retrieved articles by:
relevance
publication date
+
Language
And with languages:
English
French
German
Italian
Japanese
Russian
Spanish
More languages:
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Bengali
Bosnian
Bulgarian
Catalan
Chinese
Czech
Danish
Dutch
Esperanto
Estonian
Finnish
Georgian
Scottish Gaelic
Greek, Modern
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Kinyarwanda
Korean
Latin
Latvian
Lithuanian
Macedonian
Malayalam
Maori
Malay
Multiple languages
Norwegian
Persian
Polish
Portuguese
Pushto
Romanian
Sanskrit
Serbian
Croatian
Slovak
Slovenian
Swedish
Thai
Turkish
Ukrainian
Undetermined
Urdu
Vietnamese
Welsh
+
Publication-Type
And with publication types:
Clinical Trial
Editorial
Letter
Meta-Analysis
Practice Guideline
Randomized Controlled Trial
Review
More publication types:
Addresses
Bibliography
Biography
Case Reports
Classical Article
Clinical Conference
Clinical Trial, Phase I
Clinical Trial, Phase II
Clinical Trial, Phase III
Clinical Trial, Phase IV
Comment
Comparative Study
Congresses
Consensus Development Conference
Consensus Development Conference, NIH
Controlled Clinical Trial
Corrected and Republished Article
Dictionary
Directory
Duplicate Publication
English Abstract
Evaluation Studies
Festschrift
Government Publications
Guideline
Historical Article
Interactive Tutorial
Interview
Introductory Journal Article
In Vitro
Journal Article
Lectures
Legal Cases
Legislation
Multicenter Study
News
Newspaper Article
Overall
Patient Education Handout
Periodical Index
Portraits
Published Erratum
Retracted Publication
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Retraction of Publication
Scientific Integrity Review
Technical Report
Twin Study
Validation Studies
+
Species
And for:
Humans
Animals
+
Gender
And for:
Male
Female
+
Age
And for these age groups:
Newborn: birth to 1 month
Infant: 1 to 23 months
Preschool child: 2 to 5 years
Child: 6 to 12 years
Adolescent: 13 to 18 years
Adult: 19 to 44 years
Middle aged: 45 to 64 years
Aged: 65+ years
80 and over: 80+ years
+
Title
And for this query matching the titles:
+
Transliterated-Title
And for this query matching the title in original language:
+
Abstract
And for this query matching the abstratcs:
+
Major-Mesh
And for this query matching the MeSH-Major terms:
+
Mesh
And for this query matching any MeSH terms:
+
Journal
And for one or more of these journal abbreviated names:
OR
OR
(see
title abbreviations
)
+
Volume
And with journal volume number:
+
Issue
And with journal issue number:
+
Page
And with page number:
+
ISSN
And with ISSN:
+
Publication-Place
And with journal's country of publication:
+
Author
And for...
all these author names:
AND
AND
(see
help
)
one or more of these author names:
OR
OR
but not having any of these unwanted author names:
NOT
NOT
+
Affiliation
And with affiliation to:
+
Has-Abstract
Find MEDLINE records with the abstract status:
has abstract
does not have abstract
include both record types
include both record types but rank higher the records having abstract (the default BML behavior)
+
PMID
Show me only articles for these PMIDs (PubMed IDs):
+
Semantic-Type
And with semantic types:
A. Entity
A1. Physical Object
A1.1. Organism
A1.1.1. Archaeon
A1.1.2. Bacterium
A1.1.3. Eukaryote
A1.1.3.1. Animal
A1.1.3.1.1. Vertebrate
A1.1.3.1.1.1. Amphibian
A1.1.3.1.1.2. Bird
A1.1.3.1.1.3. Fish
A1.1.3.1.1.4. Mammal
A1.1.3.1.1.4.1. Human
A1.1.3.1.1.5. Reptile
A1.1.3.2. Fungus
A1.1.3.3. Plant
A1.1.4. Virus
A1.2. Anatomical Structure
A1.2.1. Embryonic Structure
A1.2.2. Anatomical Abnormality
A1.2.2.1. Congenital Abnormality
A1.2.2.2. Acquired Abnormality
A1.2.3. Fully Formed Anatomical Structure
A1.2.3.1. Body Part, Organ, or Organ Component
A1.2.3.2. Tissue
A1.2.3.3. Cell
A1.2.3.4. Cell Component
A1.2.3.5. Gene or Genome
A1.3. Manufactured Object
A1.3.1. Medical Device
A1.3.1.1. Drug Delivery Device
A1.3.2. Research Device
A1.3.3. Clinical Drug
A1.4. Substance
A1.4.1. Chemical
A1.4.1.1. Chemical Viewed Functionally
A1.4.1.1.1. Pharmacologic Substance
A1.4.1.1.1.1. Antibiotic
A1.4.1.1.2. Biomedical or Dental Material
A1.4.1.1.3. Biologically Active Substance
A1.4.1.1.3.1. Neuroreactive Substance or Biogenic Amine
A1.4.1.1.3.2. Hormone
A1.4.1.1.3.3. Enzyme
A1.4.1.1.3.4. Vitamin
A1.4.1.1.3.5. Immunologic Factor
A1.4.1.1.3.6. Receptor
A1.4.1.1.4. Indicator, Reagent, or Diagnostic Aid
A1.4.1.1.5. Hazardous or Poisonous Substance
A1.4.1.2. Chemical Viewed Structurally
A1.4.1.2.1. Organic Chemical
A1.4.1.2.1.5. Nucleic Acid, Nucleoside, or Nucleotide
A1.4.1.2.1.6. Organophosphorus Compound
A1.4.1.2.1.7. Amino Acid, Peptide, or Protein
A1.4.1.2.1.8. Carbohydrate
A1.4.1.2.1.9. Lipid
A1.4.1.2.1.9.1. Steroid
A1.4.1.2.1.9.2. Eicosanoid
A1.4.1.2.2. Inorganic Chemical
A1.4.1.2.3. Element, Ion, or Isotope
A1.4.2. Body Substance
A1.4.3. Food
A2. Conceptual Entity
A2.1. Idea or Concept
A2.1.1. Temporal Concept
A2.1.2. Qualitative Concept
A2.1.3. Quantitative Concept
A2.1.4. Functional Concept
A2.1.4.1. Body System
A2.1.5. Spatial Concept
A2.1.5.1. Body Space or Junction
A2.1.5.2. Body Location or Region
A2.1.5.3. Molecular Sequence
A2.1.5.3.1. Nucleotide Sequence
A2.1.5.3.2. Amino Acid Sequence
A2.1.5.3.3. Carbohydrate Sequence
A2.1.5.4. Geographic Area
A2.2. Finding
A2.2.1. Laboratory or Test Result
A2.2.2. Sign or Symptom
A2.3. Organism Attribute
A2.3.1. Clinical Attribute
A2.4. Intellectual Product
A2.4.1. Classification
A2.4.2. Regulation or Law
A2.5. Language
A2.6. Occupation or Discipline
A2.6.1. Biomedical Occupation or Discipline
A2.7. Organization
A2.7.1. Health Care Related Organization
A2.7.2. Professional Society
A2.7.3. Self-help or Relief Organization
A2.8. Group Attribute
A2.9. Group
A2.9.1. Professional or Occupational Group
A2.9.2. Population Group
A2.9.3. Family Group
A2.9.4. Age Group
A2.9.5. Patient or Disabled Group
B. Event
B1. Activity
B1.1. Behavior
B1.1.1. Social Behavior
B1.1.2. Individual Behavior
B1.2. Daily or Recreational Activity
B1.3. Occupational Activity
B1.3.1. Health Care Activity
B1.3.1.1. Laboratory Procedure
B1.3.1.2. Diagnostic Procedure
B1.3.1.3. Therapeutic or Preventive Procedure
B1.3.2. Research Activity
B1.3.2.1. Molecular Biology Research Technique
B1.3.3. Governmental or Regulatory Activity
B1.3.4. Educational Activity
B1.4. Machine Activity
B2. Phenomenon or Process
B2.1. Human-caused Phenomenon or Process
B2.1.1. Environmental Effect of Humans
B2.2. Natural Phenomenon or Process
B2.2.1. Biologic Function
B2.2.1.1. Physiologic Function
B2.2.1.1.1. Organism Function
B2.2.1.1.1.1. Mental Process
B2.2.1.1.2. Organ or Tissue Function
B2.2.1.1.3. Cell Function
B2.2.1.1.4. Molecular Function
B2.2.1.1.4.1. Genetic Function
B2.2.1.2. Pathologic Function
B2.2.1.2.1. Disease or Syndrome
B2.2.1.2.1.1. Mental or Behavioral Dysfunction
B2.2.1.2.1.2. Neoplastic Process
B2.2.1.2.2. Cell or Molecular Dysfunction
B2.2.1.2.3. Experimental Model of Disease
B2.3. Injury or Poisoning
Page Format
Any submit button will submit all of the items you have changed.
[theme]
Use this page design theme:
original
twenty ten
[shown]
Results per page:
5
10
20
50
100
200
500
[expand/collapse]
show these sections expanded by default:
Advanced search
MeSH query
Search history
Page format
Query expansion
Articles details
Export citations
Email
[text size]
use this font size for text:
25%
50%
75%
100%
125%
150%
200%
or enter your choice of font size:
[page width]
use this page width (relative to the default initial value):
25%
50%
75%
100%
125%
150%
200%
or enter your choice of page width:
[highlight color]
use this color to highlight query words in the articles:
red
green
blue
black
purple
yellow
orange
navy
olive
maroon
none
[query history]
maximum number of queries shown in the history section:
[annotate]
Annotate these parts of each article:
title
abstract
both
none
Reset all values
Find best MeSH terms for
Search History
1
b cell non hodgkin lymphoma 2005:2010[pubdate] *count=100
14607 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
b cell non hodgkin lymphoma
' expanded to all its synonyms;
details
Email the results to the following email address:
Export the checked citations in RIS format (RIS format is used by RefWorks, Endnote, among others).
Items 1 to 100 of about 14607
1.
Kanellis G, Mollejo M, Montes-Moreno S, Rodriguez-Pinilla SM, Cigudosa JC, Algara P, Montalban C, Matutes E, Wotherspoon A, Piris MA:
Splenic diffuse red pulp small B-cell lymphoma: revision of a series of cases reveals characteristic clinico-pathological features.
Haematologica
; 2010 Jul;95(7):1122-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Splenic diffuse red pulp small B-
cell lymphoma
: revision of a series of cases reveals characteristic clinico-pathological features.
BACKGROUND: Splenic diffuse red pulp small B-
cell lymphoma
is an uncommon B-
cell lymphoma
, now recognized as a provisional entity in the 2008 update of the WHO Classification.
DESIGN AND METHODS: We have retrospectively analyzed the
disease
features in a highly selected series of 17 patients diagnosed as splenic diffuse red pulp small B-
cell lymphoma
.
Clinical
manifestations were mainly derived from splenomegaly.
All cases showed a purely diffuse pattern of splenic infiltration by monomorphous small
cells
with small round nuclei and pale cytoplasm.
Peripheral blood
cells
were small to medium-sized, with clumped chromatin and round nuclear outline and villous cytoplasm.
Neoplastic
cells
had a CD20(+), CD23(-), bcl6(-), Annexin A1- phenotype, with frequent expression of DBA44+ (15/17) and IgG (10/15).
FCM data had a B-
cell
phenotype (CD19(+), CD20(+), CD22(+)) with FMC7 (10/11) and CD11c (5/8) expression.
CONCLUSIONS: Our data suggest that splenic diffuse red pulp small B-
cell lymphoma
is a distinct entity with morphological and immunophenotypical features that differ from those of other splenic
lymphomas
.
[MeSH-major]
Lymphoma
, B-
Cell
/ pathology. Splenic Neoplasms / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Leuk Res. 1999 Nov;23(11):1041-5
[
10576509.001
]
[Cites]
Haematologica. 2008 May;93(5):670-9
[
18367492.001
]
[Cites]
Blood. 2002 Feb 15;99(4):1299-304
[
11830479.001
]
[Cites]
Histopathology. 2002 Jan;40(1):22-30
[
11903595.001
]
[Cites]
Blood. 2003 Apr 1;101(7):2464-72
[
12446449.001
]
[Cites]
Best Pract Res Clin Haematol. 2003 Mar;16(1):41-56
[
12670464.001
]
[Cites]
Lancet. 2004 Jun 5;363(9424):1869-70
[
15183626.001
]
[Cites]
Leukemia. 1987 Apr;1(4):294-8
[
3499540.001
]
[Cites]
Am J Surg Pathol. 1996 Feb;20(2):211-23
[
8554111.001
]
[Cites]
Histopathology. 1996 Dec;29(6):571-5
[
8971565.001
]
[Cites]
Semin Hematol. 1999 Apr;36(2):148-54
[
10319383.001
]
[Cites]
Am J Pathol. 1999 May;154(5):1583-9
[
10329610.001
]
[Cites]
Am J Surg Pathol. 2007 Mar;31(3):438-46
[
17325486.001
]
[Cites]
Blood. 2008 Feb 15;111(4):2253-60
[
18042795.001
]
[Cites]
Leukemia. 2008 Mar;22(3):487-95
[
18094718.001
]
[Cites]
Blood. 2001 Jun 1;97(11):3552-8
[
11369650.001
]
(PMID = 20220064.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Other-IDs]
NLM/ PMC2895036
2.
Birgersdotter A, Baumforth KR, Porwit A, Sundblad A, Falk KI, Wei W, Sjöberg J, Murray PG, Björkholm M, Ernberg I:
Three-dimensional culturing of the Hodgkin lymphoma cell-line L1236 induces a HL tissue-like gene expression pattern.
Leuk Lymphoma
; 2007 Oct;48(10):2042-53
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Three-dimensional culturing of the
Hodgkin lymphoma cell
-line L1236 induces a HL tissue-like gene expression pattern.
To overcome some limitations of in vitro established
cell
-line tumor models for
Hodgkin lymphoma
(HL), we explored whether culturing in a three-dimensional (3D) matrix could improve the quality of the model.
The gene expression profile of the 3D-cultured HL derived
cell
-line L1236 was compared with that of suspension-cultured (2D) L1236, as well as to the gene expression profile found in HL tumor samples.
To validate our results we also included a gene expression data set of laser captured
Hodgkin
-Reed - Sternberg (H-RS)
cells
.
We found that the 3D culture affected gene expression of a HL derived
cell
-line inducing a more tumor-related expression profile.
3D culture affected the expression of 500 genes in L1236, upregulating genes involved in immune response and apoptosis and downregulating genes involved in
cell
division.
[MeSH-major]
Cell
Culture Techniques / methods. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic.
Hodgkin
Disease
/ pathology. Reed-Sternberg
Cells
/ pathology
[MeSH-minor]
Apoptosis. Biopsy.
Cell
Line, Tumor. Computational Biology. Humans. Lymph Nodes / pathology. Models, Genetic. Oligonucleotide Array Sequence Analysis. Peptides / chemistry. RNA,
Neoplasm
/ metabolism
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17917972.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Peptides; 0 / RNA, Neoplasm
3.
Mito A, Ohashi N, Akita S, Shiomi K, Daga H, Arita K, Fujiwara M:
[A case of natural killer cell lymphoma with high adenosine deaminase level in pleural effusion].
Nihon Kokyuki Gakkai Zasshi
; 2005 Jun;43(6):360-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[A case of natural killer
cell lymphoma
with high adenosine deaminase level in pleural effusion].
We finally diagnosed the case as natural killer (NK)
cell lymphoma
from CT-guided needle biopsy just before death, and necropsy.
In this case, the high level of ADA in the pleural effusion suggested
lymphoma
.
[MeSH-major]
Adenosine Deaminase / metabolism. Killer
Cells
, Natural.
Lymphoma
,
Non
-
Hodgkin
/
diagnosis
. Pleural Effusion,
Malignant
/
diagnosis
[MeSH-minor]
Diagnosis
, Differential. Humans. Male. Middle Aged. Pleura / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15997786.001).
[ISSN]
1343-3490
[Journal-full-title]
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
[ISO-abbreviation]
Nihon Kokyuki Gakkai Zasshi
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
EC 3.5.4.4 / Adenosine Deaminase
Advertisement
4.
Wöhrer S, Troch M, Zwerina J, Schett G, Skrabs C, Gaiger A, Jaeger U, Zielinski CC, Raderer M:
Influence of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone on serologic parameters and clinical course in lymphoma patients with autoimmune diseases.
Ann Oncol
; 2007 Apr;18(4):647-51
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Influence of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone on serologic parameters and
clinical
course in
lymphoma
patients with autoimmune diseases.
BACKGROUND: As patients with B-
cell
lymphomas
suffering from an underlying autoimmune condition undergoing therapy with the CD20 antibody rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) offer the unique possibility of monitoring effects of therapy on various rheumatologic parameters, we have evaluated serologic autoimmune markers and the
clinical
outcome of patients with autoimmune diseases (ADs) who received
lymphoma
treatment with R-CHOP during the course of their
disease
.
PATIENTS AND METHODS: We have retrospectively analysed 13 patients with
non
-
Hodgkin
's
lymphoma
who concurrently suffered from ADs and were treated with the R-CHOP regimen.
Ten (77%) patients showed
clinical
improvement of their autoimmune symptoms, two (15%) reported no difference and one (7%) patient with rheumatoid arthritis-related worsening symptoms during therapy with R-CHOP.
In terms of
lymphoma
response, 11 patients achieved a complete remission and two a partial remission.
CONCLUSIONS: This analysis indicates that R-CHOP given for
lymphoma
treatment is also effective for therapy of concurrent rheumatoid diseases.
Both rheumatoid parameters as well as
clinical
symptoms showed a significant decrease during treatment with this immunochemotherapy.
Genetic Alliance.
consumer health - Autoimmune Diseases
.
MedlinePlus Health Information.
consumer health - Autoimmune Diseases
.
Hazardous Substances Data Bank.
RITUXIMAB
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Ann Oncol. 2007 Apr;18(4):615-8
[
17355949.001
]
(PMID = 17218490.001).
[ISSN]
0923-7534
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9009-79-4 / Rheumatoid Factor; VB0R961HZT / Prednisone
5.
Kalia S, Bansal MP:
Diethyl maleate-induced oxidative stress leads to testicular germ cell apoptosis involving Bax and Bcl-2.
J Biochem Mol Toxicol
; 2008 Nov-Dec;22(6):371-81
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Diethyl maleate-induced oxidative stress leads to testicular germ
cell
apoptosis involving Bax and
Bcl
-2.
Testicular germ
cell
apoptosis is normally a continuous process throughout life.
However, massive testicular germ
cell
loss is known to result from a wide variety of cellular stresses including toxicant exposure.
Thus, the present study was aimed to investigate the mechanisms of germ
cell
loss under stress conditions following diethyl maleate (DEM) exposure.
The germ
cell
apoptosis was found to be increased as assessed by terminal deoxynucleotidyl transferase (TdT)-mediated deoxy-UTP biotin nick end labeling (TUNEL) staining, evaluation of histoarchitechture of testis, and germ
cell
numbers.
It was found that the germ
cell
number was significantly reduced in DEM-treated sections.
RT-PCR was carried out to assess Bax/
Bcl
-2 mRNA expression levels.
Immunohistochemistry of Bax and
Bcl
-2 revealed Bax activation.
The prevalence and cellular localization of the above markers in testicular tissues of DEM-treated animals suggest the possible involvement of Bax/
Bcl
-2 in the male germ
cell
apoptosis.
[MeSH-major]
Apoptosis / drug effects. Maleates / toxicity. Oxidative Stress / drug effects. Spermatozoa / cytology. Spermatozoa / drug effects. Testis / cytology.
bcl
-2-Associated X Protein / metabolism
[MeSH-minor]
Animals.
Cell
Shape / drug effects. Gene Expression Regulation / drug effects. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Inbred BALB C. RNA, Messenger / genetics. RNA, Messenger / metabolism
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2008 Wiley Periodicals, Inc.
(PMID = 19110998.001).
[ISSN]
1099-0461
[Journal-full-title]
Journal of biochemical and molecular toxicology
[ISO-abbreviation]
J. Biochem. Mol. Toxicol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Maleates; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; G81WQB56OL / diethyl maleate
6.
Carmagnat M, Drénou B, Chahal H, Lord JM, Charron D, Estaquier J, Mooney NA:
Dissociation of caspase-mediated events and programmed cell death induced via HLA-DR in follicular lymphoma.
Oncogene
; 2006 Mar 23;25(13):1914-21
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Dissociation of caspase-mediated events and programmed
cell
death induced via HLA-DR in follicular
lymphoma
.
Human leukocyte antigens (HLA) class II antigen-mediated apoptosis has been documented in antigen-presenting
cells
and B lymphoproliferations.
Characteristics of the apoptosis include rapidity and selectivity for mature
cells
.
Follicular
lymphomas
are particularly refractory to apoptosis.
The B-
cell lymphoma
Ramos shares characteristics of this subgroup and is insensitive to apoptosis via simple HLA-DR engagement.
However, inhibition of caspase activation simply delayed the apoptotic phenotype but neither protected against
cell
death nor prevented mitochondrial injury.
Finally, blockade of caspase activation in parallel with HLA-DR mAb stimulation could provide a potent autovaccination stimulus by leading to necrotic death of B-
cell
lymphomas
.
[MeSH-major]
Apoptosis. Caspase Inhibitors. Caspases / metabolism. HLA-DR Antigens / physiology.
Lymphoma
, Follicular / genetics.
Lymphoma
, Follicular / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16301998.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Caspase Inhibitors; 0 / HLA-DR Antigens; EC 3.4.22.- / Caspases
7.
West J, Perkins J, Hok S, Balhorn R, Lightstone FC, Cosman M, DeNardo SJ, DeNardo GL:
Direct antilymphoma activity of novel, first-generation "antibody mimics" that bind HLA-DR10-positive non-Hodgkin's lymphoma cells.
Cancer Biother Radiopharm
; 2006 Dec;21(6):645-54
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Direct antilymphoma activity of novel, first-generation "antibody mimics" that bind HLA-DR10-positive
non
-
Hodgkin
's
lymphoma
cells
.
A first-generation series of novel small molecules, collectively known as selective high-affinity ligands (SHALs), were designed and synthesized to mimic the binding of Lym-1, a monoclonal antibody (mAb) shown to be an effective cytotoxic and radionuclide carrier molecule for targeting
non
-
Hodgkin
's
lymphoma
(NHL).
Micromolar concentrations of all three SHALs showed binding to Raji, an HLA-DR10-positive human
malignant
B-
cell
line but no binding to CEM or Jurkat's, HLA-DR10-negative
malignant
T-
cell
lines.
Additionally, the Raji
cell
membrane distributions of all three SHALs and of Lym-1 were remarkably similar.
Unlike Lym-1, which causes substantial growth inhibition and
cell
death in NHL
cell
lines, these SHALs had no direct antilymphoma activity.
In summary, three first-generation SHALs lacked direct antilymphoma activity, although they had selective NHL B-
cell
binding like Lym-1 mAb.
Because of their small size, these SHALs have potential as radionuclide carrier substitutes for Lym-1 mAb to target the HLA-DR10 NHL-related
cell
-surface protein.
[MeSH-major]
Antibodies, Monoclonal / chemistry. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Biomimetic Materials / chemistry. Biomimetic Materials / pharmacology. HLA-DR Antigens / metabolism.
Lymphoma
,
Non
-
Hodgkin
/ metabolism
[MeSH-minor]
Antibodies, Monoclonal, Murine-Derived.
Cell
Line, Tumor.
Cell
Survival / drug effects. Enzyme-Linked Immunosorbent Assay. HLA-DR Serological Subtypes. Humans. Ligands. Streptavidin / metabolism
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17257080.001).
[ISSN]
1084-9785
[Journal-full-title]
Cancer biotherapy & radiopharmaceuticals
[ISO-abbreviation]
Cancer Biother. Radiopharm.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 47829
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / HLA-DR Antigens; 0 / HLA-DR Serological Subtypes; 0 / HLA-DR10 antigen; 0 / Ligands; 0 / Lym-1 monoclonal antibody; 9013-20-1 / Streptavidin
8.
Sabah M, Cummins R, Leader M, Kay E:
Immunoreactivity of p53, Mdm2, p21(WAF1/CIP1) Bcl-2, and Bax in soft tissue sarcomas: correlation with histologic grade.
Appl Immunohistochem Mol Morphol
; 2007 Mar;15(1):64-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Immunoreactivity of p53, Mdm2, p21(WAF1/CIP1)
Bcl
-2, and Bax in soft tissue sarcomas: correlation with histologic grade.
Tumor growth depends on 2 distinctive pathways:
cell
proliferation and apoptosis.
The p53 pathway is an important regulator of the
cell
cycle as it triggers growth arrest or leads to apoptosis in response to cellular stress and therefore is commonly targeted during tumorigenesis.
Apoptosis is also controlled by the
Bcl
-2 family, which includes proapoptotic and antiapoptotic proteins.
Immunohistochemical stains for p21(WAF1/CIP1), p53, Mdm2,
Bcl
-2, and Bax proteins were carried out on tissue microarrays.
Expression of Bax protein was a common
finding
in soft tissue sarcoma cases.
Bcl
-2 was identified in 59 tumors (38.8%) and was more prevalent in high-grade sarcomas (low grade, 25.9%; intermediate grade, 32.5%; high grade, 55.2%).
The expression of p53, p21(WAF1/CIP1), and
Bcl
-2 is closely associated with the histologic grade of the tumor, and therefore these proteins may be used as prognostic markers.
MedlinePlus Health Information.
consumer health - Soft Tissue Sarcoma
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17536310.001).
[ISSN]
1541-2016
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
9.
Ehlers A, Oker E, Bentink S, Lenze D, Stein H, Hummel M:
Histone acetylation and DNA demethylation of B cells result in a Hodgkin-like phenotype.
Leukemia
; 2008 Apr;22(4):835-41
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Histone acetylation and DNA demethylation of B
cells
result in a
Hodgkin
-like phenotype.
A unique feature of the tumor
cells
(
Hodgkin
/Reed-Sternberg (HRS)) of classical
Hodgkin lymphoma
(cHL) is the loss of their B-
cell
phenotype despite their B-
cell
origin.
Several lines of evidence suggest that epigenomic events, especially promoter DNA methylation, are involved in this silencing of many B-
cell
-associated genes.
Here, we show that DNA demethylation alone or in conjunction with histone acetylation is not able to reconstitute the B-
cell
-gene expression program in cultured HRS
cells
.
Instead, combined DNA demethylation and histone acetylation of B-
cell
lines induce an almost complete extinction of their B-
cell
-expression program and a tremendous upregulation of numerous
Hodgkin
-characteristic genes, including key players such as Id2 known to be involved in the suppression of the B-
cell
phenotype.
Since the upregulation of
Hodgkin
-characteristic genes and the extinction of the B-
cell
-expression program occurred simultaneously, epigenetic changes may also be responsible for the
malignant
transformation of cHL.
The epigenetic upregulation of
Hodgkin
-characteristic genes thus plays--in addition to promoter DNA hypermethylation of B-
cell
-associated genes--a pivotal role for the reprogramming of HRS
cells
and explains why DNA demethylation alone is unable to reconstitute the B-
cell
-expression program in HRS
cells
.
[MeSH-major]
B-Lymphocytes / metabolism. DNA Methylation. Histones / metabolism.
Hodgkin
Disease
/ pathology
[MeSH-minor]
Acetylation.
Cell
Transformation, Neoplastic. Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Phenotype
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18256685.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Histones
10.
Wessely MA, Kettner N, Pierre-Jerome C:
Postlymphoproliferative disorder affecting bone after a renal transplantation.
J Manipulative Physiol Ther
; 2005 Jan;28(1):64-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Postlymphoproliferative
disorder
affecting bone after a renal transplantation.
OBJECTIVE: To illustrate a posttransplant lymphoproliferative
lymphoma
presenting as a solitary osseous lesion situated in the rib.
CLINICAL
FEATURES: A 53-year-old man was referred to a surgical department because of persistent local pain over the lower part of his left posterior hemithorax.
The histological study of the surgically removed tissue revealed diffuse infiltration of the marrow by lymphoid-like
cells
.
There was evidence of interstitial fibrosis, and further immunohistochemical examination showed the presence of B
cells
in the specimen confirming the
diagnosis
of B-
cell lymphoma
.
CONCLUSION: This case report discusses an unusual presentation of a
lymphoma
induced by immunosuppressive therapy in a patient who had received an organ transplant.
[MeSH-major]
Bone Neoplasms / etiology. Immunosuppression / adverse effects. Kidney Transplantation.
Lymphoma
, B-
Cell
/ etiology. Ribs
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Kidney Transplantation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15726037.001).
[ISSN]
1532-6586
[Journal-full-title]
Journal of manipulative and physiological therapeutics
[ISO-abbreviation]
J Manipulative Physiol Ther
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
11.
Kojima M, Nakamura N, Shimizu K, Tamaki Y, Itoh H, Nakamura S:
Marginal zone B-Cell lymphoma among primary B-Cell lymphoma of Waldeyer's ring: histopathologic and immunohistochemical study of 16 tonsillectomy specimens.
Int J Surg Pathol
; 2008 Apr;16(2):164-70
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Marginal zone B-
Cell lymphoma
among primary B-
Cell lymphoma
of Waldeyer's ring: histopathologic and immunohistochemical study of 16 tonsillectomy specimens.
Two subtypes of marginal zone B-
cell lymphoma
(eg, mucosa-associated lymphoid tissue [MALT]
type
and splenic
type
) have been reported in the lymph node.
To determine the presence or absence of marginal zone B-
cell lymphoma
of MALT
type
and the splenic
type
among Waldeyer's ring (WR)
lymphomas
, 16 tonsillectomy specimens were studied.
Ten cases (63%) were marginal zone B-
cell lymphoma
.
Among marginal zone B-
cell lymphoma
, 7 were the MALT
type
and the remaining 3 cases of marginal zone B-
cell lymphoma
were the splenic
type
.
Moreover, 4 cases of 7 MALT-
type lymphomas
contained numerous large
cells
(diffuse large B-
cell lymphoma
arising from a low-grade marginal zone B-
cell lymphoma
of MALT
type
).
The low incidence of primary mucosa-associated lymphoid tissue
type
lymphoma
of WR in previous reports may be because it is difficult to correctly identify the characteristic histologic findings of MALT-
type
lymphoma
because of the small biopsy size.
[MeSH-major]
Lymphoid Tissue / pathology.
Lymphoma
, B-
Cell
, Marginal Zone / pathology. Tonsillar Neoplasms / pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18417673.001).
[ISSN]
1066-8969
[Journal-full-title]
International journal of surgical pathology
[ISO-abbreviation]
Int. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
12.
Riccioni R, Carulli G, de Maria M, Pacini S, Cagno C, Selli C, Petrini M:
Primary lymphoma of the bladder: case report.
Am J Hematol
; 2006 Jan;81(1):77-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Primary
lymphoma
of the bladder: case report.
[MeSH-major]
Antineoplastic Agents, Alkylating / administration & dosage. Cyclophosphamide / administration & dosage.
Lymphoma
, B-
Cell
/ drug therapy.
Lymphoma
,
Non
-
Hodgkin
/ drug therapy. Urinary Bladder Neoplasms / drug therapy
MedlinePlus Health Information.
consumer health - Bladder Cancer
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16369978.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
13.
Hirt C, Dölken G, Janz S, Rabkin CS:
Distribution of t(14;18)-positive, putative lymphoma precursor cells among B-cell subsets in healthy individuals.
Br J Haematol
; 2007 Aug;138(3):349-53
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Distribution of t(14;18)-positive, putative
lymphoma
precursor
cells
among B-
cell
subsets in healthy individuals.
The t(14;18)(q32;q21) is the characteristic chromosomal translocation of follicular
lymphoma
(FL).
The aim of this study was to determine the immunophenotypic markers of t(14;18)-positive
cells
in HI and to relate these features to lymphocyte maturation.
B
cells
from 10 subjects with t(14;18)-positive and three subjects with t(14;18)-negative peripheral blood mononuclear
cells
(PBMC) were fluorescence-activated
cell
sorted for antigen-naïve (CD27(-)), immunoglobulin M (IgM) memory (IgM(+)CD27(+)) and switched memory (IgM(-) CD27(+))
cells
. t(14;18)-recombinations were detected by quantitative PCR.
Among PBMC-positive subjects, t(14;18)-frequency was significantly higher in IgM memory (median: 380/10(6)) than in antigen-naïve (median: 16/10(6)) or switched memory (median: 5/10(6)) B
cells
.
All PBMC-negative subjects nevertheless had detectable t(14;18) in sorted B
cells
; levels were lower than in PBMC-positive subjects, but had the same relative predominance.
These results suggest that t(14;18) is generated during early B-
cell
development in the bone marrow and that affected
cells
may mature and expand in germinal centres. t(14;18)-frequency was highest in IgM memory
cells
, a B-
cell
subset that shares immunophenotypic similarities with FL.
