BioMedLib Search Engine
[ goto HOMEPAGE ]
Search the biomedical literature, for the most relevant articles.
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Clarify the query
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 leukemias acute 2005:2010[pubdate] *count=100
1012 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
acute
' expands to
3 meanings
. Choose the one you intended:
Concept C0205178: acuteness qualifier value;
details
Concept C1547229: acute triage code;
details
Concept C1547295: admission level of care code acute;
details
'
b cell leukemias
' 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 1012
1.
Abdallah E, Hajji Z, Mellal Z, Belmekki M, Bencherifa F, Berraho A:
[Macular serous detachment revealing acute lymphoblastic leukemia].
J Fr Ophtalmol
; 2005 Jan;28(1):39-44
[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]
[Macular serous detachment revealing
acute
lymphoblastic
leukemia
].
BACKGROUND:
Leukemias
are a group of malignant diseases caused by immature hematopoietic cells proliferating in the blood marrow.
OBSERVATION: We report a case
of a
42-year-old women presenting with loss of vision caused by serous macular detachment.
The investigations showed the diagnosis of
acute
lymphoblastic
leukemia
.
DISCUSSION: Ocular involvement is seen in 28%-80%
of leukemia
cases.
Serous detachment of the neuroepithelium is seldom reported, and can be the first symptom of the
disease
.
CONCLUSION: Ocular manifestations
of leukemia
are frequent but rarely reveal the
disease
.
However, the diagnosis
of leukemia
should be considered in case of pigmentary epithelium involvement.
[MeSH-major]
Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / complications. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis. Retinal Detachment / etiology
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
MedlinePlus Health Information.
consumer health - Retinal Detachment
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15767897.001).
[ISSN]
0181-5512
[Journal-full-title]
Journal français d'ophtalmologie
[ISO-abbreviation]
J Fr Ophtalmol
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
2.
Faber J, Gregory RI, Armstrong SA:
Linking miRNA regulation to BCR-ABL expression: the next dimension.
Cancer Cell
; 2008 Jun;13(6):467-9
[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.
The introduction of tyrosine kinase inhibitors in the treatment of BCR-ABL1-rearranged malignancies has revolutionized therapy, but the prognosis for
acute leukemias
remains suboptimal.
In this issue of Cancer
Cell
, Bueno et al. (2008) add a new dimension to the regulation of ABL1 expression.
The authors demonstrate that ABL1 is a direct target of miR-203, miR-203 is silenced by genetic and epigenetic mechanisms in hematopoietic malignancies expressing either ABL1 or BCR-ABL1, and restoration of miR-203 expression reduces ABL1 and BCR-ABL1 levels and inhibits
cell
proliferation.
[MeSH-minor]
Animals. Antineoplastic Agents / therapeutic use.
Cell
Line, Tumor.
Cell
Proliferation. Gene Expression Regulation, Leukemic. Humans.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / metabolism.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, T-
Cell
/ genetics. Lymphoma, T-
Cell
/ metabolism. Lymphoma, T-
Cell
/ pathology. Mice. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / metabolism. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / pathology. Protein Kinase Inhibitors / therapeutic use. Up-Regulation
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
[CommentOn]
Cancer Cell. 2008 Jun;13(6):496-506
[
18538733.001
]
(PMID = 18538729.001).
[ISSN]
1878-3686
[Journal-full-title]
Cancer cell
[ISO-abbreviation]
Cancer Cell
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / MicroRNAs; 0 / Protein Kinase Inhibitors; 0 / abl-bcr fusion protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
3.
Chowdhury T, Brady HJ:
Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
Blood Cells Mol Dis
; 2008 Mar-Apr;40(2):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]
Insights from clinical studies into the role of the MLL gene in infant and childhood
leukemia
.
Translocations involving the Mixed Lineage
Leukemia
(MLL) gene at 11q23 are found in both
acute
lymphoblastic
leukemia
(ALL) and
acute
myeloblastic
leukemia
(AML), but have different prognostic implications depending on the phenotype of the
leukemia
in
de
novo pediatric cases.
The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged
leukemias
is shedding light on the molecular mechanisms and potential therapeutic targets of these
leukemias
.
[MeSH-major]
Gene Rearrangement.
Leukemia
, Myeloid,
Acute
/ genetics. Myeloid-Lymphoid
Leukemia
Protein / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17905612.001).
[ISSN]
1079-9796
[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; Review
[Publication-country]
United States
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Number-of-references]
82
Advertisement
4.
Migkou M, Dimopoulos MA, Gavriatopoulou M, Terpos E:
Applications of monoclonal antibodies for the treatment of hematological malignancies.
Expert Opin Biol Ther
; 2009 Feb;9(2):207-20
[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.
BACKGROUND: The introduction of mAbs has changed the clinical approach to patients with lymphoma and
leukemia
.
RESULTS: Rituximab (anti-CD20) was the first mAb developed for the treatment of B-
cell
lymphomas.
Several randomized studies have demonstrated its efficacy in lymphomas and low toxicity profile; rituximab also has significant activity in chronic
lymphocytic leukemia
(CLL).
Alemtuzumab (anti-CD52) has shown efficacy in previously untreated or refractory CLL patients, while gemtuzumab ozogamicin (anti-CD33) appears to have significant activity in
acute
myeloid
leukemias
and myelodysplastic syndromes.
CONCLUSIONS: In the next few years, investigations will be concentrated on the improvement of the older mAbs, and the development of new mAbs, targeting molecules important for malignant
cell
cycle and survival in an attempt to further improve patient survival.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ drug therapy. Lymphoma, Non-Hodgkin / drug therapy
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19236251.001).
[ISSN]
1744-7682
[Journal-full-title]
Expert opinion on biological therapy
[ISO-abbreviation]
Expert Opin Biol Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
[Number-of-references]
107
5.
Lü SQ, Yang JM, Wang JM:
[Effects of proteasome inhibitors on leukemias].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Aug;15(4):896-900
[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]
[Effects of proteasome inhibitors on
leukemias
].
A lot of studies on effects of proteasome inhibitors on
leukemias
, including plasma
cell
leukemia
; chronic
lymphocytic leukemia
, adult T
cell
lymphoma/
leukemia
, chronic myeloid
leukemia
and
acute
myeloid
leukemia
, were reviewed in this article.
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17708829.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
China
[Chemical-registry-number]
0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
[Number-of-references]
27
6.
Diakos C, Zhong S, Xiao Y, Zhou M, Vasconcelos GM, Krapf G, Yeh RF, Zheng S, Kang M, Wiencke JK, Pombo-de-Oliveira MS, Panzer-Grümayer R, Wiemels JL:
TEL-AML1 regulation of survivin and apoptosis via miRNA-494 and miRNA-320a.
Blood
; 2010 Dec 2;116(23):4885-93
[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.
We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood
leukemia
, on miRNA expression and the leukemic phenotype.
These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be Dicer-dependent. miRNAs-494 and -320a are expressed at lower levels in TEL-AML1+
leukemias
compared with immunophenotype-matched nonTEL-AML1
acute
lymphoblastic
leukemia
subtypes, and within TEL-AML1+
leukemias
their expression is correlated to survivin levels.
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
[Cites]
Int J Cancer. 2008 Mar 1;122(5):969-77
[
18098138.001
]
[Cites]
Science. 2008 Jan 18;319(5861):336-9
[
18202291.001
]
[Cites]
Curr Top Microbiol Immunol. 2008;320:77-97
[
18268840.001
]
[Cites]
Nature. 2008 Feb 28;451(7182):1125-9
[
18278031.001
]
[Cites]
Science. 2008 Mar 28;319(5871):1789-90
[
18369137.001
]
[Cites]
Oncogene. 2008 Apr 10;27(17):2412-21
[
17968314.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15535-40
[
18832181.001
]
[Cites]
Blood. 2009 Jan 8;113(2):412-21
[
18941112.001
]
[Cites]
J Clin Invest. 2009 Apr;119(4):826-36
[
19287094.001
]
[Cites]
Blood. 2009 May 7;113(19):4586-94
[
19202128.001
]
[Cites]
Semin Immunol. 2005 Apr;17(2):155-65
[
15737576.001
]
[Cites]
Nat Methods. 2004 Oct;1(1):47-53
[
15782152.001
]
[Cites]
Nature. 2005 Jun 9;435(7043):834-8
[
15944708.001
]
[Cites]
Oncogene. 2005 Nov 17;24(51):7579-91
[
16044150.001
]
[Cites]
Mol Cancer Ther. 2006 May;5(5):1087-98
[
16731740.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15166-71
[
17015828.001
]
[Cites]
Blood. 2006 Dec 1;108(12):3646-53
[
16882713.001
]
[Cites]
Blood. 2007 Mar 15;109(6):2607-10
[
17095626.001
]
[Cites]
J Biol Chem. 2007 Mar 30;282(13):9703-12
[
17259635.001
]
[Cites]
DNA Cell Biol. 2007 May;26(5):273-82
[
17504023.001
]
[Cites]
Mol Cell Biol. 2007 Jun;27(11):3995-4005
[
17371837.001
]
[Cites]
Paediatr Drugs. 2007;9(3):149-56
[
17523695.001
]
[Cites]
Nature. 2007 Jun 28;447(7148):1130-4
[
17554337.001
]
[Cites]
Mol Cell. 2007 Jul 6;27(1):91-105
[
17612493.001
]
[Cites]
J Exp Med. 2007 Jul 9;204(7):1603-11
[
17576776.001
]
[Cites]
Haematologica. 2007 Aug;92(8):1043-50
[
17640858.001
]
[Cites]
Clin Cancer Res. 2007 Oct 15;13(20):5991-4
[
17947459.001
]
[Cites]
Cancer Cell. 2007 Nov;12(5):457-66
[
17996649.001
]
[Cites]
Lancet. 1999 Oct 30;354(9189):1499-503
[
10551495.001
]
[Cites]
Curr Opin Oncol. 2000 Jan;12(1):3-12
[
10687723.001
]
[Cites]
Curr Opin Hematol. 2001 Jul;8(4):197-200
[
11561155.001
]
[Cites]
Cancer Genet Cytogenet. 2001 Oct 15;130(2):93-104
[
11675129.001
]
[Cites]
Int J Hematol. 2001 Oct;74(3):258-65
[
11721960.001
]
[Cites]
Oncogene. 2002 May 13;21(21):3475-95
[
12032783.001
]
[Cites]
Curr Opin Hematol. 2002 Jul;9(4):345-52
[
12042710.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8242-7
[
12048236.001
]
[Cites]
Cancer Cell. 2002 Mar;1(2):133-43
[
12086872.001
]
[Cites]
Mol Cell. 2003 Jun;11(6):1587-98
[
12820971.001
]
[Cites]
Oncogene. 2004 May 24;23(24):4275-83
[
15156184.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8443-8
[
15155899.001
]
[Cites]
Biochim Biophys Acta. 1996 Aug 8;1288(1):M7-10
[
8764840.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4584-8
[
9539781.001
]
[Cites]
Blood. 1999 Aug 1;94(3):1057-62
[
10419898.001
]
[Cites]
Int J Hematol. 2004 Oct;80(3):232-8
[
15540897.001
]
(PMID = 20807887.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R03-CA137829; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NCI NIH HHS / CA / R03 CA137829; United States / NCI NIH HHS / CA / R01-CA89032; United States / NCI NIH HHS / CA / CA137829-02; United States / NCI NIH HHS / CA / R03 CA137829-02; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NCI NIH HHS / CA / CA137829-01A1; United States / NCI NIH HHS / CA / R03 CA137829-01A1
[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 / BIRC5 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / MicroRNAs; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein
[Other-IDs]
NLM/ PMC3265147
7.
Schwonzen M, Diehl V, Dellanna M, Staib P:
Immunophenotyping of surface antigens in acute myeloid leukemia by flow cytometry after red blood cell lysis.
Leuk Res
; 2007 Jan;31(1):113-6
[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]
Immunophenotyping of surface antigens in
acute
myeloid
leukemia
by flow cytometry after red blood
cell
lysis.
Immunophenotyping of
acute
leukemia
using flow cytometry after density gradient separation (dg-sep) of mononuclear cells is the international gold standard.
Both methods revealed congruent results in phenotyping of 26 cases of
acute
myeloid
leukemias
by testing CD4, CD7, CD11b, CD11c, CD13, CD14, CD15, CD33, CD34, CD65s, Glycophorin A and HLA-DR antigens.
[MeSH-major]
Antigens, CD / analysis. Antigens, Surface / analysis.
Leukemia
, Myeloid,
Acute
/ genetics
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16730795.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Surface; 0 / Glycophorin; 0 / HLA-DR Antigens
8.
Cairoli R, Beghini A, Grillo G, Nadali G, Elice F, Ripamonti CB, Colapietro P, Nichelatti M, Pezzetti L, Lunghi M, Cuneo A, Viola A, Ferrara F, Lazzarino M, Rodeghiero F, Pizzolo G, Larizza L, Morra E:
Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study.
Blood
; 2006 May 1;107(9):3463-8
[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]
Prognostic impact
of c
-KIT mutations in core binding factor
leukemias
: an Italian retrospective study.
Distinct forms of tyrosine kinase domain (TKD), juxtamembrane domain, exon 8, and internal tandem duplication (ITD) mutations
of c
-KIT, were observed in about 46% of core binding factor
leukemia
(CBFL) patients.
In
acute
myeloid
leukemia
(AML) with t(8;21), the presence
of c
-KIT TKD mutation at codon 816 (TKD(816)) was associated with a high white blood
cell
count at diagnosis (median, 29.60 x 10(9)/L) and a higher incidence (33%) of extramedullary
leukemia
(EML) during the course of the
disease
.
[MeSH-major]
Core Binding Factors / genetics.
Leukemia
, Myeloid,
Acute
/ genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16384925.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
9.
Ishii E, Oda M, Kinugawa N, Oda T, Takimoto T, Suzuki N, Kosaka Y, Ohara A, Ogawa A, Ishii M, Sakata N, Okamura T, Koike K, Kojima S, Horibe K, Mizutani S:
Features and outcome of neonatal leukemia in Japan: experience of the Japan infant leukemia study group.
Pediatr Blood Cancer
; 2006 Sep;47(3):268-72
[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]
Features and outcome of neonatal
leukemia
in Japan: experience of the Japan infant
leukemia
study group.
BACKGROUND: Neonatal
leukemia
characterized by early stem
cell
origin and extramedullary infiltration in the first 4 weeks of life is rare.
We analyzed the features and outcome of neonatal
leukemia
in Japan to establish an appropriate treatment strategy for this rare disorder.
PROCEDURE: Patients with infant
leukemia
registered and treated in the Japan Infant
Leukemia
Study between 1996 and 2001 were analyzed.
RESULTS: Among 162 infant
leukemia
patients, 11 exhibited neonatal
leukemia
; frequencies for all infant
leukemias
were 6.9% (8/116) for
acute
lymphoblastic
leukemia
(ALL) and 7.3% (3/41) for
acute
myeloid
leukemia
(AML).
Acute
monoblastic
leukemia
was apparent in all three patients with AML (M5a in the FAB classification).
Four patients (one with AML, and three with ALL) have survived following stem
cell
transplantation (SCT); however, growth impairment related to SCT was observed in these patients.
CONCLUSIONS: These results suggest an improvement attributable to treatment of neonatal
leukemia
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
, Myeloid / therapy. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / therapy. Stem
Cell
Transplantation
[MeSH-minor]
Acute
Disease
. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Japan / epidemiology. Male. Myeloid-Lymphoid
Leukemia
Protein / genetics. Registries. Survival Rate. Treatment Outcome
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Pediatr Blood Cancer. 2006 Sep;47(3):234-5
[
16206196.001
]
(PMID = 16333820.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
10.
Miller AL, Komak S, Webb MS, Leiter EH, Thompson EB:
Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids.
Cancer Cell Int
; 2007 Nov 28;7:18
[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.
By activating the glucocorticoid receptor (GR), GCs evoke apoptosis through transcriptional regulation
of a
complex, interactive gene network over a period of time preceding activation of the apoptotic enzymes.
Pediatric CD4+/CD8+ T-
cell
leukemia
was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.
GC-sensitive pediatric B-
cell
leukemia
was represented by the SUP-B15 line and adult B-
cell
leukemia
by RS4;11 cells.
Kasumi-1 cells gave an example of the rare Dex-sensitive
acute
myeloblastic
leukemia
(AML).
To test the generality of the correlations in malignant
cell
gene sets, we compared with GC effects on mouse non-transformed thymocytes.
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
[Cites]
Cell Growth Differ. 1995 May;6(5):505-13
[
7647033.001
]
[Cites]
Leuk Res. 1997 Jan;21(1):45-50
[
9029185.001
]
[Cites]
Cancer Res. 1998 Aug 15;58(16):3684-93
[
9721879.001
]
[Cites]
Blood. 1998 Oct 15;92(8):2730-41
[
9763557.001
]
[Cites]
Int Immunol. 1998 Dec;10(12):1807-17
[
9885901.001
]
[Cites]
Blood. 1999 Aug 15;94(4):1209-17
[
10438708.001
]
[Cites]
Science. 1999 Nov 26;286(5445):1735-8
[
10576740.001
]
[Cites]
Cell Death Differ. 1999 Dec;6(12):1182-9
[
10637434.001
]
[Cites]
Hum Mol Genet. 2000 Jul 1;9(11):1681-90
[
10861295.001
]
[Cites]
Oncogene. 2001 Jul 19;20(32):4324-36
[
11466613.001
]
[Cites]
Oncogene. 2002 Feb 21;21(9):1346-58
[
11857078.001
]
[Cites]
Mol Cell Biol. 2002 Apr;22(7):2283-93
[
11884613.001
]
[Cites]
Neoplasia. 2002 Jan-Feb;4(1):68-81
[
11922393.001
]
[Cites]
Biochem Biophys Res Commun. 2002 May 17;293(4):1254-61
[
12054511.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jan;88(1):277-84
[
12519866.001
]
[Cites]
Leukemia. 2003 Jan;17(1):17-25
[
12529655.001
]
[Cites]
J Biol Chem. 2003 Jun 27;278(26):23861-7
[
12676946.001
]
[Cites]
J Biol Chem. 2003 Jul 18;278(29):27053-8
[
12736248.001
]
[Cites]
Genomics. 2003 Jun;81(6):543-55
[
12782123.001
]
[Cites]
Recent Prog Horm Res. 2003;58:175-97
[
12795419.001
]
[Cites]
Cancer. 1965 Apr;18:522-9
[
14278051.001
]
[Cites]
Eur J Endocrinol. 2004 Jan;150(1):41-7
[
14713278.001
]
[Cites]
J Biol Chem. 2004 May 14;279(20):20858-65
[
14996839.001
]
[Cites]
Mol Cell Endocrinol. 2004 Apr 15;218(1-2):49-55
[
15130510.001
]
[Cites]
J Biol Chem. 2004 Dec 31;279(53):55809-17
[
15509554.001
]
[Cites]
Blood. 2005 Mar 15;105(6):2519-26
[
15572593.001
]
[Cites]
Ann Acad Med Singapore. 2004 Sep;33(5 Suppl):S21-2
[
15651190.001
]
[Cites]
Mol Endocrinol. 2005 Jun;19(6):1569-83
[
15817653.001
]
[Cites]
Clin Cancer Res. 2005 Aug 15;11(16):6050-6
[
16115950.001
]
[Cites]
Blood. 2005 Dec 15;106(13):4131-8
[
16118324.001
]
[Cites]
Anticancer Res. 2005 May-Jun;25(3B):2253-8
[
16158972.001
]
[Cites]
Blood. 2006 Mar 1;107(5):2061-9
[
16293608.001
]
[Cites]
Oncogene. 2006 Mar 23;25(13):1903-13
[
16301999.001
]
[Cites]
Leukemia. 2006 Jun;20(6):987-93
[
16598301.001
]
[Cites]
FEBS Lett. 2006 Jun 12;580(14):3539-44
[
16730715.001
]
[Cites]
J Pharmacol Exp Ther. 2006 Nov;319(2):887-97
[
16914556.001
]
[Cites]
J Dermatol. 2006 Oct;33(10):662-9
[
17040494.001
]
[Cites]
J Biol Chem. 2006 Dec 22;281(51):39051-61
[
17062574.001
]
[Cites]
Leukemia. 2007 Feb;21(2):281-7
[
17151701.001
]
[Cites]
Blood. 2007 May 1;109(9):3929-35
[
17218380.001
]
[Cites]
Ann Rheum Dis. 2007 Oct;66(10):1289-95
[
17267514.001
]
[Cites]
Cancer Cell Int. 2007;7:3
[
17391526.001
]
[Cites]
Cancer Res. 2007 May 1;67(9):4482-90
[
17483364.001
]
[Cites]
Steroids. 2007 Sep;72(9-10):673-81
[
17606285.001
]
[Cites]
Blood. 1991 May 1;77(9):2031-6
[
2018839.001
]
[Cites]
J Steroid Biochem Mol Biol. 1991 May;38(5):561-8
[
2039752.001
]
[Cites]
Cancer Res. 1988 May 15;48(10):2876-9
[
3162827.001
]
[Cites]
Blood. 1985 Jan;65(1):21-31
[
3917311.001
]
[Cites]
Int J Cancer. 1985 Aug 15;36(2):241-6
[
3926660.001
]
[Cites]
Leukemia. 1995 Oct;9(10):1771-8
[
7564524.001
]
(PMID = 18045478.001).