The significance of these
cells
as
lymphoma
precursors or indicators of
lymphoma
risk remains to be established.
[MeSH-minor]
Clone
Cells
. Gene Frequency. Genes, Immunoglobulin. Genes,
bcl
-2. Humans. Immunologic Memory. Immunophenotyping.
Lymphoma
,
Non
-
Hodgkin
/ immunology. Polymerase Chain Reaction
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17614821.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
England
14.
Kastenbaum HA, Khalbuss WE, Felgar RE, Stoller R, Monaco SE:
The spectrum of coincident entities with small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) diagnosed by cytology.
Cytojournal
; 2010;7:20
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The spectrum of coincident entities with small
lymphocytic
lymphoma
/chronic
lymphocytic
leukemia (SLL/CLL) diagnosed by cytology.
BACKGROUND: The cytologic
diagnosis
of Small
lymphocytic
lymphoma
/chronic
lymphocytic
leukemia (SLL/CLL) often relies on
finding a
small lymphoid population with the characteristic immunoprofile by ancillary testing.
MATERIALS AND METHODS: We retrospectively reviewed all FNA and TP cytology cases between January 2005 and May 2009 with
a diagnosis
of SLL/CLL to determine the presence of any coincident process.
Coincident entities were identified in nine cases (31%) and included seven (28%) neoplastic entities (
Hodgkin lymphoma
[HL], adenocarcinoma, squamous
cell
carcinoma, seminoma) and two (7%)
non
-neoplastic entities (infection and immunoglobulin containing
cells
).
Six cases (21%) suspicious for large
cell
transformation were also identified.
CONCLUSION: In our review of SLL/CLL, coincident entities were present in 31% of the cases and included a spectrum of
non
-neoplastic and neoplastic processes.
FC was the most frequently utilized ancillary test, but IHC provided important information by excluding a mantle
cell lymphoma
or confirming a coincident process.
Thus, cytomorphologic evaluation in these patients is important due to the high risk of a coincident process that may not be apparent by FC alone and may require
clinical
management.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20976208.001).
[ISSN]
1742-6413
[Journal-full-title]
CytoJournal
[ISO-abbreviation]
Cytojournal
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC2955352
[Keywords]
NOTNLM ; Chronic lymphocytic leukemia / SLL/CLL / cytopathology / small lymphocytic lymphoma
15.
Meredith RF, Knox SJ:
Clinical development of radioimmunotherapy for B-cell non-Hodgkin's lymphoma.
Int J Radiat Oncol Biol Phys
; 2006;66(2 Suppl):S15-22
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Clinical
development of radioimmunotherapy for B-
cell non
-
Hodgkin
's
lymphoma
.
Over the past several decades, several biomolecules have been investigated for their ability to deliver radiation to cancer
cells
, but antibodies have been the carriers of choice in systemic targeted radionuclide therapy (STaRT).
Food and Drug Administration for the treatment of patients with relapsed or refractory B-
cell non
-
Hodgkin
's
lymphoma
(NHL), and
clinical
trials have shown that they are effective as monotherapies in the salvage setting, producing response rates that are often higher and durations of response that are often longer than those with chemotherapy.
Escalated doses of these agents can be supported with stem
cell
transplantation and can produce high rates of complete response and greater survival in patients with relapsed NHL.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use.
Lymphoma
, B-
Cell
/ radiotherapy. Radioimmunotherapy / methods
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16979433.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / Iodine Radioisotopes; 0 / Yttrium Radioisotopes; 0 / ibritumomab tiuxetan; 0 / iodine-131 anti-B1 antibody
[Number-of-references]
45
16.
Cao X, Rodarte C, Zhang L, Morgan CD, Littlejohn J, Smythe WR:
Bcl2/bcl-xL inhibitor engenders apoptosis and increases chemosensitivity in mesothelioma.
Cancer Biol Ther
; 2007 Feb;6(2):246-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bcl2/
bcl
-xL inhibitor engenders apoptosis and increases chemosensitivity in mesothelioma.
Mesothelioma is
a neoplasm
of the pleura that is currently incurable by conventional therapies.
Previously, we demonstrated that mesothelioma overexpresses
BCL
-X(L), an anti-apoptotic member of the
BCL
-2 family.
In addition, we have shown that down regulation of
BCL
-X(L) using
a BCL
-X(L) antisense oligonucleotide engenders mesothelioma apoptotic
cell
death in vitro and in vivo.
The purpose of this study is to evaluate the efficacy of bcl2/
bcl
-x(L) inhibitor, 2-methoxy antimycin A3, in inducing apoptosis and increasing chemo-sensitivity in vitro and in vivo.
Several
bcl
-x(L) high-expression tumor
cell
lines and one normal human
cell
line were exposed to 2-methoxy antimycin A3.
2-methoxy antimycin A3 demonstrated significant growth inhibition only in these tumor
cell
lines, with little effect on normal human
cells
.
Treatment with 2-methoxy antimycin A3 alone resulted in a dramatic increase in the induction of apoptosis in the cancer
cells
.
Notably, treatment with 2-methoxy antimycin A3 does not alter
BCL
-2 family protein expression.
Together, these findings indicate that exposure of cancer
cells
to small molecule
Bcl
-2/x(L) inhibitors such as 2-methoxy antimycin A3 alone, or in the combination with other chemotherapeutics, may represent a novel therapeutic strategy in treatment of cancer, especially mesothelioma.
[MeSH-major]
Antimycin A / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Genes,
bcl
-2 / drug effects. Mesothelioma / drug therapy. Pleural Neoplasms / drug therapy.
bcl
-X Protein / drug effects
[MeSH-minor]
Apoptosis / drug effects.
Cell
Line, Tumor. Humans. In Vitro Techniques
MedlinePlus Health Information.
consumer health - Mesothelioma
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Cancer Biol Ther. 2007 Mar;6(3):465-6
[
17471026.001
]
(PMID = 17224645.001).
[ISSN]
1538-4047
[Journal-full-title]
Cancer biology & therapy
[ISO-abbreviation]
Cancer Biol. Ther.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / BCL2L1 protein, human; 0 / bcl-X Protein; 642-15-9 / Antimycin A
17.
Pilka R, Mícková I, Lubuský M, Dusková M, Rícánková M, Kudela M:
[Expression of p53, Ki-67, bcl-2, c-erb-2, estrogen, and progesterone receptors in endometrial cancer].
Ceska Gynekol
; 2008 Jul;73(4):222-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Expression of p53, Ki-67,
bcl
-2, c-erb-2, estrogen, and progesterone receptors in endometrial cancer].
[Transliterated title]
Exprese p53, Ki-67,
bcl
-2, c-erb-2, estrogenového, a progesteronového receptoru v endometriálním karcinomu.
OBJECTIVE: To assess the immunohistochemical expression of p53,
bcl
-2, c-erb-2, Ki-67, estrogen and progesterone receptors in endometrial cancer patients.
METHODS: We studied 103 cases of primary untreated endometrial carcinoma in which the p53,
bcl
-2, c-erb-2, Ki-67, estrogen and progesterone receptor antigens were investigated by an immunohistochemical method.
We evaluated the correlations among the immunohistochemical staining assessed by histoscore, and the age, grading, depth of invasion, stage of the
neoplasia
and extrauterine
disease
.
p53,
bcl
-2, c-erb-2, Ki-67, estrogen and progesterone receptors were positive in 49 (48%), 81 (79%).
There was no clear association between immunohistochemical parameters and the age of patients. p53 and Ki-67 overexpression was found to be related to poor grade of differentiation, deeper myometrial invasion, advanced stage of
neoplasia
and extrauterine spread of
disease
.
Immunostaining for
bcl
-2 correlated inversely with FIGO stage, while c-erb-2 was overexpressed in tumors with deeper myometrial invasion.
Estrogen and progesterone receptor positive tumors showed a statistically significant association with clinicopathological parameters of better
clinical
outcome.
CONCLUSION: The overexpression of p53 and Ki-67 seems to indicate more
malignant
phenotype, while
bcl
-2 and c-erb-2 may have a limited role in the identification of high-risk tumors.
Genetic Alliance.
consumer health - Endometrial cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18711961.001).
[ISSN]
1210-7832
[Journal-full-title]
Ceska gynekologie
[ISO-abbreviation]
Ceska Gynekol
[Language]
CZE
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Czech Republic
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, ErbB-2
18.
Nencioni L, De Chiara G, Sgarbanti R, Amatore D, Aquilano K, Marcocci ME, Serafino A, Torcia M, Cozzolino F, Ciriolo MR, Garaci E, Palamara AT:
Bcl-2 expression and p38MAPK activity in cells infected with influenza A virus: impact on virally induced apoptosis and viral replication.
J Biol Chem
; 2009 Jun 5;284(23):16004-15
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bcl
-2 expression and p38MAPK activity in
cells
infected with influenza A virus: impact on virally induced apoptosis and viral replication.
Previous reports have shown that various steps in the influenza A virus life cycle are impaired in
cells
expressing the antiapoptotic protein
Bcl
-2 (
Bcl
-2(+)
cells
).
We demonstrated a direct link between
Bcl
-2 and the reduced nuclear export of viral ribonucleoprotein (vRNP) complexes in these
cells
.
However, despite its negative impact on viral replication,
Bcl
-2 did not prevent host
cells
from undergoing virally triggered apoptosis.
In infected
Bcl
-2(+)
cells
, activated p38MAPK was found predominantly in the cytoplasm, colocalized with
Bcl
-2, and both
Bcl
-2 phosphorylation and virally induced apoptosis were diminished by specific inhibition of p38MAPK activity.
In contrast, in
Bcl
-2-negative (
Bcl
-2(-))
cells
, which are fully permissive to viral infection, p38MAPK activity was predominantly nuclear, and its inhibition decreased vRNP traffic, phosphorylation of viral nucleoprotein, and virus titers in
cell
supernatants, suggesting that this kinase also contributes to the regulation of vRNP export and viral replication.
This could explain why in
Bcl
-2(+)
cells
, where p38MAPK is active in the cytoplasm, phosphorylating
Bcl
-2, influenza viral replication is substantially reduced, whereas apoptosis proceeds at rates similar to those observed in
Bcl
-2(-)
cells
.
Our findings suggest that the impact of p38MAPK on the influenza virus life cycle and the apoptotic response of host
cells
to infection depends on whether or not the
cells
express
Bcl
-2, highlighting the possibility that the pathological effects of the virus are partly determined by the
cell
type
it targets.
[MeSH-major]
Influenza A Virus, H1N1
Subtype
/ physiology. Kidney / physiology. Proto-Oncogene Proteins c-
bcl
-2 / genetics. p38 Mitogen-Activated Protein Kinases / metabolism
[MeSH-minor]
Animals. Apoptosis.
Cell
Line. DNA Primers. Dogs. Down-Regulation. Humans. Life Cycle Stages. Plasmids. Polymerase Chain Reaction. RNA, Small Interfering / genetics. Transfection. Virus Replication
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Gen Virol. 2000 Jan;81(Pt 1):135-42
[
10640551.001
]
[Cites]
Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):6961-5
[
1871110.001
]
[Cites]
Life Sci. 2000 Jan 14;66(8):663-73
[
10680575.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 May 9;92(10):4507-11
[
7753834.001
]
[Cites]
J Virol. 1996 Jan;70(1):663-6
[
8523590.001
]
[Cites]
J Virol. 1997 Dec;71(12):9690-700
[
9371635.001
]
[Cites]
EMBO J. 1998 Jan 2;17(1):288-96
[
9427762.001
]
[Cites]
J Immunol. 1998 May 1;160(9):4175-81
[
9574517.001
]
[Cites]
Am J Respir Cell Mol Biol. 1998 Jun;18(6):794-9
[
9618384.001
]
[Cites]
Virology. 1998 Jun 20;246(1):1-23
[
9656989.001
]
[Cites]
Pharmacol Ther. 1999 May-Jun;82(2-3):389-97
[
10454214.001
]
[Cites]
Cell Mol Life Sci. 1999 Aug 15;55(10):1230-54
[
10487205.001
]
[Cites]
Am J Respir Crit Care Med. 2005 Apr 1;171(7):764-72
[
15618464.001
]
[Cites]
J Infect Dis. 2005 May 15;191(10):1719-29
[
15838800.001
]
[Cites]
J Immunol. 2000 Mar 15;164(6):3222-8
[
10706714.001
]
[Cites]
Biochem Biophys Res Commun. 2000 Nov 30;278(3):753-9
[
11095980.001
]
[Cites]
EMBO J. 2000 Dec 15;19(24):6751-8
[
11118210.001
]
[Cites]
J Virol. 2001 Jan;75(1):408-19
[
11119609.001
]
[Cites]
J Virol. 2001 Mar;75(6):2710-28
[
11222695.001
]
[Cites]
Nat Cell Biol. 2001 Mar;3(3):301-5
[
11231581.001
]
[Cites]
Leukemia. 2001 Jun;15(6):869-74
[
11417471.001
]
[Cites]
J Biol Chem. 2001 Oct 19;276(42):39027-36
[
11495898.001
]
[Cites]
Virus Res. 2002 Mar 20;84(1-2):37-44
[
11900837.001
]
[Cites]
J Gen Virol. 2002 Apr;83(Pt 4):723-34
[
11907320.001
]
[Cites]
Trends Mol Med. 2003 Feb;9(2):46-52
[
12615037.001
]
[Cites]
FASEB J. 2003 Apr;17(6):758-60
[
12594179.001
]
[Cites]
EMBO J. 2003 Jun 2;22(11):2717-28
[
12773387.001
]
[Cites]
Vet Microbiol. 2003 Aug 29;95(1-2):1-13
[
12860072.001
]
[Cites]
Biochem Biophys Res Commun. 2003 Aug 8;307(4):870-6
[
12878192.001
]
[Cites]
Virus Res. 2003 Sep;95(1-2):3-12
[
12921991.001
]
[Cites]
EMBO J. 2003 Sep 15;22(18):4646-55
[
12970177.001
]
[Cites]
J Virol. 2004 Feb;78(3):1263-70
[
14722281.001
]
[Cites]
Appl Microbiol. 1968 Apr;16(4):588-94
[
5647517.001
]
[Cites]
J Gen Virol. 1989 Sep;70 ( Pt 9):2421-31
[
2778438.001
]
[Cites]
J Immunol Methods. 1991 Jun 3;139(2):271-9
[
1710634.001
]
[Cites]
Nature. 1993 Feb 25;361(6414):739-42
[
8441470.001
]
[Cites]
J Cell Biol. 1994 Jan;124(1-2):1-6
[
8294493.001
]
[Cites]
J Virol. 1994 Jun;68(6):3667-73
[
8189504.001
]
[Cites]
Am J Pathol. 1994 Jun;144(6):1195-202
[
8203460.001
]
[Cites]
Antimicrob Agents Chemother. 2000 Jan;44(1):200-4
[
10602750.001
]
[Cites]
J Virol. 2005 Aug;79(16):10147-54
[
16051807.001
]
[Cites]
J Virol. 2005 Sep;79(18):11788-800
[
16140756.001
]
[Cites]
Brain Res Bull. 2006 Feb 15;68(6):406-13
[
16459194.001
]
[Cites]
Cell Microbiol. 2006 Mar;8(3):375-86
[
16469051.001
]
[Cites]
J Biol Chem. 2006 Jul 28;281(30):21353-61
[
16714293.001
]
[Cites]
FASEB J. 2006 Aug;20(10):1683-5
[
16790527.001
]
[Cites]
Intervirology. 2007;50(2):99-107
[
17139186.001
]
[Cites]
Virus Res. 2007 Mar;124(1-2):12-21
[
17081640.001
]
[Cites]
J Virol. 2007 Dec;81(23):12730-9
[
17881440.001
]
[Cites]
PLoS Pathog. 2008 May;4(5):e1000018
[
18516228.001
]
[Cites]
J Virol. 2000 Feb;74(4):1781-6
[
10644350.001
]
(PMID = 19336399.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
[Other-IDs]
NLM/ PMC2708894
19.
Marmey B, Boix C, Barbaroux JB, Dieu-Nosjean MC, Diebold J, Audouin J, Fridman WH, Mueller CG, Molina TJ:
CD14 and CD169 expression in human lymph nodes and spleen: specific expansion of CD14+CD169- monocyte-derived cells in diffuse large B-cell lymphomas.
Hum Pathol
; 2006 Jan;37(1):68-77
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
CD14 and CD169 expression in human lymph nodes and spleen: specific expansion of CD14+CD169- monocyte-derived
cells
in diffuse large B-
cell
lymphomas
.
The mononuclear phagocyte system of human lymphoid tissue comprises macrophages and dendritic
cells
(DCs).
The heterogeneity of the
non
-DC mononuclear phagocyte population in human lymphoid tissue has been little addressed.
Here, we studied the expression of 2 monocyte-derived markers, CD14 and CD169 (sialoadhesin), in reactive human lymphoid tissue as well as in a series of 51 B-
cell
lymphomas
by immunohistochemistry on paraffin-embedded tissue.
We confirmed that lymph node sinusoidal monocyte-derived
cells
were the only population staining for CD169.
Although most sinusoidal histiocytes also expressed CD14, monocyte-derived
cells
with phagocytosis such as erythrophagocytosis, anthracosis, or tingible bodies macrophage lacked CD14 and CD169.
Among B-
cell
lymphomas
, splenic marginal zone
lymphoma
was the only one associated with an expansion of the CD14(+)CD169(+)
cells
in the cords.
With respect to nodal B-
cell
lymphomas
, CD14(+)
cells
were rare among B-chronic
lymphocytic
leukemia, follicular
lymphoma
(FL), mantle
cell lymphoma
(MCL).
However, strikingly, we found a strong expansion of CD14(+)CD169(-)
cells
in numerous diffuse large B-
cell
lymphomas
(DLBCLs), except in cases associated with numerous mitoses, apoptotic bodies, and tingible bodies macrophages.
When cultivated in granulocyte/macrophage colony stimulating factor/interleukin 4, DLBCL purified CD14(+)
cells
differentiate into plasmacytoid
cells
, expressing DC-specific intercellular adhesion molecule 3-grabbing nonintegrin, suggesting dendritic
cell
differentiation potential.
[MeSH-major]
Antigens, CD14 / metabolism. Lymph Nodes / metabolism.
Lymphoma
, B-
Cell
/ metabolism.
Lymphoma
, Large B-
Cell
, Diffuse / metabolism. Membrane Glycoproteins / metabolism. Monocytes / metabolism. Receptors, Immunologic / metabolism. Spleen / metabolism
[MeSH-minor]
Biomarkers, Tumor / metabolism.
Cell
Separation. Dendritic
Cells
/ metabolism. Dendritic
Cells
/ pathology. Flow Cytometry. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Lymphadenitis / metabolism. Lymphadenitis / pathology. Sialic Acid Binding Ig-like Lectin 1
Genetic Alliance.
consumer health - B-Cell Lymphomas
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16360418.001).
[ISSN]
0046-8177
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD14; 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; 0 / SIGLEC1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 1
20.
Sørensen RB, Hadrup SR, Køllgaard T, Svane IM, thor Straten P, Andersen MH:
Efficient tumor cell lysis mediated by a Bcl-X(L) specific T cell clone isolated from a breast cancer patient.
Cancer Immunol Immunother
; 2007 Apr;56(4):527-33
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Efficient tumor
cell
lysis mediated by
a Bcl
-X(L) specific T
cell
clone isolated from a breast cancer patient.
Based on the detection of spontaneous immune responses in cancer patients with cancer of different origin,
Bcl
-X(L) was recently described as a highly interesting tumor antigen recognized by CD8 positive cytotoxic T lymphocytes.
To further characterize
Bcl
-X(L) as a tumor antigen we isolated and expanded
Bcl
-X(L) specific T
cells
from the peripheral blood of a breast cancer patient hosting a strong
Bcl
-X(L) specific T
cell
response.
We describe that HLA-A2 restricted
Bcl
-X(L) specific T
cell
clones very efficiently lyse peptide pulsed T2
cells
.
Furthermore, tumor
cell
lines of different origin, i.e., breast cancer, colon cancer, and melanoma, are efficiently lysed in an HLA-dependent manner.
Finally, ex vivo-isolated leukemia
cells
, but not
non
-
malignant
B and T
cells
are killed by
Bcl
-X(L) specific T
cells
.
Our data underline
Bcl
-X(L) as an universal tumor antigen widely applicable in specific anticancer immunotherapy.
[MeSH-major]
Antigens,
Neoplasm
/ immunology. Breast Neoplasms / immunology. Neoplasms / immunology. T-Lymphocytes, Cytotoxic / immunology.
bcl
-X Protein / immunology
[MeSH-minor]
Clone
Cells
. Cytotoxicity, Immunologic. Female. Flow Cytometry. HLA-A2 Antigen. Humans. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Breast Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16850344.001).
[ISSN]
0340-7004
[Journal-full-title]
Cancer immunology, immunotherapy : CII
[ISO-abbreviation]
Cancer Immunol. Immunother.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / HLA-A2 Antigen; 0 / bcl-X Protein
21.
Takada E, Hata K, Mizuguchi J:
Requirement for JNK-dependent upregulation of BimL in anti-IgM-induced apoptosis in murine B lymphoma cell lines WEHI-231 and CH31.
Exp Cell Res
; 2006 Nov 15;312(19):3728-38
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Requirement for JNK-dependent upregulation of BimL in anti-IgM-induced apoptosis in murine
B lymphoma cell
lines WEHI-231 and CH31.
The cross-linking of
B cell
receptor (BCR) undergoes growth arrest, accompanied by apoptosis, in the CH31 and WEHI-231
B lymphoma
cells
, a model representing primary immature B
cells
.
In unstimulated
cells
, BimL protein was complexed with
Bcl
-x(L) and changed the partner to associate with Bax on the mitochondrial membrane after ligation of BCR, leading to initiation of apoptotic processes.
Retroviral transduction of BimL into WEHI-231
cells
overexpressing dominant-negative form of JNK1 (dnJNK1) resulted in a comparable level of apoptotic
cells
to control
cells
, whereas the BimL-mediated apoptosis was partially prevented by
Bcl
-x(L).
[MeSH-major]
Apoptosis Regulatory Proteins / genetics. JNK Mitogen-Activated Protein Kinases / metabolism.
Lymphoma
, B-
Cell
/ metabolism. Membrane Proteins / genetics. Proto-Oncogene Proteins / genetics
[MeSH-minor]
Animals. Antibodies, Anti-Idiotypic / administration & dosage. Apoptosis / immunology. Base Sequence. Biological Transport, Active.
Cell
Line, Tumor. DNA Primers / genetics. Immunoglobulin M. Mice. Protein Isoforms / genetics. Protein Isoforms / metabolism. Receptors, Antigen, B-
Cell
/ metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transduction, Genetic. Up-Regulation.
bcl
-2-Associated X Protein / metabolism.
bcl
-X Protein / metabolism
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17007835.001).
[ISSN]
0014-4827
[Journal-full-title]
Experimental cell research
[ISO-abbreviation]
Exp. Cell Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Anti-Idiotypic; 0 / Apoptosis Regulatory Proteins; 0 / Bax protein, mouse; 0 / Bcl-2-like protein 11; 0 / Bcl2l1 protein, mouse; 0 / DNA Primers; 0 / Immunoglobulin M; 0 / Membrane Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Receptors, Antigen, B-Cell; 0 / Recombinant Proteins; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
22.
Klemke CD, Goerdt S, Schrama D, Becker JC:
New insights into the molecular biology and targeted therapy of cutaneous T-cell lymphomas.
J Dtsch Dermatol Ges
; 2006 May;4(5):395-406
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
New insights into the molecular biology and targeted therapy of cutaneous T-
cell
lymphomas
.
Cutaneous T-
cell lymphoma
is an extra-nodal
non
-
Hodgkin lymphoma
of mature T
cells
.
These tumor
cells
home to and persist in the skin,producing a broad spectrum of
clinical
entities.
Recent results of basic research on tumor biology and tumor immunology as well as molecular genetics of cutaneous T-
cell lymphoma
have fostered the development of new therapeutic approaches.
Several
clinical
trials testing these targeted therapies have shown encouraging results.
This article provides an overview of recent research developments and therapeutic strategies for cutaneous T-
cell lymphoma
.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Drug Delivery Systems / trends. Genetic Therapy / trends.
Lymphoma
, T-
Cell
/ drug therapy.
Lymphoma
, T-
Cell
/ physiopathology. Skin Neoplasms / drug therapy. Skin Neoplasms / physiopathology
Genetic Alliance.
consumer health - Cutaneous T-Cell Lymphoma
.
MedlinePlus Health Information.
consumer health - Genes and Gene Therapy
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16686607.001).
[ISSN]
1610-0379
[Journal-full-title]
Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG
[ISO-abbreviation]
J Dtsch Dermatol Ges
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
90
23.
Filippi AR, Franco P, Galliano M, Ricardi U:
Peripheral blood complete remission after splenic irradiation in mantle-cell lymphoma with 11q22-23 deletion and ATM inactivation.
Radiat Oncol
; 2006;1:35
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Peripheral blood complete remission after splenic irradiation in mantle-
cell lymphoma
with 11q22-23 deletion and ATM inactivation.
Mantle
Cell Lymphoma
(MCL) is a well-known histological and
clinical subtype
of B-
cell non
-
Hodgkin
'
s Lymphomas
.
It is usually characterized by an aggressive
disease
course, presenting with advanced stage
disease
at
diagnosis
and with low response rates to therapy.
We herein report a case of MCL with splenomegaly and peripheral blood involvement as main
clinical
features.
Mainly advocated mechanisms responsible for this phenomenon are considered direct radiation-induced apoptotic
cell
death, immune modulation via proportional changes of lymphocyte subsets due to known differences in intrinsic radiosensitivity and a radiation-induced cytokine release.
The peculiar intrinsic radiosensitivity pattern of lymphoid
cells
could probably be explained by well-defined individual genetic and molecular features.
In this context, among NHLs, MCL
subtype
has the highest rate of ATM (Ataxia Teleangiectasia Mutated) inactivation.
While the ATM gene is thought to play a key-role in detecting radiation-induced DNA damage (especially Double Strand Breaks), recent in vitro data support the hypothesis that ATM loss may actually contribute to the radiosensitivity of MCL
cells
.
[MeSH-major]
Cell
Cycle Proteins / genetics. Chromosome Deletion. Chromosomes, Human, Pair 11. DNA-Binding Proteins / genetics.
Lymphoma
, Mantle-
Cell
/ genetics.
Lymphoma
, Mantle-
Cell
/ radiotherapy. Protein-Serine-Threonine Kinases / genetics. Spleen / radiation effects. Tumor Suppressor Proteins / genetics
Genetic Alliance.
consumer health - Mantle cell lymphoma
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
University of Turin Instituional Repository AperTO.
Full Text from
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Radiother Oncol. 2001 Mar;58(3):235-46
[
11230883.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2773-8
[
10706620.001
]
[Cites]
Eur J Cancer. 2002 Feb;38(3):401-8
[
11818206.001
]
[Cites]
Am J Clin Pathol. 2002 Feb;117(2):237-45
[
11863220.001
]
[Cites]
Am J Clin Oncol. 2003 Apr;26(2):178-83
[
12714892.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5372-7
[
12697903.001
]
[Cites]
Oncogene. 2003 Sep 11;22(39):7905-12
[
12970738.001
]
[Cites]
Tumori. 1982 Dec 31;68(6):511-4
[
6820205.001
]
[Cites]
Acta Haematol. 1983;70(1):59-62
[
6408868.001
]
[Cites]
Radiother Oncol. 1985 Aug;4(1):45-54
[
3898236.001
]
[Cites]
Int J Radiat Biol Relat Stud Phys Chem Med. 1985 Dec;48(6):943-61
[
3877700.001
]
[Cites]
Cancer. 1986 Sep 15;58(6):1204-7
[
2427184.001
]
[Cites]
Am J Hematol. 1989 Mar;30(3):188-9
[
2916562.001
]
[Cites]
Eur J Haematol. 1991 Apr;46(4):202-4
[
2015875.001
]
[Cites]
Br J Haematol. 1990 Oct;76(2):305-6
[
2094335.001
]
[Cites]
Eur J Cancer. 1992;28A(10):1729-34
[
1389495.001
]
[Cites]
Am J Hematol. 1994 Jun;46(2):65-71
[
8172197.001
]
[Cites]
Br J Radiol. 1995 Sep;68(813):997-1003
[
7496700.001
]
[Cites]
Leuk Lymphoma. 1997 Jul;26(3-4):395-8
[
9322903.001
]
[Cites]
Semin Hematol. 1999 Apr;36(2):115-27
[
10319380.001
]
[Cites]
Blood Rev. 1999 Sep;13(3):163-70
[
10527268.001
]
[Cites]
Cancer Treat Rev. 2005 May;31(3):159-72
[
15923088.001
]
[Cites]
Lancet Oncol. 2005 Jul;6(7):520-8
[
15992701.001
]
[Cites]
J Clin Oncol. 2005 Sep 10;23(26):6409-14
[
16155027.001
]
[Cites]
Mutat Res. 2006 May 11;597(1-2):113-8
[
16413041.001
]
[Cites]
Blood. 1999 Nov 1;94(9):3262-4
[
10556216.001
]
[Cites]
Blood. 2002 Jan 1;99(1):238-44
[
11756177.001
]
(PMID = 16956411.001).
[ISSN]
1748-717X
[Journal-full-title]
Radiation oncology (London, England)
[ISO-abbreviation]
Radiat Oncol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
[Other-IDs]
NLM/ PMC1569379
[General-notes]
NLM/ Original DateCompleted: 20070726
24.
Reid-Nicholson M, Kavuri S, Ustun C, Crawford J, Nayak-Kapoor A, Ramalingam P:
Plasmablastic lymphoma: Cytologic findings in 5 cases with unusual presentation.
Cancer
; 2008 Oct 25;114(5):333-41
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Plasmablastic
lymphoma
: Cytologic findings in 5 cases with unusual presentation.
BACKGROUND: Plasmablastic
lymphoma
(PBL) is a rare form of
non
-
Hodgkin lymphoma
that was once believed to occur primarily in the oral cavity of human immunodeficiency virus-positive individuals.
The presence of the following was evaluated: cellularity, plasmablastic
cells
, background necrosis (BN), single-
cell
necrosis (SCN), lymphoglandular bodies (LGB), tingible-body macrophages (TBM), 3-dimensional clusters/sheets, and cytoplasmic vacuoles.
Two patients had the acquired immunodeficiency syndrome and 3 had second
non
-PBL related malignancies including endometrial carcinoma, lung adenocarcinoma, and small
lymphocytic
lymphoma
.
The most common cytologic features were hypercellularity (80%), plasmablastic
cells
(73%), SCN (73%), BN (87%), and LGB (66%).
These include hypercellular specimens with abundant plasmablastic
cells
, LGB, SCN, and BN.
However, although these findings may suggest PBL, a definitive
diagnosis
requires adjunctive studies including immunohistochemistry and flow cytometry.
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/ metabolism.
Lymphoma
,
Non
-
Hodgkin
/ pathology
HIV InSite.
treatment guidelines - Human Herpesvirus-8
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2008 American Cancer Society.
(PMID = 18683216.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
25.
Okur FV, Krance R:
Stem cell transplantation in childhood non-Hodgkin's lymphomas.
Curr Hematol Malig Rep
; 2010 Oct;5(4):192-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Stem
cell
transplantation in childhood
non
-
Hodgkin
'
s lymphomas
.
Despite the high cure rates achieved with intensified primary therapies for childhood
non
-
Hodgkin
'
s lymphomas
(NHL), the prognosis for children with relapsed or refractory
disease
is poor.
Dose intensification followed by stem
cell
transplantation has been used in these circumstances and may provide a curative treatment option for these patients, but the number of children treated using this approach is relatively small and its effectiveness has been difficult to judge.
We summarize the current experience for stem
cell
transplantation in childhood NHL and offer our recommendations.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation.
Lymphoma
,
Non
-
Hodgkin
/ therapy
[MeSH-minor]
Child.
Clinical
Trials as Topic. Humans.
Lymphoma
, B-
Cell
/ therapy.