[ISSN]
1475-2867
[Journal-full-title]
Cancer cell international
[ISO-abbreviation]
Cancer Cell Int.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA041407
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2228275
11.
Kojima K, Burks JK, Arts J, Andreeff M:
The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias.
Mol Cancer Ther
; 2010 Sep;9(9):2545-57
[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 novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in
acute
myeloid and lymphoid
leukemias
.
The development of small-molecule activators of p53 is currently focused on malignancies containing a wild-type p53 genotype, which is present in most
leukemias
.
Here, we report the effects of JNJ-26854165 in
acute leukemias
.
JNJ-26854165 treatment induced p53-mediated apoptosis in
acute
leukemia
cells with wild-type p53, in which p53 rapidly drives transcription-independent apoptosis followed by activation
of a
transcription-dependent pathway.
Apoptotic activity of JNJ-26854165 against primary
acute
leukemia
cells was maintained in
leukemia
/stroma cocultures, unlike doxorubicin, which has reduced cytrotoxicity in coculture systems.
Our data suggest that JNJ-26854165 may provide a novel therapeutic approach for the treatment of
acute leukemias
.
[MeSH-major]
Apoptosis / drug effects. E2F1 Transcription Factor / metabolism. Genes, p53.
Leukemia
, Myeloid,
Acute
/ drug therapy. Tryptamines / pharmacology
[MeSH-minor]
Cell
Line, Tumor. Humans. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / metabolism. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / pathology. Transfection
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 2010 Jan 14;115(2):306-14
[
19897582.001
]
[Cites]
Biochemistry. 2009 Dec 29;48(51):12159-68
[
19916559.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):552-8
[
12766778.001
]
[Cites]
Mol Cancer Res. 2003 Dec;1(14):1001-8
[
14707283.001
]
[Cites]
Science. 2004 Feb 6;303(5659):844-8
[
14704432.001
]
[Cites]
J Biol Chem. 2004 Mar 5;279(10):8627-34
[
14684737.001
]
[Cites]
Mol Cell Biol. 2004 Aug;24(15):6728-41
[
15254240.001
]
[Cites]
Adv Enzyme Regul. 1984;22:27-55
[
6382953.001
]
[Cites]
Science. 1991 Jul 5;253(5015):49-53
[
1905840.001
]
[Cites]
Blood. 1993 Nov 1;82(9):2617-23
[
8219216.001
]
[Cites]
Oncogene. 1998 Mar 26;16(12):1513-23
[
9569018.001
]
[Cites]
Cell Death Differ. 2005 Apr;12(4):377-83
[
15706352.001
]
[Cites]
Blood. 2005 Nov 1;106(9):3150-9
[
16014563.001
]
[Cites]
Oncogene. 2005 Nov 3;24(48):7238-47
[
16170383.001
]
[Cites]
Blood. 2006 May 15;107(10):4122-9
[
16439677.001
]
[Cites]
Blood. 2006 Aug 1;108(3):993-1000
[
16543464.001
]
[Cites]
Nat Chem Biol. 2006 Sep;2(9):474-9
[
16862141.001
]
[Cites]
Mod Pathol. 2007 Jan;20(1):54-62
[
17143258.001
]
[Cites]
Hum Mutat. 2007 Jun;28(6):622-9
[
17311302.001
]
[Cites]
Oncogene. 2007 May 24;26(24):3473-81
[
17146434.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3933-8
[
18316739.001
]
[Cites]
Leukemia. 2008 Apr;22(4):730-9
[
18273046.001
]
[Cites]
Br J Haematol. 2008 May;141(4):445-53
[
18341636.001
]
[Cites]
Cancer Cell. 2008 May;13(5):454-63
[
18455128.001
]
[Cites]
Leukemia. 2008 Sep;22(9):1728-36
[
18548093.001
]
[Cites]
Oncogene. 2008 Sep 11;27(40):5303-14
[
18521084.001
]
[Cites]
Blood. 2008 Nov 1;112(9):3827-34
[
18682598.001
]
[Cites]
Expert Opin Investig Drugs. 2008 Dec;17(12):1865-82
[
19012502.001
]
[Cites]
Nat Rev Drug Discov. 2008 Dec;7(12):979-87
[
19043449.001
]
[Cites]
Cancer Cell. 2009 Mar 3;15(3):171-83
[
19249676.001
]
[Cites]
Apoptosis. 2009 Apr;14(4):597-606
[
19259822.001
]
[Cites]
Int J Oncol. 2009 May;34(5):1395-402
[
19360352.001
]
[Cites]
Blood. 2009 Apr 30;113(18):4300-8
[
19190243.001
]
[Cites]
Nature. 2009 Apr 30;458(7242):1127-30
[
19407794.001
]
[Cites]
Cell Cycle. 2009 Jun 1;8(11):1711-9
[
19411846.001
]
[Cites]
Lancet Oncol. 2009 Sep;10(9):913-9
[
19717093.001
]
[Cites]
Blood. 2009 Nov 12;114(20):4451-9
[
19759355.001
]
[Cites]
Methods. 2001 Dec;25(4):402-8
[
11846609.001
]
(PMID = 20736344.001).
[ISSN]
1538-8514
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA89346; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA089346-03; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / P01 CA049639-09A19007; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA055164-09; United States / NCI NIH HHS / CA / R01 CA089346; United States / NCI NIH HHS / CA / P30 CA016672-22S29015; United States / NCI NIH HHS / CA / P01 CA055164-08; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA055164
[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 / E2F1 Transcription Factor; 0 / Tryptamines
[Other-IDs]
NLM/ NIHMS231527; NLM/ PMC2949269
12.
Zwaan MC, Reinhardt D, Hitzler J, Vyas P:
Acute leukemias in children with Down syndrome.
Pediatr Clin North Am
; 2008 Feb;55(1):53-70, x
[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]
Acute leukemias
in children with Down syndrome.
Children with Down syndrome have an increased risk for developing both
acute
myeloid as well as lymphoblastic
leukemia
.
These
leukemias
differ in presenting characteristics and underlying biology when compared with
leukemias
occurring in non-Down syndrome children.
Myeloid
leukemia
in children with Down syndrome is preceded by a preleukemic clone (transient
leukemia
or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.
Twenty percent of children with transient
leukemia
subsequently develop myeloid
leukemia
.
This transition offers a unique model to study the stepwise development
of leukemia
, and of gene dosage effects mediated by aneuploidy.
[MeSH-major]
Down Syndrome / complications.
Leukemia
, Myeloid / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic.
Disease
Progression. Humans. Infant. Infant, Newborn. Mutation
Genetic Alliance.
consumer health - Down Syndrome
.
MedlinePlus Health Information.
consumer health - Down Syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18242315.001).
[ISSN]
0031-3955
[Journal-full-title]
Pediatric clinics of North America
[ISO-abbreviation]
Pediatr. Clin. North Am.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
83
13.
Radomska HS, Bassères DS, Zheng R, Zhang P, Dayaram T, Yamamoto Y, Sternberg DW, Lokker N, Giese NA, Bohlander SK, Schnittger S, Delmotte MH, Davis RJ, Small D, Hiddemann W, Gilliland DG, Tenen DG:
Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.
J Exp Med
; 2006 Feb 20;203(2):371-81
[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]
Block
of C
/EBP alpha function by phosphorylation in
acute
myeloid
leukemia
with FLT3 activating mutations.
Mutations constitutively activating FLT3 kinase are detected in approximately 30% of
acute
myelogenous
leukemia
(AML) patients and affect downstream pathways such as extracellular signal-regulated kinase (ERK)1/2.
In contrast, there was no effect when serine 21 was mutated to aspartate (S21D), which mimics phosphorylation
of C
/EBPalpha.
Thus, our results suggest that therapies targeting the MEK/ERK cascade or development of protein therapies based on transduction of constitutively active C/EBPalpha may prove effective in treatment of FLT3 mutant
leukemias
resistant to the FLT3 inhibitor therapies.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
PhosphoSitePlus.
gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource
.
Hazardous Substances Data Bank.
L-SERINE
.
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 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
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 2002 Oct 15;100(8):2717-23
[
12351377.001
]
[Cites]
Blood. 2002 Dec 15;100(13):4372-80
[
12393388.001
]
[Cites]
Leukemia. 2003 Jan;17(1):120-4
[
12529668.001
]
[Cites]
Blood. 2003 Feb 15;101(4):1494-504
[
12406902.001
]
[Cites]
Nat Rev Cancer. 2003 Feb;3(2):89-101
[
12563308.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74
[
9012825.001
]
[Cites]
Leuk Res. 1997 Apr;21(4):327-35
[
9150350.001
]
[Cites]
Leukemia. 1997 Sep;11(9):1469-77
[
9305600.001
]
[Cites]
Leukemia. 1997 Oct;11(10):1605-9
[
9324277.001
]
[Cites]
Mol Cell Biol. 1998 Jan;18(1):322-33
[
9418879.001
]
[Cites]
Mol Cell Biol. 1998 Jul;18(7):4301-14
[
9632814.001
]
[Cites]
Blood. 1999 May 1;93(9):3074-80
[
10216104.001
]
[Cites]
Leukemia. 2003 Feb;17(2):343-9
[
12592334.001
]
[Cites]
Genes Chromosomes Cancer. 2003 May;37(1):72-8
[
12661007.001
]
[Cites]
Blood. 2003 Apr 15;101(8):3164-73
[
12468433.001
]
[Cites]
Hematol J. 2003;4(1):31-40
[
12692518.001
]
[Cites]
Blood. 2003 Jun 15;101(12):4667-79
[
12623839.001
]
[Cites]
Oncogene. 2000 Feb 3;19(5):624-31
[
10698507.001
]
[Cites]
Nature. 2000 Mar 9;404(6774):193-7
[
10724173.001
]
[Cites]
Leukemia. 2000 Apr;14(4):675-83
[
10764154.001
]
[Cites]
J Pharmacol Exp Ther. 2000 Oct;295(1):139-45
[
10991971.001
]
[Cites]
Leukemia. 2000 Oct;14(10):1766-76
[
11021752.001
]
[Cites]
Genes Dev. 2000 Oct 1;14(19):2501-14
[
11018017.001
]
[Cites]
Blood. 2000 Dec 1;96(12):3907-14
[
11090077.001
]
[Cites]
Br J Haematol. 2000 Oct;111(1):190-5
[
11091200.001
]
[Cites]
Int J Oncol. 2001 Mar;18(3):559-65
[
11179487.001
]
[Cites]
Nat Genet. 2001 Mar;27(3):263-70
[
11242107.001
]
[Cites]
Nat Med. 2001 Apr;7(4):444-51
[
11283671.001
]
[Cites]
Blood. 2001 Apr 15;97(8):2434-9
[
11290608.001
]
[Cites]
Clin Cancer Res. 2003 Jun;9(6):2140-50
[
12796379.001
]
[Cites]
Leukemia. 2003 Jul;17(7):1263-93
[
12835716.001
]
[Cites]
Leukemia. 2003 Sep;17(9):1783-93
[
12970778.001
]
[Cites]
Blood. 2003 Oct 15;102(8):2763-7
[
12843001.001
]
[Cites]
Blood. 2003 Nov 1;102(9):3163-71
[
12869508.001
]
[Cites]
Semin Oncol. 2003 Oct;30(5 Suppl 16):105-16
[
14613031.001
]
[Cites]
Clin Cancer Res. 2003 Nov 15;9(15):5465-76
[
14654525.001
]
[Cites]
Mol Cell Biol. 2004 Jan;24(2):675-86
[
14701740.001
]
[Cites]
J Clin Oncol. 2004 Feb 15;22(4):624-33
[
14726504.001
]
[Cites]
Blood. 2004 Mar 1;103(5):1883-90
[
14592841.001
]
[Cites]
Eur J Cancer. 2004 Mar;40(5):707-21, discussion 722-4
[
15010072.001
]
[Cites]
Blood. 2004 Apr 1;103(7):2744-52
[
14656889.001
]
[Cites]
Blood. 2004 May 15;103(10):3669-76
[
14726387.001
]
[Cites]
Ann Hematol. 2004;83 Suppl 1:S89-90
[
15124689.001
]
[Cites]
Nature. 1970 Aug 15;227(5259):680-5
[
5432063.001
]
[Cites]
Blood. 1987 Jul;70(1):192-9
[
3496132.001
]
[Cites]
J Immunol. 1987 Nov 15;139(10):3348-54
[
3500218.001
]
[Cites]
Int J Cancer. 1988 Mar 15;41(3):456-61
[
3162233.001
]
[Cites]
Science. 1991 Jan 18;251(4991):288-92
[
1987644.001
]
[Cites]
Leukemia. 1995 Dec;9(12):2058-66
[
8609717.001
]
[Cites]
Oncogene. 1995 Dec 7;11(11):2365-74
[
8570188.001
]
[Cites]
Leukemia. 1996 Feb;10(2):238-48
[
8637232.001
]
[Cites]
Leukemia. 1996 Dec;10(12):1911-8
[
8946930.001
]
[Cites]
Blood. 1999 Jul 15;94(2):560-71
[
10397723.001
]
[Cites]
Methods Enzymol. 2001;332:319-36
[
11305107.001
]
[Cites]
Mol Cell Biol. 2001 Jun;21(11):3789-806
[
11340171.001
]
[Cites]
Best Pract Res Clin Haematol. 2001 Mar;14(1):19-47
[
11355922.001
]
[Cites]
Br J Haematol. 2001 Jun;113(4):983-8
[
11442493.001
]
[Cites]
Leukemia. 2001 Jul;15(7):1001-10
[
11455967.001
]
[Cites]
Blood. 2001 Aug 1;98(3):885-7
[
11468194.001
]
[Cites]
Blood. 2001 Sep 15;98(6):1752-9
[
11535508.001
]
[Cites]
Cancer Res. 2001 Oct 1;61(19):7233-9
[
11585760.001
]
[Cites]
Nat Genet. 2002 Jan;30(1):48-58
[
11753385.001
]
[Cites]
Blood. 2002 Jan 1;99(1):310-8
[
11756186.001
]
[Cites]
Blood. 2002 Feb 15;99(4):1332-40
[
11830484.001
]
[Cites]
Blood. 2002 Jun 1;99(11):3885-91
[
12010785.001
]
[Cites]
Blood. 2002 Jun 15;99(12):4406-12
[
12036869.001
]
[Cites]
Cancer Cell. 2002 Jun;1(5):421-32
[
12124172.001
]
[Cites]
Cancer Cell. 2002 Jun;1(5):433-43
[
12124173.001
]
[Cites]
Blood. 2002 Sep 1;100(5):1532-42
[
12176867.001
]
(PMID = 16446383.001).
[ISSN]
0022-1007
[Journal-full-title]
The Journal of experimental medicine
[ISO-abbreviation]
J. Exp. Med.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / K01 DK062064; United States / NCI NIH HHS / CA / P01 CA072009; United States / NIDDK NIH HHS / DK / DK62064; United States / NCI NIH HHS / CA / P01 CA72009
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Piperazines; 0 / Quinazolines; 452VLY9402 / Serine; E1IO3ICJ9A / tandutinib; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1
[Other-IDs]
NLM/ PMC2118199
14.
Pratz KW, Cho E, Levis MJ, Karp JE, Gore SD, McDevitt M, Stine A, Zhao M, Baker SD, Carducci MA, Wright JJ, Rudek MA, Smith BD:
A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.
Leukemia
; 2010 Aug;24(8):1437-44
[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 pharmacodynamic study of sorafenib in patients with relapsed and refractory
acute leukemias
.
We report the results
of a
phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory
acute
leukemia
patients using an intermittent dosing regimen.
Fifteen patients with advanced
leukemia
(12 with
acute
myeloid
leukemia
, 2 with
acute
lymphoblastic
leukemia
, 1 with biphenotypic) and a median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.
Out of 15 patients, 11 experienced stable
disease
as best response.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use.
Leukemia
, Myeloid,
Acute
/ drug therapy. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
Hazardous Substances Data Bank.
NICOTINAMIDE
.
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
[Cites]
Onkologie. 2002 Dec;25(6):511-8
[
12566895.001
]
[Cites]
J Clin Oncol. 2003 Dec 15;21(24):4642-9
[
14673054.001
]
[Cites]
Blood. 2004 May 15;103(10):3669-76
[
14726387.001
]
[Cites]
Br J Clin Pharmacol. 2004 Aug;58(2):212-6
[
15255805.001
]
[Cites]
Blood. 2004 Aug 15;104(4):1145-50
[
15126317.001
]
[Cites]
Blood. 2004 Sep 15;104(6):1841-9
[
15166029.001
]
[Cites]
Cancer Res. 2004 Oct 1;64(19):7099-109
[
15466206.001
]
[Cites]
J Pharm Sci. 1972 Jun;61(6):952-4
[
5046120.001
]
[Cites]
Eur J Drug Metab Pharmacokinet. 1991 Oct-Dec;16(4):249-55
[
1823867.001
]
[Cites]
Blood. 2005 Jan 15;105(2):812-20
[
15374878.001
]
[Cites]
J Clin Oncol. 2005 Feb 10;23(5):965-72
[
15613696.001
]
[Cites]
Br J Cancer. 2005 May 23;92(10):1855-61
[
15870716.001
]
[Cites]
Clin Cancer Res. 2005 Aug 1;11(15):5472-80
[
16061863.001
]
[Cites]
Blood. 2005 Aug 15;106(4):1154-63
[
15870183.001
]
[Cites]
Leukemia. 2005 Sep;19(9):1543-9
[
16001087.001
]
[Cites]
Ann Oncol. 2005 Oct;16(10):1688-94
[
16006586.001
]
[Cites]
Blood. 2005 Oct 1;106(7):2484-90
[
15956279.001
]
[Cites]
Oncogene. 2005 Oct 20;24(46):6861-9
[
16007148.001
]
[Cites]
Cancer Chemother Pharmacol. 2006 May;57(5):685-92
[
16133532.001
]
[Cites]
Expert Opin Pharmacother. 2006 Mar;7(4):453-61
[
16503817.001
]
[Cites]
Cytometry B Clin Cytom. 2006 May;70(3):107-14
[
16498671.001
]
[Cites]
J Clin Oncol. 2006 Sep 10;24(26):4293-300
[
16908937.001
]
[Cites]
Blood. 2006 Oct 1;108(7):2358-65
[
16763210.001
]
[Cites]
Blood. 2006 Nov 15;108(10):3477-83
[
16857987.001
]
[Cites]
Clin Cancer Res. 2006 Dec 15;12(24):7271-8
[
17189398.001
]
[Cites]
J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Feb 1;846(1-2):1-7
[
16798122.001
]
[Cites]
Oncologist. 2007 Apr;12(4):426-37
[
17470685.001
]
[Cites]
J Biol Chem. 2007 Oct 12;282(41):29831-46
[
17698840.001
]
[Cites]
J Natl Cancer Inst. 2008 Feb 6;100(3):184-98
[
18230792.001
]
[Cites]
Curr Opin Hematol. 2008 Jul;15(4):400-7
[
18536580.001
]
[Cites]
Leuk Res. 2009 Feb;33(2):348-50
[
18573526.001
]
[Cites]
Blood. 2009 Apr 23;113(17):3938-46
[
19029442.001
]
[Cites]
Blood. 2009 Jun 25;113(26):6567-71
[
19389879.001
]
[Cites]
Blood. 2010 Feb 18;115(7):1425-32
[
20007803.001
]
(PMID = 20535150.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
[Other-IDs]
NLM/ NIHMS201571; NLM/ PMC2921005
15.
Lu L, Zhang L, Xiao Z, Lu S, Yang R, Han ZC:
Neuropilin-1 in acute myeloid leukemia: expression and role in proliferation and migration of leukemia cells.
Leuk Lymphoma
; 2008 Feb;49(2):331-8
[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]
Neuropilin-1 in
acute
myeloid
leukemia
: expression and role in proliferation and migration
of leukemia
cells.
The role of NRP-1 in the growth and progression
of leukemia
is unknown.
Our results showed that NRP-1 mRNA was expressed in six of seven leukemic
cell
lines and primary
leukemias
derived from all 24 patients with
acute
myeloid
leukemia
(AML).
Reduced NRP-1 expression by RNA interference led to a decrease of VEGF-mediated mitogenic and migration responses in
acute
myeloid leukemic
cell
line HEL.
Our data demonstrated that a higher
level of
NRP-1 mRNA was expressed in
leukemias
and NRP-1 promoted proliferation and chemotaxis of leukemic cells in response to VEGF.
[MeSH-major]
Cell
Movement.
Cell
Proliferation. Gene Expression Regulation, Leukemic.
Leukemia
, Myeloid,
Acute
/ pathology. Neuropilin-1 / analysis. Vascular Endothelial Growth Factor A / physiology
[MeSH-minor]
Adolescent. Adult. Aged.
Cell
Survival. Chemotaxis. Child. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18231921.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 144713-63-3 / Neuropilin-1
16.
Yamamoto JF, Goodman MT:
Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
Cancer Causes Control
; 2008 May;19(4):379-90
[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]
Patterns
of leukemia
incidence in the United States by subtype and demographic characteristics, 1997-2002.
OBJECTIVE: Efforts to prevent
leukemia
have been hampered by an inability to identify significant risk factors.
Exploring incidence patterns
of leukemia
subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns
of leukemia
incidence by subtype, sex, age, race and ethnicity.
RESULTS: A total of 144,559
leukemia
cases were identified, including 66,067 (46%)
acute
and 71,860 (50%) chronic
leukemias
.
The highest rates of
acute
myeloid
leukemia
with and without maturation were observed in Asian-Pacific Islanders (API).
Hispanics had a higher incidence of
acute
lymphocytic leukemia
, particularly in childhood, and promyelocytic
leukemia
than did non-Hispanics.
African-Americans had the highest rates of HTLV-1 positive adult T-
cell
leukemia
/lymphoma.
A sharp increase in the incidence of chronic myeloid
leukemia
was observed for both APIs and Hispanics, 85 years and older.
CONCLUSION: Known risk factors are unlikely to explain the observed disparities in
leukemia
incidence.
Further studies of differences in environmental and genetic risk factors in these populations by specific
leukemia
subtype may provide clues to the etiologies of these malignancies.
[MeSH-major]
Leukemia
/ ethnology
Genetics Home Reference.
consumer health - acute promyelocytic leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18064533.001).
[ISSN]
0957-5243
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
Netherlands
17.
Qi H, Xiao L, Lingyun W, Ying T, Yi-Zhi L, Shao-Xu Y, Quan P:
Expression of type 1 insulin-like growth factor receptor in marrow nucleated cells in malignant hematological disorders: correlation with apoptosis.
Ann Hematol
; 2006 Feb;85(2):95-101
[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.
To verify the expression of type 1 insulin-like growth factor receptor (IGF-IR) and its impact on hematopoietic cells apoptosis in myelodysplastic syndromes (MDS) and
acute
myeloid
leukemias
(AML), marrow samples from 16 patients with MDS and 16 patients with AML were examined along with 16 healthy donors as controls.
Immunocytochemical methods (alkaline phosphatase anti-alkaline phosphatase) and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (fluorescence) were used simultaneously on nucleated
cell
cytospins.
In MDS nucleated cells, IGF-IR showed stronger expression in refractory anemia with excess blasts (RAEB)/RAEB in transformation/chronic myelomonocytic
leukemia
subgroup when compared to RA/RA with ringed sideroblasts cases (64.1+/-3.2 vs 53.5+/-16.2%) (P>0.05).
When analyzed by groups,
cell
number with IGF-IR expression showed a negative correlation to apoptotic cells amount (r=-0.852; P<0.01) but positive correlation to their blast count (r=0.677; P<0.01).
In conclusion, overexpression of IGF-IR existed in hematopoietic cells in MDS and AML marrows, which appeared to be contributed to
disease
progress.
[MeSH-major]
Apoptosis. Bone Marrow Cells / cytology. Gene Expression Regulation, Neoplastic. Hematologic Neoplasms / metabolism.
Leukemia
, Myeloid,
Acute
/ metabolism. Myelodysplastic Syndromes / metabolism. Receptor, IGF Type 1 / biosynthesis
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Anemia / metabolism.
Cell
Transformation, Neoplastic. Child. Female. Humans. Male. Middle Aged
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Myelodysplastic Syndromes
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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 = 16328478.001).
[ISSN]
0939-5555
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
EC 2.7.10.1 / Receptor, IGF Type 1
18.
Zhang X, Huang H, Xu Z, Zhan R:
2-Methoxyestradiol blocks cell-cycle progression at the G2/M phase and induces apoptosis in human acute T lymphoblastic leukemia CEM cells.
Acta Biochim Biophys Sin (Shanghai)
; 2010 Sep;42(9):615-22
[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]
2-Methoxyestradiol blocks
cell
-cycle progression at the G2/M phase and induces apoptosis in human
acute
T lymphoblastic
leukemia
CEM cells.
The current study sought to determine the mechanism of anti-cancer activity of 2-ME2 in human
acute
T lymphoblastic
leukemia
CEM cells.
Exposure to 2-ME2 led to G(2)/M phase
cell
-cycle arrest, which preceded apoptosis characterized by the appearance
of a
sub-G(1)
cell
population.
Moreover, the expression
level of
p21 protein was upregulated, whereas Bcl-2 and dysfunctional p53 protein were downregulated, which also contributed to 2-ME2-induced apoptosis.
Our findings revealed that 2-ME2 might be a potent natural candidate for chemotherapeutic treatment of human
acute
T lymphoblastic
leukemia
when the precise effects of 2-ME2 were investigated further in other T
leukemia
cell
lines and in primary T-
cell leukemias
.
[MeSH-major]
Apoptosis / drug effects.
Cell
Cycle / drug effects. Estradiol / analogs & derivatives
[MeSH-minor]
Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / metabolism. Blotting, Western.
Cell
Division / drug effects.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. G2 Phase / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Membrane Potential, Mitochondrial / drug effects. Precursor T-
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor T-
Cell
Lymphoblastic
Leukemia
-Lymphoma / metabolism. Precursor T-
Cell
Lymphoblastic
Leukemia
-Lymphoma / pathology. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tubulin Modulators / pharmacology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Hazardous Substances Data Bank.
ESTRADIOL
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20732853.001).
[ISSN]
1745-7270
[Journal-full-title]
Acta biochimica et biophysica Sinica
[ISO-abbreviation]
Acta Biochim. Biophys. Sin. (Shanghai)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tubulin Modulators; 0 / Tumor Suppressor Protein p53; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
19.
Clappier E, Cuccuini W, Cayuela JM, Vecchione D, Baruchel A, Dombret H, Sigaux F, Soulier J:
Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias.
Leukemia
; 2006 Jan;20(1):82-6
[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]
Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-
cell acute
lymphoblastic
leukemias
.
While the cyclin D1 and D3 genes (CCND1 and CCND3) are recurrently involved in genomic rearrangements, especially in B-
cell
lymphoid neoplasias, no clear involvement of the cyclin D2 gene (CCND2) has been reported to date.
Here, we identified chromosomal translocations targeting the CCND2 locus at 12p13, and the T-
cell
receptor beta (TCRB) or the TCRA/D loci in T-
cell acute
lymphoblastic
leukemias
(T-ALLs).
In order to evaluate dysregulation in T-ALL with respect to normal T-
cell
differentiation, we analyzed CCND2 expression in normal purified human thymic subpopulations.
CCND2 levels were downregulated through progression from the early stages of human T-
cell
differentiation, further suggesting that the massive and sustained expression in the CCND2-rearranged T-ALL cases was oncogenic.
This report is the first clear evidence
of a
direct involvement of cyclin D2 in human cancer due to recurrent somatic genetic alterations.
[MeSH-major]
Chromosomes, Human, Pair 12 / genetics. Cyclins / biosynthesis. Cyclins / genetics.
Leukemia
-Lymphoma, Adult T-
Cell
/ genetics. Receptors, Antigen, T-
Cell
/ genetics. Translocation, Genetic
[MeSH-minor]
Adult.
Cell
Separation. Child. Cyclin D2. Cytogenetic Analysis. DNA Mutational Analysis. Gene Rearrangement. Humans
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
(PMID = 16270038.001).
[ISSN]
0887-6924
[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 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell
20.
Aikawa Y, Katsumoto T, Zhang P, Shima H, Shino M, Terui K, Ito E, Ohno H, Stanley ER, Singh H, Tenen DG, Kitabayashi I:
PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
Nat Med
; 2010 May;16(5):580-5, 1p following 585
[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]
PU.1-mediated upregulation of CSF1R is crucial for
leukemia
stem
cell
potential induced by MOZ-TIF2.
Leukemias
and other cancers possess self-renewing stem cells that help to maintain the cancer.
Cancer stem
cell
eradication is thought to be crucial for successful anticancer therapy.
Using an
acute
myeloid
leukemia
(AML) model induced by the
leukemia
-associated monocytic
leukemia
zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation
of leukemia
stem cells.
Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent
leukemia
-initiating activity.
Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced
leukemia
.
Thus, in this subtype of AML,
leukemia
stem cells are contained within the CSF1R(high)
cell
population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
SciCrunch.
OMIM: Data: Gene Annotation
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Immunity. 2002 Nov;17(5):665-76
[
12433372.001
]
[Cites]
Blood. 2007 Jul 1;110(1):323-33
[
17360941.001
]
[Cites]
Cancer Cell. 2003 Mar;3(3):259-71
[
12676584.001
]
[Cites]
J Leukoc Biol. 2004 Apr;75(4):612-23
[
14726498.001
]
[Cites]
Cancer Res. 1987 Feb 1;47(3):874-80
[
2433029.001
]
[Cites]
Nature. 1987 Sep 17-23;329(6136):259-61
[
3476856.001
]
[Cites]
Cell. 1987 Nov 20;51(4):663-73
[
2824063.001
]
[Cites]
J Clin Invest. 1988 Apr;81(4):1030-5
[
2832442.001
]
[Cites]
J Cell Physiol. 1988 Apr;135(1):133-8
[
3259234.001
]
[Cites]
Mol Cell Biol. 1994 Jan;14(1):373-81
[
8264604.001
]
[Cites]
Mol Cell Biol. 1996 Mar;16(3):1231-40
[
8622667.001
]
[Cites]
Nat Genet. 1996 Sep;14(1):33-41
[
8782817.001
]
[Cites]
Nat Med. 1997 Jul;3(7):730-7
[
9212098.001
]
[Cites]
EMBO J. 1998 Jul 1;17(13):3714-25
[
9649441.001
]
[Cites]
Cancer Cell. 2004 Dec;6(6):587-96
[
15607963.001
]
[Cites]
Blood. 2005 Apr 15;105(8):3127-32
[
15637141.001
]
[Cites]
Blood. 2005 Sep 1;106(5):1590-600
[
15914556.001
]
[Cites]
Cell Cycle. 2005 Jul;4(7):851-3
[
15917650.001
]
[Cites]
Oncogene. 2006 Jan 5;25(1):147-51
[
16170366.001
]
[Cites]
Genes Dev. 2006 May 1;20(9):1175-86
[
16651658.001
]
[Cites]
Cancer Res. 2007 Nov 15;67(22):10677-85
[
18006809.001
]
[Cites]
Cancer Sci. 2008 Aug;99(8):1523-7
[
18754862.001
]
[Cites]
Haematologica. 2008 Oct;93(10):1591-3
[
18698081.001
]
[Cites]
Blood. 2009 Jul 9;114(2):299-309
[
19339695.001
]
[Cites]
Gene Ther. 2000 Jun;7(12):1063-6
[
10871756.001
]
[Cites]
Nature. 2001 Nov 1;414(6859):105-11
[
11689955.001
]
[Cites]
EMBO J. 2001 Dec 17;20(24):7184-96
[
11742995.001
]
[Cites]
Blood. 2002 Jan 1;99(1):111-20
[
11756160.001
]
[Cites]
Genes Dev. 2006 May 15;20(10):1321-30
[
16702405.001
]
[Cites]
Mol Cancer Ther. 2006 Nov;5(11):2634-43
[
17121910.001
]
[Cites]
Blood. 2007 May 1;109(9):3998-4005
[
17227832.001
]
[Cites]
Nucleic Acids Res. 2003 Feb 15;31(4):e12
[
12582257.001
]
(PMID = 20418886.001).
[ISSN]
1546-170X
[Journal-full-title]
Nature medicine
[ISO-abbreviation]
Nat. Med.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719
[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 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
[Other-IDs]
NLM/ NIHMS265702; NLM/ PMC3039870
21.
Chen E, Kwon YT, Lim MS, Dubé ID, Hough MR:
Loss of Ubr1 promotes aneuploidy and accelerates B-cell lymphomagenesis in TLX1/HOX11-transgenic mice.
Oncogene
; 2006 Sep 21;25(42):5752-63
[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]
Loss of Ubr1 promotes aneuploidy and accelerates B-
cell
lymphomagenesis in TLX1/HOX11-transgenic mice.
The TLX1/HOX11 homeobox gene was originally identified at the recurrent t(10;14)(q24;q11) translocation breakpoint, a chromosomal abnormality observed in 5-7% of T-
cell acute
lymphoblastic
leukemias
(T-ALLs).
Proviral insertional mutagenesis studies performed on transgenic mice ectopically expressing TLX1/HOX11 in B
lymphocytes
(IgHmu-HOX11(Tg) mice) revealed the Ubr1 gene locus as a frequent site of proviral insertion, concomitant with accelerated development of diffuse large B-
cell
lymphoma.
Loss or reduced levels of Ubr1 expression was associated with 5/14 spontaneous B-
cell
lymphomas in IgHmu-HOX11(Tg) mice and one of nine primary human T-ALLs.
IgHmu-HOX11(Tg)/Ubr1(-/-) mice exhibited a modest but statistically significant acceleration
of disease onset
relative to IgHmu-HOX11(Tg)/Ubr1(+/-) mice.
Moreover, micronucleus assays to detect for chromosome missegregation were conducted and revealed increased presence of micronuclei in IgHmu-HOX11(Tg)/Ubr1(-/-) primary B lymphocyte cultures, and in both TLX1/HOX11-overexpressing T
cell
lines and fibroblast cultures following transfection with short interfering RNAs (siRNAs) targeting Ubr1.
[MeSH-major]
Homeodomain Proteins / genetics. Lymphoma, B-
Cell
/ genetics. Proto-Oncogene Proteins / genetics. Ubiquitin-Protein Ligases / deficiency
[MeSH-minor]
Animals. Blotting, Southern. DNA Primers. Genome, Viral. Humans.
Lymphocytes
/ physiology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Micronucleus Tests. Mitosis. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16862188.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / GM69482
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 143275-75-6 / TLX1 protein, human; EC 6.3.2.19 / UBR1 protein, mouse; EC 6.3.2.19 / Ubiquitin-Protein Ligases
22.
Hsu KC, Gooley T, Malkki M, Pinto-Agnello C, Dupont B, Bignon JD, Bornhäuser M, Christiansen F, Gratwohl A, Morishima Y, Oudshoorn M, Ringden O, van Rood JJ, Petersdorf E, International Histocompatibility Working Group:
KIR ligands and prediction of relapse after unrelated donor hematopoietic cell transplantation for hematologic malignancy.
Biol Blood Marrow Transplant
; 2006 Aug;12(8):828-36
[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]
KIR ligands and prediction of relapse after unrelated donor hematopoietic
cell
transplantation for hematologic malignancy.
Recurrent malignancy remains a significant complication after allogeneic hematopoietic
cell
transplantation (HCT).
Efforts to decrease relapse have included donor lymphocyte infusion to stimulate donor anti-recipient T-
cell
allorecognition of major and minor histocompatibility differences.
Recently, alloreactive effects of donor natural killer
cell
-mediated inhibitory killer immunoglobulin-like receptor (KIR) recognition of recipient HLA-C and -B ligands have been described.
We examined KIR ligand effects on risk of relapse in 1770 patients undergoing myeloablative T-replete HCT from HLA-matched or -mismatched unrelated donors for the treatment of myeloid and lymphoid
leukemias
.
The decrease in hazard of relapse in patients with
acute
myelogenous
leukemia
was similar to that in patients with chronic myelogenous
leukemia
and
acute
lymphoblastic
leukemia
(P = .95).
Recipient homozygosity for HLA-B or -C epitopes that define KIR ligands is likely to be a predictive factor for
leukemia
relapse after myeloablative HCT from HLA-mismatched unrelated donors.