Lymphoma
, Large-
Cell
, Anaplastic / therapy. Precursor
Cell
Lymphoblastic Leukemia-
Lymphoma
/ therapy
Genetic Alliance.
consumer health - Transplantation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 2005 Feb 15;105(4):1622-31
[
15507526.001
]
[Cites]
J Clin Oncol. 1994 May;12(5):899-908
[
8164040.001
]
[Cites]
J Clin Oncol. 2004 Jun 1;22(11):2172-6
[
15169805.001
]
[Cites]
Blood. 2003 Dec 1;102(12):3871-9
[
12933571.001
]
[Cites]
Blood. 2007 Apr 1;109(7):2773-80
[
17132719.001
]
[Cites]
J Clin Oncol. 2001 Jun 1;19(11):2927-36
[
11387366.001
]
[Cites]
Blood. 2000 Jan 15;95(2):416-21
[
10627444.001
]
[Cites]
J Clin Oncol. 1995 Feb;13(2):359-72
[
7844597.001
]
[Cites]
Blood. 2006 May 15;107(10):4047-52
[
16424389.001
]
[Cites]
Int J Hematol. 2006 Jan;83(1):66-73
[
16443556.001
]
[Cites]
J Clin Oncol. 1999 Mar;17(3):825-31
[
10071273.001
]
[Cites]
Ann Oncol. 1997;8 Suppl 1:37-42
[
9187427.001
]
[Cites]
Ann Oncol. 2000 Jan;11(1):53-8
[
10690387.001
]
[Cites]
Br J Haematol. 2006 Apr;133(2):176-82
[
16611309.001
]
[Cites]
Br J Haematol. 2006 Mar;132(5):594-7
[
16445832.001
]
[Cites]
Blood. 2005 Feb 1;105(3):948-58
[
15486066.001
]
[Cites]
J Clin Oncol. 2006 Jan 20;24(3):491-9
[
16421426.001
]
[Cites]
Am J Clin Pathol. 2004 Apr;121(4):496-506
[
15080301.001
]
[Cites]
Semin Oncol. 2009 Oct;36(5):381-418
[
19835736.001
]
[Cites]
Haematologica. 2007 Nov;92(11):1533-48
[
18024402.001
]
[Cites]
J Clin Oncol. 1996 Apr;14(4):1252-61
[
8648381.001
]
[Cites]
Blood. 2001 Jun 1;97(11):3370-9
[
11369626.001
]
[Cites]
Blood. 1999 Jun 1;93(11):3913-21
[
10339500.001
]
[Cites]
J Clin Oncol. 1997 Feb;15(2):509-17
[
9053472.001
]
[Cites]
Bone Marrow Transplant. 2003 Aug;32(3):317-24
[
12858205.001
]
[Cites]
Bone Marrow Transplant. 1999 Mar;23(5):437-42
[
10100556.001
]
[Cites]
J Clin Oncol. 1993 Jun;11(6):1024-32
[
8501488.001
]
[Cites]
Blood. 2007 Apr 1;109(7):2736-43
[
17138821.001
]
[Cites]
Bone Marrow Transplant. 2002 May;29(9):769-75
[
12040475.001
]
[Cites]
Ann Oncol. 1999 Dec;10(12):1419-32
[
10643532.001
]
[Cites]
Ann Oncol. 2006 Jan;17(1):123-30
[
16236753.001
]
[Cites]
Biol Blood Marrow Transplant. 2010 Feb;16(2):223-30
[
19800015.001
]
[Cites]
Bone Marrow Transplant. 1995 Mar;15(3):353-9
[
7599558.001
]
[Cites]
J Clin Oncol. 2006 Jul 1;24(19):3121-7
[
16754935.001
]
[Cites]
Br J Haematol. 2001 Sep;114(4):741-60
[
11564061.001
]
[Cites]
Blood. 1997 Oct 15;90(8):2921-30
[
9376572.001
]
[Cites]
J Clin Oncol. 2009 Jul 10;27(20):3363-9
[
19433688.001
]
[Cites]
Br J Haematol. 2005 Oct;131(1):39-49
[
16173961.001
]
[Cites]
Blood. 2008 Jan 15;111(2):537-43
[
17971487.001
]
[Cites]
Blood. 2008 Feb 1;111(3):1560-6
[
17957029.001
]
[Cites]
Nature. 2000 Feb 3;403(6769):503-11
[
10676951.001
]
[Cites]
Blood. 2004 Feb 1;103(3):777-83
[
12907446.001
]
[Cites]
Br J Haematol. 2009 Jan;144(1):24-40
[
19087093.001
]
[Cites]
Leukemia. 2005 Jun;19(6):945-52
[
15800666.001
]
[Cites]
Rev Prat. 1993 Sep 1;43(13):1665-8
[
8303185.001
]
[Cites]
Bone Marrow Transplant. 2005 Sep;36(5):437-41
[
15980879.001
]
[Cites]
Ann Hematol. 2006 Nov;85(11):787-94
[
16932891.001
]
[Cites]
Blood. 2003 Apr 1;101(7):2476-82
[
12456505.001
]
[Cites]
J Clin Oncol. 2009 Oct 20;27(30):5056-61
[
19738127.001
]
[Cites]
Blood. 2004 Sep 15;104(6):1624-30
[
15178574.001
]
[Cites]
Bone Marrow Transplant. 2003 Apr;31(8):667-78
[
12692607.001
]
[Cites]
N Engl J Med. 2002 Jan 24;346(4):235-42
[
11807147.001
]
[Cites]
Cancer. 2003 Sep 15;98(6):1283-91
[
12973853.001
]
[Cites]
Blood. 2007 Oct 15;110(8):2838-45
[
17609424.001
]
[Cites]
J Clin Oncol. 2003 Mar 1;21(5):897-906
[
12610191.001
]
[Cites]
Pediatr Blood Cancer. 2008 Sep;51(3):369-74
[
18493992.001
]
[Cites]
Leukemia. 2007 Dec;21(12):2563-6
[
17597802.001
]
[Cites]
Blood. 2001 Jun 15;97(12):3699-706
[
11389005.001
]
[Cites]
Cancer. 2005 Nov 15;104(10):2133-40
[
16211546.001
]
[Cites]
Lancet Oncol. 2006 May;7(5):379-91
[
16648042.001
]
[Cites]
J Clin Oncol. 2005 Apr 1;23(10):2240-7
[
15800314.001
]
[Cites]
Br J Haematol. 2006 Jun;133(6):634-7
[
16704438.001
]
(PMID = 20661786.001).
[ISSN]
1558-822X
[Journal-full-title]
Current hematologic malignancy reports
[ISO-abbreviation]
Curr Hematol Malig Rep
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
26.
Diao LP, Yu XM, Gao YH, Li Y, Liu HS, Liu LH, Zhou RM, Wang N, Wu LL, Wang SJ:
Association of VEGF genetic polymorphisms with the clinical characteristics of non-Hodgkin's lymphoma.
J Cancer Res Clin Oncol
; 2009 Nov;135(11):1473-81
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Association of VEGF genetic polymorphisms with the
clinical
characteristics of
non
-
Hodgkin
's
lymphoma
.
We investigated the possible associations of two polymorphisms (-2578C/A and +936C/T) in the VEGF gene with the clinicopathologic parameters for patients with
non
-
Hodgkin
's
lymphoma
(NHL).
RESULTS: The -2578A allele was significantly associated with less frequent
clinical
staging III, IV and bone marrow involvement (The odds ratio (OR) 0.59; 95% confidence interval (CI) 0.43-0.82; and OR 0.66; 95% CI 0.48-0.91, respectively).
The TT genotype of the +936C/T polymorphism was significantly associated with less frequent T
cell
histological
type
,
clinical
staging III, IV and bone marrow involvement (OR 0.25; 95% CI 0.07-0.89; OR 0.37; 95% CI 0.15-0.89; and OR 0.31; 95% CI 0.10-0.96, respectively).
The +936 T allele was marginally associated with less frequent bone marrow involvement and with
Clinical
staging III, IV (OR 0.71; 95% CI 0.49-1.01; and OR 0.70; 95% CI 0.49-1.00, respectively).
None of the evaluated genotypes of -2578C/A was significantly associated with the gender, age, tumor size, B symptoms and immunohistological
subtype
.
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/ genetics. Vascular Endothelial Growth Factor A / genetics
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Female. Genotype. Humans. Male. Middle Aged.
Neoplasm
Staging. Polymorphism, Genetic
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Clin Cancer Res. 2005 May 15;11(10):3647-53
[
15897560.001
]
[Cites]
J Cancer Res Clin Oncol. 2008 Mar;134(3):381-7
[
17694324.001
]
[Cites]
Eur Urol. 2007 Oct;52(4):1147-55
[
17287073.001
]
[Cites]
J Cancer Res Clin Oncol. 2007 Oct;133(10):787-91
[
17564725.001
]
[Cites]
Crit Rev Oncol Hematol. 2007 May;62(2):105-18
[
17188504.001
]
[Cites]
Nucleic Acids Res. 1988 Feb 11;16(3):1215
[
3344216.001
]
[Cites]
Gynecol Oncol. 2007 May;105(2):385-9
[
17289129.001
]
[Cites]
Endocr Rev. 1997 Feb;18(1):4-25
[
9034784.001
]
[Cites]
Clin Cancer Res. 2007 Feb 1;13(3):898-901
[
17289883.001
]
[Cites]
Nat Med. 2003 Jun;9(6):669-76
[
12778165.001
]
[Cites]
J Surg Oncol. 2006 Dec 1;94(7):624-30
[
17111394.001
]
[Cites]
J Vasc Res. 2000 Nov-Dec;37(6):443-8
[
11146397.001
]
[Cites]
Cytokine. 2000 Aug;12(8):1232-5
[
10930302.001
]
[Cites]
Semin Oncol. 2005 Feb;32(1 Suppl 1):S36-43
[
15786024.001
]
[Cites]
Leuk Lymphoma. 2007 Mar;48(3):584-95
[
17454603.001
]
[Cites]
Leuk Lymphoma. 2003 Dec;44(12):2089-93
[
14959852.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1148-52
[
16775174.001
]
[Cites]
Appl Immunohistochem Mol Morphol. 2002 Dec;10(4):316-21
[
12607599.001
]
[Cites]
Lung Cancer. 2004 Dec;46(3):293-8
[
15541813.001
]
[Cites]
Cancer Res. 2002 Jun 15;62(12):3369-72
[
12067976.001
]
[Cites]
Clin Cancer Res. 2005 Jan 1;11(1):154-61
[
15671540.001
]
[Cites]
Cancer Res. 2003 Feb 15;63(4):812-6
[
12591731.001
]
[Cites]
Ann Diagn Pathol. 2003 Feb;7(1):1-8
[
12616467.001
]
[Cites]
Blood. 2000 Dec 1;96(12):3712-8
[
11090051.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):571-5
[
15767331.001
]
[Cites]
Genes Immun. 2002 Jun;3(4):229-32
[
12058259.001
]
[Cites]
Urology. 2005 Jan;65(1):70-5
[
15667866.001
]
[Cites]
Int J Cancer. 2003 Sep 10;106(4):468-71
[
12845639.001
]
(PMID = 19649652.001).
[ISSN]
1432-1335
[Journal-full-title]
Journal of cancer research and clinical oncology
[ISO-abbreviation]
J. Cancer Res. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Vascular Endothelial Growth Factor A
27.
CpG 7909: PF 3512676, PF-3512676.
Drugs R D
; 2006;7(5):312-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
CpG 7909, acting through the TLR9 receptor present in B
cells
and plasmacytoid dendritic
cells
, stimulates human B-
cell
proliferation, enhances antigen-specific antibody production and induces interferon-alpha production, interleukin-10 secretion and natural killer
cell
activity.
In 2002, GlaxoSmithKline (GSK) was granted a worldwide,
non
-exclusive licence to Coley's CpG immunostimulatory oligonucleotides, including CpG 7909 [VaxImmune], for their use as adjuvants for cancer vaccines.
A phase I/II trial in patients with NHL has also been conducted in 24 patients with relapsed or refractory
disease
at the University of Iowa.
These trials are evaluating CpG 7909 in combination with chemotherapy versus chemotherapy alone as a first-line treatment for patients with advanced (stage IIIb or IV)
non
-small-
cell
lung cancer (NSCLC).
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/ drug therapy. Oligodeoxyribonucleotides / administration & dosage. Oligodeoxyribonucleotides / adverse effects
[MeSH-minor]
Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / adverse effects. Anthrax Vaccines / administration & dosage. Anthrax Vaccines / adverse effects. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects.
Clinical
Trials, Phase I as Topic. Humans. Rituximab. Toll-Like Receptor 9 / agonists
Hazardous Substances Data Bank.
RITUXIMAB
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16922592.001).
[ISSN]
1174-5886
[Journal-full-title]
Drugs in R&D
[ISO-abbreviation]
Drugs R D
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
New Zealand
[Chemical-registry-number]
0 / Adjuvants, Immunologic; 0 / Anthrax Vaccines; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Oligodeoxyribonucleotides; 0 / ProMune; 0 / TLR9 protein, human; 0 / Toll-Like Receptor 9; 4F4X42SYQ6 / Rituximab
[Number-of-references]
14
28.
Khan F, Bauer F, Gazi G, Bilgrami S:
Regression of large B-cell non-Hodgkin's lymphoma of stomach with HAART: case report and review.
Leuk Lymphoma
; 2006 Apr;47(4):750-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Regression of large B-
cell non
-
Hodgkin
's
lymphoma
of stomach with HAART: case report and review.
[MeSH-major]
Antiretroviral Therapy, Highly Active.
Lymphoma
, AIDS-Related / drug therapy.
Lymphoma
, Large B-
Cell
, Diffuse / drug therapy.
Lymphoma
,
Non
-
Hodgkin
/ drug therapy. Stomach Neoplasms / drug therapy
MedlinePlus Health Information.
consumer health - HIV/AIDS Medicines
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
HIV InSite.
treatment guidelines - Human Herpesvirus-8
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16886274.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
29.
Xie XT, Jiang SY, Li BS, Yang LL:
[Relationship between the expression of the genes encoding the key enzymes for cytarabine metabolism and the pharmacokinetics of cytarabine in the treatment of childhood acute leukemia with high-dose cytarabine].
Zhonghua Er Ke Za Zhi
; 2008 Apr;46(4):276-80
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
OBJECTIVE: It has been reported that high-dose cytarabine (HD-AraC) was very effective for childhood hematological malignancies, especially for improving the long-term survival of high-risk acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), and T-
cell
lymphoid malignancies (T-ALL, T-
cell non
-
Hodgkin
's
lymphoma
).
METHODS: The drug levels of Ara-C in plasma and cerebrospinal fluid were detected with HPLC while HD-AraC was used, the expression of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) mRNA in human leukemia
cell
lines and the bone marrow
cells
were investigated in 48 cases of childhood hematological malignancies with RT-PCR methods, and the relationship between the expression of these enzymes mRNA and the outcome of the patients was analyzed. RESULTS:.
There were no significant differences in expressions of dCK in T-ALL and B lineage ALL. (3) In vitro study found that the expressions of dCK and CDA mRNA did not change in leukemia
cell
lines incubated at different doses and times of Ara-C.
[MeSH-minor]
Child. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Gene Expression. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism.
Lymphoma
,
Non
-
Hodgkin
/ drug therapy.
Lymphoma
,
Non
-
Hodgkin
/ genetics.
Lymphoma
,
Non
-
Hodgkin
/ metabolism. Precursor
Cell
Lymphoblastic Leukemia-
Lymphoma
/ drug therapy. Precursor
Cell
Lymphoblastic Leukemia-
Lymphoma
/ genetics. Precursor
Cell
Lymphoblastic Leukemia-
Lymphoma
/ metabolism
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
CYTARABINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19099730.001).
[ISSN]
0578-1310
[Journal-full-title]
Zhonghua er ke za zhi = Chinese journal of pediatrics
[ISO-abbreviation]
Zhonghua Er Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.5.4.5 / Cytidine Deaminase
30.
Yamamoto R, Hashiguchi K, Iwai A, Satoh S, Hanaoka N, Okudaira K, Inoue T, Miyazaki J, Matsuzaki K, Tsuzuki Y, Kawaguchi A, Nagao S, Itoh K, Miura S, Hatano B:
[A case of secondary non-Hodgkin's lymphoma of the colon after the treatment for Hodgkin's disease].
Nihon Shokakibyo Gakkai Zasshi
; 2005 Jan;102(1):53-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[A case of secondary
non
-
Hodgkin
's
lymphoma
of the colon after the treatment for
Hodgkin
'
s disease
].
[MeSH-major]
Colonic Neoplasms / etiology.
Hodgkin
Disease
/ therapy.
Lymphoma
,
Non
-
Hodgkin
/ etiology. Neoplasms, Second Primary / etiology
[MeSH-minor]
Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Female. Humans. Peripheral Blood Stem
Cell
Transplantation. Prednisone / administration & dosage. Procarbazine / administration & dosage. Radiotherapy Dosage. Remission Induction. Vincristine / administration & dosage
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
Hazardous Substances Data Bank.
PROCARBAZINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15682817.001).
[ISSN]
0446-6586
[Journal-full-title]
Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
[ISO-abbreviation]
Nihon Shokakibyo Gakkai Zasshi
[Language]
jpn
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; COPP protocol
31.
Andréasson U, Ek S, Merz H, Rosenquist R, Andersen N, Jerkeman M, Dictor M, Borrebaeck CA:
B cell lymphomas express CX3CR1 a non-B cell lineage adhesion molecule.
Cancer Lett
; 2008 Feb 8;259(2):138-45
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
B cell
lymphomas
express CX3CR1 a
non
-
B cell
lineage adhesion molecule.
To study the differential expression of
cell
membrane-bound receptors and their potential role in growth and/or survival of the tumor
cells
, highly purified follicular
lymphoma
cells
were analyzed, using gene expression analysis, and compared to
non
-
malignant
B cell
populations.
Filtering the genome for overexpressed genes coding for
cell
membrane-bound proteins/receptors resulted in a hit list of 27 identified genes.
Among these, we have focused on the aberrant over expression of CX3CR1, in different types of
B cell lymphoma
, as compared to
non
-
malignant
B
cells
.
We show that CX3CR1, which normally is not expressed on B
cells
, is expressed both at the mRNA and protein level in several subtypes of
lymphoma
.
CX3CR1 has also shown to be involved in the homing to specific tissues that express the ligand, CX3CL1, in breast and prostate cancer and may thus be involved in dissemination of
lymphoma
.
[MeSH-major]
B-Lymphocytes / immunology.
Lymphoma
, Follicular / immunology.
Lymphoma
, Mantle-
Cell
/ immunology. Palatine Tonsil / immunology. Receptors, Chemokine / analysis
[MeSH-minor]
Cell
Separation. Flow Cytometry. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis
Genetic Alliance.
consumer health - B-Cell Lymphomas
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18060687.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / CX3CR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Chemokine
32.
Hara T, Omura-Minamisawa M, Chao C, Nakagami Y, Ito M, Inoue T:
Bcl-2 inhibitors potentiate the cytotoxic effects of radiation in Bcl-2 overexpressing radioresistant tumor cells.
Int J Radiat Oncol Biol Phys
; 2005 Feb 1;61(2):517-28
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bcl
-2 inhibitors potentiate the cytotoxic effects of radiation in
Bcl
-2 overexpressing radioresistant tumor
cells
.
PURPOSE:
Bcl
-2, an inhibitor of apoptosis frequently shows elevated expression in human tumors, thus resulting in resistance to radiation therapy.
Therefore, inhibiting
Bcl
-2 function may enhance the radiosensitivity of tumor
cells
.
Tetrocarcin A (TC-A) and
bcl
-2 antisense oligonucleotides exhibit antitumor activity by inhibiting
Bcl
-2 function and transcription, respectively.
We investigated whether these antitumor agents would enhance the cytotoxic effects of radiation in tumor
cells
overexpressing
Bcl
-2.
METHODS AND MATERIALS: We used HeLa/
bcl
-2
cells
, a stable
Bcl
-2-expressing
cell
line derived from wild-
type
HeLa (HeLa/wt)
cells
.
Cells
were incubated with TC-A and
bcl
-2 antisense oligonucleotides for 24 h after irradiation, and
cell
viability was then determined.
Apoptotic
cells
were quantified by flow cytometric assay.
RESULTS: The HeLa/
bcl
-2
cells
were more resistant to radiation than HeLa/wt
cells
.
At concentrations that are not inherently cytotoxic, both TC-A and
bcl
-2 antisense oligonucleotides increased the cytotoxic effects of radiation in HeLa/
bcl
-2
cells
, but not in HeLa/wt
cells
.
However, in HeLa/
bcl
-2
cells
, additional treatment with TC-A in combination with radiation did not significantly increase apoptosis.
CONCLUSIONS: The present results suggest that TC-A and
bcl
-2 antisense oligonucleotides reduce radioresistance of tumor
cells
overexpressing
Bcl
-2.
Therefore, a combination of radiotherapy and
Bcl
-2 inhibitors may prove to be a useful therapeutic approach for treating tumors that overexpress
Bcl
-2.
[MeSH-major]
Aminoglycosides / pharmacology. Apoptosis. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-
bcl
-2 / antagonists & inhibitors. Radiation Tolerance / drug effects. Radiation-Sensitizing Agents / pharmacology
[MeSH-minor]
Analysis of Variance.
Cell
Survival / drug effects.
Cell
Survival / radiation effects. HeLa
Cells
/ drug effects. HeLa
Cells
/ metabolism. HeLa
Cells
/ radiation effects. Humans. RNA, Messenger / antagonists & inhibitors. Tumor Stem
Cell
Assay
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15667975.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; 73666-84-9 / tetrocarcin A
33.
Vose JM:
Personalized immunotherapy for the treatment of non-Hodgkin's lymphoma: a promising approach.
Hematol Oncol
; 2006 Jun;24(2):47-55
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Personalized immunotherapy for the treatment of
non
-
Hodgkin
's
lymphoma
: a promising approach.
In patients with B-
cell
lymphomas
, particularly indolent
lymphoma
, the use of passive immunotherapy, such as the anti-CD20 monoclonal antibody rituximab, has made an impressive impact on patient outcome.
Personalized immunotherapy, a method that triggers the immune system to mount a response against tumor
cells
, has shown promising results in early
clinical
trials in hematologic malignancies.
Currently, 3 large phase III studies are evaluating the efficacy and safety of personalized immunotherapy in patients with follicular
lymphoma
.
It is hoped that the results of these studies will lead to the incorporation of this promising approach into the standard treatment of patients with
lymphoma
.
[MeSH-major]
Cancer Vaccines.
Hodgkin
Disease
/ immunology. Immunotherapy / methods
[MeSH-minor]
Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Clinical
Trials as Topic. Combined Modality Therapy. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Humans
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16447298.001).
[ISSN]
0278-0232
[Journal-full-title]
Hematological oncology
[ISO-abbreviation]
Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Cancer Vaccines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
[Number-of-references]
64
34.
Kvansakul M, Yang H, Fairlie WD, Czabotar PE, Fischer SF, Perugini MA, Huang DC, Colman PM:
Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands.
Cell Death Differ
; 2008 Oct;15(10):1564-71
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Vaccinia virus anti-apoptotic F1L is a novel
Bcl
-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands.
Some viruses express proteins homologous in sequence and function to mammalian pro-survival
Bcl
-2 proteins.
Anti-apoptotic F1L expressed by vaccinia virus is essential for survival of infected
cells
, but it bears no discernable sequence homology to proteins other than its immediate orthologues in related pox viruses.
Here we report that the crystal structure of F1L reveals
a Bcl
-2-like fold with an unusual N-terminal extension.
Structural comparison of F1L with other
Bcl
-2 family members reveals a novel sequence signature that redefines the BH4 domain as a structural motif present in both pro- and anti-apoptotic
Bcl
-2 members, including viral
Bcl
-2-like proteins.
[MeSH-major]
Protein Structure, Quaternary. Protein Structure, Tertiary. Proto-Oncogene Proteins c-
bcl
-2 / chemistry. Viral Proteins / chemistry. Viral Proteins / metabolism
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18551131.001).
[ISSN]
1350-9047
[Journal-full-title]
Cell death and differentiation
[ISO-abbreviation]
Cell Death Differ.
[Language]
eng
[Databank-accession-numbers]
PDB/ 2VTY
[Grant]
United States / NCI NIH HHS / CA / CA43540; United States / NCI NIH HHS / CA / CA80188
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / F1L protein, vaccinia virus; 0 / Ligands; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 0 / Viral Proteins
35.
Paoluzzi L, Gonen M, Bhagat G, Furman RR, Gardner JR, Scotto L, Gueorguiev VD, Heaney ML, Manova K, O'Connor OA:
The BH3-only mimetic ABT-737 synergizes the antineoplastic activity of proteasome inhibitors in lymphoid malignancies.
Blood
; 2008 Oct 1;112(7):2906-16
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Overexpression of antiapoptotic members of the
Bcl
-2 family is observed in approximately 80% of B-
cell
lymphomas
, contributing to intrinsic and acquired drug resistance.
ABT-737 is a BH3-only mimetic and potent inhibitor of the antiapoptotic
Bcl
-2 family members
Bcl
-2,
Bcl
-X(L), and
Bcl
-w.
In vitro, ABT-737 exhibited concentration-dependent cytotoxicity against a broad panel of
lymphoma cell
lines including mantle
cell lymphoma
(MCL) and diffuse large B-
cell lymphoma
(DLBCL).
ABT-737 showed synergism when combined with the proteasome inhibitors bortezomib or carfilzomib in select
lymphoma cell
lines and induced potent mitochondrial membrane depolarization and apoptosis when combined with either.
ABT-737 plus bortezomib also induced significant apoptosis in primary samples of MCL, DLBCL, and chronic
lymphocytic
leukemia (CLL) but no significant cytotoxic effect was observed in peripheral blood mononuclear
cells
from healthy donors.
Collectively, these data suggest that ABT-737 alone or in combination with a proteasome inhibitor represents a novel and potentially important platform for the treatment of B-
cell
malignancies.
[MeSH-major]
Antineoplastic Agents / pharmacology. Biphenyl Compounds / pharmacology. Enzyme Inhibitors / pharmacology.
Lymphoma
/ enzymology.
Lymphoma
/ pathology. Molecular Mimicry / drug effects. Nitrophenols / pharmacology. Proteasome Inhibitors. Sulfonamides / pharmacology
[MeSH-minor]
Animals. Boronic Acids / pharmacology. Bortezomib.
Cell
Death / drug effects.
Cell
Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance,
Neoplasm
/ drug effects. Drug Synergism. Health. Humans. Leukemia,
Lymphocytic
, Chronic, B-
Cell
/ pathology. Leukocytes, Mononuclear / drug effects.
Lymphoma
, Large B-
Cell
, Diffuse / pathology.
Lymphoma
, Mantle-
Cell
/ pathology. Membrane Potential, Mitochondrial / drug effects. Mice. Microscopy, Confocal. Piperazines / pharmacology. Proto-Oncogene Proteins c-
bcl
-2 / metabolism. Pyrazines / pharmacology. Tissue Donors. Xenograft Model Antitumor Assays
MedlinePlus Health Information.
consumer health - Lymphoma
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18591385.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ABT-737; 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitrophenols; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Sulfonamides; 69G8BD63PP / Bortezomib
36.
Takakuwa T, Miyauchi A, Aozasa K:
Aberrant somatic hypermutations in thyroid lymphomas.
Leuk Res
; 2009 May;33(5):649-54
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Aberrant somatic hypermutations in thyroid
lymphomas
.
To determine a possible role of aberrant somatic hypermutation (ASHM) in the pathogenesis of thyroid
lymphoma
(TL), mutational status of genes affected by ASHM, including c-MYC, PIM-1, PAX-5 and RhoH/TTF, was analyzed.
Tumor specimens from 33 patients with thyroid B-
cell lymphoma
and 14 with chronic
lymphocytic
thyroiditis (CLTH), an autoimmune thyroiditis known to provide a basis for TL development, was examined.
Occurrence of ASHM in PIM-1, RhoH/TTF, and c-MYC was a constant
finding
in follicular
lymphoma
(FL) (all of 11 cases) but not so frequent in diffuse large B-
cell lymphoma
(DLBCL) (4 (33.3%) of 12 cases) and Marginal zone B-
cell lymphoma
(MZBCL) (1 (10.0%) of 10 cases).
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/ genetics. Mutation. Thyroid Neoplasms / genetics
MedlinePlus Health Information.
consumer health - Thyroid Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19019431.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
37.
Chang PM, Chen PM, Hsieh SL, Tzeng CH, Liu JH, Chiou TJ, Wang WS, Yen CC, Gau JP, Yang MH:
Expression of a soluble decoy receptor 3 in patients with diffuse large B-cell lymphoma predicts clinical outcome.
Int J Oncol
; 2008 Sep;33(3):549-54
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression of a soluble decoy receptor 3 in patients with diffuse large B-
cell lymphoma
predicts
clinical
outcome.
It is regarded as a decoy receptor released from tumor
cells
to escape host immune response by neutralizing the cytotoxic and immunomodulatory effects of FasL, LIGHT and TL1A.
Overexpression of DcR3 has been observed in several human malignancies; however, only limited information exists on the role of DcR3 in
non
-
Hodgkin lymphoma
especially for B-
cell
origin.
In the current study, the expression profile of DcR3 was analyzed by RT-PCR and immunohistochemistry (IHC) in a set of
lymphoma cell
lines including T-
cell
and B-
cell
lymphomas
.
The result demonstrated that overexpression of DcR3 was detected in most T-
cell lymphoma
cells
, which was consistent with previous reports.
Interestingly, overexpression of DcR3 was also detected both in the B-
cell lymphoma cell
lines and diffuse large
B cell lymphoma
(DLBCL) patients.
An in vitro study showed that neutralization of DcR3 increased the percentage of doxorubicin-mediated apoptosis in two B-
cell lymphoma cell
lines, which indicated the possibility of DcR3 mediated chemo-resistance in B-
cell
lymphomas
.
We suggest that overexpression of DcR3 is associated with a worse prognosis in DLBCL and the possible mechanism may act through the increase of chemo-resistance of
lymphoma
cells
.
[MeSH-major]
Biomarkers, Tumor / analysis. Drug Resistance,
Neoplasm
/ genetics.
Lymphoma
, Large B-
Cell
, Diffuse / metabolism. Receptors, Tumor Necrosis Factor, Member 6b / biosynthesis
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Gene Expression. Humans. Immunohistochemistry. Kaplan-Meier Estimate.
Lymphoma
, T-
Cell
/ metabolism.
Lymphoma
, T-
Cell
/ mortality.
Lymphoma
, T-
Cell
/ pathology. Male. Middle Aged. Prednisone / therapeutic use. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Vincristine / therapeutic use
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18695885.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
38.
Utkan G, Tek I, Kocer M, Muallaoglu S, Durnal AG, Arslan UY, Celenkoglu G, Tokluoglu S, Alkis N:
Blood viscosity in patients with diffuse large B cell non-Hodgkin's lymphoma.
Exp Oncol
; 2006 Dec;28(4):326-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Blood viscosity in patients with diffuse large
B cell non
-
Hodgkin
's
lymphoma
.
The aim of the study was to evaluate blood viscosity as possible marker of
disease
progression in patients with newly diagnosed
non
-
Hodgkin
's
lymphoma
(NHL).
[MeSH-major]
Blood Viscosity.
Lymphoma
, B-
Cell
/ blood.
Lymphoma
, Large B-
Cell
, Diffuse / blood
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17285120.001).
[ISSN]
1812-9269
[Journal-full-title]
Experimental oncology
[ISO-abbreviation]
Exp. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Ukraine
39.
Hirose A, Yamane T, Nakajima Y, Manabe M, Kanashima H, Hagihara K, Sakamoto E, Nakamae M, Terada Y, Kosaka S, Aoyama Y, Sakamoto C, Kumura T, Koh KR, Hirai M, Ohta K, Nakao Y, Mugitani A, Teshima H, Hino M:
[Autologous hematopoietic stem cell transplantation for aggressive B-cell non-Hodgkin's lymphoma].
Gan To Kagaku Ryoho
; 2005 Dec;32(13):2059-64
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Autologous hematopoietic stem
cell
transplantation for aggressive B-
cell non
-
Hodgkin
's
lymphoma
].
To evaluate the results of high-dose chemotherapy (HDT) and autologous hematopoietic stem
cell
transplantation (ASCT) in patients with diffuse B-
cell
aggressive
non
-
Hodgkin
's
lymphoma
(NHL).
The 5-year probability of
disease
-free survival for patients in the low-risk group and in the high-risk group was 68.8% and 60.0%,respectively (p = 0.9 6).
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation.
Lymphoma
, B-
Cell
/ therapy.
Lymphoma
, Large B-
Cell
, Diffuse / therapy. Transplantation, Autologous
[MeSH-minor]
Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage.
Disease
-Free Survival. Drug Administration Schedule. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Nitrosourea Compounds / administration & dosage. Remission Induction. Treatment Outcome
Genetic Alliance.
consumer health - Transplantation
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16352929.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Nitrosourea Compounds; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; RYH2T97J77 / ranimustine
40.
Hajdu M, Kopper L, Sebestyén A:
Notch-regulation upon Dll4-stimulation of TGFb-induced apoptosis and gene expression in human B-cell non-Hodgkin lymphomas.
Scand J Immunol
; 2010 Jan;71(1):29-37
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Notch-regulation upon Dll4-stimulation of TGFb-induced apoptosis and gene expression in human B-
cell non
-
Hodgkin
lymphomas
.
Notch-signalling has been implicated as a pathogenetic factor and a therapeutical target in T-
cell
leukaemias and in some
lymphomas
of B-
cell
origin.
Our aim was to investigate the role of Notch-signalling in apoptosis regulation in human
non
-
Hodgkin B
-
cell lymphoma
(B-NHL)
cell
lines and in primary chronic lymhocytic leukaemia (CLL)
cells
using Delta-like 4 (Dll4) ligand mediated Notch activation and gamma-secretase inhibitor (GSI) mediated Notch inhibition in vitro.