[MeSH-major]
HLA-B Antigens / genetics. Hematologic Neoplasms / genetics. Hematopoietic Stem
Cell
Transplantation. Isoantigens / genetics. Living Donors. Lymphocyte Transfusion
[MeSH-minor]
Disease
-Free Survival. Epitopes / genetics. Epitopes / immunology. Female. Follow-Up Studies. HLA-C Antigens / genetics. HLA-C Antigens / immunology. Humans. Killer Cells, Natural / immunology. Ligands. Male. Receptors, Immunologic / agonists. Receptors, Immunologic / genetics. Receptors, Immunologic / immunology. Receptors, KIR. Recurrence. Risk Factors. Survival Rate. T-
Lymphocytes
/ immunology. Transplantation, Homologous
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Organ Donation
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16864053.001).
[ISSN]
1083-8791
[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
[Grant]
United States / NCI NIH HHS / CA / P01 CA 023766; United States / NIAID NIH HHS / AI / U24 AI 49215; United States / NIAID NIH HHS / AI / U24 AI49213; United States / NIAID NIH HHS / AI / UO1 AI 069197
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Epitopes; 0 / HLA-B Antigens; 0 / HLA-Bw4 antigen; 0 / HLA-C Antigens; 0 / Isoantigens; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR
23.
Okuya M, Kurosawa H, Kikuchi J, Furukawa Y, Matsui H, Aki D, Matsunaga T, Inukai T, Goto H, Altura RA, Sugita K, Arisaka O, Look AT, Inaba T:
Up-regulation of survivin by the E2A-HLF chimera is indispensable for the survival of t(17;19)-positive leukemia cells.
J Biol Chem
; 2010 Jan 15;285(3):1850-60
[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]
Up-regulation of survivin by the E2A-HLF chimera is indispensable for the survival of t(17;19)-positive
leukemia
cells.
The E2A-HLF fusion transcription factor generated by t(17;19)(q22;p13) translocation is found in a small subset of pro-
B cell acute
lymphoblastic
leukemias
(ALLs) and promotes leukemogenesis by substituting for the antiapoptotic function of cytokines.
Forced expression of E2A-HLF in t(17;19)(-)
leukemia
cells up-regulated Survivin expression, suggesting that Survivin is a downstream target of E2A-HLF.
Analysis using a counterflow centrifugal elutriator revealed that t(17;19)+ ALL cells express Survivin throughout the
cell
cycle.
Reporter assays revealed that E2A-HLF induces survivin expression at the transcriptional
level
likely through indirect down-regulation
of a
cell
cycle-dependent cis element in the promoter region.
Down-regulation of Survivin function by a dominant negative mutant of Survivin or reduction of Survivin expression induced massive apoptosis throughout the
cell
cycle in t(17;19)+ cells mainly through caspase-independent pathways involving translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus.
These data indicated that reversal of AIF translocation by Survivin, which is induced by E2A-HLF throughout the
cell
cycle, is one of the key mechanisms in the protection of t(17;19)+
leukemia
cells from apoptosis.
[MeSH-major]
Basic Helix-Loop-Helix Transcription Factors / metabolism. Basic-Leucine Zipper Transcription Factors / metabolism. Microtubule-Associated Proteins / genetics. Precursor B-
Cell
Lymphoblastic
Leukemia
-Lymphoma / pathology. Recombinant Fusion Proteins / metabolism. Translocation, Genetic / genetics. Up-Regulation
[MeSH-minor]
Animals. Apoptosis. Base Sequence. Caspases / metabolism.
Cell
Cycle / genetics.
Cell
Line, Tumor.
Cell
Survival / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 19 / genetics. Humans. Inhibitor of Apoptosis Proteins. Mice. Molecular Sequence Data. Mutation. Precursor Cells, B-Lymphoid / cytology. Precursor Cells, B-Lymphoid / metabolism. Promoter Regions, Genetic / genetics. Transcriptional Activation
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Cell. 2002 Oct;2(4):279-88
[
12398892.001
]
[Cites]
J Cell Biochem. 2008 Oct 1;105(2):381-90
[
18553460.001
]
[Cites]
Nat Genet. 2003 Mar;33(3):401-6
[
12590264.001
]
[Cites]
Oncogene. 2003 Jul 3;22(27):4266-80
[
12833149.001
]
[Cites]
J Cell Physiol. 2003 Oct;197(1):8-29
[
12942537.001
]
[Cites]
Blood. 2003 Dec 1;102(12):4179-86
[
12920030.001
]
[Cites]
Cancer Res. 2003 Nov 15;63(22):7724-32
[
14633697.001
]
[Cites]
Oncogene. 2004 Jan 8;23(1):39-48
[
14712209.001
]
[Cites]
Blood. 2004 Apr 15;103(8):3185-91
[
15070701.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7183-90
[
15492230.001
]
[Cites]
Science. 1992 Jul 24;257(5069):531-4
[
1386162.001
]
[Cites]
Genes Dev. 1992 Sep;6(9):1608-20
[
1516826.001
]
[Cites]
Mol Cell Biol. 1994 May;14(5):3403-13
[
8164688.001
]
[Cites]
EMBO J. 1995 Jan 16;14(2):266-75
[
7835337.001
]
[Cites]
Blood. 1996 Feb 15;87(4):1211-24
[
8608207.001
]
[Cites]
Nature. 1996 Aug 8;382(6591):541-4
[
8700228.001
]
[Cites]
Nature. 1996 Aug 8;382(6591):545-7
[
8700229.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2609-14
[
9122243.001
]
[Cites]
Biochem J. 1999 Dec 1;344 Pt 2:305-11
[
10567210.001
]
[Cites]
J Natl Cancer Inst. 2001 Oct 17;93(20):1541-52
[
11604477.001
]
[Cites]
Science. 2002 Jul 12;297(5579):259-63
[
12114629.001
]
[Cites]
Blood. 1997 Jun 1;89(11):3980-90
[
9166836.001
]
[Cites]
Nat Med. 1997 Aug;3(8):917-21
[
9256286.001
]
[Cites]
Mol Cell Biol. 1998 Oct;18(10):6035-43
[
9742120.001
]
[Cites]
Cancer Res. 1998 Dec 1;58(23):5315-20
[
9850056.001
]
[Cites]
Nature. 1998 Dec 10;396(6711):580-4
[
9859993.001
]
[Cites]
Blood. 1999 Jan 1;93(1):321-32
[
9864177.001
]
[Cites]
Nature. 1999 Feb 4;397(6718):441-6
[
9989411.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1457-62
[
9990045.001
]
[Cites]
Mol Cell Biol. 1999 Apr;19(4):2754-62
[
10082541.001
]
[Cites]
Mol Cell. 1999 Sep;4(3):309-19
[
10518212.001
]
[Cites]
Mol Cell. 1999 Sep;4(3):343-52
[
10518215.001
]
[Cites]
Neoplasma. 2006;53(3):206-12
[
16652189.001
]
[Cites]
Trends Cell Biol. 2006 May;16(5):264-72
[
16621561.001
]
[Cites]
Mol Cancer Ther. 2006 May;5(5):1087-98
[
16731740.001
]
[Cites]
J Cell Physiol. 2006 Sep;208(3):476-86
[
16557517.001
]
[Cites]
J Invest Dermatol. 2006 Oct;126(10):2247-56
[
16728972.001
]
[Cites]
Leukemia. 2007 Feb;21(2):288-96
[
17183364.001
]
[Cites]
Mol Cell Biol. 2007 Jul;27(13):4844-62
[
17470554.001
]
[Cites]
Stem Cells. 2007 Oct;25(10):2439-47
[
17600109.001
]
[Cites]
Nat Rev Cancer. 2008 Jan;8(1):61-70
[
18075512.001
]
[Cites]
Tohoku J Exp Med. 2008 Sep;216(1):25-34
[
18719335.001
]
[Cites]
Nat Rev Cancer. 2003 Jan;3(1):46-54
[
12509766.001
]
(PMID = 19887369.001).
[ISSN]
1083-351X
[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 / BIRC5 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / HLF protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF3 protein, human; EC 3.4.22.- / Caspases
[Other-IDs]
NLM/ PMC2804343
24.
Sadananda Adiga MN, Chandy S, Ramachandra N, Appaji L, Aruna Kumari BS, Ramaswamy G, Savithri HS, Krishnamoorthy L:
Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children.
Indian J Cancer
; 2010 Jan-Mar;47(1):40-5
[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]
Methylenetetrahydrofolate reductase gene polymorphisms and risk of
acute
lymphoblastic
leukemia
in children.
Leukemias
are malignancies arising from rapidly proliferating hematopoietic cells having great requirement of DNA synthesis.
This case-control study was undertaken to analyze the association of the MTHFR gene polymorphisms 677 C"T and 1298 A"C and the risk of
acute
lymphoblastic
leukemia
in children.
MATERIALS AND METHODS: Eighty-six patients aged below 15 years with a confirmed diagnosis of
acute
lymphoblastic
leukemia
(ALL) and 99 matched controls were taken for this study.
[MeSH-major]
Genetic Predisposition to
Disease
. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20071789.001).
[ISSN]
1998-4774
[Journal-full-title]
Indian journal of cancer
[ISO-abbreviation]
Indian J Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Chemical-registry-number]
EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
25.
Hu J, Fang J, Dong Y, Chen SJ, Chen Z:
Arsenic in cancer therapy.
Anticancer Drugs
; 2005 Feb;16(2):119-27
[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.
Arsenic, a natural substance that has been used as a drug for over 2000 years, has been revived because of its remarkable therapeutic efficacy in patients with
acute
promyelocytic
leukemia
(APL).
Specific degradation of the leukemogenic PML-RARalpha fusion protein induced by arsenic leads to the differentiation
of leukemia
cells.
Preliminary in vitro studies have also extended the potential anti-cancer effect of arsenic to non-APL
leukemias
, lymphoid malignancies and other cancers.
In vitro and in vivo studies demonstrate that arsenic exerts a broad spectrum of anti-cancer effects by induction of apoptosis, inhibition of
cell
proliferation, anti-angiogenesis and possible immunomodulation.
[MeSH-minor]
Animals. Apoptosis / drug effects. Clinical Trials as Topic. Dose-Response Relationship, Drug. Humans.
Leukemia
/ drug therapy. Lymphoma / drug therapy. Multiple Myeloma / drug therapy
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15655408.001).
[ISSN]
0959-4973
[Journal-full-title]
Anti-cancer drugs
[ISO-abbreviation]
Anticancer Drugs
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Arsenicals
[Number-of-references]
65
26.
Sollars VE, Pequignot E, Rothstein JL, Buchberg AM:
Analysis of expansion of myeloid progenitors in mice to identify leukemic susceptibility genes.
Mamm Genome
; 2006 Aug;17(8):808-21
[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.
The myeloid progenitor
cell
compartment (MPC) exhibits pronounced expansion in human myeloid
leukemias
.
It is becoming more apparent that progression of myelodysplastic syndromes and myeloproliferative diseases to
acute
myelogenous
leukemia
is the result of defects in progenitor
cell
maturation.
The MPC of bone marrow was analyzed in mice using a
cell
culture assay for measuring the relative frequency of proliferative myeloid progenitors.
Given the importance of this
cell
compartment in
leukemia
progression and the soon to be released genomic sequence of 15 mouse strains, these differences may provide a valuable tool for research into
leukemia
.
[MeSH-major]
Cell
Proliferation. Genetic Predisposition to
Disease
.
Leukemia
/ genetics. Myeloid Progenitor Cells / metabolism
[MeSH-minor]
Animals. Bone Marrow / growth & development.
Cell
Size. Chromosomes, Mammalian. Cytokines / metabolism. Flow Cytometry. Linkage Disequilibrium. Male. Mice. Mice, Inbred Strains. Stem Cells
MedlinePlus Health Information.
consumer health - Leukemia
.
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)
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 2002 Jan 15;99(2):561-6
[
11781239.001
]
[Cites]
Cancer Res. 1989 Jan 1;49(1):149-53
[
2783241.001
]
[Cites]
Blood. 2004 Mar 15;103(6):2343-50
[
14630819.001
]
[Cites]
Annu Rev Immunol. 1990;8:303-33
[
1693082.001
]
[Cites]
PLoS Biol. 2004 Dec;2(12):e393
[
15534693.001
]
[Cites]
FASEB J. 1999 Apr;13(6):707-13
[
10094931.001
]
[Cites]
Blood. 2001 Mar 1;97(5):1274-81
[
11222370.001
]
[Cites]
J Virol. 1981 Aug;39(2):632-40
[
6268848.001
]
[Cites]
Blood. 1995 May 1;85(9):2331-6
[
7727767.001
]
[Cites]
Blood. 1999 May 15;93(10):3294-301
[
10233881.001
]
[Cites]
Blood. 2002 Jun 1;99(11):3947-54
[
12010793.001
]
[Cites]
Exp Hematol. 2000 Apr;28(4):442-50
[
10781902.001
]
[Cites]
Exp Hematol. 1999 May;27(5):928-35
[
10340409.001
]
[Cites]
J Exp Med. 1996 Mar 1;183(3):1141-50
[
8642256.001
]
[Cites]
Arterioscler Thromb Vasc Biol. 2003 Jan 1;23(1):117-22
[
12524234.001
]
[Cites]
Nat Med. 2005 Jun;11(6):630-7
[
15908956.001
]
[Cites]
N Engl J Med. 2004 Aug 12;351(7):657-67
[
15306667.001
]
[Cites]
Br J Haematol. 1997 Jun;97(4):920-6
[
9217198.001
]
[Cites]
J Exp Med. 1997 Aug 18;186(4):529-36
[
9254651.001
]
[Cites]
Cell. 1983 Dec;35(3 Pt 2):639-45
[
6652681.001
]
[Cites]
Blood. 1997 Mar 1;89(5):1543-50
[
9057635.001
]
[Cites]
Science. 2001 Jun 8;292(5523):1915-8
[
11397946.001
]
[Cites]
Physiol Genomics. 2002 Dec 3;11(3):185-93
[
12419856.001
]
[Cites]
Nat Rev Genet. 2006 Jan;7(1):21-33
[
16369569.001
]
[Cites]
Mamm Genome. 2003 Jan;14(1):81-5
[
12532271.001
]
[Cites]
J Virol. 1984 Sep;51(3):586-94
[
6088784.001
]
[Cites]
Blood. 1993 Sep 15;82(6):1720-3
[
7691233.001
]
[Cites]
J Virol. 1988 Mar;62(3):839-46
[
2828679.001
]
[Cites]
Cancer Res. 1994 Jan 15;54(2):399-402
[
8275475.001
]
[Cites]
Nat Genet. 1999 Nov;23(3):348-53
[
10610183.001
]
[Cites]
J Mol Cell Immunol. 1987;3(1):29-36
[
3509920.001
]
[Cites]
Blood. 2003 Jul 1;102(1):94-101
[
12623852.001
]
[Cites]
Blood. 1997 Apr 15;89(8):2736-44
[
9108391.001
]
[Cites]
J Virol. 1982 May;42(2):379-88
[
6283161.001
]
[Cites]
Blood. 2000 Apr 1;95(7):2446-8
[
10733521.001
]
[Cites]
Cell Struct Funct. 2002 Apr;27(2):81-9
[
12207049.001
]
[Cites]
Stem Cells. 2002;20(5):460-9
[
12351816.001
]
[Cites]
Blood. 1991 Aug 15;78(4):961-6
[
1714329.001
]
[Cites]
Blood. 2000 Apr 1;95(7):2449-51
[
10733522.001
]
[Cites]
J Exp Med. 2005 Mar 21;201(6):881-90
[
15781580.001
]
(PMID = 16897342.001).
[ISSN]
0938-8990
[Journal-full-title]
Mammalian genome : official journal of the International Mammalian Genome Society
[ISO-abbreviation]
Mamm. Genome
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / T32-CA09678
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytokines
27.
Catalina P, Bueno C, Montes R, Nieto A, Ligero G, Sanchez L, Jara M, Rasillo A, Orfao A, Cigudosa J, Hovatta O, Greaves M, Menendez P:
Genetic stability of human embryonic stem cells: A first-step toward the development of potential hESC-based systems for modeling childhood leukemia.
Leuk Res
; 2009 Jul;33(7):980-90
[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]
Genetic stability of human embryonic stem cells: A first-step toward the development of potential hESC-based systems for modeling childhood
leukemia
.
Of interest, are the human childhood
acute leukemias
harboring specific fusion oncogenes such as MLL-AF4, TEL-AML1 or BCR-ABL wherein clinically significant manifestations arise in utero.
The mechanisms of transformation are not amenable to analysis with patient samples and, many mouse models for pediatric
leukemias
have fallen short in illuminating the human
disease
because they do not recapitulate key aspects of the actual
disease
, suggesting that the mouse models are missing essential components of oncogenesis present in the human embryo.
Prior to using hESCs as a tentative system for modeling
leukemia
, robust studies aimed at demonstrating their genetic stability are required; otherwise, cooperating mutations already present could prime hESCs susceptible to transformation.
This data should encourage stem
cell
researchers to implement robust cytogenetic tools when assessing hESC genetic stability, in order to detect tiny but relevant biological functional or structural chromosome abnormalities and, paves the way for generating fusion oncogene-expressing transgenic hESCs as a human-specific system for studying the early in utero events leading to normal hematopoietic specification versus childhood leukemic transformation.
[MeSH-major]
Cell
Differentiation / genetics.
Cell
Lineage / genetics.
Disease
Models, Animal. Embryo, Mammalian / cytology. Embryonic Stem Cells / physiology. Genomic Instability
[MeSH-minor]
Acute
Disease
. Adult. Animals. Cells, Cultured. Child. Comparative Genomic Hybridization. Flow Cytometry. Humans. Immunoenzyme Techniques. Karyotyping.
Leukemia
/ genetics. Male. Mice. Mice, SCID. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Spectral Karyotyping. fms-Like Tyrosine Kinase 3 / genetics
Cellosaurus - a cell line knowledge resource.
culture/stock collections - Cellosaurus - a cell line knowledge resource
.
Cellosaurus - a cell line knowledge resource.
culture/stock collections - Cellosaurus - a cell line knowledge resource
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18930318.001).
[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
[Chemical-registry-number]
0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
28.
Jeeninga RE, Jan B, van den Berg H, Berkhout B:
Construction of doxycyline-dependent mini-HIV-1 variants for the development of a virotherapy against leukemias.
Retrovirology
; 2006 Sep 27;3:64
[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]
Construction of doxycyline-dependent mini-HIV-1 variants for the development
of a
virotherapy against
leukemias
.
T-
cell acute
lymphoblastic
leukemia
(T-ALL) is a high-risk type of blood-
cell
cancer.
We describe the improvement
of a
candidate therapeutic virus for virotherapy of leukemic cells.
Virotherapy is based on the exclusive replication
of a
virus in leukemic cells, leading to the selective removal of these malignant cells.
These minimized HIV-rtTA variants contain up to 7 deletions/inactivating mutations (TAR, Tat, vif, vpR, vpU, nef and U3) and replicate efficiently in the leukemic SupT1 T
cell
line, but do not replicate in normal peripheral blood mononuclear cells.
The therapeutic viruses use CD4 and CXCR4 for
cell
entry and could potentially be used against CXCR4 expressing malignancies such as T-lymphoblastic
leukemia
/lymphoma, NK
leukemia
and some myeloid
leukemias
.
Genetic Alliance.
consumer health - HIV
.
MedlinePlus Health Information.
consumer health - Leukemia
.
HIV InSite.
treatment guidelines - Human Herpesvirus-8
.
Hazardous Substances Data Bank.
DOXYCYCLINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Gen Virol. 2002 Mar;83(Pt 3):491-502
[
11842243.001
]
[Cites]
Hum Gene Ther. 2001 Dec 10;12(18):2155-65
[
11779400.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9503-8
[
12093916.001
]
[Cites]
J Neurovirol. 2002 Dec;8 Suppl 2:134-7
[
12491165.001
]
[Cites]
Cancer Gene Ther. 2003 May;10(5):341-52
[
12719704.001
]
[Cites]
J Clin Invest. 2003 May;111(10):1547-54
[
12750404.001
]
[Cites]
J Virol. 2004 Mar;78(6):3099-109
[
14990729.001
]
[Cites]
J Biol Chem. 2004 Apr 30;279(18):18776-82
[
14761948.001
]
[Cites]
Methods Enzymol. 2004;388:359-79
[
15289083.001
]
[Cites]
Cancer Gene Ther. 2004 Oct;11(10):643-64
[
15286681.001
]
[Cites]
Cancer Res. 1984 Dec;44(12 Pt 1):5657-60
[
6437672.001
]
[Cites]
Nature. 1988 Jul 14;334(6178):165-7
[
3386755.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 May;86(10):3862-6
[
2542949.001
]
[Cites]
J Virol. 1989 Dec;63(12):5501-4
[
2479775.001
]
[Cites]
Virology. 1992 May;188(1):391-5
[
1566581.001
]
[Cites]
Nucleic Acids Res. 1993 Nov 11;21(22):5020-4
[
8255755.001
]
[Cites]
EMBO J. 1994 Jun 1;13(11):2650-9
[
8013464.001
]
[Cites]
AIDS Res Hum Retroviruses. 1994 Apr;10(4):343-50
[
8068414.001
]
[Cites]
Science. 1995 Nov 10;270(5238):988-91
[
7481804.001
]
[Cites]
Science. 1996 Oct 18;274(5286):373-6
[
8832876.001
]
[Cites]
Nucleic Acids Res. 1996 Nov 1;24(21):4356-7
[
8932394.001
]
[Cites]
Virology. 1997 Oct 27;237(2):228-36
[
9356335.001
]
[Cites]
J Virol. 1999 Feb;73(2):1138-45
[
9882315.001
]
[Cites]
J Virol. 1999 Jan;73(1):81-91
[
9847310.001
]
[Cites]
J Virol. 1999 Apr;73(4):2781-9
[
10074125.001
]
[Cites]
J Natl Cancer Inst. 1964 Jan;32:135-63
[
14114965.001
]
[Cites]
Cancer Res. 2005 Apr 15;65(8):3347-55
[
15833868.001
]
[Cites]
J Virol. 2005 Jul;79(14):9180-91
[
15994812.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14034-9
[
16172403.001
]
[Cites]
Cancer Res. 2005 Oct 1;65(19):9056-63
[
16204080.001
]
[Cites]
Cancer Res. 2005 Oct 15;65(20):9463-72
[
16230410.001
]
[Cites]
Nat Rev Cancer. 2005 Dec;5(12):965-76
[
16294217.001
]
[Cites]
J Virol. 2006 Feb;80(3):1067-76
[
16414984.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3369-74
[
16492778.001
]
[Cites]
Mol Ther. 2006 Aug;14(2):268-75
[
16697708.001
]
[Cites]
Virology. 2001 May 10;283(2):294-305
[
11336554.001
]
[Cites]
Nat Med. 2000 Aug;6(8):879-85
[
10932224.001
]
[Cites]
J Virol. 2000 Nov;74(22):10581-8
[
11044102.001
]
[Cites]
Cancer Res. 2000 Nov 15;60(22):6359-66
[
11103798.001
]
[Cites]
J Virol. 2001 Jan;75(2):979-87
[
11134311.001
]
[Cites]
J Virol. 2001 Jun;75(12):5443-7
[
11356950.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 May 22;98(11):6342-7
[
11353837.001
]
[Cites]
J Clin Virol. 2001 Oct;22(3):263-70
[
11564591.001
]
[Cites]
J Virol. 2002 Mar;76(6):3084-8
[
11861878.001
]
(PMID = 17005036.001).
[ISSN]
1742-4690
[Journal-full-title]
Retrovirology
[ISO-abbreviation]
Retrovirology
[Language]
ENG
[Grant]
United States / PHS HHS / / R21-A147017-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-Bacterial Agents; 0 / Antigens, CD4; 0 / Gene Products, tat; 0 / Receptors, CXCR4; 0 / tat Gene Products, Human Immunodeficiency Virus; N12000U13O / Doxycycline
[Other-IDs]
NLM/ PMC1592508
29.
Patel A, Dharmarajan V, Vought VE, Cosgrove MS:
On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex.
J Biol Chem
; 2009 Sep 4;284(36):24242-56
[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]
On the mechanism of multiple lysine methylation by the human mixed lineage
leukemia
protein-1 (MLL1) core complex.
The mixed lineage
leukemia
protein-1 (MLL1) is a member of the SET1 family of H3K4 methyltransferases and is frequently rearranged in
acute leukemias
.
Single turnover kinetic experiments reveal that the reaction leading to H3K4 dimethylation involves the transient accumulation
of a
monomethylated species, suggesting that the MLL1 core complex uses a non-processive mechanism to catalyze multiple lysine methylation.
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
Hazardous Substances Data Bank.
L-Lysine
.
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
[Cites]
Biophys J. 2000 Mar;78(3):1606-19
[
10692345.001
]
[Cites]
J Biol Chem. 2008 Dec 12;283(50):35258-64
[
18840606.001
]
[Cites]
Nature. 2000 Aug 10;406(6796):593-9
[
10949293.001
]
[Cites]
Science. 2001 Sep 28;293(5539):2453-5
[
11498546.001
]
[Cites]
Genes Dev. 2001 Dec 15;15(24):3286-95
[
11751634.001
]
[Cites]
Curr Opin Genet Dev. 2002 Apr;12(2):198-209
[
11893494.001
]
[Cites]
Nature. 2002 Sep 26;419(6905):407-11
[
12353038.001
]
[Cites]
Cell. 2002 Oct 4;111(1):91-103
[
12372303.001
]
[Cites]
Cell. 2002 Oct 4;111(1):105-15
[
12372304.001
]
[Cites]
Cell. 2002 Oct 4;111(1):117-27
[
12372305.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1107-17
[
12453418.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1119-28
[
12453419.001
]
[Cites]
Mol Cell Biol. 2003 Jan;23(1):140-9
[
12482968.001
]
[Cites]
Nature. 2003 Feb 6;421(6923):652-6
[
12540855.001
]
[Cites]
Nat Struct Biol. 2003 Mar;10(3):187-96
[
12567185.001
]
[Cites]
Cell. 2003 Mar 7;112(5):711-23
[
12628190.001
]
[Cites]
Mol Cell. 2003 Mar;11(3):709-19
[
12667453.001
]
[Cites]
Genes Dev. 2003 Apr 1;17(7):896-911
[
12670868.001
]
[Cites]
Nat Struct Biol. 2003 Jul;10(7):545-52
[
12819771.001
]
[Cites]
Mol Cell. 2003 Jul;12(1):177-85
[
12887903.001
]
[Cites]
Mol Cell. 2003 Nov;12(5):1325-32
[
14636589.001
]
[Cites]
Mol Cell. 2003 Dec;12(6):1591-8
[
14690610.001
]
[Cites]
Mol Cell. 2004 Feb 27;13(4):587-97
[
14992727.001
]
[Cites]
PLoS Biol. 2004 Jul;2(7):E171
[
15252442.001
]
[Cites]
Mol Cell Biol. 1993 Oct;13(10):6357-66
[
8413234.001
]
[Cites]
EMBO J. 1994 Aug 15;13(16):3822-31
[
7915232.001
]
[Cites]
Mech Dev. 1995 Aug;52(2-3):209-23
[
8541210.001
]
[Cites]
Nature. 1995 Nov 30;378(6556):505-8
[
7477409.001
]
[Cites]
Anal Biochem. 1996 Jun 1;237(2):260-73
[
8660575.001
]
[Cites]
Mol Biol Cell. 1997 Dec;8(12):2421-36
[
9398665.001
]
[Cites]
Protein Expr Purif. 1999 Feb;15(1):34-9
[
10024467.001
]
[Cites]
Nature. 2005 Jan 27;433(7024):434-8
[
15647753.001
]
[Cites]
J Biol Chem. 2005 Feb 18;280(7):5563-70
[
15590646.001
]
[Cites]
Cell. 2005 Jun 17;121(6):873-85
[
15960975.001
]
[Cites]
Genes Dev. 2005 Jun 15;19(12):1444-54
[
15933069.001
]
[Cites]
Genes Dev. 2005 Jun 15;19(12):1455-65
[
15933070.001
]
[Cites]
Biophys J. 2005 Jul;89(1):619-34
[
15863475.001
]
[Cites]
Genome Biol. 2005;6(8):227
[
16086857.001
]
[Cites]
Mol Cell. 2009 Jan 30;33(2):181-91
[
19187761.001
]
[Cites]
Biochemistry. 2000 Nov 14;39(45):13633-40
[
11076501.001
]
[Cites]
Cell. 2005 Aug 26;122(4):517-27
[
16122420.001
]
[Cites]
Plant Cell. 2005 Sep;17(9):2439-53
[
16100335.001
]
[Cites]
Mol Cell. 2005 Sep 16;19(6):849-56
[
16168379.001
]
[Cites]
PLoS Biol. 2005 Oct;3(10):e328
[
16122352.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14765-70
[
16199523.001
]
[Cites]
J Biol Chem. 2005 Dec 16;280(50):41725-31
[
16253997.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6629-34
[
16618927.001
]
[Cites]
J Mol Biol. 2006 May 26;359(1):86-96
[
16603186.001
]
[Cites]
Nature. 2006 Jul 6;442(7098):96-9
[
16728974.001
]
[Cites]
Nature. 2006 Jul 6;442(7098):86-90
[
16728976.001
]
[Cites]
Nat Struct Mol Biol. 2006 Aug;13(8):713-9
[
16878130.001
]
[Cites]
Nat Struct Mol Biol. 2006 Sep;13(9):852-4
[
16892064.001
]
[Cites]
Nat Genet. 2007 Mar;39(3):311-8
[
17277777.001
]
[Cites]
Biochemistry. 2007 Mar 27;46(12):3905-15
[
17338551.001
]
[Cites]
Mutat Res. 2007 May 1;618(1-2):102-15
[
17374386.001
]
[Cites]
J Biol Chem. 2007 May 4;282(18):13419-28
[
17355966.001
]
[Cites]
J Biol Chem. 2007 Jul 13;282(28):20395-406
[
17500065.001
]
[Cites]
Curr Opin Genet Dev. 2008 Apr;18(2):159-68
[
18281209.001
]
[Cites]
J Biol Chem. 2008 Nov 21;283(47):32162-75
[
18829457.001
]
[Cites]
J Biol Chem. 2008 Nov 21;283(47):32158-61
[
18829459.001
]
[Cites]
Anal Chem. 2000 Jul 15;72(14):3311-9
[
10939405.001
]
(PMID = 19556245.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA140522
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ASH2L protein, human; 0 / DNA-Binding Proteins; 0 / DPY30 protein, human; 0 / Histones; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / RBP5 protein, human; 0 / Retinol-Binding Proteins, Cellular; 0 / Transcription Factors; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine
[Other-IDs]
NLM/ PMC2782018
30.
Krug U, Yasmeen A, Beger C, Bäumer N, Dugas M, Berdel WE, Müller-Tidow C:
Cyclin A1 regulates WT1 expression in acute myeloid leukemia cells.
Int J Oncol
; 2009 Jan;34(1):129-36
[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]
Cyclin A1 regulates WT1 expression in
acute
myeloid
leukemia
cells.
Cyclin A1 is a
cell
cycle protein that is expressed in testes, brain and CD34-positive hematopoietic progenitor cells.
Cyclin A1 is overexpressed in a variety of myeloid leukemic
cell
lines and in myeloid leukemic blasts.
Transgenic cyclin A1 overexpressing mice develop
acute
myeloid
leukemia
with low frequency.
Repression of WT1 expression was confirmed on the mRNA and protein
level
.
In addition, overexpression of the WT1-/+ isoform induced a G1
cell
cycle arrest which was abrogated upon cotransfection with cyclin A1.
This study identified WT1 as a repressed target of cyclin A1 and suggests that the suppression of WT1 in cyclin A1-overexpressing
leukemias
might play a role in the growth and suppression of apoptosis in these leukemic cells.
[MeSH-minor]
Animals. Blotting, Western. Bone Marrow / metabolism.
Cell
Line, Tumor. Colony-Forming Units Assay. Cyclin A1. G1 Phase / physiology. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Oligonucleotide Array Sequence Analysis. Protein Isoforms. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells / metabolism
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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 = 19082485.001).
[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 / CCNA1 protein, human; 0 / Ccna1 protein, mouse; 0 / Cyclin A; 0 / Cyclin A1; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / WT1 Proteins
31.
Yee KW, Hagey A, Verstovsek S, Cortes J, Garcia-Manero G, O'Brien SM, Faderl S, Thomas D, Wierda W, Kornblau S, Ferrajoli A, Albitar M, McKeegan E, Grimm DR, Mueller T, Holley-Shanks RR, Sahelijo L, Gordon GB, Kantarjian HM, Giles FJ:
Phase 1 study of ABT-751, a novel microtubule inhibitor, in patients with refractory hematologic malignancies.
Clin Cancer Res
; 2005 Sep 15;11(18):6615-24
[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.
A phase 1 study was conducted to determine the maximum tolerated dose and toxicities of ABT-751 in patients with advanced myelodysplastic syndrome and relapsed or refractory
acute leukemias
.
RESULTS: Dose-limiting toxicity consisted of ileus in one patient at 200 mg/m(2), with a subsequent patient developing grade 2 constipation at the same dose
level
.
One patient with relapsed
acute
myelogenous
leukemia
achieved a complete remission that was sustained for 2 months.
Four other patients had transient hematologic improvements, consisting
of a
decrease in peripheral blood blasts and improvements in platelet counts.
CONCLUSION: Further assessment of ABT-751, especially in combination with other agents, in patients with
acute leukemias
is warranted.
[MeSH-minor]
Acute
Disease
. Adult. Aged. Antigens, CD / analysis. Antigens, CD146. Antigens, CD31 / analysis. Antigens, CD45 / analysis. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Constipation / chemically induced. Diarrhea / chemically induced. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Endothelial Cells / chemistry. Female. Glycoproteins / analysis. Humans.
Leukemia
/ blood.
Leukemia
/ drug therapy.
Leukemia
/ genetics. Male. Microtubules / metabolism. Middle Aged. Mutation. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Nausea / chemically induced. Neoplasm Recurrence, Local. Neoplastic Cells, Circulating / chemistry. Neural
Cell
Adhesion Molecules / analysis. Peptides / analysis. Treatment Outcome. Tubulin / genetics. Vomiting / chemically induced
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16166440.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ABT751; 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD146; 0 / Antigens, CD31; 0 / Antineoplastic Agents; 0 / Glycoproteins; 0 / Neural Cell Adhesion Molecules; 0 / Peptides; 0 / Sulfonamides; 0 / Tubulin; EC 3.1.3.48 / Antigens, CD45
32.
Fiegl M, Samudio I, Clise-Dwyer K, Burks JK, Mnjoyan Z, Andreeff M:
CXCR4 expression and biologic activity in acute myeloid leukemia are dependent on oxygen partial pressure.
Blood
; 2009 Feb 12;113(7):1504-12
[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]
CXCR4 expression and biologic activity in
acute
myeloid
leukemia
are dependent on oxygen partial pressure.
In
acute
myeloid
leukemia
(AML), elevated expression of CXCR4 has been shown to correlate with shortened survival.
At this pO(2), CXCR4 surface and total expression were up-regulated within 10 hours in leukemic
cell
lines and patient samples as shown by Western blotting, fluorescence-activated
cell
sorting, and microscopy.
Given the importance of CXCR4 in
cell
signaling, survival, and adhesion in
leukemia
, the results suggest that pO(2) be considered a critical variable in conducting and interpreting studies of CXCR4 expression and regulation in
leukemias
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
OXYGEN
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Res. 2007 Sep 15;67(18):8605-14
[
17875700.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5431-6
[
17374716.001
]
[Cites]
J Biol Chem. 2008 May 23;283(21):14177-81
[
18385130.001
]
[Cites]
Oncogene. 2008 Aug 14;27(35):4768-78
[
18438433.001
]
[Cites]
Blood. 2002 Jan 1;99(1):394
[
11783438.001
]
[Cites]
J Clin Oncol. 2002 Feb 1;20(3):680-7
[
11821448.001
]
[Cites]
J Immunol. 2002 Apr 15;168(8):4121-6
[
11937572.001
]
[Cites]
Nat Rev Immunol. 2002 Aug;2(8):569-79
[
12154376.001
]
[Cites]
J Exp Med. 2003 May 5;197(9):1221-7
[
12732664.001
]
[Cites]
J Clin Invest. 2003 Jul;112(1):126-35
[
12840067.001
]
[Cites]
J Exp Med. 2003 Nov 3;198(9):1391-402
[
14597738.001
]
[Cites]
J Biol Chem. 2003 Dec 12;278(50):50791-802
[
14523017.001
]
[Cites]
Mol Immunol. 2004 Jun;41(4):399-409
[
15163537.001
]
[Cites]
J Mol Histol. 2004 Mar;35(3):233-45
[
15339043.001
]
[Cites]
Acta Med Scand. 1976;199(3):185-90
[
3948.001
]
[Cites]
J Biol Chem. 1983 Jan 10;258(1):339-43
[
6848505.001
]
[Cites]
Exp Pathol. 1988;33(1):59-63
[
3384068.001
]
[Cites]
Stroke. 1990 Nov;21(11 Suppl):III71-4
[
2146782.001
]
[Cites]
Mol Chem Neuropathol. 1993 May-Jun;19(1-2):95-106
[
8363708.001
]
[Cites]
Blood. 1993 Oct 1;82(7):2031-7
[
8104535.001
]
[Cites]
J Mol Cell Cardiol. 1995 Jan;27(1):453-8
[
7760365.001
]
[Cites]
Am J Physiol. 1995 Nov;269(5 Pt 1):C1105-11
[
7491897.001
]
[Cites]
Cancer Res. 1996 Oct 1;56(19):4509-15
[
8813149.001
]
[Cites]
Int J Cancer. 1998 Aug 21;79(4):365-9
[
9699528.001
]
[Cites]
Br J Cancer. 1998 Sep;78(6):822-7
[
9743308.001
]
[Cites]
Stem Cells. 2004;22(6):1015-29
[
15536192.001
]
[Cites]
Blood. 2006 Mar 1;107(5):1761-7
[
16269611.001
]
[Cites]
Cancer Immunol Immunother. 2006 Jul;55(7):808-18
[
16283305.001
]
[Cites]
Cancer Res. 2006 Nov 15;66(22):11013-20
[
17108140.001
]
[Cites]
Mol Cancer Ther. 2006 Dec;5(12):3113-21
[
17172414.001
]
[Cites]
Blood. 2007 Jan 15;109(2):786-91
[
16888090.001
]
[Cites]
Cancer. 2007 Mar 15;109(6):1152-6
[
17315232.001
]
[Cites]
Mol Cancer Res. 2008 Mar;6(3):446-57
[
18337451.001
]
(PMID = 18957686.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P01 CA55164
[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 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Receptors, CXCR4; S88TT14065 / Oxygen
[Other-IDs]
NLM/ PMC2644078
33.