Modulation of Notch-signalling by itself did not change the rate of apoptosis in B-NHL
cell
lines and in CLL
cells
.
TGFb-induced apoptosis was decreased - but not completely abolished - by GSI in TGFb-sensitive
cell
lines, but resistance to the apoptotic effects of TGFb were not reversed by Notch activation or inhibition.
We identified Hairy/Enhancer of Split (HES)-1 as a TGFb target gene in selected - TGFb-sensitive - B-NHL
cell
lines.
[MeSH-major]
Apoptosis / drug effects. Intercellular Signaling Peptides and Proteins / pharmacology.
Lymphoma
, B-
Cell
/ pathology. Receptors, Notch / physiology. Transforming Growth Factor beta / pharmacology
[MeSH-minor]
Amyloid Precursor Protein Secretases / antagonists & inhibitors. Basic Helix-Loop-Helix Transcription Factors / genetics.
Cell
Line, Tumor. Dipeptides / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Homeodomain Proteins / genetics. Humans. Leukemia,
Lymphocytic
, Chronic, B-
Cell
/ pathology. Repressor Proteins / genetics. Signal Transduction
Genetic Alliance.
consumer health - B-Cell Lymphomas
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20017807.001).
[ISSN]
1365-3083
[Journal-full-title]
Scandinavian journal of immunology
[ISO-abbreviation]
Scand. J. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DLL4 protein, human; 0 / Dipeptides; 0 / HEY2 protein, human; 0 / Homeodomain Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / N-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester; 0 / Receptors, Notch; 0 / Repressor Proteins; 0 / Transforming Growth Factor beta; 149348-15-2 / HES1 protein, human; EC 3.4.- / Amyloid Precursor Protein Secretases
41.
Cypel M, Belfort R Jr, Moraes N, Muccioli C:
[Primary intraocular B-cell lymphoma: case report].
Arq Bras Oftalmol
; 2007 Jul-Aug;70(4):709-12
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Primary intraocular B-
cell lymphoma
: case report].
[Transliterated title]
Linfoma
intra-ocular primário
de
células tipo B: relato
de
caso.
Ocular
non
-
Hodgkin
's
lymphoma
is a rare condition that can involve the retina, the vitreous and the optic nerve.
It can occur alone or can be associated with
lymphoma
of the central nervous system and a frequent manifestation is a posterior uveitis of difficult treatment.
This kind of ocular tumor is difficult and a challenge to
diagnosis
.
We describe a case of
non
-
Hodgkin
's intraocular B-
cell lymphoma
in a 47-year-old woman who had a posterior uveitis as the first manifestation.
We emphasize the importance of a careful investigation and of the general
clinical
examination since this is the most common
type
in the eye.
We expect to call the attention to this
disease
that many times appears in an unspecific form with unspecific symptoms.
[MeSH-major]
Eye Neoplasms /
diagnosis
.
Lymphoma
, B-
Cell
/
diagnosis
[MeSH-minor]
Female. Humans.
Lymphoma
,
Non
-
Hodgkin
/
diagnosis
. Middle Aged. Uveitis /
diagnosis
MedlinePlus Health Information.
consumer health - Eye Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17906772.001).
[ISSN]
0004-2749
[Journal-full-title]
Arquivos brasileiros de oftalmologia
[ISO-abbreviation]
Arq Bras Oftalmol
[Language]
por
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Brazil
42.
Lin P, Jetly R, Lennon PA, Abruzzo LV, Prajapati S, Medeiros LJ:
Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature.
Hum Pathol
; 2008 Nov;39(11):1664-72
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Translocation (18;22)(q21;q11) in B-
cell
lymphomas
: a report of 4 cases and review of the literature.
Follicular
lymphomas
characteristically carry t(14;18)(q32;q21) which results in IGH-
BCL
-2 fusion.
Variant translocations that juxtapose the
BCL
-2 gene with the immunoglobulin kappa (2p11) and lambda (22q11) light chain genes are rare.
We report 4 cases of B-
cell lymphoma
/leukemia associated with t(18;22)(q21;q11).
Three cases were classified as chronic
lymphocytic
leukemia, and one as follicular
lymphoma
based on morphology and immunophenotype.
Fluorescence in situ hybridization analysis was performed on all 4 cases using
a BCL
-2 breakapart probe.
The
BCL
-2 gene was rearranged in all cases.
These cases illustrate that t(18;22)(q21;q11) is more commonly observed in chronic
lymphocytic
leukemia and may represent either an initial or secondary genetic event.
[MeSH-major]
Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 22. Leukemia,
Lymphocytic
, Chronic, B-
Cell
/ genetics.
Lymphoma
, B-
Cell
/ genetics
[MeSH-minor]
Aged. Fatal Outcome. Female. Gene Rearrangement, B-Lymphocyte. Genes,
bcl
-2. Humans. Male. Middle Aged. Translocation, Genetic
Genetic Alliance.
consumer health - B-Cell Lymphomas
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18656237.001).
[ISSN]
1532-8392
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
25
43.
Autorino R, Lamendola MG, De Sio M, Di Trolio RA, Ferraraccio F, Di Lorenzo G:
A complete response with rituximab in metastatic diffuse large B-cell lymphoma of the testis: case report.
Int J Immunopathol Pharmacol
; 2007 Apr-Jun;20(2):401-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A complete response with rituximab in metastatic diffuse large B-
cell lymphoma
of the testis: case report.
Primary testicular
lymphoma
is an uncommon testicular tumour.
We present a case of a primary
non
-
Hodgkin lymphoma
of the testis, describing its
clinical
and pathological features and discussing our treatment strategy.
Light microscopy demonstrated the classic appearance of a diffuse large B-
cell lymphoma
.
The immunohistochemical study showed tumour
cells
intensively positive for CD45, Ki67 and CD20.
No evidence of extra-testicular involvement by
lymphoma
was found.
At 6 months, a TC-PET showed
a clinical
relapse in lung and abdominal lymphonodes, while
clinical
examination demonstrated a single, indolent and erythematous nodule in the left foot.
The histologic analysis confirmed
diagnosis
of CD-20 positive B-
cell lymphoma
.
After 3 months a complete response was observed in all sites of
disease
.
The patient was free from
disease
at 12 months follow-up.
[MeSH-major]
Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology.
Lymphoma
, B-
Cell
/ drug therapy.
Lymphoma
, Large B-
Cell
, Diffuse / drug therapy. Testicular Neoplasms / drug therapy
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
Hazardous Substances Data Bank.
RITUXIMAB
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17624254.001).
[ISSN]
0394-6320
[Journal-full-title]
International journal of immunopathology and pharmacology
[ISO-abbreviation]
Int J Immunopathol Pharmacol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
44.
Meyer J, Delay J, Bienzle D:
Clinical, laboratory, and histopathologic features of equine lymphoma.
Vet Pathol
; 2006 Nov;43(6):914-24
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Clinical
, laboratory, and histopathologic features of equine
lymphoma
.
Clinical
, laboratory and tissue findings from 37 horses with
lymphoma
were investigated.
Tumor
cell
morphology was heterogeneous in 17 tumors, and 8 tumors had marked histiocytic and multinucleated giant
cell
infiltrates.
Extensive necrosis or focal fibrosis was present in 22 and 4
lymphomas
, respectively.
Staining of tumor sections with antibodies against CD3 and CD79alpha molecules resulted in classification of T-
cell
(n = 26) or B-
cell
(n = 7) origin.
Most T-
cell
tumors comprised small to medium CD3(+) lymphocytes, whereas 5 of 7 B-
cell
tumors were infiltrated by numerous small T lymphocytes and classified as T-
cell
-rich B-
cell lymphoma
.
Fresh tumor
cells
from 6 horses bound antibodies reactive with equine CD4, CD5, CD8, CD21, or major histocompatibility class II molecules, confirming T-
cell
(n = 5) or B-
cell
origin (n = 1).
These findings suggest that T-
cell lymphoma
is more common than B-
cell lymphoma
in horses and that inflammation, possibly from tumor cytokine production, is frequent.
[MeSH-major]
Horse Diseases / pathology.
Lymphoma
/ veterinary
MedlinePlus Health Information.
consumer health - Lymphoma
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17099148.001).
[ISSN]
0300-9858
[Journal-full-title]
Veterinary pathology
[ISO-abbreviation]
Vet. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
45.
Chang CM, Schroeder JC, Huang WY, Dunphy CH, Baric RS, Olshan AF, Dorsey KC, Dent GA, Cerhan JR, Lynch CF, Rothman N, Cantor KP, Blair A:
Non-Hodgkin lymphoma (NHL) subtypes defined by common translocations: utility of fluorescence in situ hybridization (FISH) in a case-control study.
Leuk Res
; 2010 Feb;34(2):190-5
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Non
-
Hodgkin lymphoma
(NHL) subtypes defined by common translocations: utility of fluorescence in situ hybridization (FISH) in a case-control study.
We used fluorescence in situ hybridization (FISH) assays to identify t(14;18) translocations in archival paraffin-embedded tumor sections from
non
-
Hodgkin lymphoma
(NHL) cases enrolled in a population-based study. t(14;18) was identified in 54% of 152 cases, including 39% of diffuse large
cell
lymphomas
(26 of 66 cases) and 84% of follicular
lymphomas
(36 of 43 cases).
Eighty-seven percent of t(14;18)-positive cases and 57% of t(14;18)-negative cases expressed
bcl
-2.
FISH assays detected twice as many t(14;18)-positive follicular
lymphomas
as PCR assays.
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
Genetic Alliance.
consumer health - Non-Hodgkin Lymphoma
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2009 Elsevier Ltd. All rights reserved.
[Cites]
Cancer Genet Cytogenet. 2003 May;143(1):73-9
[
12742158.001
]
[Cites]
Arch Pathol Lab Med. 2008 Aug;132(8):1355-61
[
18684042.001
]
[Cites]
Int J Hematol. 2003 Aug;78(2):154-9
[
12953811.001
]
[Cites]
Cancer. 2003 Dec 25;99(6):385-93
[
14681948.001
]
[Cites]
Pathology. 2004 Feb;36(1):19-44
[
14757555.001
]
[Cites]
Cancer Genet Cytogenet. 2004 Apr 1;150(1):22-6
[
15041219.001
]
[Cites]
Am J Pathol. 2004 Jul;165(1):159-66
[
15215171.001
]
[Cites]
Histopathology. 2004 Nov;45(5):501-10
[
15500654.001
]
[Cites]
J Natl Cancer Inst. 1987 Apr;78(4):675-8
[
3470542.001
]
[Cites]
J Natl Cancer Inst. 1987 Jun;78(6):1137-44
[
3473254.001
]
[Cites]
Am J Public Health. 1988 May;78(5):570-1
[
3354743.001
]
[Cites]
Cancer Res. 1990 Oct 15;50(20):6585-91
[
2208120.001
]
[Cites]
Arch Environ Health. 1991 Mar-Apr;46(2):70-4
[
2006896.001
]
[Cites]
Leuk Res. 1991;15(5):305-14
[
2046383.001
]
[Cites]
Cancer Res. 1992 Oct 1;52(19 Suppl):5522s-5528s
[
1394167.001
]
[Cites]
Cancer Res. 1992 Oct 1;52(19 Suppl):5529s-5540s
[
1394168.001
]
[Cites]
Am J Ind Med. 1993 Feb;23(2):301-12
[
8427258.001
]
[Cites]
Blood. 1994 Sep 1;84(5):1361-92
[
8068936.001
]
[Cites]
J Clin Oncol. 1996 Mar;14(3):963-9
[
8622046.001
]
[Cites]
Blood Cells Mol Dis. 1998 Mar;24(1):62-72
[
9616042.001
]
[Cites]
Cancer Sci. 2005 Feb;96(2):77-82
[
15723651.001
]
[Cites]
Leukemia. 2005 Jun;19(6):1058-63
[
15815725.001
]
[Cites]
Am J Surg Pathol. 2005 Aug;29(8):1067-73
[
16006802.001
]
[Cites]
Anticancer Res. 2005 Sep-Oct;25(5):3179-82
[
16101124.001
]
[Cites]
Am J Clin Pathol. 2005 Sep;124(3):421-9
[
16191511.001
]
[Cites]
Eur J Haematol. 2006 Apr;76(4):284-93
[
16519699.001
]
[Cites]
Cancer. 2006 Jun 25;108(3):198-204
[
16671111.001
]
[Cites]
Mod Pathol. 2006 Aug;19(8):1027-33
[
16680153.001
]
[Cites]
Blood. 2006 Aug 15;108(4):1363-9
[
16621961.001
]
[Cites]
Hum Pathol. 2007 Feb;38(2):365-72
[
17134735.001
]
[Cites]
Am J Epidemiol. 2007 Mar 15;165(6):652-9
[
17204518.001
]
[Cites]
Leuk Res. 2008 May;32(5):737-42
[
17964648.001
]
[Cites]
Cancer Causes Control. 2008 Oct;19(8):859-67
[
18386141.001
]
[Cites]
Cancer Res. 1992 Oct 1;52(19 Suppl):5456s-5462s; discussion 5462s-5464s
[
1394154.001
]
[Cites]
Genes Chromosomes Cancer. 2000 Jan;27(1):85-94
[
10564590.001
]
[Cites]
Arch Pathol Lab Med. 1999 Dec;123(12):1189-207
[
10583924.001
]
[Cites]
Br J Haematol. 2001 May;113(2):383-90
[
11380403.001
]
[Cites]
Epidemiology. 2001 Nov;12(6):701-9
[
11679800.001
]
[Cites]
Blood. 2002 Apr 1;99(7):2285-90
[
11895757.001
]
[Cites]
Cancer Causes Control. 2002 Mar;13(2):159-68
[
11936822.001
]
[Cites]
Leukemia. 2003 Jan;17(1):255-9
[
12529690.001
]
[Cites]
J Mol Diagn. 2003 Aug;5(3):168-75
[
12876207.001
]
(PMID = 19505720.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
ENG
[Grant]
United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / R21 CA107966-01; United States / NICHD NIH HHS / HD / R24 HD050924; United States / NCI NIH HHS / CA / R03 CA71617-01; United States / NIEHS NIH HHS / ES / P30ES10126; United States / NCI NIH HHS / CA / CA107966-01
[Publication-type]
Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Proto-Oncogene Proteins c-bcl-2
[Other-IDs]
NLM/ NIHMS157999; NLM/ PMC2815151
46.
Westphal D, Ledgerwood EC, Hibma MH, Fleming SB, Whelan EM, Mercer AA:
A novel Bcl-2-like inhibitor of apoptosis is encoded by the parapoxvirus ORF virus.
J Virol
; 2007 Jul;81(13):7178-88
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A novel
Bcl
-2-like inhibitor of apoptosis is encoded by the parapoxvirus ORF virus.
Apoptotic
cell
death forms part of the host defense against virus infection.
We tested orf virus, a member of the poxvirus family, for the ability to inhibit apoptosis and found that orf virus-infected
cells
were fully resistant to UV-induced changes in
cell
morphology, caspase activation, and DNA fragmentation.
These features are comparable to the antiapoptotic properties of the mitochondrial regulator
Bcl
-2.
Furthermore, bioinformatic analyses revealed sequence and secondary-structure similarities to
Bcl
-2 family members, including characteristic residues of all four
Bcl
-2 homology domains.
Consistent with this, the viral protein inhibited the UV-induced activation of the proapoptotic
Bcl
-2 family members Bax and Bak.
ORFV125 is the first parapoxvirus apoptosis inhibitor to be identified, and we propose that it is a new antiapoptotic member of the
Bcl
-2 family.
[MeSH-minor]
Apoptosis. Caspases / metabolism. DNA Fragmentation / radiation effects. Enzyme Activation / genetics. Enzyme Activation / radiation effects. HeLa
Cells
. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Mitochondria / metabolism. Protein Structure, Secondary. Protein Structure, Tertiary. Ultraviolet Rays.
bcl
-2 Homologous Antagonist-Killer Protein / genetics.
bcl
-2 Homologous Antagonist-Killer Protein / metabolism.
bcl
-2-Associated X Protein / genetics.
bcl
-2-Associated X Protein / metabolism
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2000 May 15;60(10):2666-72
[
10825139.001
]
[Cites]
J Virol. 2004 Jan;78(1):353-66
[
14671117.001
]
[Cites]
J Gen Virol. 2000 Nov;81(Pt 11):2803-11
[
11038395.001
]
[Cites]
Protein Sci. 2000 Dec;9(12):2528-34
[
11206074.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3012-7
[
11248023.001
]
[Cites]
Mol Biol Cell. 2002 May;13(5):1615-25
[
12006657.001
]
[Cites]
Curr Opin Microbiol. 2002 Aug;5(4):395-402
[
12160859.001
]
[Cites]
Genes Dev. 2002 Oct 1;16(19):2465-78
[
12368257.001
]
[Cites]
J Gen Virol. 2000 Apr;81(Pt 4):1087-97
[
10725436.001
]
[Cites]
J Virol. 2000 Apr;74(8):3815-31
[
10729156.001
]
[Cites]
J Exp Med. 2000 May 1;191(9):1487-98
[
10790424.001
]
[Cites]
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):83-94
[
14996493.001
]
[Cites]
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):95-105
[
14996494.001
]
[Cites]
J Virol. 2004 Jul;78(13):7097-111
[
15194786.001
]
[Cites]
Science. 2004 Jul 30;305(5684):626-9
[
15286356.001
]
[Cites]
Arch Virol. 1982;71(1):43-55
[
6279055.001
]
[Cites]
Nucleic Acids Res. 1987 Sep 11;15(17):7192
[
2821498.001
]
[Cites]
Arch Virol. 1988;101(3-4):255-9
[
3178493.001
]
[Cites]
J Virol. 1994 Dec;68(12):7728-37
[
7966562.001
]
[Cites]
Nature. 1996 May 23;381(6580):335-41
[
8692274.001
]
[Cites]
Cell. 1996 Jul 12;86(1):147-57
[
8689682.001
]
[Cites]
Science. 1997 Feb 14;275(5302):983-6
[
9020082.001
]
[Cites]
Oncogene. 1997 Jan 30;14(4):405-14
[
9053837.001
]
[Cites]
Virology. 1997 Mar 3;229(1):193-200
[
9123861.001
]
[Cites]
Biochem J. 1998 Jan 1;329 ( Pt 1):95-9
[
9405280.001
]
[Cites]
Virology. 1998 May 10;244(2):365-96
[
9601507.001
]
[Cites]
Virus Genes. 1998;17(2):107-15
[
9857983.001
]
[Cites]
Trends Microbiol. 1999 Apr;7(4):160-5
[
10217831.001
]
[Cites]
Curr Opin Cell Biol. 2004 Dec;16(6):647-52
[
15530776.001
]
[Cites]
J Virol. 2005 Jan;79(2):1084-98
[
15613337.001
]
[Cites]
Bioinformatics. 2005 Apr 1;21(7):951-60
[
15531603.001
]
[Cites]
Cancer Biol Ther. 2005 Feb;4(2):139-63
[
15725726.001
]
[Cites]
Biochem J. 2005 Jul 1;389(Pt 1):83-9
[
15727562.001
]
[Cites]
FEBS Lett. 2005 Jul 4;579(17):3503-7
[
15949801.001
]
[Cites]
J Virol. 2005 Nov;79(22):14031-43
[
16254338.001
]
[Cites]
Curr Opin Cell Biol. 2005 Dec;17(6):617-25
[
16243507.001
]
[Cites]
J Virol. 2006 Feb;80(3):1140-51
[
16414991.001
]
[Cites]
Virus Res. 2006 Mar;116(1-2):146-58
[
16274827.001
]
[Cites]
Cell Death Differ. 2006 Sep;13(9):1423-33
[
16676004.001
]
[Cites]
Cell Death Differ. 2006 Oct;13(10):1651-62
[
16439990.001
]
[Cites]
J Biol Chem. 2006 Dec 22;281(51):39728-39
[
17074758.001
]
[Cites]
Mol Cell. 2007 Mar 23;25(6):933-42
[
17386268.001
]
[Cites]
Oncogene. 2000 May 4;19(19):2286-95
[
10822379.001
]
[Cites]
J Cell Biol. 2003 Jan 6;160(1):53-64
[
12515824.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2432-7
[
12591950.001
]
[Cites]
Cell Death Differ. 2003 Jan;10 Suppl 1:S68-76
[
12655348.001
]
[Cites]
EMBO J. 2003 Apr 1;22(7):1497-507
[
12660157.001
]
[Cites]
Bioessays. 2003 Sep;25(9):888-96
[
12938178.001
]
[Cites]
J Cell Biol. 2003 Sep 1;162(5):877-87
[
12952938.001
]
[Cites]
Immunity. 2003 Sep;19(3):341-52
[
14499110.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14345-50
[
14610284.001
]
[Cites]
J Virol. 2004 Jan;78(1):168-77
[
14671098.001
]
[Cites]
Trends Cell Biol. 2000 Sep;10(9):369-77
[
10932094.001
]
(PMID = 17475653.001).
[ISSN]
0022-538X
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Inhibitor of Apoptosis Proteins; 0 / Viral Proteins; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases
[Other-IDs]
NLM/ PMC1933275
47.
Horning SJ, Younes A, Jain V, Kroll S, Lucas J, Podoloff D, Goris M:
Efficacy and safety of tositumomab and iodine-131 tositumomab (Bexxar) in B-cell lymphoma, progressive after rituximab.
J Clin Oncol
; 2005 Feb 1;23(4):712-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Efficacy and safety of tositumomab and iodine-131 tositumomab (Bexxar) in B-
cell lymphoma
, progressive after rituximab.
PURPOSE: To determine overall response (OR) and complete response (CR) rates, response duration, progression-free (PFS) and overall survival and safety with the tositumomab and iodine-131 tositumomab ((131)I tositumomab) therapeutic regimen in patients with indolent, follicular large-
cell
, or transformed B-
cell lymphoma
, progressive after rituximab.
CONCLUSION: (131)I tositumomab is effective in CD20-positive
lymphoma
progressive after rituximab, with a 65% OR rate and median PFS of 24.5 months for responders.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use.
Lymphoma
, B-
Cell
/ radiotherapy. Radioimmunotherapy
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
RITUXIMAB
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15613695.001).
[ISSN]
0732-183X
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / iodine-131 anti-B1 antibody; 4F4X42SYQ6 / Rituximab
48.
Ascani S, Massone C, Ferrara G, Rongioletti F, Papini M, Pileri S, Cerroni L:
CD4-negative variant of CD4+/CD56+ hematodermic neoplasm: description of three cases.
J Cutan Pathol
; 2008 Oct;35(10):911-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
CD4-negative variant of CD4+/CD56+ hematodermic
neoplasm
: description of three cases.
BACKGROUND: CD4+/CD56+ hematodermic
neoplasm
(HN) (blastic natural killer (NK)-
cell lymphoma
) is a rare entity characterized by dense, monomorphous infiltrates of medium-sized
cells
with blastic appearance and a characteristic immunophenotype (positivity for CD4, CD56 and CD123).
The term 'CD4+/CD56+ hematodermic
neoplasm
' adopted in the World Health Organization-European Organization for Research and Treatment of Cancer classification of cutaneous
lymphomas
may be misleading and should probably be revised in the light of all data published in the literature.
[MeSH-major]
Antigens, CD4 / metabolism. Antigens, CD56 / metabolism. Killer
Cells
, Natural / pathology.
Lymphoma
,
Non
-
Hodgkin
/ pathology. Skin Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Skin Cancer
.
COS Scholar Universe.
author profiles
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18494823.001).
[ISSN]
1600-0560
[Journal-full-title]
Journal of cutaneous pathology
[ISO-abbreviation]
J. Cutan. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Antigens, CD4; 0 / Antigens, CD56; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
49.
Xiao W, Li L, Zhou R, Xiao R, Wang Y, Ji X, Wu M, Wang L, Huang W, Zheng X, Tan X, Chen L, Xiong T, Xiong J, Jin Y, Tan J, He Y:
EBV-induced human CD8(+) NKT cells synergise CD4(+) NKT cells suppressing EBV-associated tumours upon induction of Th1-bias.
Cell Mol Immunol
; 2009 Oct;6(5):367-79
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
EBV-induced human CD8(+) NKT
cells
synergise CD4(+) NKT
cells
suppressing EBV-associated tumours upon induction of Th1-bias.
CD8(+) natural killer T (NKT)
cells
from EBV-associated tumour patients are quantitatively and functionally impaired.
EBV-induced CD8(+) NKT
cells
drive syngeneic T
cells
into a Th1-bias response to suppress EBV-associated malignancies.
IL-4-biased CD4(+) NKT
cells
do not affect either syngeneic T
cell
cytotoxicity or Th cytokine secretion.
Circulating mDC1
cells
from patients with EBV-associated malignancies impair the production of IFN-gamma by CD8(+) NKT
cells
.
In this study, we have established a human-thymus-SCID chimaera model to further investigate the underlying mechanism of EBV-induced CD8(+) NKT
cells
in suppressing EBV-associated malignancies.
In the human-thymus-SCID chimera, EBV-induced CD8(+) NKT
cells
suppress EBV-associated malignancies in a manner dependent on the Th1-bias response and syngeneic CD3(+) T
cells
.
However, adoptive transfer with CD4(+) NKT
cells
alone inhibits T
cell
immunity.
Interestingly, CD4(+) NKT
cells
themselves secrete high levels of IL-2, enhancing the persistence of adoptively transferred CD8(+) NKT
cells
and T
cells
, thereby leading to a more pronounced T
cell
anti-tumour response in chimaeras co-transferred with CD4(+) and CD8(+) NKT
cells
.
Thus, immune reconstitution with EBV-induced CD4(+) and CD8(+) NKT
cells
synergistically enhances T
cell
tumour immunity, providing a potential prophylactic and therapeutic treatment for EBV-associated malignancies.
[MeSH-major]
Antigens, CD8 / immunology. Cytotoxicity, Immunologic. Epstein-Barr Virus Infections / immunology. Herpesvirus 4, Human / immunology.
Hodgkin
Disease
/ immunology.
Hodgkin
Disease
/ therapy.
Lymphoma
, B-
Cell
/ immunology.
Lymphoma
, B-
Cell
/ therapy. Nasopharyngeal Neoplasms / immunology. Nasopharyngeal Neoplasms / therapy. Natural Killer T-
Cells
/ immunology. Th1
Cells
/ immunology
[MeSH-minor]
Adoptive Transfer. Animals. Antigens, CD4 / immunology.
Cell
Line, Tumor. Chimera. Humans. Interferon-gamma / metabolism. Interleukin-2 / metabolism. Interleukin-4 / immunology. Lymphocyte Activation. Mice. Mice, SCID. T-Lymphocyte Subsets / immunology. T-Lymphocyte Subsets / metabolism
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Cell Mol Immunol. 2011 Jul;8(4):368
(PMID = 19887050.001).
[ISSN]
2042-0226
[Journal-full-title]
Cellular & molecular immunology
[ISO-abbreviation]
Cell. Mol. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Interleukin-2; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
[Other-IDs]
NLM/ PMC4003220
50.
Hariprasad R, Kumar L, Bhatla DM, Kukreja M, Papaiah S:
Primary uterine lymphoma: report of 2 cases and review of literature.
Am J Obstet Gynecol
; 2006 Jul;195(1):308-13
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Primary uterine
lymphoma
: report of 2 cases and review of literature.
Primary uterine
non
-
Hodgkin
's
lymphoma
is a rare malignancy.
We here describe 2 patients who presented with cervical growth, stage IE, diffuse large
B cell
histology.
They achieved complete
clinical
and radiological response.
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/ drug therapy. Uterine Neoplasms / drug therapy
[MeSH-minor]
Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Middle Aged.
Neoplasm
Staging. Prednisone / therapeutic use. Radiotherapy Dosage. Vincristine / therapeutic use
MedlinePlus Health Information.
consumer health - Uterine Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16813759.001).
[ISSN]
1097-6868
[Journal-full-title]
American journal of obstetrics and gynecology
[ISO-abbreviation]
Am. J. Obstet. Gynecol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
[Number-of-references]
30
51.
Sansonno D, Tucci FA, Lauletta G, De Re V, Montrone M, Troiani L, Sansonno L, Dammacco F:
Hepatitis C virus productive infection in mononuclear cells from patients with cryoglobulinaemia.
Clin Exp Immunol
; 2007 Feb;147(2):241-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Hepatitis C virus productive infection in mononuclear
cells
from patients with cryoglobulinaemia.
HCV minus strand RNA, the viral replicative intermediate, was searched for by a polyA(+) tract strand-specific Tth-based reverse transcriptase-polymerase chain reaction (RT-PCR) in lymphoid
cells
of 46 patients with acute and chronic infection.
The HCV replicating form in lymphoid
cells
was associated strictly with mixed cryoglobulinaemia (MCG), in that it was found in six of 13 (46%) MCG patients, including two with
B cell non
-
Hodgkin
's
lymphoma
(NHL).
These results emphasize the direct role of the virus in the pathogenesis of MCG and support the contention that HCV is not specifically lymphotropic, its entry and replication in lymphoid
cells
being determined largely by selective interactions.
[MeSH-minor]
Acute
Disease
. Adult. Aged. Bone Marrow
Cells
/ virology. Female. Hepatitis C, Chronic / complications. Humans.
Lymphoma
, B-
Cell
/ virology. Male. Middle Aged. RNA, Viral / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Virus Replication
Genetic Alliance.
consumer health - Hepatitis
.
MedlinePlus Health Information.
consumer health - Hepatitis C
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Viral Hepat. 2004 Jul;11(4):310-8
[
15230853.001
]
[Cites]
Curr Top Microbiol Immunol. 2000;242:55-84
[
10592656.001
]
[Cites]
Arch Virol. 1994;134(3-4):293-302
[
7510473.001
]
[Cites]
Virology. 1994 Aug 1;202(2):606-14
[
8030225.001
]
[Cites]
Blood. 1995 Sep 1;86(5):1887-92
[
7655017.001
]
[Cites]
J Hepatol. 1995 Jun;22(6):696-9
[
7560864.001
]
[Cites]
J Virol. 1995 Dec;69(12):8079-83
[
7494326.001
]
[Cites]
Clin Exp Immunol. 1996 Mar;103(3):414-21
[
8608640.001
]
[Cites]
J Clin Invest. 1996 Feb 1;97(3):845-51
[
8609243.001
]
[Cites]
Blood. 1996 Dec 15;88(12):4638-45
[
8977256.001
]
[Cites]
Blood. 1998 Nov 1;92(9):3328-37
[
9787170.001
]
[Cites]
J Hepatol. 2005 Apr;42(4):491-8
[
15763335.001
]
[Cites]
Science. 2005 Jul 22;309(5734):623-6
[
15947137.001
]
[Cites]
J Virol. 2000 May;74(10):4824-30
[
10775621.001
]
[Cites]
Hepatology. 2000 Aug;32(2):382-7
[
10915746.001
]
[Cites]
Adv Virus Res. 2000;55:231-69
[
11050944.001
]
[Cites]
Eur J Clin Invest. 2001 Jul;31(7):628-38
[
11454019.001
]
[Cites]
Cell. 2002 Mar 8;108(5):717-25
[
11893341.001
]
[Cites]
EMBO J. 2002 Oct 1;21(19):5017-25
[
12356718.001
]
[Cites]
Blood. 2003 Jan 1;101(1):52-7
[
12393733.001
]
[Cites]
J Virol. 2003 Mar;77(5):3007-19
[
12584326.001
]
[Cites]
J Exp Med. 2003 Mar 3;197(5):633-42
[
12615904.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7271-6
[
12761383.001
]
[Cites]
J Virol. 2003 Oct;77(19):10432-6
[
12970428.001
]
[Cites]
Eur J Immunol. 2004 Jan;34(1):126-36
[
14971038.001
]
[Cites]
Hepatology. 2005 Nov;42(5):1019-27
[
16231354.001
]
[Cites]
J Hepatol. 2006 Feb;44(2):436-9
[
16360233.001
]
[Cites]
J Virol. 2006 Feb;80(4):1734-41
[
16439530.001
]
[Cites]
Gastroenterology. 2006 Apr;130(4):1107-16
[
16618405.001
]
[Cites]
Clin Exp Immunol. 2006 Feb;143(2):288-96
[
16412053.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12766-71
[
10535997.001
]
[Cites]
Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2451-5
[
1848704.001
]
(PMID = 17223964.001).
[ISSN]
0009-9104
[Journal-full-title]
Clinical and experimental immunology
[ISO-abbreviation]
Clin. Exp. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Viral
[Other-IDs]
NLM/ PMC1810461
52.
Trümper L, Zwick C, Ziepert M, Hohloch K, Schmits R, Mohren M, Liersch R, Bentz M, Graeven U, Wruck U, Hoffmann M, Metzner B, Hasenclever D, Loeffler M, Pfreundschuh M, German High-Grade Non-Hodgkin's Lymphoma Study Group (DSHNHL):
Dose-escalated CHOEP for the treatment of young patients with aggressive non-Hodgkin's lymphoma: I. A randomized dose escalation and feasibility study with bi- and tri-weekly regimens.