Invernizzi R, Travaglino E, Benatti C, Malcovati L, Della Porta M, Cazzola M, Ascari E:
Survivin expression, apoptosis and proliferation in chronic myelomonocytic leukemia.
Eur J Haematol
; 2006 Jun;76(6):494-501
[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]
Survivin expression, apoptosis and proliferation in chronic myelomonocytic
leukemia
.
We analyzed the expression of the inhibitor of apoptosis survivin by immunocytochemistry in bone marrow cells from patients with chronic myelomonocytic
leukemia
(CMML) to evaluate possible abnormalities in comparison with other myelodysplastic (MDS) and myeloproliferative syndromes, and to investigate a possible correlation between survivin expression and altered apoptosis or proliferation, or relevant laboratory and clinical findings.
Thirty-four patients with CMML [18 MDS-CMML and 16 myeloproliferative disorder (MPD)-CMML], 90 with MDS, 41 with
acute
myeloid
leukemia
(AML), 19 with chronic MPD and 25 control subjects were studied.
In CMML and MDS apoptosis was significantly higher compared to normal controls and all other subtypes of
leukemias
(P < 0.0001).
In CMML there was no correlation between survivin expression and blast
cell
percentage, apoptosis or proliferation, FAB or WHO subgroup.
Survivin overexpression, by disrupting the balance between
cell
proliferation/differentiation and apoptosis, may play an important role in its pathophysiology.
[MeSH-major]
Leukemia
, Myelomonocytic, Chronic / pathology. Microtubule-Associated Proteins / physiology. Neoplasm Proteins / physiology
[MeSH-minor]
Acute
Disease
. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis.
Cell
Division.
Disease
Progression. Female. Humans. Inhibitor of Apoptosis Proteins.
Leukemia
, Myeloid / classification.
Leukemia
, Myeloid / metabolism.
Leukemia
, Myeloid / pathology. Male. Middle Aged. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / pathology
Genetic Alliance.
consumer health - Chronic Myelomonocytic Leukemia
.
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 = 16529600.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
34.
Zhang W, Konopleva M, Ruvolo VR, McQueen T, Evans RL, Bornmann WG, McCubrey J, Cortes J, Andreeff M:
Sorafenib induces apoptosis of AML cells via Bim-mediated activation of the intrinsic apoptotic pathway.
Leukemia
; 2008 Apr;22(4):808-18
[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.
Raf/MEK/Erk signaling is activated in the majority of
acute
myeloid
leukemias
(AMLs), providing rationale for targeting this pathway with therapeutic intent.
Our studies demonstrated that sorafenib significantly inhibited the phosphorylation levels of Raf downstream target proteins MEK1/2 and Erk, induced apoptosis and inhibited colony formation in AML
cell
lines and in primary AML samples.
Combination of sorafenib with cytarabine or the novel small molecule Bcl-2 inhibitor ABT-737 synergistically induced
cell
death in AML
cell
lines.
[MeSH-major]
Apoptosis / drug effects. Apoptosis Regulatory Proteins / metabolism. Benzenesulfonates / pharmacology.
Leukemia
, Myeloid,
Acute
/ drug therapy. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Pyridines / pharmacology. Signal Transduction / drug effects
[MeSH-minor]
Cell
Line. Drug Synergism. Humans. Mitochondria / metabolism. Niacinamide / analogs & derivatives. Phenylurea Compounds
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
NICOTINAMIDE
.
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
.
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 = 18200035.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA55164
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Benzenesulfonates; 0 / Membrane Proteins; 0 / Phenylurea Compounds; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
35.
Wananukul S, Nuchprayoon I, Siripanich H:
Mucocutaneous findings in febrile neutropenic children with acute leukemias.
J Med Assoc Thai
; 2005 Jun;88(6):817-23
[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]
Mucocutaneous findings in febrile neutropenic children with
acute leukemias
.
Febrile neutropenia is common in children with
leukemia
.
The authors prospectively examined children with fever with neutropenia in
acute
leukemia
, aged 1-15 years, who were admitted to the Department of Pediatrics, King Chulalongkorn Memorial Hospital, between September 2000 and August 2001.
The prevalence of infection was found in severe neutropenia (absolute neutrophil count, ANC less than 500
cell
/cu mm), moderate neutropenia (ANC, 500-1000
cell
/cu mm) and mild neutropenia (ANC, 1001-1500
cell
/cu mm) was 72%, 9% and 5%, respectively.
Daily physical examination of skin and mucous membrane are suggested for proper and prompt diagnosis and treatment of febrile neutropenic children with
acute
leukemia
to reduce mortality and morbidity in these patients.
A Guideline for the use of antimicrobial agents in neutropenic patients with
acute
leukemia
is proposed In conclusion, infection was commonly found in severe neutropenia.
Mucocutaneous infection was the most common site of infection infebrile neutropenia in children with
leukemia
.
[MeSH-major]
Fever. Neutropenia / diagnosis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis. Skin Diseases / etiology
MedlinePlus Health Information.
consumer health - Fever
.
MedlinePlus Health Information.
consumer health - Skin Conditions
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16083222.001).
[ISSN]
0125-2208
[Journal-full-title]
Journal of the Medical Association of Thailand = Chotmaihet thangphaet
[ISO-abbreviation]
J Med Assoc Thai
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Thailand
36.
Jeeninga RE, Jan B, van der Linden B, van den Berg H, Berkhout B:
Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-cell lines: towards a new virotherapy approach.
Cancer Res
; 2005 Apr 15;65(8):3347-55
[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]
Construction
of a
minimal HIV-1 variant that selectively replicates in leukemic derived T-
cell
lines: towards a new virotherapy approach.
T-
cell acute
lymphoblastic
leukemia
is a high-risk type of blood-
cell
cancer.
We analyzed the possibility of developing virotherapy for T-
cell acute
lymphoblastic
leukemia
.
Virotherapy is based on the exclusive replication
of a
virus in leukemic cells, leading to the selective removal of these malignant cells.
This mini-HIV virus has five deletions (vif, vpR, vpU, nef, and U3) and replicated in the SupT1
cell
line, but did not replicate in normal peripheral blood mononuclear cells.
The mini-HIV variant that uses CD4 and CXCR4 for
cell
entry could potentially be used against CXCR4-expressing malignancies such as T-lymphoblastic
leukemia
/lymphoma, natural killer
leukemia
, and some myeloid
leukemias
.
[MeSH-major]
HIV-1 / physiology.
Leukemia
-Lymphoma, Adult T-
Cell
/ therapy.
Leukemia
-Lymphoma, Adult T-
Cell
/ virology. T-
Lymphocytes
/ virology
[MeSH-minor]
Antigens, CD4 / biosynthesis.
Cell
Line, Tumor. Female. Gene Deletion. Genes, nef / genetics. Genes, vif / genetics. Genes, vpr / genetics. Genes, vpu / genetics. HIV Long Terminal Repeat / genetics. Humans. Jurkat Cells. Receptors, CXCR4 / biosynthesis. Virus Replication
Genetic Alliance.
consumer health - HIV
.
HIV InSite.
treatment guidelines - Women and HIV
.
HIV InSite.
treatment guidelines - Human Herpesvirus-8
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15833868.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / R21-AI47017-01
[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 / Antigens, CD4; 0 / Receptors, CXCR4
37.
Raponi S, De Propris MS, Wai H, Intoppa S, Elia L, Diverio D, Vitale A, Foà R, Guarini A:
An accurate and rapid flow cytometric diagnosis of BCR-ABL positive acute lymphoblastic leukemia.
Haematologica
; 2009 Dec;94(12):1767-70
[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]
An accurate and rapid flow cytometric diagnosis of BCR-ABL positive
acute
lymphoblastic
leukemia
.
Tyrosine kinase inhibitors have profoundly modified the treatment and prognosis of chronic myeloid
leukemia
and Ph(+)
acute
lymphoblastic
leukemia
.
A rapid and accurate detection of the BCR-ABL fusion protein is paramount today for an optimal management of Ph(+)
acute
lymphoblastic
leukemia
.
We have utilized a recently described and commercialized immunoassay that identifies qualitatively the presence of the BCR-ABL protein in leukemic
cell
lysates.
The assay was applied to 101 primary patient samples (94
acute leukemias
and 7 chronic myeloid
leukemia
blast crisis) and the results of the immunoassay were concordant with those obtained by conventional molecular techniques.
This flow cytometric immunoassay has important implications for perfecting the management of Ph(+)
acute
lymphoblastic
leukemia
patients worldwide.
[MeSH-major]
Flow Cytometry / methods. Fusion Proteins, bcr-abl / analysis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
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
[Cites]
N Engl J Med. 2000 Apr 6;342(14):998-1006
[
10749961.001
]
[Cites]
Crit Rev Oncol Hematol. 2000 Oct;36(1):49-58
[
10996522.001
]
[Cites]
Blood. 2002 Sep 15;100(6):1965-71
[
12200353.001
]
[Cites]
Haematologica. 2003 Mar;88(3):275-9
[
12651265.001
]
[Cites]
Nature. 1982 Dec 23;300(5894):765-7
[
6960256.001
]
[Cites]
Blood. 1996 Oct 1;88(7):2375-84
[
8839828.001
]
[Cites]
Blood. 2005 May 1;105(9):3434-41
[
15650057.001
]
[Cites]
Mayo Clin Proc. 2005 Nov;80(11):1517-27
[
16295033.001
]
[Cites]
J Clin Oncol. 2006 Jan 20;24(3):460-6
[
16344315.001
]
[Cites]
Curr Opin Oncol. 2006 Nov;18(6):652-9
[
16988590.001
]
[Cites]
Blood. 2007 May 1;109(9):3676-8
[
17213285.001
]
[Cites]
Cancer. 2007 May 15;109(10):2068-76
[
17429836.001
]
[Cites]
Blood. 2007 May 15;109(10):4143-50
[
17264298.001
]
[Cites]
Clin Adv Hematol Oncol. 2007 Apr;5(4):270-2, 292
[
17607286.001
]
[Cites]
Blood. 2008 Dec 15;112(13):4808-17
[
19064740.001
]
[Cites]
Leukemia. 2009 Jun;23(6):1106-17
[
19387467.001
]
[CommentIn]
Haematologica. 2009 Dec;94(12):1639-41
[
19996114.001
]
(PMID = 19608682.001).
[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
[Chemical-registry-number]
EC 2.7.10.2 / Fusion Proteins, bcr-abl
[Other-IDs]
NLM/ PMC2791932
38.
Kaufmann SH, Karp JE, Letendre L, Kottke TJ, Safgren S, Greer J, Gojo I, Atherton P, Svingen PA, Loegering DA, Litzow MR, Sloan JA, Reid JM, Ames MM, Adjei AA, Erlichman C:
Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory acute leukemia.
Clin Cancer Res
; 2005 Sep 15;11(18):6641-9
[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]
Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory
acute
leukemia
.
PURPOSE: To assess the maximum tolerated dose, toxicities, pharmacokinetics, and antileukemic activity of topotecan and carboplatin in adults with recurrent or refractory
acute leukemias
.
Among 45 evaluable patients, there were 7 complete remissions, 2 partial remissions, 1 incomplete complete remission, and 1 reversion to chronic-phase chronic myelogenous
leukemia
.
Leukemic
cell
levels of topoisomerase I, checkpoint kinase 1, checkpoint kinase 2, and Mcl-1 correlated with proliferating
cell
nuclear antigen but not with response.
Responses seem to correlate with low pretreatment blast
cell
Bcl-2 expression.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
/ drug therapy
[MeSH-minor]
Acute
Disease
. Adult. Aged. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Carboplatin / administration & dosage. Carboplatin / adverse effects. Carboplatin / pharmacokinetics.
Cell
Cycle Proteins / metabolism. Combined Modality Therapy. DNA Topoisomerases, Type I / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. HL-60 Cells. Hematopoietic Stem
Cell
Transplantation. Humans. Immunoblotting. Infusions, Intravenous. Male. Middle Aged. Neoplasm Recurrence, Local. Proliferating
Cell
Nuclear Antigen / metabolism. Topotecan / administration & dosage. Topotecan / adverse effects. Topotecan / pharmacokinetics. Treatment Outcome
MedlinePlus Health Information.
consumer health - Leukemia
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
Topotecan
.
Hazardous Substances Data Bank.
CARBOPLATIN
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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 = 16166443.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA73709; United States / NCI NIH HHS / CA / U01 CA69854; United States / NCI NIH HHS / CA / U01 CA69912
[Publication-type]
Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / Proliferating Cell Nuclear Antigen; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin; EC 5.99.1.2 / DNA Topoisomerases, Type I
39.
Kurosu T, Ohki M, Wu N, Kagechika H, Miura O:
Sorafenib induces apoptosis specifically in cells expressing BCR/ABL by inhibiting its kinase activity to activate the intrinsic mitochondrial pathway.
Cancer Res
; 2009 May 1;69(9):3927-36
[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.
Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous
leukemia
and Philadelphia chromosome-positive (Ph+)
acute
lymphoblastic
leukemia
, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.
Thus, sorafenib may provide an effective therapeutic measure to treat Ph+
leukemias
, particularly those expressing the T315I mutant, which is totally resistant to imatinib and the second generation BCR/ABL inhibitors.
[MeSH-major]
Apoptosis / drug effects. Benzenesulfonates / pharmacology. Fusion Proteins, bcr-abl / antagonists & inhibitors.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mitochondria / drug effects. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines / pharmacology
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
Hazardous Substances Data Bank.
NICOTINAMIDE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
antibodies-online.
View related products from antibodies-online.com
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19366808.001).
[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 / ABT-737; 0 / Acetophenones; 0 / Benzamides; 0 / Benzenesulfonates; 0 / Benzopyrans; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Interleukin-3; 0 / Nitrophenols; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrazines; 0 / Pyridines; 0 / Pyrimidines; 0 / Sulfonamides; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; E29LP3ZMUH / rottlerin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / Caspases
40.
Derwich K, Sedek L, Meyer C, Pieczonka A, Dawidowska M, Gaworczyk A, Wachowiak J, Konatkowska B, Witt M, Marschalek R, Szczepański T:
Infant acute bilineal leukemia.
Leuk Res
; 2009 Jul;33(7):1005-8
[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]
Infant
acute
bilineal
leukemia
.
Most cases of
acute
leukemia
can be assigned to the myeloid, B or T lineage.
There are rare cases of
acute
leukemia
, which cannot be clearly classified, because either blasts express antigens of more than one lineage (
acute
biphenotypic
leukemias
) or distinct blast populations of two lineages co-exist (
acute
bilineal
leukemias
, aBLL).
We present a 10-month-old infant with
de
novo aBLL, characterized by blasts of monocytic and B-
cell
precursor lineages.
Despite poor initial response, both to
acute
lymphoblastic
leukemia
(ALL) induction treatment and
acute
myeloid
leukemia
induction blocks, the child reached complete clinical remission with minimal residual
disease
negative status and was transplanted.
This case report illustrates that aBLL is a very aggressive type of
acute
leukemia
that should be individually treated and monitored, particularly in children less than 1 year of age.
[MeSH-major]
B-
Lymphocytes
/ pathology.
Leukemia
, Biphenotypic,
Acute
/ diagnosis.
Leukemia
, Myeloid,
Acute
/ diagnosis. Neoplasm, Residual / diagnosis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis
[MeSH-minor]
Cell
Lineage. Hematopoietic Stem
Cell
Transplantation. Humans. Infant. Male. Remission Induction. Treatment Outcome
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19286255.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
41.
Nakamura S, Okinaka K, Hirano I, Ono T, Sugimoto Y, Shigeno K, Fujisawa S, Shinjo K, Ohnishi K:
KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.
Leuk Res
; 2008 Sep;32(9):1358-65
[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]
KIS induces proliferation and the
cell
cycle progression through the phosphorylation of p27Kip1 in
leukemia
cells.
The mRNA expressions of KIS were successfully reduced in all
cell
lines.
We showed that KIS protein directly interacted with p27(Kip1) protein, and reduction of KIS inhibited the S10 phosphorylation of p27(Kip1) in
leukemia
cells.
On these cells transfected with siRNA KIS, the inhibition of S10 phosphorylation of p27(Kip1) was strongly suppressed
cell
proliferation in a time-dependent manner.
These data demonstrated that the KIS activity was induced during G0/G1, and it promotes
cell
cycle progression by phosphorylation of S10 on p27(Kip1).
We showed that KIS mRNA expression was increased in primary
leukemia
specimens (
acute
myelogenous
leukemia
(AML); 37, myelodysplastic syndrome (MDS); 72,
acute
lymphoblastic
leukemia
(ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.
Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various
leukemias
, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).
This study demonstrates that the elevated levels of KIS protein in
leukemia
cells promote the
cell
cycle progression in
leukemia
cells.
[MeSH-major]
Cell
Cycle / physiology.
Cell
Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Intracellular Signaling Peptides and Proteins / physiology.
Leukemia
, Myeloid,
Acute
/ metabolism. Myelodysplastic Syndromes / metabolism. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / metabolism. Protein-Serine-Threonine Kinases / physiology
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Myelodysplastic Syndromes
.
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 = 18384876.001).
[ISSN]
0145-2126
[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
[Chemical-registry-number]
0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human
42.
Kurosu T, Tsuji K, Kida A, Koyama T, Yamamoto M, Miura O:
Rottlerin synergistically enhances imatinib-induced apoptosis of BCR/ABL-expressing cells through its mitochondrial uncoupling effect independent of protein kinase C-delta.
Oncogene
; 2007 May 10;26(21):2975-87
[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.
Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid
leukemia
(CML) and Philadelphia-chromosome positive
acute
lymphoblastic
leukemia
(ALL), relapse with emerging imatinib-resistance mutations in the BCR/ABL kinase domain poses a significant problem.
Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a
cell
line expressing the imatinib-resistant E255K BCR/ABL mutant.
The present study indicates that rottlerin synergistically enhances imatinib-induced apoptosis through its mitochondrial uncoupling effect independent of PKCdelta and may contribute to the development of new treatment strategy to overcome the imatinib resistance and to cure the BCR/ABL expressing
leukemias
.
[MeSH-minor]
Animals. Benzamides. Drug Synergism. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. K562 Cells.
Leukemia
, Erythroblastic,
Acute
/ drug therapy.
Leukemia
, Erythroblastic,
Acute
/ enzymology. Mice. Mitochondria / drug effects. Mitochondria / enzymology. Mitochondria / metabolism. Up-Regulation / drug effects
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17130834.001).
[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 / Acetophenones; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzopyrans; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Uncoupling Agents; 8A1O1M485B / Imatinib Mesylate; E29LP3ZMUH / rottlerin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.13 / Protein Kinase C-delta
43.
Alzani R, Pedrini O, Albanese C, Ceruti R, Casolaro A, Patton V, Colotta F, Rambaldi A, Introna M, Pesenti E, Ciomei M, Golay J:
Therapeutic efficacy of the pan-cdk inhibitor PHA-793887 in vitro and in vivo in engraftment and high-burden leukemia models.
Exp Hematol
; 2010 Apr;38(4):259-269.e2
[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]
Therapeutic efficacy of the pan-cdk inhibitor PHA-793887 in vitro and in vivo in engraftment and high-burden
leukemia
models.
MATERIALS AND METHODS: Thirteen leukemic
cell
lines bearing different cytogenetic abnormalities and normal hematopoietic cells were used in cytotoxicity and colony assays.
The drug activity at the molecular
level
was analyzed by Western blotting.
PHA-793887 was also tested in vivo in several
leukemia
xenograft models.
RESULTS: PHA-793887 was cytotoxic for leukemic
cell
lines in vitro, with IC(50) ranging from 0.3 to 7 microM (mean: 2.9 microM), regardless of any specific chromosomal aberration.
Interestingly, in colony assays PHA-793887 showed very high activity against
leukemia
cell
lines, with an IC(50) <0.1 microM (mean: 0.08 microM), indicating that it has efficient and prolonged antiproliferative activity.
PHA-793887 induced
cell
-cycle arrest, inhibited Rb and nucleophosmin phosphorylation, and modulated cyclin E and cdc6 expression at low doses (0.2-1 microM) and induced apoptosis at the highest dose (5 microM).
It was also effective in vivo in both subcutaneous xenograft and primary leukemic disseminated models that better mimic naturally occurring human
disease
.
Interestingly, in one disseminated model derived from a relapsed Philadelphia-positive
acute
lymphoid
leukemia
patient, PHA-793887 showed strong therapeutic activity also when treatment was started after establishment of high
disease
burden.
CONCLUSIONS: We conclude that PHA-793887 has promising therapeutic activity against
acute leukemias
in vitro and in vivo.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors.
Leukemia
/ drug therapy
[MeSH-minor]
Animals. Apoptosis. Blotting, Western.
Cell
Cycle / drug effects.
Cell
Line, Tumor.
Disease
Models, Animal. Drug Screening Assays, Antitumor. Humans. Immunohistochemistry. Inhibitory Concentration 50. Mice. Mice, SCID
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Leukemia
.
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
(PMID = 20167248.001).
[ISSN]
1873-2399
[Journal-full-title]
Experimental hematology
[ISO-abbreviation]
Exp. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; EC 2.7.11.22 / Cyclin-Dependent Kinases
44.
Pichiorri F, Trapasso F, Palumbo T, Aqeilan RI, Drusco A, Blaser BW, Iliopoulos D, Caligiuri MA, Huebner K, Croce CM:
Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35.
Clin Cancer Res
; 2006 Jun 01;12(11 Pt 1):3494-501
[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]
Preclinical assessment of FHIT gene replacement therapy in human
leukemia
using a chimeric adenovirus, Ad5/F35.
Adenovirus 5 (Ad5) virus or adeno-associated viral vectors have been used to study the tumor suppressor function of FHIT in solid tumors, but these tools have not been effective in
leukemias
.
EXPERIMENTAL DESIGN: Infection efficiency of Ad5/F35-FHIT and Ad5/F35-GFP viruses was tested in
leukemia
cell
lines that lacked FHIT expression, and biological effects of successful infection were assessed.
An
acute
myelogenous
leukemia
, a chronic myelogenous
leukemia
, and four
acute
lymphoblastic
leukemia
human
cell
lines were examined as well as two EBV-transformed B lymphoblastoid
cell
lines that expressed endogenous FHIT.
RESULTS: Two of four
acute
lymphoblastic
leukemia
cell
lines, Jurkat and MV4;11, which were efficiently infected with Ad5/F35-FHIT, underwent growth suppression and massive induction of apoptosis without apparent activation of caspase-8 or caspase-2 and late activation of caspase-3.
The two remaining infected
acute
lymphoblastic
leukemia
cell
lines, Molt-3 and RS4;11, were apparently unaffected.
Restoration of FHIT expression in the chronic myelogenous
leukemia
K562
cell
line and the
acute
myelogenous
leukemia
KG1a
cell
line also induced apoptosis but at later time points than seen in the
acute
lymphoblastic
leukemia
Jurkat and MV4;11
cell
lines. I.v. injection of Ad5/F35-FHIT-infected Jurkat cells resulted in abrogation of tumorigenicity in the NOD/SCID xenogeneic engraftment model.
CONCLUSION: FHIT restoration in some FHIT-deficient
leukemia
cells induces both antiproliferative and proapoptotic effects involving the intrinsic caspase apoptotic pathway.
[MeSH-major]
Acid Anhydride Hydrolases / genetics. Adenoviruses, Human / genetics. Gene Expression Regulation, Neoplastic / genetics. Genetic Therapy / methods.
Leukemia
/ genetics. Neoplasm Proteins / genetics
[MeSH-minor]
Animals. Apoptosis / drug effects. Apoptosis / genetics.
Cell
Cycle.
Cell
Line, Tumor.
Cell
Proliferation / drug effects.
Disease
Models, Animal. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Gene Transfer Techniques. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Humans. Kinetics. Mice. Mice, Inbred NOD. Mice, SCID. Structure-Activity Relationship. Transplantation, Heterologous. Xenograft Model Antitumor Assays
MedlinePlus Health Information.
consumer health - Genes and Gene Therapy
.
MedlinePlus Health Information.
consumer health - Leukemia
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Clin Cancer Res. 2016 Dec 15;22(24):6304
[
27856602.001
]
(PMID = 16740775.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA56036; United States / NCI NIH HHS / CA / CA77738; United States / NCI NIH HHS / CA / CA78890; United States / NCI NIH HHS / CA / CA89341
[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 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.6.- / Acid Anhydride Hydrolases
45.
Haferlach T, Kohlmann A, Wieczorek L, Basso G, Kronnie GT, Béné MC, De Vos J, Hernández JM, Hofmann WK, Mills KI, Gilkes A, Chiaretti S, Shurtleff SA, Kipps TJ, Rassenti LZ, Yeoh AE, Papenhausen PR, Liu WM, Williams PM, Foà R:
Clinical utility of microarray-based gene expression profiling in the diagnosis and subclassification of leukemia: report from the International Microarray Innovations in Leukemia Study Group.
J Clin Oncol
; 2010 May 20;28(15):2529-37
[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]
Clinical utility of microarray-based gene expression profiling in the diagnosis and subclassification
of leukemia
: report from the International Microarray Innovations in
Leukemia
Study Group.
PURPOSE: The Microarray Innovations in
Leukemia
study assessed the clinical utility of gene expression profiling as a single test to subtype
leukemias
into conventional categories of myeloid and lymphoid malignancies.
An exploratory retrospective stage I study was designed for biomarker discovery and generated whole-genome expression profiles from 2,143 patients with
leukemias
and myelodysplastic syndromes.
In a second cohort of 1,152 prospectively collected patients, a classification scheme reached 95.6% median sensitivity and 99.8% median specificity for 14 standard subtypes of
acute
leukemia
(eight
acute
lymphoblastic
leukemia
and six
acute
myeloid
leukemia
classes, n = 693).
Our comprehensive gene expression data set will be submitted to the public domain to foster research focusing on the molecular understanding of
leukemias
.
[MeSH-major]
Leukemia
/ classification.
Leukemia
/ genetics
MedlinePlus Health Information.
consumer health - Leukemia
.
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
[CommentIn]
Nat Rev Clin Oncol. 2010 Aug;7(8):422
[
20700897.001
]
[Cites]
J Clin Oncol. 2008 Nov 1;26(31):5078-87
[
18809607.001
]
[Cites]
Cancer. 2008 Jan 1;112(1):4-16
[
18000811.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8
[
9843981.001
]
[Cites]
Blood. 2004 Dec 1;104(12):3679-87
[
15226186.001
]
[Cites]
Blood. 2004 Apr 1;103(7):2771-8
[
14684422.001
]
[Cites]
Leukemia. 2004 Jan;18(1):63-71
[
14603332.001
]
[Cites]
BMC Genomics. 2007 Jun 22;8:188
[
17587440.001
]
[Cites]
Blood. 2005 Aug 15;106(4):1189-98
[
15878973.001
]
[Cites]
Blood. 2007 Nov 15;110(10):3706-14
[
17671232.001
]
[Cites]
Blood. 2003 Oct 15;102(8):2951-9
[
12730115.001
]
[Cites]
Clin Chem. 2008 Oct;54(10):1705-15
[
18719197.001
]
[Cites]
Genes Chromosomes Cancer. 2003 Aug;37(4):396-405
[
12800151.001
]
[Cites]
Blood. 2006 Sep 1;108(5):1677-83
[
16670265.001
]
[Cites]
Blood. 2008 Nov 15;112(10):4193-201
[
18716133.001
]
[Cites]
Leukemia. 2008 Dec;22(12):2193-200
[
18754029.001
]
[Cites]
J Clin Oncol. 2008 Oct 1;26(28):4595-602
[
18559874.001
]
[Cites]
Blood. 2005 Aug 1;106(3):899-902
[
15831697.001
]
[Cites]
Blood. 2009 Jan 8;113(2):291-8
[
18703705.001
]
[Cites]
Blood. 2005 Dec 1;106(12):3747-54
[
16109776.001
]
[Cites]
Blood. 2008 Feb 1;111(3):1552-9
[
17940205.001
]
[Cites]
N Engl J Med. 2004 Apr 15;350(16):1617-28
[
15084694.001
]
[Cites]
Blood. 2002 Dec 15;100(13):4325-36
[
12393746.001
]
[Cites]
Br J Haematol. 2008 Sep;142(5):802-7
[
18573112.001
]
[Cites]
Cancer Cell. 2002 Mar;1(2):133-43
[
12086872.001
]
[Cites]
J Theor Biol. 2006 Nov 21;243(2):273-8
[
16889801.001
]
[Cites]
Nat Genet. 2002 Jan;30(1):41-7
[
11731795.001
]
[Cites]
Genes Chromosomes Cancer. 2005 Jul;43(3):227-38
[
15846790.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10008-13
[
12105272.001
]
[Cites]
N Engl J Med. 2004 Apr 15;350(16):1605-16
[
15084693.001
]
[Cites]
Nucleic Acids Res. 2005 Jan 1;33(Database issue):D562-6
[
15608262.001
]
[Cites]
Blood. 2004 Sep 1;104(5):1474-81
[
15142876.001
]
[Cites]
Blood. 2001 Sep 1;98 (5):1312-20
[
11520776.001
]
[Cites]
Blood. 2008 May 1;111(9):4490-5
[
18309032.001
]
[Cites]
Science. 1999 Oct 15;286(5439):531-7
[
10521349.001
]
(PMID = 20406941.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA081534
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
46.
Parovichnikova EN, Savchenko VG, Verniuk MA, Vinogradova OA, Misiurin AV, Vorob'ev IA, Domracheva EV, Tikhonova LIu, Rukavitsyn OA, Rossiev VA, Kliasova GA, Turkina AG, Liubimova LS, Mendeleeva LP, Isaev VG:
[Acute lymphoblastic leukemias with aberrations of BCR-ABL genes].
Ter Arkh
; 2005;77(7):11-6
[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]
[
Acute
lymphoblastic
leukemias
with aberrations of BCR-ABL genes].
AIM: To develop an original therapeutic strategy in Ph-positive
acute
lymphoblastic
leukemia
(ALL).
[MeSH-major]
Fusion Proteins, bcr-abl / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16116902.001).
[ISSN]
0040-3660
[Journal-full-title]
Terapevticheskiĭ arkhiv
[ISO-abbreviation]
Ter. Arkh.
[Language]
rus
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
47.
Kazemi T, Asgarian-Omran H, Memarian A, Shabani M, Sharifian RA, Vossough P, Ansaripour B, Rabbani H, Shokri F:
Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.
Cancer Immunol Immunother
; 2009 Jun;58(6):989-96
[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]
Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with
acute
lymphoblastic
leukemia
.
Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-
cell
lineage expression, in some chronic B-
cell leukemias
with possible implication for classification and/or targeted immunotherapy.
[MeSH-major]
Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics. Receptors,
Cell
Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18802695.001).
[ISSN]
1432-0851
[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 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic
48.
Fei F, Stoddart S, Groffen J, Heisterkamp N:
Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive acute lymphoblastic leukemias.
Mol Cancer Ther
; 2010 May;9(5):1318-27
[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]
Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive
acute
lymphoblastic
leukemias
.
The emergence of resistance to tyrosine kinase inhibitors due to point mutations in Bcr/Abl is a challenging problem for Philadelphia chromosome-positive (Ph-positive)
acute
lymphoblastic
leukemia
(ALL) patients, especially for those with the T315I mutation, against which neither nilotinib or dasatinib shows significant activity.
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
[Cites]
Science. 2001 Aug 3;293(5531):876-80
[
11423618.001
]
[Cites]
Leukemia. 2010 Apr;24(4):813-20
[
20111071.001
]
[Cites]
Semin Hematol. 2003 Apr;40(2 Suppl 2):4-10
[
12783368.001
]
[Cites]
Nat Rev Mol Cell Biol. 2003 Nov;4(11):842-54
[
14625535.001
]
[Cites]
Curr Opin Hematol. 2004 Jan;11(1):35-43
[
14676625.001
]
[Cites]
Leukemia. 2004 Jan;18(1):23-8
[
14603339.001
]
[Cites]
Nat Med. 2004 Mar;10(3):262-7
[
14981513.001
]
[Cites]
Science. 2004 Jul 16;305(5682):399-401
[
15256671.001
]
[Cites]
J Med Chem. 2004 Dec 30;47(27):6658-61
[
15615512.001
]
[Cites]
Cancer Cell. 2005 Feb;7(2):129-41
[
15710326.001
]
[Cites]
Blood. 2005 Apr 1;105(7):2640-53
[
15618470.001
]
[Cites]
Cancer Res. 2005 Jun 1;65(11):4500-5
[
15930265.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11011-6
[
16046538.001
]
[Cites]
Cancer Res. 2006 Jan 15;66(2):1007-14
[
16424036.001
]
[Cites]
Curr Opin Genet Dev. 2006 Feb;16(1):92-9
[
16343892.001
]
[Cites]
Cancer Res. 2006 May 15;66(10):5387-93
[
16707466.001
]
[Cites]
Leukemia. 2006 Jun;20(6):1061-6
[
16642048.001
]
[Cites]
Blood. 2007 Jan 15;109(2):500-2
[
16990603.001
]
[Cites]
Mol Cancer Res. 2007 Jan;5(1):1-10
[
17259342.001
]
[Cites]
Leukemia. 2007 Jun;21(6):1189-97
[
17392819.001
]
[Cites]
Mol Cancer. 2007;6:67
[
17958915.001
]
[Cites]
Clin Cancer Res. 2008 Jan 15;14(2):352-9
[
18223208.001
]
[Cites]
Haematologica. 2008 May;93(5):662-9
[
18367484.001
]
[Cites]
Blood. 2008 Aug 1;112(3):793-804
[
18505786.001
]
[Cites]
Cancer. 2008 Sep 1;113(5):985-94
[
18615627.001
]
[Cites]
Clin Cancer Res. 2008 Oct 1;14(19):6106-15
[
18829489.001
]
[Cites]
J Biol Chem. 2008 Nov 14;283(46):31785-90
[
18801727.001
]
[Cites]
Exp Cell Res. 2009 Apr 15;315(7):1085-99
[
19233169.001
]
[Cites]
Biochem Pharmacol. 2010 Mar 1;79(5):688-97
[
19874801.001
]
[Cites]
Blood. 2002 Mar 1;99(5):1860-2
[
11861307.001
]
(PMID = 20388735.001).
[ISSN]
1538-8514
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
ENG
[Grant]
None / None / / R01 CA090321-08S1; United States / NCI NIH HHS / CA / CA090321; United States / NCI NIH HHS / CA / R01 CA090321-08S1; United States / NCI NIH HHS / CA / R01 CA090321; United States / NCI NIH HHS / CA / R01 CA090321-08; None / None / / R01 CA090321-08
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 639089-54-6 / VX680; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; RBZ1571X5H / Dasatinib
[Other-IDs]
NLM/ NIHMS185920; NLM/ PMC2868097
49.
Fu JF, Liang DC, Shih LY:
Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL.
Am J Clin Pathol
; 2007 Jan;127(1):24-30
[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]
Analysis of
acute leukemias
with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL.
t(11;19)(q23;p13.3); is one of the common chromosomal translocations in
acute leukemias
involving MLL rearrangements.
In a study of
acute leukemias
, 148 patients were identified to have MLL rearrangements by Southern blot analysis.
Of 15 patients with MLL/ENL, 7 had precursor B-
cell acute
lymphoblastic
leukemia
, 4 had T-
cell acute
lymphoblastic
leukemia
, and 4 had
acute
myeloid
leukemia
.
[MeSH-major]
Leukemia
, Myeloid / genetics. Myeloid-Lymphoid
Leukemia
Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Fusion / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17145626.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
50.
Savani BN, Mielke S, Adams S, Uribe M, Rezvani K, Yong AS, Zeilah J, Kurlander R, Srinivasan R, Childs R, Hensel N, Barrett AJ:
Rapid natural killer cell recovery determines outcome after T-cell-depleted HLA-identical stem cell transplantation in patients with myeloid leukemias but not with acute lymphoblastic leukemia.
Leukemia
; 2007 Oct;21(10):2145-52
[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]
Rapid natural killer
cell
recovery determines outcome after T-
cell
-depleted HLA-identical stem
cell
transplantation in patients with myeloid
leukemias
but not with
acute
lymphoblastic
leukemia
.
Natural killer (NK) cells are the first
lymphocytes
to recover after allogeneic stem
cell
transplantation (SCT) and can exert powerful graft-versus-
leukemia
(GVL) effects determining transplant outcome.
Conditions governing NK
cell
alloreactivity and the role of NK recovery in sibling SCT are not well defined.
NK cells on day 30 post-transplant (NK30) were measured in 54 SCT recipients with
leukemia
and donor and recipient killer immunoglobulin-like receptor (KIR) genotype determined.
NK30 counts also correlated directly with the transplant CD34
cell
dose and inversely with the CD3+
cell
dose.
Patients with NK30 >150/microl had less relapse (HR 18.3, P=0.039),
acute
graft-versus-host
disease
(HR 3.2, P=0.03), non-relapse mortality (HR 10.7, P=0.028) and improved survival (HR 11.4, P=0.03).
Results suggest that T
cell
-depleted SCT might be improved and the GVL effect enhanced by selecting donors with favorable KIR genotype, and by optimizing CD34 and CD3 doses.
[MeSH-major]
HLA Antigens / metabolism. Killer Cells, Natural / cytology.
Leukemia
, Myeloid / metabolism. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / metabolism. Stem
Cell
Transplantation / methods. T-
Lymphocytes
/ metabolism
[MeSH-minor]
Adolescent. Adult. Antigens, CD3 / biosynthesis. Antigens, CD34 / biosynthesis. Child. Cohort Studies. Female. Genotype. Graft vs
Leukemia
Effect. Humans. Male. Middle Aged. Monomeric GTP-Binding Proteins / metabolism. Transplantation Conditioning. Transplantation, Homologous
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Genetic Alliance.
consumer health - Transplantation
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17673900.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD3; 0 / Antigens, CD34; 0 / HLA Antigens; EC 3.6.5.2 / GEM protein, human; EC 3.6.5.2 / Monomeric GTP-Binding Proteins
51.