Ann Oncol
; 2008 Mar;19(3):538-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Dose-escalated CHOEP for the treatment of young patients with aggressive
non
-
Hodgkin
's
lymphoma
: I. A randomized dose escalation and feasibility study with bi- and tri-weekly regimens.
BACKGROUND: To determine the maximum tolerated dose of a bi- and tri-weekly combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone plus etoposide (CHOEP) regimen without stem-
cell
support.
PATIENTS AND METHODS: Randomized phase I/II multicenter four-level (cyclophosphamide: 1000-1200-1400-1600 mg/m2; doxorubicin: 55-60-65-70 mg/m2; etoposide: 375-450-525-600 mg/m2) dose escalation study with CHOEP-14 and CHOEP-21 in young patients (18-60 years) with newly diagnosed aggressive
non
-
Hodgkin
's
lymphoma
.
MedlinePlus Health Information.
consumer health - Blood Disorders
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISOLONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18212092.001).
[ISSN]
1569-8041
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
53.
Al-Abbadi MA, Hattab EM, Tarawneh MS, Amr SS, Orazi A, Ulbright TM:
Primary testicular diffuse large B-cell lymphoma belongs to the nongerminal center B-cell-like subgroup: A study of 18 cases.
Mod Pathol
; 2006 Dec;19(12):1521-7
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Primary testicular diffuse large B-
cell lymphoma
belongs to the nongerminal center B-
cell
-like subgroup: A study of 18 cases.
The most common
type
of primary testicular
lymphoma
is diffuse large B-
cell
type
, which has the potential for aggressive
clinical
behavior.
Diffuse large B-
cell lymphoma
can be further subclassified into two major prognostic categories: germinal center B-
cell
-like and nongerminal center B-
cell
-like.
Such distinction is made possible using the immunohistochemical expression of CD10,
Bcl
-6 and MUM1.
The aim of this study was to stratify primary testicular
lymphoma
of the diffuse large B-
cell
type
according to this scheme.
Immunohistochemical stains for CD10,
Bcl
-6 and MUM1 were performed on 18 cases of primary testicular
lymphoma
of diffuse large B-
cell
type
.
Subclassification was carried out as previously described where CD10 and/or
Bcl
-6 positivity and negativity for MUM1 were considered indicative of germinal center B-
cell
-like
type
and the opposite expression as nongerminal center B-
cell
-like
type
.
Of 18 cases, 16 (89%) were found to belong to the nongerminal center B-
cell
-like
type
.
Two cases (11%) were classified as germinal center B-
cell
-like
type
; one had a CD10-positive,
Bcl
-6-positive and MUM1-negative profile, and the other was CD10 negative,
Bcl
-6 positive and MUM1 negative.
We conclude that most (89%) primary testicular
lymphomas
of the diffuse large B-
cell
type
belong to the nongerminal center B-
cell
-like subgroup and have high proliferative activity.
[MeSH-major]
Lymphoma
, B-
Cell
/ pathology.
Lymphoma
,
Non
-
Hodgkin
/ pathology. Testicular Neoplasms / pathology
[MeSH-minor]
Adult. Aged. Biomarkers, Tumor / analysis. DNA-Binding Proteins / analysis. Humans. Immunoenzyme Techniques. Interferon Regulatory Factors / analysis. Male. Middle Aged.
Neoplasm
Staging. Neprilysin / analysis. Prognosis. Survival Rate. Testis / chemistry. Testis / pathology
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16998463.001).
[ISSN]
0893-3952
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
54.
Kohlhof JK, Driemel O, Müller-Richter UD:
[Re-re-relapse of a MALT lymphoma of the conjunctiva].
Klin Monbl Augenheilkd
; 2008 Aug;225(8):727-30
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Re-re-relapse of a MALT
lymphoma
of the conjunctiva].
BACKGROUND: The MALT
lymphoma
(mucosa-associated lymphoid-like tissue
lymphomas
) is a rare entity and belongs to the low-grade
non
-
Hodgkin
(NHL)
lymphomas
.
In some cases a MALT
lymphoma
of the conjunctiva is misdiagnosed as chronic conjunctivitis.
Mostly a MALT
lymphoma
of the conjunctiva can be cured by radiation and has a good prognosis.
The medical history revealed treatment for a MALT
lymphoma
4 years previously and a relapse 3 years previously.
CLINICAL
COURSE: To confirm the
diagnosis a
biopsy was done.
The histological examination demonstrated a relapse of the MALT
lymphoma
.
CONCLUSION: This case shows that a relapse of the MALT
lymphoma
may arise although the previous tumour and its relapse were resected totally.
[MeSH-major]
Conjunctival Neoplasms /
diagnosis
.
Lymphoma
, B-
Cell
, Marginal Zone /
diagnosis
.
Neoplasm
Recurrence, Local /
diagnosis
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18712659.001).
[ISSN]
1439-3999
[Journal-full-title]
Klinische Monatsblätter für Augenheilkunde
[ISO-abbreviation]
Klin Monbl Augenheilkd
[Language]
ger
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Germany
55.
Li B, Shi S, Qian W, Zhao L, Zhang D, Hou S, Zheng L, Dai J, Zhao J, Wang H, Guo Y:
Development of novel tetravalent anti-CD20 antibodies with potent antitumor activity.
Cancer Res
; 2008 Apr 1;68(7):2400-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Despite the effectiveness of the anti-CD20 monoclonal antibody (mAb) Rituximab (C2B8) in the treatment of B-
cell lymphoma
, its efficacy remains variable and often modest.
Unfortunately, all the current anti-CD20 mAbs effective in CDC are relatively inactive in signaling
cell
death and vice versa.
TetraMcAbs, with a molecular mass only 25 kDa higher than native divalent antibodies (DiMcAb), were shown not only to be as effective in mediating CDC and antibody-dependent cellular cytotoxicity against B-
lymphoma
cells
as DiMcAbs but also to have antiproliferative and apoptosis-inducing activity markedly superior to that of DiMcAbs.
Interestingly, whereas 2F2 and C2B8 were equally effective in inducing
cell
growth arrest and apoptosis, the functions of their tetravalent versions, 2F2(ScFvHL)(4)-Fc and C2B8(ScFvHL)(4)-Fc, were significantly different.
Immunotherapeutic studies further showed that 2F2(ScFvHL)(4)-Fc was far more effective in prolonging the survival of severe combined immunodeficient mice bearing systemic Daudi or Raji tumors than C2B8, 2F2, and C2B8(ScFvHL)(4)-Fc, suggesting that it might be a promising therapeutic agent for B-
cell lymphoma
.
[MeSH-major]
Antibodies, Monoclonal / pharmacology. Antigens, CD30 / immunology. Antineoplastic Agents / pharmacology. Burkitt
Lymphoma
/ therapy.
Lymphoma
, B-
Cell
/ therapy
[MeSH-minor]
Animals. Antibodies, Monoclonal, Murine-Derived. CHO
Cells
.
Cell
Line, Tumor. Cricetinae. Cricetulus. Female. Humans.
Lymphoma
, T-
Cell
/ immunology.
Lymphoma
, T-
Cell
/ therapy. Mice. Mice, Inbred BALB C. Mice, Inbred ICR. Mice, SCID. Rituximab. Xenograft Model Antitumor Assays
Hazardous Substances Data Bank.
RITUXIMAB
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18381448.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD30; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
56.
Ci W, Polo JM, Melnick A:
B-cell lymphoma 6 and the molecular pathogenesis of diffuse large B-cell lymphoma.
Curr Opin Hematol
; 2008 Jul;15(4):381-90
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
B-
cell lymphoma
6 and the molecular pathogenesis of diffuse large B-
cell lymphoma
.
PURPOSE OF REVIEW: The B-
cell lymphoma
6 transcriptional repressor is the most commonly involved oncogene in B-
cell
lymphomas
.
Sustained expression of B-
cell lymphoma
6 causes
malignant
transformation of germinal center B
cells
.
Understanding the mechanism of action of B-
cell lymphoma
6 is crucial for the study of how aberrant transcriptional programming leads to lymphomagenesis and development of targeted antilymphoma therapy.
RECENT FINDINGS: Identification of B-
cell lymphoma
6 target genes indicates a critical role for B-
cell lymphoma
6 in facilitating a state of physiological genomic instability required for germinal center B
cells
to undergo affinity maturation, and suggests its contribution to several additional cellular functions.
The discovery of several layers of counterregulatory mechanisms reveals how B
cells
can control and fine-tune the potentially lymphomagenic actions of B-
cell lymphoma
6.
From the biochemical standpoint, B-
cell lymphoma
6 can regulate distinct biological pathways through different cofactors.
This observation explains how the biological actions of B-
cell lymphoma
6 can be physiologically controlled through separate mechanisms and affords the means for improved therapeutic targeting.
The fact that patients with B-
cell lymphoma
6-dependent
lymphoma
can be identified on the basis of gene signatures suggests that therapeutic trials of B-
cell lymphoma
6 inhibitors could be personalized to these individuals.
SUMMARY: B-
cell lymphoma
6 plays a fundamental role in lymphomagenesis and is an excellent therapeutic target for development of improved antilymphoma therapeutic regimens.
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nature. 2004 Dec 2;432(7017):635-9
[
15577913.001
]
[Cites]
Blood Cells Mol Dis. 2008 Jul-Aug;41(1):95-9
[
18346918.001
]
[Cites]
Nat Med. 2004 Dec;10(12):1329-35
[
15531890.001
]
[Cites]
J Immunol. 2005 Jan 1;174(1):205-14
[
15611242.001
]
[Cites]
Clin Cancer Res. 2005 Jan 1;11(1):28-40
[
15671525.001
]
[Cites]
Blood. 2005 Mar 1;105(5):1851-61
[
15550490.001
]
[Cites]
Cancer Cell. 2005 May;7(5):445-55
[
15894265.001
]
[Cites]
Nat Immunol. 2005 Oct;6(10):1054-60
[
16142238.001
]
[Cites]
Mol Immunol. 2006 May;43(12):1965-71
[
16423395.001
]
[Cites]
Oncogene. 2006 Apr 6;25(15):2223-33
[
16331266.001
]
[Cites]
Mol Cell Biol. 2006 Sep;26(18):6880-9
[
16943429.001
]
[Cites]
Oncogene. 2007 Jan 11;26(2):224-33
[
16819511.001
]
[Cites]
Nature. 2000 Feb 3;403(6769):503-11
[
10676951.001
]
[Cites]
Cancer Invest. 2000;18(4):356-65
[
10808372.001
]
[Cites]
Genes Dev. 2000 Jul 15;14(14):1810-23
[
10898795.001
]
[Cites]
J Exp Med. 2000 Dec 18;192(12):1841-8
[
11120780.001
]
[Cites]
Nat Immunol. 2000 Sep;1(3):214-20
[
10973278.001
]
[Cites]
Nature. 2001 Jul 19;412(6844):341-6
[
11460166.001
]
[Cites]
Science. 2007 Jan 26;315(5811):528-31
[
17185562.001
]
[Cites]
Mol Cell. 2003 Dec;12(6):1551-64
[
14690607.001
]
[Cites]
Blood. 2004 Feb 15;103(4):1454-63
[
14551142.001
]
[Cites]
J Immunol. 2004 Jul 15;173(2):1158-65
[
15240705.001
]
[Cites]
Cell. 2004 Oct 1;119(1):75-86
[
15454082.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14198-203
[
15375218.001
]
[Cites]
Blood. 1996 Jun 15;87(12):5257-68
[
8652841.001
]
[Cites]
Science. 1997 Apr 25;276(5312):589-92
[
9110977.001
]
[Cites]
Nat Genet. 1997 Jun;16(2):161-70
[
9171827.001
]
[Cites]
Nature. 2007 Mar 1;446(7131):83-7
[
17268470.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3207-12
[
17360630.001
]
[Cites]
J Exp Med. 2007 Apr 16;204(4):819-30
[
17403935.001
]
[Cites]
Mol Cell Proteomics. 2007 May;6(5):820-34
[
17296600.001
]
[Cites]
Nat Immunol. 2007 Jul;8(7):705-14
[
17558410.001
]
[Cites]
Oncogene. 2007 Aug 13;26(37):5439-49
[
17694085.001
]
[Cites]
J Pathol. 2007 Sep;213(1):106-15
[
17573669.001
]
[Cites]
Blood. 2007 Sep 15;110(6):2067-74
[
17545502.001
]
[Cites]
Cancer Cell. 2007 Sep;12(3):280-92
[
17785208.001
]
[Cites]
Nat Immunol. 2007 Oct;8(10):1132-9
[
17828269.001
]
[Cites]
Eur J Cell Biol. 2007 Oct;86(10):581-9
[
17651861.001
]
[Cites]
Leukemia. 2007 Nov;21(11):2332-43
[
17625604.001
]
[Cites]
Nat Genet. 2008 Jan;40(1):108-12
[
18066064.001
]
[Cites]
Blood. 2008 Feb 1;111(3):1515-23
[
17951530.001
]
[Cites]
J Pathol. 2008 Mar;214(4):498-507
[
18189332.001
]
[Cites]
Nature. 2008 Feb 14;451(7180):841-5
[
18273020.001
]
[Cites]
Mol Cell. 2008 Feb 15;29(3):384-91
[
18280243.001
]
[Cites]
Mol Cell Biol. 2008 Apr;28(7):2175-86
[
18212045.001
]
[Cites]
Blood. 2008 Apr 1;111(7):3701-13
[
18160665.001
]
[Cites]
Cancer Res. 2008 May 1;68(9):3361-9
[
18451163.001
]
[Cites]
Leuk Lymphoma. 2008 May;49(5):874-82
[
18452090.001
]
[Cites]
Blood. 2004 Dec 15;104(13):4088-96
[
15331443.001
]
(PMID = 18536578.001).
[ISSN]
1531-7048
[Journal-full-title]
Current opinion in hematology
[ISO-abbreviation]
Curr. Opin. Hematol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA104348-05; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / R01 CA104348-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Proto-Oncogene Proteins c-bcl-6
[Number-of-references]
51
[Other-IDs]
NLM/ NIHMS126312; NLM/ PMC2748732
57.
Benmiloud S, Steffens M, Beauloye V, de Wandeleer A, Devogelaer JP, Brichard B, Vermylen C, Maiter D:
Long-term effects on bone mineral density of different therapeutic schemes for acute lymphoblastic leukemia or non-Hodgkin lymphoma during childhood.
Horm Res Paediatr
; 2010;74(4):241-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Long-term effects on bone mineral density of different therapeutic schemes for acute lymphoblastic leukemia or
non
-
Hodgkin lymphoma
during childhood.
METHODS: Bone mineral density (BMD) was evaluated at lumbar spine (LS), total hip and femoral neck in 89 patients (44 men) more than 5 years after remission of childhood acute lymphoblastic leukemia (ALL) or
non
-
Hodgkin lymphoma
(NHL).
A multivariate analysis showed independent significant influences of male gender at LS (p < 0.001) and of
type
of treatment and dexamethasone at the hip (p < 0.05).
[MeSH-major]
Antineoplastic Agents / adverse effects. Bone Density / drug effects. Bone Density / radiation effects.
Lymphoma
,
Non
-
Hodgkin
/ therapy. Precursor
Cell
Lymphoblastic Leukemia-
Lymphoma
/ therapy
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia, Childhood
.
Genetic Alliance.
consumer health - Acute Non Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
Genetic Alliance.
consumer health - Hodgkin lymphoma, childhood
.
Genetic Alliance.
consumer health - Lymphoblastic lymphoma
.
Genetic Alliance.
consumer health - Non-Hodgkin lymphoma, childhood
.
Genetic Alliance.
consumer health - Non-Hodgkin Lymphoma
.
MedlinePlus Health Information.
consumer health - Bone Density
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
METHYLPREDNISOLONE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 S. Karger AG, Basel.
(PMID = 20395671.001).
[ISSN]
1663-2826
[Journal-full-title]
Hormone research in pædiatrics
[ISO-abbreviation]
Horm Res Paediatr
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone; X4W7ZR7023 / Methylprednisolone
58.
Roullet MR, Bagg A:
Recent insights into the biology of Hodgkin lymphoma: unraveling the mysteries of the Reed-Sternberg cell.
Expert Rev Mol Diagn
; 2007 Nov;7(6):805-20
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Recent insights into the biology of
Hodgkin lymphoma
: unraveling the mysteries of the Reed-Sternberg
cell
.
The microscopic pathology of
Hodgkin lymphoma
has been recognized for well over a century; however, only in the past 15 years has the enigmatic nature of this peculiar
neoplasm
been somewhat unraveled.
This has been accomplished via a combination of the acquisition, via microdissection, of the prototypically rare
malignant cells
and their subsequent analysis via a variety of modalities, including genomic studies and expression profiling.
This has facilitated the elucidation of the surreptitiously concealed B-
cell
origin of the
cells
, their complex but vital relationships with the surrounding micro- and macroenvironment, as well as multiple pathways involved in the pathobiology of this
lymphoma
.
[MeSH-major]
Hodgkin
Disease
. Reed-Sternberg
Cells
/ physiology
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
MedlinePlus Health Information.
consumer health - Hodgkin Disease
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18020910.001).
[ISSN]
1744-8352
[Journal-full-title]
Expert review of molecular diagnostics
[ISO-abbreviation]
Expert Rev. Mol. Diagn.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / NF-kappa B
[Number-of-references]
164
59.
Nemet AY, Deckel Y, Kourt G:
Orbital invasion of frontal sinus lymphoma.
Orbit
; 2006 Jun;25(2):149-51
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Orbital invasion of frontal sinus
lymphoma
.
Paranasal sinus
lymphoma
is an uncommon malignancy and is often difficult to diagnose.
Early
diagnosis
is essential for effective treatment.
Ophthalmological symptoms and signs occur early in the
disease
process due to the close proximity of the orbit to the paranasal sinuses.
We report a case of frontal sinus
lymphoma
that presented as a superior-nasal orbital mass in an 84 year old man.
Histology revealed diffuse large
B cell non Hodgkin
's
lymphoma
.
[MeSH-major]
Frontal Sinus / pathology.
Lymphoma
, B-
Cell
/ pathology.
Lymphoma
, Large B-
Cell
, Diffuse / pathology. Orbit / pathology. Paranasal Sinus Neoplasms / pathology
[MeSH-minor]
Aged, 80 and over. Humans. Male.
Neoplasm
Invasiveness
Genetic Alliance.
consumer health - Orbital lymphoma
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16754228.001).
[ISSN]
0167-6830
[Journal-full-title]
Orbit (Amsterdam, Netherlands)
[ISO-abbreviation]
Orbit
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
60.
Walls KC, Ghosh AP, Ballestas ME, Klocke BJ, Roth KA:
bcl-2/Adenovirus E1B 19-kd interacting protein 3 (BNIP3) regulates hypoxia-induced neural precursor cell death.
J Neuropathol Exp Neurol
; 2009 Dec;68(12):1326-38
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
bcl
-2/Adenovirus E1B 19-kd interacting protein 3 (BNIP3) regulates hypoxia-induced neural precursor
cell
death.
In addition to producing neuron death, HI causes death of neural precursor
cells
(NPCs) in the developing brain.
To characterize the molecular pathways that regulate hypoxia-induced death of NPCs, we treated a mouse neural stem
cell
line (C17.2
cells
) and fibroblastic growth factor II-expanded primary NPCs derived from wild-
type
or gene-disrupted mice, with oxygen glucose deprivation or the hypoxia mimetics desferrioxamine or cobalt chloride.
Neural precursor
cells
undergoing hypoxia exhibited time- and concentration-dependent caspase-3 activation and
cell
death, which was significantly reduced by treatment with a broad caspase inhibitor or protein synthesis inhibition.
Oxygen glucose deprivation or hypoxia-mimetic exposure also resulted in increased hypoxia-inducible factor alpha and
bcl
-2/adenovirus E1B 19-kd interacting protein 3 (BNIP3) expression.
BNIP3 shRNA treatment failed to affect hypoxia-induced caspase-3 activation but inhibited
cell
death and nuclear translocation of apoptosis-inducing factor, indicating that BNIP3 is an important regulator of caspase-independent NPC death after hypoxia.
These studies demonstrate that hypoxia activates both caspase-dependent and -independent NPC death pathways that are critically regulated by multiple
Bcl
-2 family members.
MedlinePlus Health Information.
consumer health - Stem Cells
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Biol Chem. 1999 Nov 12;274(46):32631-7
[
10551817.001
]
[Cites]
Am J Physiol Heart Circ Physiol. 2008 Nov;295(5):H2025-31
[
18790835.001
]
[Cites]
Mol Cell Biol. 2000 Aug;20(15):5454-68
[
10891486.001
]
[Cites]
FEBS Lett. 2001 Feb 23;491(1-2):85-90
[
11226425.001
]
[Cites]
Science. 2001 Apr 20;292(5516):464-8
[
11292862.001
]
[Cites]
Science. 2001 Apr 20;292(5516):468-72
[
11292861.001
]
[Cites]
EMBO Rep. 2001 Jul;2(7):615-20
[
11454738.001
]
[Cites]
Cell. 2001 Oct 5;107(1):43-54
[
11595184.001
]
[Cites]
Science. 2004 Feb 13;303(5660):1010-4
[
14963330.001
]
[Cites]
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):189-203
[
14996503.001
]
[Cites]
Cancer Res. 2004 Jun 15;64(12):4286-93
[
15205343.001
]
[Cites]
Anat Embryol (Berl). 1990;181(3):195-213
[
2186664.001
]
[Cites]
Cell. 1992 Jan 10;68(1):33-51
[
1732063.001
]
[Cites]
Science. 1995 Oct 6;270(5233):96-9
[
7569956.001
]
[Cites]
Nature. 1998 Mar 26;392(6674):405-8
[
9537326.001
]
[Cites]
J Biol Chem. 1999 Jan 1;274(1):7-10
[
9867803.001
]
[Cites]
Cancer Cell. 2004 Dec;6(6):597-609
[
15607964.001
]
[Cites]
Neuroscience. 2005;131(1):55-65
[
15680691.001
]
[Cites]
Oncogene. 2005 Feb 3;24(6):980-91
[
15592527.001
]
[Cites]
FASEB J. 2005 Aug;19(10):1308-10
[
15941769.001
]
[Cites]
Cell. 2005 Sep 23;122(6):927-39
[
16179260.001
]
[Cites]
Apoptosis. 2006 Jan;11(1):67-77
[
16374551.001
]
[Cites]
Cell Death Differ. 2006 Oct;13(10):1727-39
[
16514420.001
]
[Cites]
J Neuropathol Exp Neurol. 2007 Jan;66(1):66-74
[
17204938.001
]
[Cites]
Cell Death Differ. 2007 Apr;14(4):775-84
[
17039248.001
]
[Cites]
Cell Biochem Biophys. 2007;47(1):11-20
[
17406056.001
]
[Cites]
Stroke. 2007 May;38(5):1606-13
[
17379825.001
]
[Cites]
Free Radic Biol Med. 2007 Jul 1;43(1):117-27
[
17561100.001
]
[Cites]
Biochem J. 2007 Aug 1;405(3):407-15
[
17447897.001
]
[Cites]
J Exp Med. 2007 Aug 6;204(8):1741-8
[
17635954.001
]
[Cites]
Mol Cell Biol. 2007 Sep;27(17):6229-42
[
17576813.001
]
[Cites]
J Clin Invest. 2007 Oct;117(10):2825-33
[
17909626.001
]
[Cites]
Autophagy. 2007 Nov-Dec;3(6):616-9
[
17786027.001
]
[Cites]
J Neurochem. 2007 Nov;103(3):1121-31
[
17711427.001
]
[Cites]
Autophagy. 2008 Feb;4(2):195-204
[
18059169.001
]
[Cites]
J Biol Chem. 2008 Apr 18;283(16):10892-903
[
18281291.001
]
[Cites]
FASEB J. 2008 Aug;22(8):2662-75
[
18375543.001
]
[Cites]
J Biol Chem. 2000 Jan 14;275(2):1439-48
[
10625696.001
]
(PMID = 19915483.001).
[ISSN]
1554-6578
[Journal-full-title]
Journal of neuropathology and experimental neurology
[ISO-abbreviation]
J. Neuropathol. Exp. Neurol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / P30 NS047466; United States / NINDS NIH HHS / NS / NS047466-05; United States / NINDS NIH HHS / NS / R01 NS035107-11; United States / NINDS NIH HHS / NS / R01 NS041962; United States / NINDS NIH HHS / NS / P30 NS057098; United States / NINDS NIH HHS / NS / P30 NS047466-05; United States / NINDS NIH HHS / NS / R01 NS041962-06; United States / NINDS NIH HHS / NS / NS57098; United States / NINDS NIH HHS / NS / R01 NS035107; United States / NINDS NIH HHS / NS / NS057098-04; United States / NINDS NIH HHS / NS / NS35107; United States / NINDS NIH HHS / NS / NS035107-11; United States / NINDS NIH HHS / NS / NS47466; United States / NINDS NIH HHS / NS / NS41962; United States / NINDS NIH HHS / NS / NS041962-06; United States / NINDS NIH HHS / NS / P30 NS057098-04
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / BNip3 protein, mouse; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Mitochondrial Proteins; EC 3.4.22.- / Caspase 3
[Other-IDs]
NLM/ NIHMS161285; NLM/ PMC2791349
61.
Vose JM, Bierman PJ, Loberiza FR, Lynch JC, Bociek GR, Weisenburger DD, Armitage JO:
Long-term outcomes of autologous stem cell transplantation for follicular non-Hodgkin lymphoma: effect of histological grade and Follicular International Prognostic Index.
Biol Blood Marrow Transplant
; 2008 Jan;14(1):36-42
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Long-term outcomes of autologous stem
cell
transplantation for follicular
non
-
Hodgkin lymphoma
: effect of histological grade and Follicular International Prognostic Index.
Although results of autologous stem
cell
transplantation (SCT) for recurrent follicular
non
-
Hodgkin lymphoma
(NHL) have been previously reported, the long-term results and evaluation of prognostic factors in a large patient population receiving this therapy are difficult to find in the literature.
At the time of transplantation, 88 of the patients (35%) had a Follicular
Lymphoma
International Prognostic Index (FLIPI) score of low risk, 87 (35%) had an intermediate-risk FLIPI score, 37 (15%) had a high-risk FLIPI score, and 36 (15%) had at least 1 missing value, preventing calculation of the FLIPI score.
In addition, the use of a transplantation regimen including a monoclonal antibody decreased the relative risk of progressive
lymphoma
.
These data suggest that transplantation earlier in the course of the
disease
for patients with follicular
lymphoma
with use of a monoclonal antibody-based regimen may lead to improved outcomes.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem
Cell
Transplantation / adverse effects. Hematopoietic Stem
Cell
Transplantation / methods.
Lymphoma
, Follicular / therapy. Severity of Illness Index
[MeSH-minor]
Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / adverse effects. Combined Modality Therapy / methods.
Disease
-Free Survival. Female. Humans. Longitudinal Studies. Male. Middle Aged. Risk Assessment. Transplantation Conditioning / adverse effects. Transplantation Conditioning / methods. Transplantation, Autologous / adverse effects. Transplantation, Autologous / methods. Treatment Outcome. Whole-Body Irradiation / adverse effects
Genetic Alliance.
consumer health - Follicular Lymphoma
.
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
Genetic Alliance.
consumer health - Transplantation
.
Genetic Alliance.
consumer health - Non-Hodgkin Lymphoma
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18158959.001).
[ISSN]
1523-6536
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal
62.
Henrich M, Hecht W, Weiss AT, Reinacher M:
A new subgroup of immunoglobulin heavy chain variable region genes for the assessment of clonality in feline B-cell lymphomas.
Vet Immunol Immunopathol
; 2009 Jul 15;130(1-2):59-69
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A new subgroup of immunoglobulin heavy chain variable region genes for the assessment of clonality in feline B-
cell
lymphomas
.
In human medicine, PCR-amplification of the complementarity determining region 3 of the immunoglobulin heavy chain genes followed by polyacrylamide gel electrophoresis (PAGE) is an accepted method to assess clonality in B-
cell
lymphomas
and thereby facilitates the differentiation of neoplasias from benign hyperplasias or reactive infiltrates.
To generate a basis for the development of a PCR-based assay for the assessment of clonality in feline B-
cell
lymphomas
we analyzed 28 transcripts (cDNA) of the feline immunoglobulin heavy chain variable region genes (IGHV).
With these four sets of primers, the assay was able to detect monoclonality in 7/10 (70%) cats with histologically and immunohistochemically diagnosed B-
cell
lymphomas
.
The use of a PCR-based assay in combination with standard techniques for the
diagnosis
of feline
lymphoma
is helpful and the characterization of the additional subgroup of feline variable regions genes puts this assay on a broader basis.
[MeSH-major]
Cat Diseases / immunology. Cat Diseases / pathology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics.
Lymphoma
, B-
Cell
/ veterinary
[MeSH-minor]
Amino Acid Sequence. Animals. Cats. Clone
Cells
. Molecular Sequence Data. Plasmids / genetics. RNA,
Neoplasm
/ chemistry. RNA,
Neoplasm
/ genetics. Random Amplified Polymorphic DNA Technique / veterinary. Sequence Alignment. Sequence Analysis, DNA
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19243841.001).
[ISSN]
1873-2534
[Journal-full-title]
Veterinary immunology and immunopathology
[ISO-abbreviation]
Vet. Immunol. Immunopathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / RNA, Neoplasm
63.
Tsukahara S, Yamamoto S, Tin-Tin-Win-Shwe, Ahmed S, Kunugita N, Arashidani K, Fujimaki H:
Inhalation of low-level formaldehyde increases the Bcl-2/Bax expression ratio in the hippocampus of immunologically sensitized mice.
Neuroimmunomodulation
; 2006;13(2):63-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Inhalation of low-level formaldehyde increases the
Bcl
-2/Bax expression ratio in the hippocampus of immunologically sensitized mice.
In the present study, we examined the effects of FA on apoptotic mechanisms regulating survival and death of
cells
and on N-methyl-D-aspartate (NMDA) receptors related to hippocampal functions in the mouse hippocampus.
METHODS: Western blot analyses were performed for
Bcl
-2, Bax and NMDA receptor subtypes 2A and 2B of the hippocampus taken from C3H mice exposed to 0 or 400 ppb of FA with or without ovalbumin (OVA) immunization.
RESULTS: The ratio of
Bcl
-2 to Bax expression levels significantly increased with 400-ppb FA exposure in OVA-immunized mice but not in mice without OVA immunization, although differences in each protein level were not significant among groups.
Active caspase- 3-immunoreactive
cells
were found in the hippocampus.
NMDA receptor
type
2A and 2B expression levels of FA-exposed mice were sustained at comparative levels with those for the control mice with or without OVA immunization.
CONCLUSIONS: These results indicate that changes in the
Bcl
-2/Bax expression ratio, which occurs with low-level FA exposure and immunization and may follow enhancement of nerve growth factor production, exerts a protective effect against
cell
death by apoptosis.
[MeSH-minor]
Animals. Caspase 3 / drug effects. Caspase 3 / metabolism.
Cell
Survival / drug effects.
Cell
Survival / immunology. Female. Immunization. Mice. Mice, Inbred C3H. Neurotoxins / toxicity. Ovalbumin / immunology. Proto-Oncogene Proteins c-
bcl
-2 / drug effects. Proto-Oncogene Proteins c-
bcl
-2 / metabolism. Receptors, N-Methyl-D-Aspartate / drug effects. Receptors, N-Methyl-D-Aspartate / metabolism. Up-Regulation / drug effects. Up-Regulation / immunology.
bcl
-2-Associated X Protein / drug effects.
bcl
-2-Associated X Protein / metabolism
Hazardous Substances Data Bank.
FORMALDEHYDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16888403.001).
[ISSN]
1021-7401
[Journal-full-title]
Neuroimmunomodulation
[ISO-abbreviation]
Neuroimmunomodulation
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / N-methyl D-aspartate receptor subtype 2A; 0 / NR2B NMDA receptor; 0 / Neurotoxins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, N-Methyl-D-Aspartate; 0 / bcl-2-Associated X Protein; 1HG84L3525 / Formaldehyde; 9006-59-1 / Ovalbumin; 9061-61-4 / Nerve Growth Factor; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3
64.
Bremer E, ten Cate B, Samplonius DF, Mueller N, Wajant H, Stel AJ, Chamuleau M, van de Loosdrecht AA, Stieglmaier J, Fey GH, Helfrich W:
Superior activity of fusion protein scFvRit:sFasL over cotreatment with rituximab and Fas agonists.
Cancer Res
; 2008 Jan 15;68(2):597-604
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The
clinical
efficacy of the CD20-specific chimeric monoclonal antibody rituximab is significantly hampered by intrinsic or acquired resistance to therapy.
The resultant fusion protein, designated scFvRit:sFasL, potently induced CD20-restricted apoptosis in a panel of
malignant
B-
cell
lines (10 of 11) and primary patient-derived
malignant
B
cells
(two of two
non
-
Hodgkin lymphoma
and five of six
B cell
chronic
lymphocytic
leukemia).
ScFvRit:sFasL lacked activity toward normal human B
cells
and also lacked systemic toxicity in nude mice with no elevation of aspartate aminotransferase and alanine aminotransferase levels or liver caspase-3 activity.
In conclusion, scFvRit:sFasL efficiently activates CD20 and Fas-apoptotic signaling and may be useful for the elimination of
malignant
B
cells
.
[MeSH-major]
Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fas Ligand Protein / agonists. Genetic Therapy. Leukemia,
Lymphocytic
, Chronic, B-
Cell
/ therapy.
Lymphoma
,
Non
-
Hodgkin
/ therapy. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / therapeutic use
[MeSH-minor]
Animals. Antibodies, Monoclonal, Murine-Derived. Apoptosis / drug effects. Apoptosis / genetics. B-Lymphocytes / drug effects. CHO
Cells
. Cricetinae. Cricetulus. Female. Humans. Male. Rituximab. Signal Transduction / drug effects. Signal Transduction / genetics. Single-Chain Antibodies. Tumor
Cells
, Cultured
MedlinePlus Health Information.
consumer health - Genes and Gene Therapy
.
Hazardous Substances Data Bank.
RITUXIMAB
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18199557.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Recombinant Fusion Proteins; 0 / Single-Chain Antibodies; 0 / scFvRit-sFasL protein, human; 4F4X42SYQ6 / Rituximab
65.
Weng Y, Gao ZF, Liu K, Zhang WJ, Ke XY, Li M:
[Factors affecting the prognosis of diffuse large B-cell lymphoma in Chinese].
Zhonghua Nei Ke Za Zhi
; 2005 Sep;44(9):681-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Factors affecting the prognosis of diffuse large B-
cell lymphoma
in Chinese].
OBJECTIVE: To study the correlation between
clinical
prognosis and clinicopathologic features, origin and
cell
proliferous index of diffuse large B-
cell lymphoma
(DLBCL) in China.
Immunohistochemistry stain was used to check the expression of CD(45)RO, CD(3), CD(20), CD(79)a, CD(45)RA, Ki-67, p53 and
bcl
-6.
23 patients 38.3% died during follow-up, the longest survival period lasting 108 months.16 died in the first year after establishment of
diagnosis
(16/23, 69.6%).
Ki-67, p53,
bcl
-6 were expressed in some cases (48/53, 90.6%; 26/46, 56.5%; 21/41, 51.2%).
The expression of
bcl
-6 protein was somewhat related with prognosis (P = 0.0049), but the expression of p53 was not (P = 0.5948).
Most of the cases died in the first year after establishment of
diagnosis
.
IPI can be used to predict the
clinical
outcome.
The expression of
bcl
-6 protein was somewhat related with
clinical
prognosis, but that of p53 was not.
[MeSH-major]
Lymphoma
, Large B-
Cell
, Diffuse / pathology
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over.
Cell
Proliferation. Child. China. DNA-Binding Proteins / metabolism. Female. Follow-Up Studies. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Tumor Suppressor Protein p53 / metabolism
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16202261.001).
[ISSN]
0578-1426
[Journal-full-title]
Zhonghua nei ke za zhi
[ISO-abbreviation]
Zhonghua Nei Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
66.
Yun SJ, Lee KH, Yang DW, Lee JB, Kim SJ, Lee SC, Won YH:
Primary cutaneous spindle cell B-cell lymphoma with multiple figurate erythema-like manifestation.
J Cutan Pathol
; 2009 Jan;36(1):49-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Primary cutaneous spindle
cell B
-
cell lymphoma
with multiple figurate erythema-like manifestation.
Spindle-shaped
cells
with elongated, twisted nuclei containing dispersed chromatin were also seen.
Immunohistochemical analysis showed that all of the
cells
were strongly positive for CD20, CD21, CD79a and CD45, while they were negative for CD3, CD5, CD10, CD23, CD35, CD43, CD45RO and CD68.
The spindle
cells
were also negative for smooth-muscle actin, desmin, S-100 and CD34.
They consistently expressed nuclear
bcl
-6, but did not express
bcl
-2, multiple myeloma-1 and p16.
We diagnosed him with primary cutaneous spindle
cell B
-
cell lymphoma
(PCSBCL) and treated him with six cycles of cyclophosphamide, adriamycin, vincristine, prednisone and rituximab (R-CHOP) chemotherapy; his skin lesions disappeared completely.
Immunohistochemical profiles suggest that PCSBCL is a variant of primary cutaneous follicle center
lymphoma
.
[MeSH-major]
Lymphoma
, Large B-
Cell
, Diffuse / pathology. Skin Neoplasms / pathology
MedlinePlus Health Information.
consumer health - Skin Cancer
.
Hazardous Substances Data Bank.
RITUXIMAB
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19125734.001).
[ISSN]
1600-0560
[Journal-full-title]
Journal of cutaneous pathology
[ISO-abbreviation]
J. Cutan. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone
67.
Rohde G, Kermer P, Reed JC, Bähr M, Weishaupt JH:
Neuron-specific overexpression of the co-chaperone Bcl-2-associated athanogene-1 in superoxide dismutase 1(G93A)-transgenic mice.
Neuroscience
; 2008 Dec 10;157(4):844-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Neuron-specific overexpression of the co-chaperone
Bcl
-2-associated athanogene-1 in superoxide dismutase 1(G93A)-transgenic mice.
Bcl
-2-associated athanogene-1 (BAG1) binds heat-shock protein 70 (Hsp70)/Hsc70, increases intracellular chaperone activity in neurons and proved to be protective in several models for neurodegeneration.
Moreover, expression of mtSOD1 decreases BAG1 levels in a motoneuronal
cell
line.
[MeSH-minor]
Age Factors. Amyotrophic Lateral Sclerosis / genetics. Amyotrophic Lateral Sclerosis / metabolism. Amyotrophic Lateral Sclerosis / mortality. Amyotrophic Lateral Sclerosis / pathology. Animals.
Disease
Models, Animal. Humans. Mice. Mice, Transgenic. Motor Activity / genetics. Phosphopyruvate Hydratase / metabolism. Proto-Oncogene Proteins c-
bcl
-2 / genetics. Proto-Oncogene Proteins c-
bcl
-2 / metabolism. Spinal Cord / pathology. Survival Analysis
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18955116.001).
[ISSN]
0306-4522
[Journal-full-title]
Neuroscience
[ISO-abbreviation]
Neuroscience
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / BCL2-associated athanogene 1 protein; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; EC 1.15.1.- / SOD1 G93A protein; EC 1.15.1.1 / Superoxide Dismutase; EC 4.2.1.11 / Phosphopyruvate Hydratase
68.
Cho DG, Cho KD, Jo MS:
Thoracoscopic direct suture repair of thoracic duct injury after thoracoscopic mediastinal surgery.
Surg Laparosc Endosc Percutan Tech
; 2007 Feb;17(1):60-1
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
We report herein a case of postoperative chylothorax managed successfully by early thoracoscopic direct suture repair of the site of chylous leak that developed after the thoracoscopic resection of mediastinal mass and surrounding fat with ectopic thymus in a patient with persistent myasthenia gravis with
non
-
Hodgkin lymphoma
.
[MeSH-major]
Lymphoma
, B-
Cell
/ surgery. Mediastinal Neoplasms / surgery. Suture Techniques. Thoracic Duct / injuries. Thoracoscopy
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17318061.001).
[ISSN]
1530-4515
[Journal-full-title]
Surgical laparoscopy, endoscopy & percutaneous techniques
[ISO-abbreviation]
Surg Laparosc Endosc Percutan Tech
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
69.
Senff NJ, Noordijk EM, Kim YH, Bagot M, Berti E, Cerroni L, Dummer R, Duvic M, Hoppe RT, Pimpinelli N, Rosen ST, Vermeer MH, Whittaker S, Willemze R, European Organization for Research and Treatment of Cancer, International Society for Cutaneous Lymphoma:
European Organization for Research and Treatment of Cancer and International Society for Cutaneous Lymphoma consensus recommendations for the management of cutaneous B-cell lymphomas.
Blood
; 2008 Sep 1;112(5):1600-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
European Organization for Research and Treatment of Cancer and International Society for Cutaneous
Lymphoma
consensus recommendations for the management of cutaneous B-
cell
lymphomas
.
Primary cutaneous B-
cell
lymphomas
(CBCL) represent approximately 20% to 25% of all primary cutaneous
lymphomas
.
With the advent of the World Health Organization-European Organization for Research and Treatment of Cancer (EORTC) Consensus Classification for Cutaneous
Lymphomas
in 2005, uniform terminology and classification for this rare group of neoplasms were introduced.
However, staging procedures and treatment strategies still vary between different cutaneous
lymphoma
centers, which may be because consensus recommendations for the management of CBCL have never been published.
Based on an extensive literature search and discussions within the EORTC Cutaneous
Lymphoma
Group and the International Society for Cutaneous
Lymphomas
, the present report aims to provide uniform recommendations for the management of the 3 main groups of CBCL.
Despite these limitations, there was consensus among the members of the multidisciplinary expert panel that these recommendations reflect the state-of-the-art management as currently practiced in major cutaneous
lymphoma
centers.
They may therefore contribute to uniform staging and treatment and form the basis for future
clinical
trials in patients with a CBCL.
[MeSH-major]
Lymphoma
, B-
Cell
/ therapy. Skin Neoplasms / therapy
[MeSH-minor]
Anti-Bacterial Agents / therapeutic use. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / therapeutic use. Humans. Interferon
Type
I / administration & dosage. Lyme
Disease
/ complications. Lyme
Disease
/ drug therapy.
Lymphoma
, B-
Cell
, Marginal Zone /
diagnosis
.
Lymphoma
, B-
Cell
, Marginal Zone / pathology.
Lymphoma
, B-
Cell
, Marginal Zone / therapy.
Lymphoma
, Large B-
Cell
, Diffuse /
diagnosis
.
Lymphoma
, Large B-
Cell
, Diffuse / pathology.
Lymphoma
, Large B-
Cell
, Diffuse / therapy.
Neoplasm
Staging / methods. Radiotherapy Dosage. Recombinant Proteins. Rituximab
Genetic Alliance.
consumer health - Cutaneous B-Cell Lymphomas
.
Genetic Alliance.
consumer health - B-Cell Lymphomas
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
RITUXIMAB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18567836.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Practice Guideline; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Interferon Type I; 0 / Recombinant Proteins; 4F4X42SYQ6 / Rituximab
[Number-of-references]
123
70.
Bernstein SH, Burack WR:
The incidence, natural history, biology, and treatment of transformed lymphomas.
Hematology Am Soc Hematol Educ Program
; 2009;:532-41
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The incidence, natural history, biology, and treatment of transformed
lymphomas
.
Treatment of patients with transformed
lymphoma
presents a significant challenge to the practicing physician.
Indeed, the transformation of follicular
lymphoma
to a more aggressive histology is inherent to the biology of this
disease
and is often associated with an aggressive
clinical
course, resulting in a poor prognosis.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20008238.001).
[ISSN]
1520-4383
[Journal-full-title]
Hematology. American Society of Hematology. Education Program
[ISO-abbreviation]
Hematology Am Soc Hematol Educ Program
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
57
71.
Arnaoutakis K, Oo TH:
Bronchus-associated lymphoid tissue lymphomas.
South Med J
; 2009 Dec;102(12):1229-33
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bronchus-associated lymphoid tissue
lymphomas
.
BACKGROUND: : Bronchus-associated Lymphoid Tissue (BALT)
lymphomas
are a rare
type
of extranodal marginal zone
lymphomas
.
They comprise 1% of
lymphomas
and more than two-thirds of all primary
non
-
Hodgkin lymphoma
(NHL) of the lung.
BALT
lymphomas
arise from the bronchus-associated lymphoid tissue.
METHODS: This report describes five cases of BALT
lymphoma
and discusses the pathogenesis,
diagnosis
, prognosis and treatment of BALT
lymphomas
.
DISCUSSION: BALT
lymphomas
are associated with chronic inflammation, and they are often asymptomatic.
[MeSH-major]
Bronchial Neoplasms /
diagnosis
. Bronchial Neoplasms / therapy.
Lymphoma
, B-
Cell
, Marginal Zone /
diagnosis
.
Lymphoma
, B-
Cell
, Marginal Zone / therapy
[MeSH-minor]
Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Immunotherapy / methods. Male. Middle Aged.
Neoplasm
Staging. Prognosis. Survival Analysis. Tomography, X-Ray Computed. Treatment Outcome
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20016430.001).
[ISSN]
1541-8243
[Journal-full-title]
Southern medical journal
[ISO-abbreviation]
South. Med. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
72.
Leonard JP, Friedberg JW, Hagemeister FB, Levine AM:
Combination treatment approaches and novel therapies for lymphoma.
Clin Adv Hematol Oncol
; 2007 Aug;5(8 Suppl 12):4-20; quiz 1 p following 20
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Combination treatment approaches and novel therapies for
lymphoma
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Lymphoma
,
Non
-
Hodgkin
/ therapy
[MeSH-minor]
Antibodies, Anti-Idiotypic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Bendamustine Hydrochloride. Boronic Acids / therapeutic use. Bortezomib. Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Cytokines / therapeutic use. Humans. Immunologic Factors / therapeutic use. Nitrogen Mustard Compounds / therapeutic use. Pyrazines / therapeutic use. Rituximab. Stem
Cell
Transplantation
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
Bendamustine
.
Hazardous Substances Data Bank.
RITUXIMAB
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18154235.001).
[ISSN]
1543-0790
[Journal-full-title]
Clinical advances in hematology & oncology : H&O
[ISO-abbreviation]
Clin Adv Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Anti-Idiotypic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Boronic Acids; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Immunologic Factors; 0 / Nitrogen Mustard Compounds; 0 / Pyrazines; 357613-77-5 / galiximab; 4F4X42SYQ6 / Rituximab; 69G8BD63PP / Bortezomib; 981Y8SX18M / Bendamustine Hydrochloride
[Number-of-references]
112
73.
Fuchs O, Provaznikova D, Kocova M, Kostecka A, Cvekova P, Neuwirtova R, Kobylka P, Cermak J, Brezinova J, Schwarz J, Markova J, Salaj P, Klamova H, Maaloufova J, Lemez P, Novakova L, Benesova K:
CEBPA polymorphisms and mutations in patients with acute myeloid leukemia, myelodysplastic syndrome, multiple myeloma and non-Hodgkin's lymphoma.
Blood Cells Mol Dis
; 2008 May-Jun;40(3):401-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
CEBPA polymorphisms and mutations in patients with acute myeloid leukemia, myelodysplastic syndrome, multiple myeloma and
non
-
Hodgkin
's
lymphoma
.
CEBPA mutations were found in 14/152 (9.2%) of acute myeloid leukemia (AML) patients' samples, 6/143 (4.2%) of MDS patients' samples, 2/56 (3.6%) of
non
-
Hodgkin
's
lymphoma
(NHL) patients' samples and 2/39 (5.1%) of multiple myeloma (MM) patients' samples.
No C
/EBPalpha mutations were detected in healthy donors (41 individuals).
[MeSH-major]
CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics.
Lymphoma
,
Non
-
Hodgkin
/ genetics. Multiple Myeloma / genetics. Mutation. Myelodysplastic Syndromes / genetics. Polymorphism, Genetic
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Genetic Alliance.
consumer health - Multiple myeloma
.
Genetic Alliance.
consumer health - Myelodysplastic syndromes
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Multiple Myeloma
.
MedlinePlus Health Information.
consumer health - Myelodysplastic Syndromes
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18182175.001).
[ISSN]
1096-0961
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human
74.
Watanuki J, Hatakeyama K, Sonoki T, Tatetsu H, Yoshida K, Fujii S, Mizutani M, Abo T, Kurimoto M, Matsuoka H, Matsuno F, Nakakuma H:
Bone marrow large B cell lymphoma bearing cyclin D3 expression: clinical, morphologic, immunophenotypic, and genotypic analyses of seven patients.
Int J Hematol
; 2009 Sep;90(2):217-25
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bone marrow large
B cell lymphoma
bearing cyclin D3 expression:
clinical
,
morphologic
, immunophenotypic, and genotypic analyses of seven patients.
We report seven large
B cell lymphoma
patients showing the involvement of tumor
cells
with cyclin D3 (CCND3) expression in bone marrow (BM) at the initial
diagnosis
.
The tumor
cells
were divided into those with a lymphoplasmacytoid or blastoid appearance.
Six cases were confirmed to express CD5 antigen on tumor
cells
.
Further studies are required to determine whether CCND3 expression is associated with a unique subset of diffuse large
B cell lymphoma
.
[MeSH-major]
B-Lymphocytes / physiology. Bone Marrow
Cells
/ physiology. Cyclins / genetics. Genotype.
Lymphoma
, Large B-
Cell
, Diffuse / genetics
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Pathol. 1995 Mar;48(3):189-93
[
7730473.001
]
[Cites]
Br J Haematol. 2000 Dec;111(3):826-34
[
11122144.001
]
[Cites]
Blood. 2002 Feb 1;99(3):815-21
[
11806981.001
]
[Cites]
Blood. 2001 Jul 1;98(1):217-23
[
11418483.001
]
[Cites]
Blood. 2008 Sep 1;112(5):1570-80
[
18725575.001
]
[Cites]
Int J Hematol. 2008 Oct;88(3):299-303
[
18758895.001
]
[Cites]
Int J Hematol. 2008 Dec;88(5):536-42
[
18972186.001
]
[Cites]
Blood. 2003 Oct 15;102(8):3003-9
[
12842981.001
]
[Cites]
N Engl J Med. 2005 Feb 24;352(8):804-15
[
15728813.001
]
[Cites]
J Clin Pathol. 1992 Sep;45(9):770-5
[
1401205.001
]
[Cites]
Blood. 2001 Nov 1;98(9):2837-44
[
11675358.001
]
[Cites]
Br J Haematol. 2007 Feb;136(3):351
[
17233843.001
]
[Cites]
Br J Haematol. 1991 Mar;77(3):301-10
[
2012754.001
]
[Cites]
Am J Clin Pathol. 2007 May;127(5):762-9
[
17439835.001
]
[Cites]
Mt Sinai J Med. 2003 Mar;70(2):133-8
[
12634906.001
]
[Cites]
Int J Cancer. 2007 Nov 15;121(10):2205-11
[
17657714.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13931-6
[
8943038.001
]
[Cites]
Blood. 2008 Jun 15;111(12 ):5683-90
[
18391076.001
]
[Cites]
Rinsho Ketsueki. 2002 Oct;43(10):943-8
[
12462031.001
]
[Cites]
Blood. 2007 Apr 15;109(8):3451-61
[
17170124.001
]
[Cites]
N Engl J Med. 1999 Nov 11;341(20):1520-9
[
10559454.001
]
[Cites]
Nucleic Acids Res. 2006 Jan 1;34(Database issue):D781-4
[
16381979.001
]
[Cites]
Cell. 2000 Sep 1;102(5):553-63
[
11007474.001
]
[Cites]
Br J Haematol. 1999 Aug;106(2):477-85
[
10460609.001
]
[Cites]
Br J Haematol. 1989 Oct;73(2):199-204
[
2479409.001
]
[Cites]
Int J Hematol. 1996 Jan;63(1):71-6
[
8713579.001
]
[Cites]
Clin Cancer Res. 2005 Dec 1;11(23):8265-72
[
16322284.001
]
[Cites]
Nucleic Acids Res. 1997 Sep 1;25(17):3389-402
[
9254694.001
]
[Cites]
J Exp Med. 2007 Mar 19;204(3):633-43
[
17353367.001
]
[Cites]
Leukemia. 2002 May;16(5):937-9
[
11986957.001
]
(PMID = 19639271.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / CCND3 protein, human; 0 / Cyclin D3; 0 / Cyclins
75.
Tari A, Asaoku H, Kashiwado K, Yoshino T, Kitadai Y, Tanaka S, Fujihara M:
Predictive value of endoscopy and endoscopic ultrasonography for regression of gastric diffuse large B-cell lymphomas after Helicobacter pylori eradication.
Dig Endosc
; 2009 Oct;21(4):219-27
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Predictive value of endoscopy and endoscopic ultrasonography for regression of gastric diffuse large B-
cell
lymphomas
after Helicobacter pylori eradication.
BACKGROUND: Some gastric diffuse large B-
cell
lymphomas
have been reported to regress completely after the successful eradication of Helicobacter pylori.
The aim of this study was to investigate the
clinical
characteristics of gastric diffuse large B-
cell
lymphomas
without any detectable mucosa-associated lymphoid tissue (MALT)
lymphoma
that went into complete remission after successful H. pylori eradication.
PATIENTS AND METHODS: We examined the effect of H. pylori eradication in 15 H. pylori-positive gastric diffuse large B-
cell lymphoma
patients without any evidence of an associated MALT
lymphoma
(
clinical
stage I by the Lugano classification) by endoscopic examination including biopsies, endoscopic ultrasonography, computed tomography, and bone marrow aspiration.
RESULTS: H. pylori eradication was successful in all the patients and complete remission was achieved in four patients whose
clinical
stage was I.
CONCLUSION: In gastric diffuse large B-
cell
lymphomas
without a concomitant MALT
lymphoma
but associated with H. pylori infection, only superficial cases and lesions limited to the shallow portion of the submucosa regressed completely after successful H. pylori eradication.
The endoscopic appearance and the rating of the depth of invasion by endosonography are both valuable for predicting the efficacy of H. pylori eradication in treating gastric diffuse large B-
cell
lymphomas
.
[MeSH-major]
Endoscopy. Endosonography. Helicobacter Infections / drug therapy. Helicobacter pylori.
Lymphoma
, Large B-
Cell
, Diffuse /
diagnosis
. Stomach Neoplasms /
diagnosis
Genetic Alliance.
consumer health - B-Cell Lymphomas
.
MedlinePlus Health Information.
consumer health - Endoscopy
.
MedlinePlus Health Information.
consumer health - Helicobacter Pylori Infections
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19961519.001).
[ISSN]
1443-1661
[Journal-full-title]
Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
[ISO-abbreviation]
Dig Endosc
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
[Chemical-registry-number]
0 / Anti-Bacterial Agents
76.
Tuma J:
[CME ultrasound diagnosis. Nodes in the groin. Low malignancy B-cell lymphoma, particularly follicular lymphoma, WHO grade 2].
Praxis (Bern 1994)
; 2008 Aug 27;97(17):957-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[CME ultrasound
diagnosis
. Nodes in the groin. Low malignancy B-
cell lymphoma
, particularly follicular
lymphoma
, WHO grade 2].
[Transliterated title]
CME-Sonographie 23/Auflösung. Knoten in der Leiste. Niedrig malignes
Non
-
Hodgkin
-
Lymphom
der-
Zell
-Reihe, insbesondere follikuläres
Lymphom
, WHO-Grad 2.
[MeSH-major]
Lymphatic Diseases / etiology. Lymphatic Diseases / ultrasonography.
Lymphoma
, B-
Cell
/ ultrasonography.
Lymphoma
, Follicular / ultrasonography
[MeSH-minor]
Adult.
Diagnosis
, Differential. Female. Humans. Lymph Nodes / ultrasonography
Genetic Alliance.
consumer health - Follicular Lymphoma
.
MedlinePlus Health Information.
consumer health - Lymphatic Diseases
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18777781.001).
[ISSN]
1661-8157
[Journal-full-title]
Praxis
[ISO-abbreviation]
Praxis (Bern 1994)
[Language]
ger
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
77.
Roychoudhury P, Ghosh U, Bhattacharyya NP, Chaudhuri K:
Activation of mitochondrial promoter P(H)-binding protein in a radio-resistant Chinese hamster cell strain associated with Bcl-2.
Biochem Biophys Res Commun
; 2006 Nov 17;350(2):272-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Activation of mitochondrial promoter P(H)-binding protein in a radio-resistant Chinese hamster
cell
strain associated with
Bcl
-2.
Previously, we have shown that up regulation of mitochondrial genes ND1, ND4, and COX1 transcribed from the heavy strand promoter (P(H)) has been increased in a radio-resistant
cell
strain designated as M5 in comparison with the parental Chinese hamster V79
cells
.
These genes are also up regulated in Chinese hamster V79
cells
VB13 that express exogenous human Bcl2.
In the present study, the expression of the gene ND6 that is expressed from the light strand promoter (P(L)) was found to be similar in both the
cell
lines, as determined by RT-PCR.
To test the possibility that this differential expression of mitochondrial genes under these two promoters was mediated by differences in proteins' affinity to interact with these promoters, we have carried out electrophoretic mobility shift assay (EMSA) using mitochondrial
cell
extracts from these two
cell
lines.
Our result of these experiments revealed that two different proteins formed complex with the synthetic promoters and higher amount of protein from M5
cell
extracts interacted with the P(H) promoter in comparison to that observed with
cell
extracts from Chinese hamster V79
cells
.
These results showed that differential mitochondrial gene expression observed earlier in the radio-resistant M5
cells
was due to enhanced interaction proteins with the promoters P(H) and mediated by the expression of Bcl2.
[MeSH-major]
DNA-Binding Proteins / metabolism. Genes, Mitochondrial. Mitochondrial Proteins / metabolism. Proto-Oncogene Proteins c-
bcl
-2 / metabolism. Radiation Tolerance
[MeSH-minor]
Animals.
Cell
Line. Cricetinae. Cricetulus. Electrophoretic Mobility Shift Assay. Gamma Rays. Gene Expression Regulation, Enzymologic. Humans. Male. Mitochondria / enzymology. Mitochondria / radiation effects. NADH Dehydrogenase / biosynthesis. NADH Dehydrogenase / genetics. Promoter Regions, Genetic. Protein Subunits / biosynthesis. Protein Subunits / genetics
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17007815.001).
[ISSN]
0006-291X
[Journal-full-title]
Biochemical and biophysical research communications
[ISO-abbreviation]
Biochem. Biophys. Res. Commun.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Mitochondrial Proteins; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins c-bcl-2; EC 1.6.99.3 / NADH Dehydrogenase
78.
Schulze-Bergkamen H, Ehrenberg R, Hickmann L, Vick B, Urbanik T, Schimanski CC, Berger MR, Schad A, Weber A, Heeger S, Galle PR, Moehler M:
Bcl-x(L) and Myeloid cell leukaemia-1 contribute to apoptosis resistance of colorectal cancer cells.
World J Gastroenterol
; 2008 Jun 28;14(24):3829-40
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bcl
-x(L) and Myeloid
cell
leukaemia-1 contribute to apoptosis resistance of colorectal cancer
cells
.
AIM: To explore the role of
Bcl
-x(L) and Myeloid
cell
leukaemia (Mcl)-1 for the apoptosis resistance of colorectal carcinoma (CRC)
cells
towards current treatment modalities.
METHODS:
Bcl
-x(L) and Mcl-1 mRNA and protein expression were analyzed in CRC
cell
lines as well as human CRC tissue by Western blot, quantitative PCR and immunohistochemistry.
Bcl
-x(L) and Mcl-1 protein expression was knocked down or increased in CRC
cell
lines by applying specific siRNAs or expression plasmids, respectively.
After modulation of protein expression, CRC
cells
were treated with chemotherapeutic agents, an antagonistic epidermal growth factor receptor (EGFR1) antibody, an EGFR1 tyrosine kinase inhibitor, or with the death receptor ligand TRAIL.
Apoptosis induction and
cell
viability were analyzed.
RESULTS: Here we show that in human CRC tissue and various CRC
cell
lines both
Bcl
-x(L) and Mcl-1 are expressed.
Bcl
-x(L) expression was higher in CRC tissue than in surrounding
non
-
malignant
tissue, both on protein and mRNA level.
Mcl-1 mRNA expression was significantly lower in
malignant
tissues.
Viability rates of CRC
cells
were significantly decreased after knock down of
Bcl
-x(L) expression, and, to a lower extent, after knock down of Mcl-1 expression.
Furthermore,
cells
with reduced
Bcl
-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of
Bcl
-x(L) also towards 5-FU-induced apoptosis.
On the other hand, upregulation of
Bcl
-x(L) by transfection of an expression plasmid decreased chemotherapeutic drug-induced apoptosis.
EGF treatment clearly induced
Bcl
-x(L) and Mcl-1 expression in CRC
cells
.
Apoptosis induction upon EGFR1 blockage by cetuximab or PD168393 was increased by inhibiting Mcl-1 and
Bcl
-x(L) expression.
More strikingly, CD95- and TRAIL-induced apoptosis was increased by
Bcl
-x(L) knock down.
CONCLUSION: Our data suggest that
Bcl
-x(L) and, to a lower extent, Mcl-1, are important anti-apoptotic factors in CRC.
Specific downregulation of
Bcl
-x(L) is a promising approach to sensitize CRC
cells
towards chemotherapy and targeted therapy.
[MeSH-major]
Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Proto-Oncogene Proteins c-
bcl
-2 / metabolism.
bcl
-X Protein / metabolism
[MeSH-minor]
Antigens, CD95 / metabolism. Camptothecin / analogs & derivatives. Camptothecin / pharmacology.
Cell
Line, Tumor.
Cell
Survival / drug effects. Fluorouracil / pharmacology. Humans. Myeloid
Cell
Leukemia Sequence 1 Protein. Organoplatinum Compounds / pharmacology. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / metabolism
Genetic Alliance.
consumer health - Colorectal Cancer
.
Genetic Alliance.
consumer health - Colorectal cancer 1
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nat Med. 1999 Feb;5(2):157-63
[
9930862.001
]
[Cites]
Dig Dis Sci. 1998 Dec;43(12):2641-8
[
9881495.001
]
[Cites]
Oncogene. 1999 Aug 19;18(33):4654-62
[
10467412.001
]
[Cites]
Mol Cancer Ther. 2005 Mar;4(3):451-6
[
15767554.001
]
[Cites]
Jpn J Clin Oncol. 2005 Aug;35(8):453-63
[
16024531.001
]
[Cites]
Cancer Biol Ther. 2005 Mar;4(3):267-76
[
15753661.001
]
[Cites]
Int J Oncol. 2006 Jan;28(1):25-32
[
16327976.001
]
[Cites]
J Hepatol. 2006 Jan;44(1):151-7
[
16289418.001
]
[Cites]
J Biol Chem. 2006 Apr 14;281(15):10153-63
[
16478725.001
]
[Cites]
Clin Cancer Res. 2006 Apr 15;12(8):2640-6
[
16638878.001
]
[Cites]
Semin Oncol. 2006 Aug;33(4):369-85
[
16890793.001
]
[Cites]
Oncogene. 2006 Aug 24;25(37):5145-54
[
16636678.001
]
[Cites]
BMC Cancer. 2006;6:232
[
17014711.001
]
[Cites]
FEBS Lett. 2006 Dec 11;580(28-29):6565-9
[
17113582.001
]
[Cites]
Oncogene. 2007 Feb 26;26(9):1324-37
[
17322918.001
]
[Cites]
Clin Cancer Res. 2007 Apr 1;13(7):2226-35
[
17404107.001
]
[Cites]
Curr Top Med Chem. 2007;7(10):961-5
[
17508927.001
]
[Cites]
Pathology. 2007 Jun;39(3):334-8
[
17558861.001
]
[Cites]
Cancer Cell. 2007 Jul;12(1):66-80
[
17613437.001
]
[Cites]
Int J Biochem Cell Biol. 2007;39(7-8):1462-75
[
17403612.001
]
[Cites]
Anticancer Agents Med Chem. 2007 Sep;7(5):492-503
[
17896910.001
]
[Cites]
Expert Opin Ther Targets. 2007 Oct;11(10):1299-314
[
17907960.001
]
[Cites]
Genes Dev. 2000 Jan 1;14(1):23-7
[
10640272.001
]
[Cites]
Mol Cell Biol. 2000 Apr;20(8):2687-95
[
10733571.001
]
[Cites]
Nat Med. 2000 May;6(5):513-9
[
10802706.001
]
[Cites]
Clin Cancer Res. 2000 Jun;6(6):2547-55
[
10873111.001
]
[Cites]
Science. 2000 Nov 3;290(5493):989-92
[
11062132.001
]
[Cites]
J Clin Pathol. 2002 Mar;55(3):206-11
[
11896073.001
]
[Cites]
Leukemia. 2002 Apr;16(4):444-54
[
11960321.001
]
[Cites]
Nature. 2002 Jul 11;418(6894):244-51
[
12110901.001
]
[Cites]
Genes Dev. 2003 Jun 15;17(12):1475-86
[
12783855.001
]
[Cites]
Cancer Res. 2003 Aug 15;63(16):5118-25
[
12941843.001
]
[Cites]
Lancet. 2003 Oct 25;362(9393):1401-3
[
14585643.001
]
[Cites]
Cancer Cell. 2004 Jan;5(1):37-49
[
14749125.001
]
[Cites]
Cancer Res. 2004 Feb 1;64(3):1110-3
[
14871845.001
]
[Cites]
Semin Oncol. 2004 Feb;31(1):90-119
[
14970941.001
]
[Cites]
Cancer Res. 2004 May 15;64(10):3517-24
[
15150106.001
]
[Cites]
Carcinogenesis. 2004 Oct;25(10):1867-77
[
15205359.001
]
[Cites]
Nature. 1987 May 28-Jun 3;327(6120):293-7
[
3587348.001
]
[Cites]
J Immunol Methods. 1991 Jun 3;139(2):271-9
[
1710634.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3516-20
[
7682708.001
]
[Cites]
Cell. 1994 Aug 26;78(4):539-42
[
8069905.001
]
[Cites]
Cancer Res. 1995 Jan 15;55(2):237-41
[
7812951.001
]
[Cites]
Cancer Res. 1996 May 15;56(10):2422-7
[
8625322.001
]
[Cites]
Exp Cell Res. 1998 Apr 10;240(1):107-21
[
9570926.001
]
[Cites]
Br J Cancer. 1998 Oct;78(8):1035-42
[
9792147.001
]
[Cites]
Clin Cancer Res. 1996 Jul;2(7):1215-9
[
9816290.001
]
[Cites]
J Clin Invest. 1999 Jul;104(2):155-62
[
10411544.001
]
(PMID = 18609706.001).
[ISSN]
1007-9327
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / BCL2L1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Organoplatinum Compounds; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / bcl-X Protein; 04ZR38536J / oxaliplatin; 7673326042 / irinotecan; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
[Other-IDs]
NLM/ PMC2721439
79.
Marín García D, Cárdenas Lafuente F, Utrilla Ayala Mdel C, Galán Jurado MV, Jiménez Martín JJ, García Ordóñez MA:
[Primary diffuse large B-cell lymphoma of the rectum simulating a rectal adenocarcinoma].
Gastroenterol Hepatol
; 2010 Feb;33(2):92-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Primary diffuse large B-
cell lymphoma
of the rectum simulating a rectal adenocarcinoma].
[Transliterated title]
Linfoma de
tipo B difuso
de
células grandes primario rectal que simula un adenocarcinoma
de
recto.
Colorectal
lymphoma
is an extremely infrequent entity, representing less than 0.5% of all primary colorectal neoplasms.
Colorectal localization accounts for 15-20% of all gastrointestinal
lymphomas
, after the stomach and small intestine.
Because the symptoms are
non
-specific, this
disease
is usually diagnosed in the advanced stages.
Dawson's criteria are highly useful in the differential
diagnosis
between primary colorectal involvement and gastrointestinal tract involvement secondary to systemic
lymphoma
, which is important due to the distinct prognosis and treatment of these entities.
We report the case of a B-
cell non
-
Hodgkin
's
lymphoma
that was difficult to diagnose and was treated with R-CHOP polychemotherapy.
[MeSH-major]
Adenocarcinoma /
diagnosis
.
Lymphoma
, Large B-
Cell
, Diffuse /
diagnosis
. Rectal Neoplasms /
diagnosis
[MeSH-minor]
Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonoscopy. Cyclophosphamide / therapeutic use.
Diagnosis
, Differential. Doxorubicin / therapeutic use. Humans. Immunohistochemistry. Male. Meta-Analysis as Topic. Middle Aged.
Neoplasm
Staging. Prednisone / therapeutic use. Prognosis. Radiography, Abdominal. Rectum / pathology. Tomography, X-Ray Computed. Vincristine / therapeutic use
Genetic Alliance.
consumer health - Large B cell diffuse lymphoma
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2009 Elsevier España, S.L. All rights reserved.
(PMID = 19875198.001).
[ISSN]
0210-5705
[Journal-full-title]
Gastroenterología y hepatología
[ISO-abbreviation]
Gastroenterol Hepatol
[Language]
spa
[Publication-type]
Case Reports; Comparative Study; English Abstract; Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
80.
Niwa K, Onogi K, Yun W, Hirose Y, Tamaya T:
Primary lymphoma of the uterine corpus: an unusual location for a common disease--case report.
Eur J Gynaecol Oncol
; 2007;28(6):522-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Primary
lymphoma
of the uterine corpus: an unusual location for a common
disease
--case report.
A case of a primary uterine corpus
lymphoma
in a 75-year-old woman is described.
Immunohistochemical studies showed diffuse large B-
cell
type
one.
Primary
lymphoma
of the uterine corpus is considered to be an unusual location for a common
disease
.
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/
diagnosis
. Uterine Neoplasms /
diagnosis
MedlinePlus Health Information.
consumer health - Uterine Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18179154.001).
[ISSN]
0392-2936
[Journal-full-title]
European journal of gynaecological oncology
[ISO-abbreviation]
Eur. J. Gynaecol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Italy
81.
Gobessi S, Laurenti L, Longo PG, Sica S, Leone G, Efremov DG:
ZAP-70 enhances B-cell-receptor signaling despite absent or inefficient tyrosine kinase activation in chronic lymphocytic leukemia and lymphoma B cells.
Blood
; 2007 Mar 1;109(5):2032-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
ZAP-70 enhances B-
cell
-receptor signaling despite absent or inefficient tyrosine kinase activation in chronic
lymphocytic
leukemia and
lymphoma B
cells
.
Expression of ZAP-70 is an important negative prognostic factor in chronic
lymphocytic
leukemia (CLL).
This protein tyrosine kinase is a key mediator of T-
cell
receptor (TCR) signaling and is structurally homologous to Syk, which plays an analogous role in B-
cell
receptor (BCR) signaling.
We have now compared antigen receptor-induced activation of ZAP-70 in B
cells
and T
cells
by analyzing phosphorylation of critical regulatory tyrosine residues.
We show that BCR-mediated activation of ZAP-70 is very inefficient in CLL and
lymphoma B
cells
and is negligible when compared to activation of Syk.
[MeSH-major]
Leukemia, B-
Cell
/ metabolism.
Lymphoma
, B-
Cell
/ metabolism. Protein-Tyrosine Kinases / metabolism. Receptors, Antigen, B-
Cell
/ metabolism. Signal Transduction. ZAP-70 Protein-Tyrosine Kinase / metabolism
[MeSH-minor]
Adaptor Proteins, Signal Transducing / metabolism. Enzyme Activation. Humans. Ligands. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Phosphotyrosine / metabolism. Proto-Oncogene Proteins c-cbl / metabolism. Shc Signaling Adaptor Proteins. Tumor
Cells
, Cultured
Genetic Alliance.
consumer health - Chronic Lymphocytic Leukemia
.
Genetic Alliance.
consumer health - Leukemia, B-cell, chronic
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17038529.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Ligands; 0 / Receptors, Antigen, B-Cell; 0 / SHC1 protein, human; 0 / Shc Signaling Adaptor Proteins; 21820-51-9 / Phosphotyrosine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl; EC 6.3.2.19 / CBLB protein, human
82.
Yang ZZ, Novak AJ, Stenson MJ, Witzig TE, Ansell SM:
Intratumoral CD4+CD25+ regulatory T-cell-mediated suppression of infiltrating CD4+ T cells in B-cell non-Hodgkin lymphoma.
Blood
; 2006 May 1;107(9):3639-46
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Intratumoral CD4+CD25+ regulatory T-
cell
-mediated suppression of infiltrating CD4+ T
cells
in B-
cell non
-
Hodgkin lymphoma
.
Most
non
-
Hodgkin
lymphomas
(NHLs) are of B-
cell
origin, but the tumor tissue can be variably infiltrated with T
cells
.
In the present study, we have identified a subset of CD4(+)CD25(+) T
cells
with high levels of CTLA-4 and Foxp3 (intratumoral T(reg)
cells
) that are overrepresented in biopsy specimens of B-
cell
NHL (median of 17% in
lymphoma
biopsies, 12% in inflammatory tonsil, and 6% in tumor-free lymph nodes; P = .001).
We found that these CD4(+)CD25(+) T
cells
suppressed the proliferation and cytokine (IFN-gamma and IL-4) production of infiltrating CD4(+)CD25(-) T
cells
in response to PHA stimulation.
PD-1 was found to be constitutively and exclusively expressed on a subset of infiltrating CD4(+)CD25(-) T
cells
, and B7-H1 could be induced on intratumoral CD4(+)CD25(+) T
cells
in B-
cell
NHL.
Anti-B7-H1 antibody or PD-1 fusion protein partly restored the proliferation of infiltrating CD4(+)CD25(-) T
cells
when cocultured with intratumoral T(reg)
cells
.
Finally, we found that CCL22 secreted by
lymphoma B
cells
is involved in the chemotaxis and migration of intratumoral T(reg)
cells
that express CCR4, but not CCR8.
Taken together, our results suggest that T(reg)
cells
are highly represented in the area of B-
cell
NHL and that
malignant
B
cells
are involved in the recruitment of these
cells
into the area of
lymphoma
.
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
Genetic Alliance.
consumer health - Non-Hodgkin Lymphoma
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Immunol. 1999 May 1;162(9):5317-26
[
10228007.001
]
[Cites]
J Immunol. 2004 Jan 15;172(2):834-42
[
14707053.001
]
[Cites]
N Engl J Med. 2004 Nov 18;351(21):2159-69
[
15548776.001
]
[Cites]
Clin Cancer Res. 2005 Feb 15;11(4):1467-73
[
15746048.001
]
[Cites]
Expert Rev Anticancer Ther. 2005 Jun;5(3):477-85
[
16001955.001
]
[Cites]
J Clin Oncol. 2005 Sep 10;23(26):6358-63
[
16155020.001
]
[Cites]
J Immunol. 2005 Oct 1;175(7):4180-3
[
16177055.001
]
[Cites]
J Exp Med. 2001 Sep 17;194(6):847-53
[
11560999.001
]
[Cites]
Immunol Rev. 2001 Aug;182:18-32
[
11722621.001
]
[Cites]
Nat Immunol. 2001 Dec;2(12):1126-32
[
11702067.001
]
[Cites]
Cancer Res. 2001 Dec 15;61(24):8643-6
[
11751377.001
]
[Cites]
J Immunol. 2002 May 1;168(9):4272-6
[
11970966.001
]
[Cites]
Nat Rev Immunol. 2002 Jun;2(6):389-400
[
12093005.001
]
[Cites]
J Exp Med. 2002 Jul 15;196(2):237-46
[
12119348.001
]
[Cites]
Adv Immunol. 2003;81:331-71
[
14711059.001
]
[Cites]
Blood. 2004 Mar 1;103(5):1755-62
[
14604957.001
]
[Cites]
Semin Immunol. 2004 Apr;16(2):81-8
[
15036231.001
]
[Cites]
Semin Immunol. 2004 Apr;16(2):89-98
[
15036232.001
]
[Cites]
J Immunol. 2004 Jul 15;173(2):1444-53
[
15240741.001
]
[Cites]
Nat Med. 2004 Sep;10(9):942-9
[
15322536.001
]
[Cites]
J Immunol. 1995 Aug 1;155(3):1151-64
[
7636184.001
]
[Cites]
Int Immunol. 1998 Dec;10(12):1969-80
[
9885918.001
]
[Cites]
J Immunol. 1999 Nov 15;163(10):5211-8
[
10553041.001
]
[Cites]
J Exp Med. 2000 Jul 17;192(2):295-302
[
10899916.001
]
[Cites]
J Exp Med. 2000 Jul 17;192(2):303-10
[
10899917.001
]
[Cites]
J Clin Oncol. 2001 Feb 1;19(3):720-6
[
11157023.001
]
[Cites]
Cancer Res. 2001 Jun 15;61(12):4766-72
[
11406550.001
]
[Cites]
Nat Immunol. 2001 Sep;2(9):816-22
[
11526392.001
]
[Cites]
J Exp Med. 2001 Sep 3;194(5):629-44
[
11535631.001
]
[Cites]
J Exp Med. 2001 Sep 17;194(6):823-32
[
11560997.001
]
[Cites]
J Exp Med. 2002 Jul 15;196(2):247-53
[
12119349.001
]
[Cites]
J Exp Med. 2002 Jul 15;196(2):255-60
[
12119350.001
]
[Cites]
J Exp Med. 2002 Aug 5;196(3):379-87
[
12163566.001
]
[Cites]
J Immunol. 2002 Sep 1;169(5):2756-61
[
12193750.001
]
[Cites]
Curr Opin Immunol. 2002 Dec;14(6):771-8
[
12413528.001
]
[Cites]
J Allergy Clin Immunol. 2002 Nov;110(5):693-702
[
12417876.001
]
[Cites]
J Exp Med. 2002 Nov 18;196(10):1335-46
[
12438424.001
]
[Cites]
J Immunol. 2002 Dec 1;169(11):6210-7
[
12444126.001
]
[Cites]
J Clin Invest. 2003 Feb;111(3):363-70
[
12569162.001
]
[Cites]
Science. 2003 Feb 14;299(5609):1057-61
[
12522256.001
]
[Cites]
Nat Immunol. 2003 Apr;4(4):330-6
[
12612578.001
]
[Cites]
Nat Immunol. 2003 Apr;4(4):337-42
[
12612581.001
]
[Cites]
Cancer. 2003 Sep 1;98(5):1089-99
[
12942579.001
]
[Cites]
Clin Cancer Res. 2003 Oct 1;9(12):4404-8
[
14555512.001
]
[Cites]
Curr Opin Immunol. 2003 Dec;15(6):690-6
[
14630204.001
]
[Cites]
Cancer Res. 1999 Jul 1;59(13):3128-33
[
10397255.001
]
(PMID = 16403912.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA92104; United States / NCI NIH HHS / CA / CA97274
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD274; 0 / Antigens, Surface; 0 / Apoptosis Regulatory Proteins; 0 / CD274 protein, human; 0 / PDCD1 protein, human; 0 / Programmed Cell Death 1 Receptor; 0 / Receptors, Interleukin-2; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
[Other-IDs]
NLM/ PMC1895773
83.
Ryan JL, Jones RJ, Elmore SH, Kenney SC, Miller G, Schroeder JC, Gulley ML:
Epstein-Barr virus WZhet DNA can induce lytic replication in epithelial cells in vitro, although WZhet is not detectable in many human tissues in vivo.
Intervirology
; 2009;52(1):8-16
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Epstein-Barr virus WZhet DNA can induce lytic replication in epithelial
cells
in vitro, although WZhet is not detectable in many human tissues in vivo.
We tested whether WZhet induces viral replication in epithelial
cells
, and we studied its prevalence in a wide range of lesional tissues arising in vivo.
These included specimens from patients with
Hodgkin
or
non
-
Hodgkin lymphoma
, post-transplant lymphoproliferation, nasopharyngeal or gastric adenocarcinoma, and infectious mononucleosis.
However, WZhet DNA was detected in vitro in EBV-infected AGS gastric cancer
cells
.
Additionally, transient transfection of infected AGS gastric cancer
cells
showed that viral replication could be induced by a WZhet plasmid.
CONCLUSION: This is the first evidence that WZhet induces the EBV lytic cycle in an epithelial
cell
line.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2009 S. Karger AG, Basel.
[Cites]
J Virol. 1987 May;61(5):1495-506
[
3033277.001
]
[Cites]
J Med Virol. 1986 Dec;20(4):329-39
[
3025351.001
]
[Cites]
Virology. 1993 Feb;192(2):541-50
[
8093650.001
]
[Cites]
Intervirology. 1993;36(1):11-9
[
8225907.001
]
[Cites]
J Infect Dis. 1993 Dec;168(6):1349-55
[
8245519.001
]
[Cites]
J Infect Dis. 1994 Jul;170(1):7-12
[
8014523.001
]
[Cites]
APMIS. 1994 Jul;102(7):495-500
[
7917218.001
]
[Cites]
Cancer. 1994 Nov 1;74(9):2414-24
[
7922994.001
]
[Cites]
J Infect Dis. 1998 Jun;177(6):1705-9
[
9607853.001
]
[Cites]
Int J Cancer. 1998 Oct 23;79(5):481-6
[
9761116.001
]
[Cites]
Am J Respir Crit Care Med. 1999 Apr;159(4 Pt 1):1336-41
[
10194186.001
]
[Cites]
Arch Virol. 2005 Apr;150(4):755-70
[
15785969.001
]
[Cites]
J Mol Diagn. 2001 Feb;3(1):1-10
[
11227065.001
]
[Cites]
Diagn Mol Pathol. 2001 Dec;10(4):255-64
[
11763317.001
]
[Cites]
Am J Pathol. 2002 Mar;160(3):781-6
[
11891176.001
]
[Cites]
Nat Rev Immunol. 2001 Oct;1(1):75-82
[
11905817.001
]
[Cites]
Mod Pathol. 2002 Aug;15(8):870-7
[
12181273.001
]
[Cites]
Am J Respir Crit Care Med. 2002 Aug 15;166(4):510-3
[
12186829.001
]
[Cites]
Cancer Res. 2002 Sep 1;62(17):4876-8
[
12208733.001
]
[Cites]
J Pathol. 2002 Aug;197(5):684-8
[
12210090.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15036-41
[
12409611.001
]
[Cites]
Respir Med. 2003 Mar;97(3):281-4
[
12645836.001
]
[Cites]
Neoplasma. 2003;50(1):8-12
[
12687272.001
]
[Cites]
Am J Pathol. 2003 Jul;163(1):369-70
[
12819043.001
]
[Cites]
Clin Infect Dis. 2003 Nov 1;37(9):1244-9
[
14557970.001
]
[Cites]
J Virol. 2004 Jan;78(1):544-9
[
14671137.001
]
[Cites]
J Virol. 2004 May;78(10):4983-92
[
15113878.001
]
[Cites]
Diagn Mol Pathol. 2004 Jun;13(2):61-8
[
15167006.001
]
[Cites]
J Mol Diagn. 2004 Nov;6(4):378-85
[
15507678.001
]
[Cites]
Nature. 1982 Jan 14;295(5845):160-3
[
6276755.001
]
[Cites]
Proc Natl Acad Sci U S A. 1983 May;80(9):2762-6
[
6302703.001
]
[Cites]
J Virol. 1984 Jul;51(1):199-207
[
6328039.001
]
[Cites]
Proc Natl Acad Sci U S A. 1985 Jun;82(12):4085-9
[
2987963.001
]
[Cites]
Proc Natl Acad Sci U S A. 1988 Dec;85(24):9801-5
[
2849118.001
]
(PMID = 19349713.001).
[ISSN]
1423-0100
[Journal-full-title]
Intervirology
[ISO-abbreviation]
Intervirology
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R21 CA107966; United States / NCI NIH HHS / CA / CA107966; United States / NIEHS NIH HHS / ES / T32 ES007017; United States / NIEHS NIH HHS / ES / T32-ES07017; United States / NCI NIH HHS / CA / R25 CA102618
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / DNA, Viral
[Other-IDs]
NLM/ PMC2865398
84.
Kocjan G:
Best Practice No 185. Cytological and molecular diagnosis of lymphoma.
J Clin Pathol
; 2005 Jun;58(6):561-7
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Best Practice No 185. Cytological and molecular
diagnosis
of
lymphoma
.
With the advances in molecular pathology, the
cell
as a morphological and functional unit has become essential in the
diagnosis
of
lymphoma
.
Conventional staining, preparation, and interpretation of
cells
, as seen in fine needle aspiration cytology (FNAC), often used as a first line investigation of lymphadenopathy, is being supplemented with an array of immunocytochemical and molecular analyses, aimed not only at a more precise
disease
definition, but also at recognising factors that can predict prognosis and response to treatment.
Accepting the pitfalls of conventional cytomorphology, this review looks at molecular changes characteristic to particular
lymphomas
and explores the currently available technology for their detection, with particular reference to cytological material.
Future protocols for the
diagnosis
and management of patients with lymphadenopathy should include FNAC as an initial investigation, followed by immunocytochemistry and molecular investigations.
Tissue biopsy, the conventional method of
diagnosis
, may be avoided in selected cases.
[MeSH-major]
Lymphoma
,
Non
-
Hodgkin
/
diagnosis
[MeSH-minor]
Biopsy, Fine-Needle. Chromosome Aberrations.
Diagnosis
, Differential. Gene Expression Profiling / methods. Humans. Nucleic Acid Hybridization / methods. Polymerase Chain Reaction / methods
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Genes Chromosomes Cancer. 2000 Jan;27(1):85-94
[
10564590.001
]
[Cites]
Arch Pathol Lab Med. 1999 Dec;123(12):1189-207
[
10583924.001
]
[Cites]
Cytopathology. 1999 Oct;10(5):291-7
[
10588346.001
]
[Cites]
Cancer. 1999 Dec 25;87(6):325-45
[
10603186.001
]
[Cites]
Am J Clin Pathol. 2000 May;113(5):688-99
[
10800402.001
]
[Cites]
Nature. 2000 Nov 9;408(6809):216-21
[
11089977.001
]
[Cites]
N Engl J Med. 2004 Aug 26;351(9):856-7
[
15329421.001
]
[Cites]
Blood. 1992 Oct 1;80(7):1781-7
[
1356511.001
]
[Cites]
Blood. 1992 Nov 15;80(10):2594-9
[
1384792.001
]
[Cites]
Blood. 1993 Oct 15;82(8):2289-95
[
8400281.001
]
[Cites]
Oncogene. 1993 Dec;8(12):3447-57
[
8247550.001
]
[Cites]
Science. 1994 Mar 4;263(5151):1281-4
[
8122112.001
]
[Cites]
Am J Pathol. 1994 Jun;144(6):1312-9
[
8203469.001
]
[Cites]
Blood. 1994 Sep 1;84(5):1361-92
[
8068936.001
]
[Cites]
Acta Cytol. 1995 Mar-Apr;39(2):180-6
[
7887065.001
]
[Cites]
Diagn Mol Pathol. 1995 Mar;4(1):25-31
[
7735552.001
]
[Cites]
Blood. 1996 Dec 1;88(11):4110-7
[
8943844.001
]
[Cites]
Cytopathology. 1997 Apr;8(2):114-21
[
9134337.001
]
[Cites]
Blood. 1997 Jun 1;89(11):3909-18
[
9166827.001
]
[Cites]
Monogr Pathol. 1997;(39):118-33
[
9249823.001
]
[Cites]
Diagn Mol Pathol. 1997 Jun;6(3):154-60
[
9276187.001
]
[Cites]
Blood. 1998 Mar 1;91(5):1680-7
[
9473234.001
]
[Cites]
Cancer Genet Cytogenet. 2003 May;143(1):73-9
[
12742158.001
]
[Cites]
Cancer. 2003 Jun 15;97(12):2960-71
[
12784330.001
]
[Cites]
Blood. 2003 Jun 15;101(12):4944-51
[
12595313.001
]
[Cites]
Cytopathology. 2003 Aug;14(4):186-90
[
12873310.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6
[
12900505.001
]
[Cites]
Br J Haematol. 2003 Sep;122(5):745-59
[
12930384.001
]
[Cites]
Arch Pathol Lab Med. 2003 Sep;127(9):1148-60
[
12946230.001
]
[Cites]
Blood. 2000 Dec 1;96(12):3681-95
[
11090048.001
]
[Cites]
Eur J Haematol. 2001 Feb;66(2):100-6
[
11168517.001
]
[Cites]
Mol Diagn. 2000 Dec;5(4):287-99
[
11172493.001
]
[Cites]
Blood. 2001 Apr 1;97(7):2098-104
[
11264177.001
]
[Cites]
N Engl J Med. 2001 Apr 5;344(14):1031-7
[
11287972.001
]
[Cites]
Cancer Genet Cytogenet. 2001 Apr 1;126(1):26-33
[
11343775.001
]
[Cites]
Mod Pathol. 2001 May;14(5):472-81
[
11353059.001
]
[Cites]
Cytopathology. 2001 Jun;12(3):157-67
[
11380557.001
]
[Cites]
J Clin Pathol. 2001 Jul;54(7):565-7
[
11429433.001
]
[Cites]
Int J Pediatr Otorhinolaryngol. 2001 Aug 20;60(2):135-40
[
11518591.001
]
[Cites]
Mol Diagn. 2001 Sep;6(3):161-8
[
11571709.001
]
[Cites]
Blood. 2002 Jan 15;99(2):716-8
[
11781262.001
]
[Cites]
Nat Med. 2002 Jan;8(1):68-74
[
11786909.001
]
[Cites]
Diagn Mol Pathol. 2002 Mar;11(1):47-57
[
11854602.001
]
[Cites]
Clin Cancer Res. 2002 Mar;8(3):794-801
[
11895911.001
]
[Cites]
Hematol J. 2000;1(1):53-66
[
11920170.001
]
[Cites]
Breast Cancer Res. 2002;4(3):R3
[
12052255.001
]
[Cites]
Semin Oncol. 2002 Jun;29(3):258-63
[
12063678.001
]
[Cites]
N Engl J Med. 2002 Jun 20;346(25):1937-47
[
12075054.001
]
[Cites]
Methods Mol Biol. 2002;204:143-53
[
12397796.001
]
[Cites]
Blood. 2003 Mar 15;101(6):2363-7
[
12424193.001
]
[Cites]
Cancer Cell. 2003 Feb;3(2):185-97
[
12620412.001
]
[Cites]
Br J Haematol. 2003 Apr;121(1):49-56
[
12670331.001
]
[Cites]
Diagn Cytopathol. 2003 Apr;28(4):191-5
[
12672094.001
]
[Cites]
N Engl J Med. 2003 May 1;348(18):1777-85
[
12724484.001
]
[Cites]
Acta Cytol. 2004 Mar-Apr;48(2):119-26
[
15085740.001
]
[Cites]
Diagn Cytopathol. 2004 May;30(5):332-40
[
15108231.001
]
[Cites]
Eur J Hum Genet. 2004 Jun;12(6):423
[
15162123.001
]
[Cites]
Leuk Lymphoma. 2003;44 Suppl 3:S13-20
[
15202520.001
]
[Cites]
Am J Pathol. 2004 Jul;165(1):159-66
[
15215171.001
]
[Cites]
Diagn Cytopathol. 2004 Jul;31(1):23-30
[
15236260.001
]
[Cites]
J Clin Oncol. 2004 Aug 1;22(15):3046-52
[
15284254.001
]
[Cites]
Nat Rev Cancer. 2004 Aug;4(8):644-53
[
15286744.001
]
[Cites]
Am J Hematol. 2003 Sep;74(1):78-84
[
12949897.001
]
[Cites]
Leuk Lymphoma. 2003 Aug;44(8):1385-94
[
12952233.001
]
[Cites]
Exp Hematol. 2003 Sep;31(9):784-8
[
12962724.001
]
[Cites]
Acta Cytol. 2003 Sep-Oct;47(5):744-8
[
14526672.001
]
[Cites]
Semin Hematol. 2003 Oct;40(4):296-307
[
14582080.001
]
[Cites]
Blood. 2003 Dec 1;102(12):3871-9
[
12933571.001
]
[Cites]
Histopathology. 2003 Dec;43(6):509-28
[
14636252.001
]
[Cites]
Leukemia. 2003 Dec;17(12):2257-317
[
14671650.001
]
[Cites]
Clin Cancer Res. 2003 Dec 1;9(16 Pt 1):5980-7
[
14676123.001
]
[Cites]
Cancer. 2003 Dec 25;99(6):385-93
[
14681948.001
]
[Cites]
Blood. 2004 Jan 1;103(1):275-82
[
14504078.001
]
[Cites]
Mod Pathol. 2004 Jan;17(1):131-5
[
14657953.001
]
[Cites]
J Exp Med. 2004 Jan 5;199(1):59-68
[
14707115.001
]
[Cites]
Lancet. 2004 Jan 10;363(9403):105-11
[
14726163.001
]
[Cites]
Hematol J. 2004;5(1):69-76
[
14745433.001
]
[Cites]
J Clin Oncol. 2004 Feb 1;22(3):474-83
[
14752070.001
]
[Cites]
Pathology. 2004 Feb;36(1):19-44
[
14757555.001
]
[Cites]
Semin Immunol. 1998 Apr;10(2):133-42
[
9618759.001
]
[Cites]
Cancer. 1998 Aug 25;84(4):252-61
[
9723601.001
]
[Cites]
Diagn Mol Pathol. 1998 Aug;7(4):209-14
[
9917131.001
]
[Cites]
Cell. 1999 Jan 8;96(1):35-45
[
9989495.001
]
[Cites]
Blood. 1999 Jun 1;93(11):3601-9
[
10339464.001
]
[Cites]
Diagn Cytopathol. 1999 Aug;21(2):98-104
[
10425046.001
]
[Cites]
Diagn Cytopathol. 1999 Oct;21(4):240-9
[
10495316.001
]
[Cites]
J Clin Lab Anal. 1999;13(5):224-8
[
10494131.001
]
(PMID = 15917402.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
90
[Other-IDs]
NLM/ PMC1770685
85.
Luo RF, Zhao S, Tibshirani R, Myklebust JH, Sanyal M, Fernandez R, Gratzinger D, Marinelli RJ, Lu ZS, Wong A, Levy R, Levy S, Natkunam Y:
CD81 protein is expressed at high levels in normal germinal center B cells and in subtypes of human lymphomas.
Hum Pathol
; 2010 Feb;41(2):271-80
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
CD81 protein is expressed at high levels in normal germinal center B
cells
and in subtypes of human
lymphomas
.
CD81 is a tetraspanin
cell
surface protein that regulates CD19 expression in B lymphocytes and enables hepatitis C virus infection of human
cells
.
Immunohistologic analysis in normal hematopoietic tissue showed strong staining for CD81 in normal germinal center B
cells
, a
cell
type
in which its increased expression has not been previously recognized.
High-dimensional flow cytometry analysis of normal hematopoietic tissue confirmed that among B- and T-
cell
subsets, germinal center B
cells
showed the highest level of CD81 expression.
In more than 800 neoplastic tissue samples, its expression was also found in most
non
-
Hodgkin
lymphomas
.
Staining for CD81 was rarely seen in multiple myeloma,
Hodgkin lymphoma
, or myeloid leukemia.
In hierarchical cluster analysis of diffuse large B-
cell lymphoma
, staining for CD81 was most similar to other germinal center
B cell
-associated markers, particularly LMO2.
By flow cytometry, CD81 was expressed in diffuse large B-
cell lymphoma
cells
independent of the presence or absence of CD10, another germinal center B-
cell
marker.
The detection of CD81 in routine biopsy samples and its differential expression in
lymphoma
subtypes, particularly diffuse large B-
cell lymphoma
, warrant further study to assess CD81 expression and its role in the risk stratification of patients with diffuse large B-
cell lymphoma
.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
[Cites]
Nat Med. 2002 Jan;8(1):68-74
[
11786909.001
]
[Cites]
N Engl J Med. 2002 Jan 24;346(4):235-42
[
11807147.001
]
[Cites]
N Engl J Med. 2002 Jun 20;346(25):1937-47
[
12075054.001
]
[Cites]
J Immunol. 2002 Dec 15;169(12):6691-5
[
12471100.001
]
[Cites]
Leuk Lymphoma. 2003 Jul;44(7):1113-20
[
12916862.001
]
[Cites]
J Immunol. 2003 Oct 15;171(8):4062-72
[
14530327.001
]
[Cites]
Blood. 2004 Jan 1;103(1):275-82
[
14504078.001
]
[Cites]
PLoS Biol. 2004 Apr;2(4):E108
[
15094809.001
]
[Cites]
N Engl J Med. 2004 Apr 29;350(18):1828-37
[
15115829.001
]
[Cites]
Mod Pathol. 2001 Jul;14(7):686-94
[
11455001.001
]
[Cites]
Int J Cancer. 2000 Jul 20;89(4):313-24
[
10956404.001
]
[Cites]
J Pathol. 2000 Aug;191(4):452-61
[
10918222.001
]
[Cites]
Nature. 2000 Feb 3;403(6769):503-11
[
10676951.001
]
[Cites]
Immunity. 1997 Feb;6(2):107-18
[
9047233.001
]
[Cites]
Science. 1998 Oct 30;282(5390):938-41
[
9794763.001
]
[Cites]
Nat Rev Immunol. 2005 Feb;5(2):136-48
[
15688041.001
]
[Cites]
Blood. 2005 Mar 1;105(5):1851-61
[
15550490.001
]
[Cites]
Blood. 2005 May 15;105(10):3979-86
[
15677569.001
]
[Cites]
J Virol. 2005 Jul;79(13):8079-89
[
15956553.001
]
[Cites]
J Clin Oncol. 2005 Aug 1;23(22):5027-33
[
15955905.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18544-9
[
16339892.001
]
[Cites]
J Clin Oncol. 2006 Feb 20;24(6):995-1007
[
16418498.001
]
[Cites]
Lancet Oncol. 2006 May;7(5):379-91
[
16648042.001
]
[Cites]
N Engl J Med. 2006 Jun 8;354(23):2419-30
[
16760442.001
]
[Cites]
J Clin Oncol. 2006 Jul 1;24(19):3121-7
[
16754935.001
]
[Cites]
Blood. 2007 Feb 15;109(4):1636-42
[
17038524.001
]
[Cites]
J Clin Pathol. 2007 Dec;60(12):1378-83
[
18042694.001
]
[Cites]
Nucleic Acids Res. 2008 Jan;36(Database issue):D871-7
[
17989087.001
]
[Cites]
J Clin Oncol. 2008 Jan 20;26(3):447-54
[
18086797.001
]
[Cites]
Blood. 2008 Jun 15;111(12):5509-14
[
18445689.001
]
[Cites]
J Immunol. 2008 Jul 1;181(1):174-85
[
18566382.001
]
(PMID = 20004001.001).
[ISSN]
1532-8392
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233; United States / NCI NIH HHS / CA / P01 CA034233-21; United States / NCI NIH HHS / CA / CA034233-21; United States / NCI NIH HHS / CA / CA33399; United States / NCI NIH HHS / CA / R37 CA033399
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD81; 0 / CD81 protein, human
[Other-IDs]
NLM/ NIHMS139240; NLM/ PMC2813949
86.
Chan WK, Au WY, Wong CY, Liang R, Leung AY, Kwong YL, Khong PL:
Metabolic activity measured by F-18 FDG PET in natural killer-cell lymphoma compared to aggressive B- and T-cell lymphomas.
Clin Nucl Med
; 2010 Aug;35(8):571-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Metabolic activity measured by F-18 FDG PET in natural killer-
cell lymphoma
compared to aggressive B- and T-
cell
lymphomas
.
PURPOSE: We aim to compare the metabolic activity by F-18 fluorodeoxyglucose (FDG) uptake across the various histologic subtypes of
non
-
Hodgkin lymphoma
(NHL) in a single center, with particular interest in the natural killer (NK)-
cell lymphoma
subtype
for which literature is scarce because of the rarity of these
lymphomas
in Western populations.
Mean SUV(max) of 4 major groups of NHL; aggressive B-
cell
(n = 63), indolent B-
cell
(n = 31), NK-
cell
(n = 14) and aggressive T-
cell lymphoma
(n = 9), was compared using one-way analysis of variance.
RESULTS: SUV(max) (mean +/- standard deviation) of NK-
cell lymphoma
(9.2 +/- 4.5) was significantly lower than aggressive B-
cell lymphoma
(14.1 +/- 6.4) (P = 0.013), similar to aggressive T-
cell lymphoma
(7.6 +/- 3.9) and significantly higher than that of indolent B-
cell lymphoma
(5.3 +/- 3.1) (P = 0.039).
Although NK-
cell
lymphomas
demonstrate high metabolic activity, SUV(max) is significantly lower than its aggressive B-
cell
counterparts.
This may reflect the large amount of coagulative necrosis and inflammatory component of the tumor, and the relatively slower tumor growth rate compared with aggressive B-
cell
lymphomas
.
[MeSH-major]
Fluorodeoxyglucose F18. Killer
Cells
, Natural / metabolism.
Lymphoma
, B-
Cell
/ metabolism.
Lymphoma
, B-
Cell
/ radionuclide imaging.
Lymphoma
, T-
Cell
/ metabolism.
Lymphoma
, T-
Cell
/ radionuclide imaging. Positron-Emission Tomography
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20631501.001).
[ISSN]
1536-0229
[Journal-full-title]
Clinical nuclear medicine
[ISO-abbreviation]
Clin Nucl Med
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0Z5B2CJX4D / Fluorodeoxyglucose F18
87.
Anderson LA, Gadalla S, Morton LM, Landgren O, Pfeiffer R, Warren JL, Berndt SI, Ricker W, Parsons R, Engels EA:
Population-based study of autoimmune conditions and the risk of specific lymphoid malignancies.
Int J Cancer
; 2009 Jul 15;125(2):398-405
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Logistic regression was used to derive odds ratios (ORs) comparing the prevalence of autoimmune conditions in cases and controls, by lymphoid malignancy
subtype
, adjusted for gender, age at malignancy/selection, year of malignancy/selection, race and number of physician claims.
The strongest associations observed by
non
-
Hodgkin lymphoma
(NHL) subtypes were diffuse large B-
cell lymphoma
with rheumatoid arthritis (OR 1.4, 95%CI 1.2-1.5) and Sjögren syndrome (2.0, 1.5-2.8); T-
cell lymphoma
with hemolytic anemia (9.7, 4.3-22), psoriasis (3.1, 2.5-4.0), discoid lupus erythematosus (4.4, 2.3-8.4) and celiac
disease
(5.0, 2.4-14.
); and marginal zone
lymphoma
with Sjögren syndrome (6.6, 4.6-9.5), systemic lupus erythematosus (2.8, 1.7-4.7) and hemolytic anemia (7.4, 3.1-18).
Hodgkin lymphoma
was associated with systemic lupus erythematosus (3.5, 1.9-6.7).
Several autoimmune conditions were associated with increased risk of lymphoid neoplasms, especially NHLs of diffuse large B-
cell
, marginal zone and T-
cell
subtypes.
[MeSH-major]
Autoimmune Diseases / epidemiology.
Lymphoma
/ complications. Population Surveillance
MedlinePlus Health Information.
consumer health - Autoimmune Diseases
.
MedlinePlus Health Information.
consumer health - Lymphoma
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Published 2009 UICC.
[Cites]
Clin Cancer Res. 2001 Apr;7(4):791-4
[
11309323.001
]
[Cites]
Ann Oncol. 2001 Jun;12(6):853-8
[
11484964.001
]
[Cites]
J Invest Dermatol. 2001 Dec;117(6):1531-7
[
11886519.001
]
[Cites]
Med Oncol. 2007;24(4):469-71
[
17917102.001
]
[Cites]
Arthritis Rheum. 2008 Mar;58(3):657-66
[
18311836.001
]
[Cites]
Blood. 2008 Apr 1;111(7):3388-94
[
18239085.001
]
[Cites]
Blood. 2008 Apr 15;111(8):4029-38
[
18263783.001
]
[Cites]
Annu Rev Med. 2005;56:29-44
[
15660500.001
]
[Cites]
Blood. 2000 May 1;95(9):2786-92
[
10779422.001
]
[Cites]
Int J Cancer. 2000 Nov 1;88(3):497-502
[
11054684.001
]
[Cites]
Scand J Rheumatol. 2002;31(2):66-71
[
12109649.001
]
[Cites]
Med Care. 2002 Aug;40(8 Suppl):IV-3-18
[
12187163.001
]
[Cites]
Nat Rev Immunol. 2002 Sep;2(9):647-55
[
12209133.001
]
[Cites]
J Assoc Physicians India. 2002 Sep;50:1186-8
[
12516708.001
]
[Cites]
Arthritis Rheum. 2003 Apr;48(4):963-70
[
12687538.001
]
[Cites]
Cancer Causes Control. 2004 May;15(4):419-28
[
15141141.001
]
[Cites]
Cancer. 2004 Aug 15;101(4):790-5
[
15305411.001
]
[Cites]
Am J Med Sci. 1978 Jan-Feb;275(1):93-8
[
665715.001
]
[Cites]
Br J Cancer. 1989 May;59(5):810-3
[
2736218.001
]
[Cites]
Cancer. 1993 Feb 1;71(3):745-50
[
8431855.001
]
[Cites]
BMJ. 1998 Jul 18;317(7152):180-1
[
9665898.001
]
[Cites]
Ann Intern Med. 1999 Apr 6;130(7):591-601
[
10189330.001
]
[Cites]
Gut. 2005 Jan;54(1):54-9
[
15591504.001
]
[Cites]
Clin Chem Lab Med. 2005;43(10):1158-63
[
16197314.001
]
[Cites]
Arch Intern Med. 2005 Nov 14;165(20):2337-44
[
16287762.001
]
[Cites]
Am J Epidemiol. 2005 Dec 15;162(12):1153-61
[
16251389.001
]
[Cites]
Blood. 2006 Jan 1;107(1):265-76
[
16150940.001
]
[Cites]
J Natl Cancer Inst. 2006 Jan 4;98(1):51-60
[
16391371.001
]
[Cites]
Arthritis Rheum. 2006 Mar;54(3):692-701
[
16508929.001
]
[Cites]
Int J Cancer. 2006 Jun 15;118(12):3095-8
[
16395700.001
]
[Cites]
Korean J Intern Med. 2006 Mar;21(1):46-9
[
16646565.001
]
[Cites]
AIDS. 2006 Aug 1;20(12):1645-54
[
16868446.001
]
[Cites]
J Invest Dermatol. 2006 Oct;126(10):2194-201
[
16741509.001
]
[Cites]
J Natl Cancer Inst. 2006 Sep 20;98(18):1321-30
[
16985251.001
]
[Cites]
Eur J Cancer. 2006 Nov;42(17):3028-33
[
16945522.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2069-77
[
17119030.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):405-8
[
17337643.001
]
[Cites]
Rheumatology (Oxford). 2007 May;46(5):830-2
[
17255135.001
]
[Cites]
Leuk Lymphoma. 2007 Jun;48(6):1139-49
[
17577777.001
]
[Cites]
Blood. 2007 Jul 15;110(2):695-708
[
17389762.001
]
[Cites]
Clin Rheumatol. 2007 Sep;26(9):1491-4
[
17297594.001
]
[Cites]
Nat Clin Pract Rheumatol. 2007 Oct;3(10):561-9
[
17906611.001
]
[Cites]
J Clin Epidemiol. 2000 Dec;53(12):1258-67
[
11146273.001
]
[Cites]
J Leukoc Biol. 2001 Mar;69(3):331-9
[
11261778.001
]
[Cites]
Dermatologica. 1989;178(4):221-4
[
2767291.001
]
[Cites]
Cancer. 1992 Dec 1;70(11):2592-6
[
1423186.001
]
[Cites]
J Natl Cancer Inst. 1993 Feb 17;85(4):307-11
[
8426374.001
]
(PMID = 19365835.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 CP010150-08
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS81238; NLM/ PMC2692814
88.
Sumida T, Kitadai Y, Masuda H, Shinagawa K, Tanaka M, Kodama M, Kuroda T, Hiyama T, Tanaka S, Nakayama H, Yoshihara M, Yoshino T, Chayama K:
Rapid progression of Epstein-Barr-virus-positive gastric diffuse large B-cell lymphoma during chemoradiotherapy: a case report.
Clin J Gastroenterol
; 2008 Oct;1(3):105-109
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Rapid progression of Epstein-Barr-virus-positive gastric diffuse large B-
cell lymphoma
during chemoradiotherapy: a case report.
Biopsy specimens showed diffuse infiltration of large atypical lymphoid
cells
in which Epstein-Barr virus (EBV) was detected by in situ hybridization.
Diffuse large B-
cell lymphoma
(DLBCL), stage II1, was diagnosed.
Partial remission was achieved by chemotherapy, but the
disease
progressed rapidly during radiotherapy.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Surg Pathol. 2003 Jan;27(1):16-26
[
12502924.001
]
[Cites]
Surgery. 1997 May;121(5):501-5
[
9142147.001
]
[Cites]
Blood. 2005 Oct 1;106(7):2444-51
[
15941916.001
]
[Cites]
Br J Haematol. 2001 Jun;113(3):814-21
[
11380475.001
]
[Cites]
Ann Surg. 2004 Jul;240(1):44-50
[
15213617.001
]
[Cites]
N Engl J Med. 1998 Jul 2;339(1):21-6
[
9647875.001
]
[Cites]
Cancer Sci. 2007 Sep;98(9):1281-7
[
17627615.001
]
[Cites]
Leuk Lymphoma. 2001 May;41(5-6):669-73
[
11378585.001
]
[Cites]
Am J Clin Pathol. 2007 Oct;128(4):579-84
[
17875508.001
]
[Cites]
Cancer Sci. 2005 Jun;96(6):349-52
[
15958057.001
]
[Cites]
Cancer Sci. 2006 Feb;97(2):163-6
[
16441428.001
]
[Cites]
Clin Cancer Res. 2002 Jan;8(1):29-34
[
11801537.001
]
[Cites]
Eur J Cancer. 1996 Dec;32A(13):2306-11
[
9038614.001
]
[Cites]
Br J Haematol. 2000 Oct;111(1):239-46
[
11091207.001
]
[Cites]
Ann Oncol. 1997;8 Suppl 1:85-8
[
9187438.001
]
[Cites]
Leuk Lymphoma. 1995 Apr;17(3-4):321-6
[
8580802.001
]
(PMID = 26193647.001).
[ISSN]
1865-7257
[Journal-full-title]
Clinical journal of gastroenterology
[ISO-abbreviation]
Clin J Gastroenterol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Keywords]
NOTNLM ; Chemoradiotherapy / Diffuse large B-cell lymphoma / Epstein-Barr virus
89.
Honeychurch J, Glennie MJ, Illidge TM:
Cyclophosphamide inhibition of anti-CD40 monoclonal antibody-based therapy of B cell lymphoma is dependent on CD11b+ cells.
Cancer Res
; 2005 Aug 15;65(16):7493-501
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cyclophosphamide inhibition of anti-CD40 monoclonal antibody-based therapy of
B cell lymphoma
is dependent on CD11b+
cells
.
We therefore assessed the efficacy of combining anti-CD40 mAb, known to elicit CTL responses against murine
lymphoma
models with the commonly used cytotoxic drug, cyclophosphamide.
In vivo tracking experiments reveal that pretreatment with cyclophosphamide leads to diminished CTL expansion, as well as an increased number of CD11b+
cells
that display an activated phenotype.
These latter
cells
are able to inhibit T-
cell
proliferation, at least in part via production of nitric oxide, but do not induce T-
cell
apoptosis.
Furthermore, adoptive transfer of the induced CD11b+
cells
is sufficient to inhibit anti-CD40 therapy in tumor-bearing recipients.
We have shown that the timing of cyclophosphamide relative to mAb administration is critical to the therapeutic outcome, and although the combination can improve survival, cyclophosphamide given prior to immunotherapy may generate a population of myeloid
cells
that can interfere with CTL responses and compromise the therapeutic outcome.
[MeSH-major]
Antibodies, Monoclonal / pharmacology. Antigens, CD11b / immunology. Antigens, CD40 / immunology. Cyclophosphamide / pharmacology. Immunosuppressive Agents / pharmacology.
Lymphoma
, B-
Cell
/ immunology.
Lymphoma
, B-
Cell
/ therapy
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
NITRIC OXIDE
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16103104.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD11b; 0 / Antigens, CD40; 0 / Immunosuppressive Agents; 31C4KY9ESH / Nitric Oxide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
90.
Chowdhury M, Endo M, Chiba T, Kudara N, Oana S, Sato K, Akasaka R, Tomita K, Fujiwara S, Mizutani T, Sugai T, Takikawa Y, Suzuki K:
Characterization of follicular lymphoma in the small intestine using double-balloon endoscopy.
Gastroenterol Res Pract
; 2009;2009:835258
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Characterization of follicular
lymphoma
in the small intestine using double-balloon endoscopy.
Follicular
lymphomas
occur rarely in the gastrointestinal tract, representing only 1-3% of all gastrointestinal tract B-
cell non
-
Hodgkin
lymphomas
.
We describe endoscopic analysis of 3 cases of follicular
lymphoma
in the small intestine using double-balloon endoscopy.
These cases are the first follicular
lymphomas
in the small intestine evaluated using narrow-band imaging or Fuji Intelligent Chromo Endoscopy to be reported.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer. 1979 Aug;44(2):645-51
[
383259.001
]
[Cites]
Chin Med J (Engl). 2008 Jun 5;121(11):977-82
[
18706244.001
]
[Cites]
Mod Pathol. 1992 Nov;5(6):631-3
[
1285443.001
]
[Cites]
Am J Pathol. 1992 May;140(5):1089-95
[
1374590.001
]
[Cites]
Am J Pathol. 1992 Jun;140(6):1327-35
[
1376556.001
]
[Cites]
Am J Surg Pathol. 1992 Jul;16(7):637-40
[
1530105.001
]
[Cites]
Semin Hematol. 1988 Apr;25(2 Suppl 2):11-6
[
2456618.001
]
[Cites]
Cancer Treat Rep. 1981 May-Jun;65(5-6):413-8
[
7016324.001
]
[Cites]
Hematol Oncol. 1995 May-Jun;13(3):153-63
[
7622145.001
]
[Cites]
J Surg Oncol. 1995 Sep;60(1):41-9
[
7666666.001
]
[Cites]
Mod Pathol. 1994 Jun;7(5):560-4
[
7937722.001
]
[Cites]
Ann Oncol. 1994 May;5(5):397-400
[
8075046.001
]
[Cites]
Gastroenterology. 1994 Apr;106(4):846-58
[
8143991.001
]
[Cites]
J Clin Gastroenterol. 1994 Mar;18(2):99-104
[
8189031.001
]
[Cites]
Am J Surg Pathol. 1996 May;20(5):627-40
[
8619427.001
]
[Cites]
Histopathology. 1996 Jun;28(6):487-95
[
8803592.001
]
[Cites]
Histopathology. 1995 Dec;27(6):501-8
[
8838329.001
]
[Cites]
Gastroenterology. 1997 Jan;112(1):7-16
[
8978336.001
]
[Cites]
Blood. 1997 Jun 1;89(11):3909-18
[
9166827.001
]
[Cites]
J Clin Oncol. 1997 Apr;15(4):1587-94
[
9193357.001
]
[Cites]
Am J Clin Pathol. 1997 Sep;108(3):302-7
[
9291459.001
]
[Cites]
Cancer. 1997 Dec 15;80(12):2311-20
[
9404709.001
]
[Cites]
Am J Surg Pathol. 2000 May;24(5):688-93
[
10800987.001
]
[Cites]
Blood. 2000 Jul 15;96(2):410-9
[
10887100.001
]
[Cites]
J Clin Oncol. 2001 Sep 15;19(18):3861-73
[
11559724.001
]
[Cites]
Am J Surg Pathol. 2002 Feb;26(2):216-24
[
11812943.001
]
[Cites]
Ann Oncol. 2003 Apr;14(4):623-9
[
12649111.001
]
[Cites]
Semin Oncol. 2003 Feb;30(1 Suppl 2):16-20
[
12652460.001
]
[Cites]
Semin Oncol. 2004 Apr;31(2 Suppl 4):66-71
[
15124137.001
]
[Cites]
Histopathology. 2005 Nov;47(5):467-78
[
16241994.001
]
[Cites]
Endoscopy. 2007 Feb;39 Suppl 1:E26-7
[
17285496.001
]
[Cites]
Dig Dis Sci. 2007 Apr;52(4):1031-5
[
17353993.001
]
[Cites]
Endoscopy. 2007 Feb;39 Suppl 1:E86-7
[
17440873.001
]
[Cites]
Intern Med. 2007;46(11):705-9
[
17541220.001
]
[Cites]
Endoscopy. 2008 Apr;40(4):343-6
[
18067068.001
]
[Cites]
Endoscopy. 2008 Sep;40 Suppl 2:E8-9
[
18278712.001
]
[Cites]
J Clin Pathol. 1992 Nov;45(11):1018-22
[
1280654.001
]
(PMID = 19901998.001).
[ISSN]
1687-630X
[Journal-full-title]
Gastroenterology research and practice
[ISO-abbreviation]
Gastroenterol Res Pract
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Egypt
[Other-IDs]
NLM/ PMC2773429
91.
Terrano DT, Upreti M, Chambers TC:
Cyclin-dependent kinase 1-mediated Bcl-xL/Bcl-2 phosphorylation acts as a functional link coupling mitotic arrest and apoptosis.
Mol Cell Biol
; 2010 Feb;30(3):640-56
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cyclin-dependent kinase 1-mediated
Bcl
-xL/
Bcl
-2 phosphorylation acts as a functional link coupling mitotic arrest and apoptosis.
Despite detailed knowledge of the components of the spindle assembly checkpoint, a molecular explanation of how
cells
die after prolonged spindle checkpoint activation, and thus how microtubule inhibitors and other antimitotic drugs ultimately elicit their lethal effects, has yet to emerge.
Mitotically arrested
cells
typically display extensive phosphorylation of two key antiapoptotic proteins,
Bcl
-x(L) and
Bcl
-2, and evidence suggests that phosphorylation disables their antiapoptotic activity.
In this report, evidence is presented that cyclin-dependent kinase 1 (CDK1)/cyclin B catalyzes mitotic-arrest-induced
Bcl
-x(L)/
Bcl
-2 phosphorylation.
When mitosis is prolonged in the absence of microtubule inhibition,
Bcl
-x(L) and
Bcl
-2 become highly phosphorylated.
Transient overexpression of nondegradable cyclin B1 caused apoptotic death, which was blocked by a phosphodefective
Bcl
-x(L) mutant but not by a phosphomimetic
Bcl
-x(L) mutant, confirming
Bcl
-x(L) as a key target of proapoptotic CDK1 signaling.
These findings suggest a model whereby a switch in the duration of CDK1 activation, from transient during mitosis to sustained during mitotic arrest, dramatically increases the extent of
Bcl
-x(L)/
Bcl
-2 phosphorylation, resulting in inactivation of their antiapoptotic function.
Thus, phosphorylation of antiapoptotic
Bcl
-2 proteins acts as a sensor for CDK1 signal duration and as a functional link coupling mitotic arrest to apoptosis.
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
Hazardous Substances Data Bank.
VINBLASTINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
FEBS Lett. 2003 Mar 13;538(1-3):41-7
[
12633850.001
]
[Cites]
J Biol Chem. 2008 Dec 19;283(51):35517-25
[
18974096.001
]
[Cites]
Cell. 1995 Jan 27;80(2):179-85
[
7834738.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 May 9;92(10):4507-11
[
7753834.001
]
[Cites]
Cancer Res. 1997 Jan 1;57(1):130-5
[
8988053.001
]
[Cites]
Eur J Biochem. 1997 Jan 15;243(1-2):527-36
[
9030781.001
]
[Cites]
Curr Opin Cell Biol. 1997 Dec;9(6):807-14
[
9425345.001
]
[Cites]
Cell Growth Differ. 1998 Jan;9(1):23-9
[
9438385.001
]
[Cites]
Mol Cell Biol. 1998 Jun;18(6):3509-17
[
9584191.001
]
[Cites]
Cancer Res. 1998 Aug 1;58(15):3331-8
[
9699663.001
]
[Cites]
J Biol Chem. 1998 Nov 13;273(46):30777-84
[
9804855.001
]
[Cites]
Mol Cell. 1998 Nov;2(5):581-91
[
9844631.001
]
[Cites]
J Cell Biol. 1999 Mar 8;144(5):891-901
[
10085289.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Apr 27;96(9):4797-802
[
10220373.001
]
[Cites]
Mol Cell Biol. 1999 Dec;19(12):8469-78
[
10567572.001
]
[Cites]
J Biol Chem. 2000 Jul 14;275(28):21661-7
[
10766756.001
]
[Cites]
Cell. 2000 Aug 4;102(3):279-91
[
10975519.001
]
[Cites]
J Biol Chem. 2000 Sep 29;275(39):29980-5
[
10913135.001
]
[Cites]
Cell. 2000 Oct 13;103(2):239-52
[
11057897.001
]
[Cites]
Cancer Res. 2000 Nov 15;60(22):6403-7
[
11103805.001
]
[Cites]
Neoplasia. 2001 Jan-Feb;3(1):70-9
[
11326318.001
]
[Cites]
Curr Biol. 2001 Jun 5;11(11):R431-5
[
11516665.001
]
[Cites]
Oncogene. 2001 Sep 27;20(43):6172-80
[
11593425.001
]
[Cites]
Nat Cell Biol. 2002 Aug;4(8):556-64
[
12134156.001
]
[Cites]
Cancer Cell. 2002 Jul;2(1):43-54
[
12150824.001
]
[Cites]
Cell Death Differ. 2002 Dec;9(12):1287-93
[
12478465.001
]
[Cites]
Dev Cell. 2004 Nov;7(5):637-51
[
15525526.001
]
[Cites]
Nature. 2004 Nov 18;432(7015):316-23
[
15549093.001
]
[Cites]
Oncogene. 2005 Jan 6;24(1):107-17
[
15531923.001
]
[Cites]
Cancer Cell. 2005 Jul;8(1):7-12
[
16023594.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Jul 11;103(28):10660-5
[
16818887.001
]
[Cites]
Nat Rev Mol Cell Biol. 2007 May;8(5):379-93
[
17426725.001
]
[Cites]
Mol Cell. 2007 Apr 27;26(2):301-10
[
17466630.001
]
[Cites]
J Cell Biol. 2007 Nov 19;179(4):671-85
[
18025303.001
]
[Cites]
Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59
[
18097445.001
]
[Cites]
Nat Rev Cancer. 2008 Feb;8(2):121-32
[
18202696.001
]
[Cites]
Cell Cycle. 2008 May 15;7(10):1449-61
[
18418077.001
]
[Cites]
Apoptosis. 2003 Oct;8(5):413-50
[
12975575.001
]
(PMID = 19917720.001).
[ISSN]
1098-5549
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA109821; United States / NCI NIH HHS / CA / CA-109821
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Protein Kinase Inhibitors; 0 / Tubulin Modulators; 0 / bcl-X Protein; 5V9KLZ54CY / Vinblastine; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2 Protein Kinase; EC 2.7.12.2 / MAP Kinase Kinase 4
[Other-IDs]
NLM/ PMC2812246
92.
Singh F, Weinberg JM:
Partial remission of psoriasis following rituximab therapy for non-Hodgkin lymphoma.
Cutis
; 2005 Sep;76(3):186-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Partial remission of psoriasis following rituximab therapy for
non
-
Hodgkin lymphoma
.
Rituximab, a human-mouse, chimeric, monoclonal antibody that targets the B-
cell
CD20 antigen and causes rapid and specific B-
cell
depletion, is indicated for the treatment of low-grade or follicular, relapsed or refractory, CD20+ B-
cell
,
non
-
Hodgkin lymphoma
(NHL).
We report the case of a middle-aged woman with psoriasis who experienced a partial sustained remission of her psoriasis after treatment with rituximab for NHL and discuss potential pathophysiologic mechanisms for this unexpected effect in a condition known to be mediated by T
cells
.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use.
Lymphoma
,
Non
-
Hodgkin
/ drug therapy. Psoriasis / drug therapy
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
Genetic Alliance.
consumer health - Psoriasis
.
Genetic Alliance.
consumer health - Non-Hodgkin Lymphoma
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Psoriasis
.
Hazardous Substances Data Bank.
RITUXIMAB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16268262.001).
[ISSN]
0011-4162
[Journal-full-title]
Cutis
[ISO-abbreviation]
Cutis
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
93.
Pan J, Huang H, Sun L, Fang B, Yeung SC:
Bcl-2-associated X protein is the main mediator of manumycin a-induced apoptosis in anaplastic thyroid cancer cells.
J Clin Endocrinol Metab
; 2005 Jun;90(6):3583-91
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bcl
-2-associated X protein is the main mediator of manumycin a-induced apoptosis in anaplastic thyroid cancer
cells
.
We previously demonstrated that the combination of paclitaxel and manumycin A, a farnesyltransferase inhibitor, enhanced apoptosis of anaplastic thyroid cancer (ATC)
cells
.
We also found that manumycin induced translocation of
Bcl
-2-associated X protein (Bax), another possible mediator of cytochrome c release, from the cytosol to the mitochondria.
Using a binary adenoviral vector system, we found that overexpression of Bax enhanced manumycin-induced apoptosis of ATC
cells
, and the combination of manumycin and overexpression of Bax increased inhibition of ATC xenograft growth in nude mice.
Thus, we concluded that manumycin-induced apoptosis in ATC
cells
was primarily mediated by Bax and that increasing Bax expression may sensitize ATC
cells
to manumycin.
[MeSH-major]
Apoptosis / drug effects. Polyenes / toxicity. Proto-Oncogene Proteins c-
bcl
-2 / physiology. Thyroid Neoplasms / pathology. Thyroid Neoplasms / physiopathology
[MeSH-minor]
Animals. Carcinoma.
Cell
Line, Tumor. Enzyme Inhibitors / toxicity. Humans. Mice. Mice, Nude. Mitochondria / drug effects. Mitochondria / pathology. Mitochondria / ultrastructure. Paclitaxel / toxicity. Polyunsaturated Alkamides. Transplantation, Heterologous.
bcl
-X Protein
Genetic Alliance.
consumer health - Thyroid cancer, anaplastic
.
Genetic Alliance.
consumer health - Thyroid Cancer
.
MedlinePlus Health Information.
consumer health - Thyroid Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
TAXOL
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15769983.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 16672
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Enzyme Inhibitors; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 52665-74-4 / manumycin; P88XT4IS4D / Paclitaxel
94.
Yano S, Asai O, Dobashi N, Osawa H, Takei Y, Takahara S, Otsubo H, Ogasawara Y, Yamaguchi Y, Saito T, Minami J, Hoshi Y, Usui N:
Long-term follow-up of autologous stem cell transplantation for patients with aggressive non-Hodgkin lymphoma who had bone marrow involvement at initial diagnosis in the pre-rituximab era.
Clin Lymphoma Myeloma
; 2007 Mar;7(5):361-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Long-term follow-up of autologous stem
cell
transplantation for patients with aggressive
non
-
Hodgkin lymphoma
who had bone marrow involvement at initial
diagnosis
in the pre-rituximab era.
BACKGROUND: High-dose therapy (HDT) followed by autologous stem
cell
transplantation (ASCT) is an important treatment option for selected patients with aggressive
non
-
Hodgkin lymphoma
; however, the effectiveness of HDT for patients with bone marrow (BM) involvement of
lymphoma
cells
is not well defined.
PATIENTS AND METHODS: Between February 1991 and December 2001, 57 patients with aggressive
non
-
Hodgkin lymphoma
were treated with HDT and ASCT.
Thirteen of 57 patients who had BM infiltration at initial
diagnosis
were analyzed.
Meanwhile, the probability of OS at 10 years for 44 patients who did not have BM
disease
was 60%.
There was no significant difference in OS (P=0.895) between patients with or without BM
disease
at initial
diagnosis
.
CONCLUSION: High-dose therapy treatment followed by ASCT might save some groups of patients with
lymphoma
regardless of BM involvement at initial
diagnosis
.
[MeSH-major]
Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms /
diagnosis
. Hematopoietic Stem
Cell
Transplantation.
Lymphoma
,
Non
-
Hodgkin
/ therapy
[MeSH-minor]
Adult. Antibodies, Monoclonal, Murine-Derived.
Disease
Progression. Dose-Response Relationship, Drug. Follow-Up Studies. Humans. Middle Aged. Remission Induction. Rituximab. Survival Rate. Time. Transplantation, Autologous. Treatment Outcome
Genetic Alliance.
consumer health - Hodgkin lymphoma
.
Genetic Alliance.
consumer health - Transplantation
.
Genetic Alliance.
consumer health - Non-Hodgkin Lymphoma
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
Hazardous Substances Data Bank.
RITUXIMAB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17562246.001).
[ISSN]
1557-9190
[Journal-full-title]
Clinical lymphoma & myeloma
[ISO-abbreviation]
Clin Lymphoma Myeloma
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
95.
Wu LX, La Rose J, Chen L, Neale C, Mak T, Okkenhaug K, Wange R, Rottapel R:
CD28 regulates the translation of Bcl-xL via the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway.
J Immunol
; 2005 Jan 1;174(1):180-94
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
CD28 regulates the translation of
Bcl
-xL via the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway.
In concert with the TCR, CD28 promotes T
cell
survival by regulating the expression of the antiapoptotic protein
Bcl
-x(L).
The mechanism by which CD28 mediates the induction of
Bcl
-x(L) remains unknown.
We show that although signaling through the TCR is sufficient to stimulate transcription of
Bcl
-x(L) mRNA, CD28, by activating PI3K and mammalian target of rapamycin, provides a critical signal that regulates the translation of
Bcl
-x(L) transcripts.
We observe that CD28 induced 4E-binding protein-1 phosphorylation, an inhibitor of the translational machinery, and that CD28 costimulation directly augmented the translation of
a Bcl
-x(L) 5'-untranslated region reporter construct.
Lastly, costimulation by CD28 shifted the distribution of
Bcl
-x(L) mRNA transcripts from the pretranslation complex to the translationally active polyribosomes.
These results demonstrate that CD28 relieves the translational inhibition of
Bcl
-x(L) in a PI3K/mammalian target of rapamycin-dependent manner.
[MeSH-major]
Antigens, CD28 / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Protein Biosynthesis / immunology. Proto-Oncogene Proteins c-
bcl
-2 / metabolism. T-Lymphocytes / immunology
[MeSH-minor]
Animals. Antigens, CD3 / immunology. Antigens, CD3 / metabolism. Blotting, Northern.
Cell
Death / physiology.
Cells
, Cultured. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Flow Cytometry. Humans. Immunosuppressive Agents / pharmacology. Interleukin-2 / biosynthesis. Interleukin-2 / immunology. Jurkat
Cells
. Mice. Mice, Transgenic. Morpholines / pharmacology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sirolimus / pharmacology. Transfection.
bcl
-X Protein
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
SIROLIMUS
.
KOMP Repository.