Sancho JM, Morgades M, Arranz R, Fernández-Abellán P, Deben G, Alonso N, Blanes M, Rodríguez MJ, Nicolás C, Sánchez E, Fernández de Sevilla A, Conde E, Ribera JM, QUIT Study (PETHEMA, GELTAMO and GOTEL Groups):
Practice of central nervous system prophylaxis and treatment in acute leukemias in Spain. Prospective registry study.
Med Clin (Barc)
; 2008 Oct 4;131(11):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]
Practice of central nervous system prophylaxis and treatment in
acute leukemias
in Spain. Prospective registry study.
BACKGROUND AND OBJECTIVE: Central nervous system (CNS) involvement in patients diagnosed with
acute leukemias
(AL) is an uncommon complication with poor prognosis.
For
acute
lymphoblastic
leukemia
patients (n = 158), CNS therapy was given to 12 cases (10 at diagnosis and 2 at relapse) and consisted of triple intrathecal therapy (TIT, methotrexate, cytarabine and hydrocortisone) in 11 and liposomal depot cytarabine in one.
In
acute
myeloblastic
leukemia
patients (n = 107), CNS therapy was administered to 17 cases (9 at diagnosis and 8 at relapse).
[MeSH-major]
Central Nervous System Neoplasms / prevention & control.
Leukemia
, Myeloid,
Acute
/ drug therapy. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Registries
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
HYDROCORTISONE
.
Hazardous Substances Data Bank.
METHOTREXATE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18928719.001).
[ISSN]
0025-7753
[Journal-full-title]
Medicina clínica
[ISO-abbreviation]
Med Clin (Barc)
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
Spain
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; 0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 04079A1RDZ / Cytarabine; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
52.
Yamane K, Kinsella TJ:
Casein kinase 2 regulates both apoptosis and the cell cycle following DNA damage induced by 6-thioguanine.
Clin Cancer Res
; 2005 Mar 15;11(6):2355-63
[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]
Casein kinase 2 regulates both apoptosis and the
cell
cycle following DNA damage induced by 6-thioguanine.
PURPOSE: The purine antimetabolite, 6-thioguanine (6-TG), is an effective drug in the management of
acute leukemias
.
Control and CK2 activity-reduced cells were cultured with 6-TG and assessed by flow cytometry to measure apoptosis and
cell
cycle profiles.
Additionally, transfection of Cdc2 with a mutation at Ser(39) to Ala, which is the CK2 phosphorylation site, partially inhibits
cell
cycle progression in G(1) to G(2) phase following 6-TG treatment.
[MeSH-major]
Apoptosis / drug effects. Casein Kinase II / pharmacology. Caspases / metabolism.
Cell
Cycle / drug effects. DNA Damage / drug effects. Thioguanine / pharmacology
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
THIOGUANINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15788687.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 84578; United States / NCI NIH HHS / CA / P30 CA 43703-12
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; EC 2.7.11.1 / Casein Kinase II; EC 3.4.22.- / Caspases; FTK8U1GZNX / Thioguanine
53.
Kröger N, Bacher U, Bader P, Böttcher S, Borowitz MJ, Dreger P, Khouri I, Macapinlac HA, Olavarria E, Radich J, Stock W, Vose JM, Weisdorf D, Willasch A, Giralt S, Bishop MR, Wayne AS:
NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: report from the Committee on Disease-Specific Methods and Strategies for Monitoring Relapse following Allogeneic Stem Cell Transplantation. Part I: Methods, acute leukemias, and myelodysplastic syndromes.
Biol Blood Marrow Transplant
; 2010 Sep;16(9):1187-211
[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]
NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem
Cell
Transplantation: report from the Committee on
Disease
-Specific Methods and Strategies for Monitoring Relapse following Allogeneic Stem
Cell
Transplantation. Part I: Methods,
acute leukemias
, and myelodysplastic syndromes.
Relapse has become the major cause of treatment failure after allogeneic stem
cell
transplantation.
To detect early relapse or minimal residual
disease
, sensitive methods such as molecular genetics, tumor-specific molecular primers, fluorescein in situ hybridization, and multiparameter flow cytometry (MFC) are commonly used after allogeneic stem
cell
transplantation to monitor patients, but not all of them are included in the commonly employed
disease
-specific response criteria.
Here, we summarize the current knowledge about the utilization of such sensitive monitoring techniques based on tumor-specific markers and donor
cell
chimerism and how these methods might augment the standard definitions of posttransplant remission, persistence, progression, relapse, and the prediction of relapse.
Critically important is the need for standardization of the different residual
disease
techniques and to assess the clinical relevance of minimal residual
disease
and chimerism surveillance in individual diseases, which in turn, must be followed by studies to assess the potential impact of specific interventional strategies.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation.
Leukemia
/ therapy. Myelodysplastic Syndromes / therapy
[MeSH-minor]
Acute
Disease
. Chimerism. Chromosome Banding.
Disease
Progression. Humans. Neoplasm Recurrence, Local / diagnosis. Transplantation Conditioning. Treatment Outcome
Genetic Alliance.
consumer health - Myelodysplastic syndromes
.
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Leukemia
.
MedlinePlus Health Information.
consumer health - Myelodysplastic Syndromes
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2010 American Society for Blood and Marrow Transplantation. All rights reserved.
[ErratumIn]
Biol Blood Marrow Transplant. 2010 Dec;16(12):1752. Macapintac, Homer [corrected to Macapinlac, Homer A]
(PMID = 20558311.001).
[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
54.
Mahmoud LA, Shamaa SS, Salem MA, Aladle DA, Goda EF:
A study for evaluation of different diagnostic approaches in acute leukemia in Egypt.
Hematology
; 2006 Apr;11(2):87-95
[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 study for evaluation of different diagnostic approaches in
acute
leukemia
in Egypt.
Cytomorphology, cytochemistry, immunophenotyping, in addition to cytogenetic and molecular analyses have specific roles in the diagnosis and management of
acute leukemias
.
This work was designed as a comparative study of different available methods for diagnosis of
acute
leukemia
.
The study comprised 47 cases with
acute
leukemia
(21 cases with ALL and 26 cases with AML).
The results of the study revealed that careful examination of Romanowsky-stained peripheral blood and BM films is fundamental in the diagnosis of
acute leukemias
, and when considered together with clinical and hematological features, indicates which of the more specialized techniques are most likely to be useful.
The major role of cytochemistry was in the diagnosis of AML, while the major role of immunophenotyping was in the diagnosis of
acute
leukemia
, which is not obviously myeloid.
Apart from identification of chromosomal abnormalities unique to specific subtypes
of leukemia
, cytogenetic analysis had a salient impact on anticipating the prognosis and treatment outcome in
acute leukemias
.
[MeSH-major]
Leukemia
, Myeloid,
Acute
/ diagnosis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16753847.001).
[ISSN]
1024-5332
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Genetic Markers
55.
Lilljebjörn H, Soneson C, Andersson A, Heldrup J, Behrendtz M, Kawamata N, Ogawa S, Koeffler HP, Mitelman F, Johansson B, Fontes M, Fioretos T:
The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias.
Hum Mol Genet
; 2010 Aug 15;19(16):3150-8
[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]
The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood
acute
lymphoblastic
leukemias
.
The ETV6/RUNX1 fusion gene, present in 25% of B-lineage childhood
acute
lymphoblastic
leukemia
(ALL), is thought to represent an initiating event, which requires additional genetic changes for
leukemia
development.
As previously demonstrated, alterations targeting genes involved in B-
cell
development were common (present in 28% of cases).
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
SciCrunch.
ArrayExpress: Data: Microarray
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Haematol. 2008 Mar;140(6):665-72
[
18241254.001
]
[Cites]
Genes Chromosomes Cancer. 2008 Apr;47(4):333-40
[
18181181.001
]
[Cites]
Genes Chromosomes Cancer. 2008 Dec;47(12):1118-25
[
18767146.001
]
[Cites]
Genes Chromosomes Cancer. 2009 Jan;48(1):1-9
[
18767147.001
]
[Cites]
Int J Cancer. 2009 Jun 15;124(12):2864-71
[
19267402.001
]
[Cites]
Genes Chromosomes Cancer. 2009 Aug;48(8):637-60
[
19415723.001
]
[Cites]
Leukemia. 2009 Jul;23(7):1209-18
[
19242497.001
]
[Cites]
Hum Genet. 2009 Oct;126(4):511-20
[
19484265.001
]
[Cites]
Leukemia. 2007 Oct;21(10):2137-44
[
17690704.001
]
[Cites]
Lancet. 1999 Oct 30;354(9189):1499-503
[
10551495.001
]
[Cites]
Cancer Res. 2000 Nov 15;60(22):6503-9
[
11103820.001
]
[Cites]
J Comput Biol. 2000;7(6):789-803
[
11382362.001
]
[Cites]
Nucleic Acids Res. 2002 Jan 1;30(1):207-10
[
11752295.001
]
[Cites]
Bioinformatics. 2004 May 22;20(8):1233-40
[
14871870.001
]
[Cites]
Cancer Genet Cytogenet. 1982 Oct;7(2):137-52
[
7172163.001
]
[Cites]
Nature. 1995 Jul 20;376(6537):263-7
[
7542362.001
]
[Cites]
Leukemia. 1995 Dec;9(12):1985-9
[
8609706.001
]
[Cites]
Mol Cell Biol. 1996 Jun;16(6):2898-905
[
8649400.001
]
[Cites]
Blood. 1996 Dec 1;88(11):4252-8
[
8943861.001
]
[Cites]
J Comput Biol. 1999 Spring;6(1):37-51
[
10223663.001
]
[Cites]
Nature. 1999 Oct 7;401(6753):556-62
[
10524622.001
]
[Cites]
Mol Cell Biol. 2005 Jan;25(1):324-35
[
15601853.001
]
[Cites]
Bioinformatics. 2007 Mar 15;23(6):657-63
[
17234643.001
]
[Cites]
Cancer Sci. 2007 May;98(5):698-706
[
17374122.001
]
[Cites]
Nature. 2007 Apr 12;446(7137):758-64
[
17344859.001
]
[Cites]
Leukemia. 2007 Jun;21(6):1258-66
[
17443227.001
]
[Cites]
Blood. 2008 Jan 15;111(2):776-84
[
17890455.001
]
[Cites]
Science. 2008 Jan 18;319(5861):336-9
[
18202291.001
]
[Cites]
Nature. 2008 May 1;453(7191):110-4
[
18408710.001
]
(PMID = 20513752.001).
[ISSN]
1460-2083
[Journal-full-title]
Human molecular genetics
[ISO-abbreviation]
Hum. Mol. Genet.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
[Other-IDs]
NLM/ PMC3146010
56.
Weir EG, Ali Ansari-Lari M, Batista DA, Griffin CA, Fuller S, Smith BD, Borowitz MJ:
Acute bilineal leukemia: a rare disease with poor outcome.
Leukemia
; 2007 Nov;21(11):2264-70
[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]
Acute
bilineal
leukemia
: a rare
disease
with poor outcome.
Most cases of
acute
leukemia
can be assigned to the myeloid, B or T lineage.
A subset of these, referred to as
acute
bilineal
leukemias
(aBLLs), is characterized by the presence of more than one population of blasts, each comprising a single lineage.
Of 16 patients with outcome data, only six achieved complete remission and only two remain free
of disease
2.5 and 4.5 years after chemotherapy or stem
cell
transplantation. aBLL is a rare
disease
that combines B or T and myeloid blasts.
[MeSH-major]
Leukemia
, Biphenotypic,
Acute
/ diagnosis.
Leukemia
, Biphenotypic,
Acute
/ therapy
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17611554.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
57.
Issa JP, Byrd JC:
Decitabine in chronic leukemias.
Semin Hematol
; 2005 Jul;42(3 Suppl 2):S43-9
[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]
Decitabine in chronic
leukemias
.
Indeed, promising clinical results have been observed in
acute
myeloid
leukemia
(AML) and the myelodysplastic syndromes (MDS).
Aberrant methylation has also been found in chronic
leukemias
, providing a rationale for investigating the use of decitabine in these diseases.
There is clear evidence of molecular (hypomethylation) as well as hematologic and cytogenetic responses to decitabine in chronic myelogenous
leukemia of
all phases, including in patients resistant to imatinib mesylate.
Clinical trials of decitabine in chronic
lymphocytic leukemia
are ongoing.
There are many unanswered questions regarding optimizing this treatment for chronic
leukemias
, but successful proof-of-concept studies for hypomethylating agents move us closer to approaches that may have a significant impact on patient outcomes.
[MeSH-major]
Azacitidine / analogs & derivatives.
Leukemia
/ drug therapy
[MeSH-minor]
Chronic
Disease
. Combined Modality Therapy. Hematopoietic Stem
Cell
Transplantation. Humans.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ drug therapy.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
MedlinePlus Health Information.
consumer health - Leukemia
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
AZACITIDINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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 = 16015505.001).
[ISSN]
0037-1963
[Journal-full-title]
Seminars in hematology
[ISO-abbreviation]
Semin. Hematol.
[Language]
eng
[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.; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
776B62CQ27 / decitabine; M801H13NRU / Azacitidine
[Number-of-references]
67
58.
Cony-Makhoul P, Bergeron A, Corm S, Dubruille V, Rea D, Rigal-Huguet F, Nicolini FE:
[Guidelines for the management of dasatinib (Sprycel)-induced side effects in chronic myelogenous leukemia and Philadelphia positive acute lymphoblastic leukemias].
Bull Cancer
; 2008 Sep;95(9):805-11
[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]
[Guidelines for the management of dasatinib (Sprycel)-induced side effects in chronic myelogenous
leukemia
and Philadelphia positive
acute
lymphoblastic
leukemias
].
[Transliterated title]
Recommandations pour la gestion des effets indésirables du traitement par dasatinib (Sprycel) au cours
de
la leucémie myéloïde chronique et des leucémies aiguës lymphoblastiques à chromosome Philadelphie.
Dasatinib (Sprycel) is a new-targeted therapy used since 2005 in the treatment of chronic myelogenous
leukemia
and
de
novo Philadelphia positive
acute
lymphoblastic leukaemia patients, intolerant or resistant to imatinib.
Despite its high efficacy in such patients in terms of hematologic, cytogenetic and molecular responses, the
onset of
frequent and sometimes serious side effects particularly in advanced phase patients, especially myelosuppressions and pleural effusions, may impair optimal administration of the drug.
Recently, dasatinib dose optimisation in chronic-phase has reduced the incidence of such adverse events without modification of the efficacy, however, their optimal overall management can efficiently reduce their severity and minimize their impact on
disease
response.
[MeSH-major]
Antineoplastic Agents / adverse effects.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Pyrimidines / adverse effects. Thiazoles / adverse effects
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Adult
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18829412.001).
[ISSN]
1769-6917
[Journal-full-title]
Bulletin du cancer
[ISO-abbreviation]
Bull Cancer
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Practice Guideline
[Publication-country]
France
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
59.
Zhang NN, Shen SH, Jiang LJ, Zhang W, Zhang HX, Sun YP, Li XY, Huang QH, Ge BX, Chen SJ, Wang ZG, Chen Z, Zhu J:
RIG-I plays a critical role in negatively regulating granulocytic proliferation.
Proc Natl Acad Sci U S A
; 2008 Jul 29;105(30):10553-8
[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.
However, we have found a significant RIG-I induction in a biological setting without active viral infection-namely, during RA-induced terminal granulocytic differentiation of
acute
myeloid
leukemias
.
Here, we present evidence that a significant Rig-I induction also occurs during normal myelopoiesis and that the disruption of the Rig-I gene in mice leads to the development
of a
progressive myeloproliferative disorder.
[MeSH-minor]
Animals.
Cell
Differentiation.
Cell
Proliferation. Exons. Hematopoietic Stem Cells / cytology. Humans. Immunity, Innate. Mice. Mice, Knockout. Mice, Transgenic. Myeloid Cells / cytology. Myeloproliferative Disorders / metabolism
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
SciCrunch.
OMIM: Data: Gene Annotation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 2000 Aug 15;96(4):1496-504
[
10942397.001
]
[Cites]
Cell Res. 2007 Oct;17(10):858-68
[
17893708.001
]
[Cites]
Immunity. 2002 Jul;17(1):63-72
[
12150892.001
]
[Cites]
J Biol Chem. 2004 Feb 20;279(8):6905-10
[
14699146.001
]
[Cites]
Nat Genet. 2004 Jun;36(6):624-30
[
15146183.001
]
[Cites]
Nat Immunol. 2004 Jul;5(7):730-7
[
15208624.001
]
[Cites]
Cell. 2004 Oct 29;119(3):431-43
[
15507213.001
]
[Cites]
Mol Cell Biol. 1993 Jul;13(7):3951-63
[
8321202.001
]
[Cites]
Cell. 1996 Oct 18;87(2):307-17
[
8861914.001
]
[Cites]
J Exp Med. 2005 Mar 21;201(6):881-90
[
15781580.001
]
[Cites]
Immunity. 2005 Jul;23(1):19-28
[
16039576.001
]
[Cites]
Cell. 2005 Sep 9;122(5):645-7
[
16143094.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 May 30;103(22):8459-64
[
16714379.001
]
[Cites]
Oncogene. 2006 Jun 22;25(26):3670-9
[
16462767.001
]
[Cites]
J Exp Med. 2006 Jul 10;203(7):1795-803
[
16785313.001
]
[Cites]
Microbes Infect. 2006 Jul;8(8):2138-44
[
16782388.001
]
[Cites]
Nat Immunol. 2007 Jun;8(6):592-600
[
17468758.001
]
[Cites]
Nature. 2007 Aug 16;448(7155):816-9
[
17653195.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):637-42
[
11805321.001
]
(PMID = 18650396.001).
[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RARRES3 protein, human; 0 / Receptors, Retinoic Acid; EC 3.6.1.- / Ddx58 protein, mouse; EC 3.6.4.13 / DEAD-box RNA Helicases
[Other-IDs]
NLM/ PMC2492484
60.
Kovacsovics T, Maziarz RT:
Philadelphia chromosome-positive acute lymphoblastic leukemia: impact of imatinib treatment on remission induction and allogeneic stem cell transplantation.
Curr Oncol Rep
; 2006 Sep;8(5):343-51
[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]
Philadelphia chromosome-positive
acute
lymphoblastic
leukemia
: impact of imatinib treatment on remission induction and allogeneic stem
cell
transplantation.
Philadelphia chromosome-positive (Ph+)
acute
lymphoblastic
leukemia
(ALL) has been associated with the worst patient survival rates of the various
acute leukemias
.
Hematopoietic stem
cell
transplantation has also integrated imatinib into its transplant strategies, with early data suggesting improved progression-free survival without clearly identifiable augmented toxicity.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Piperazines / therapeutic use. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Stem
Cell
Transplantation
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Bone Marrow Transplant. 2005 Mar;35(6):549-56
[
15756282.001
]
[Cites]
Bone Marrow Transplant. 2005 Nov;36(10):917-8
[
16113662.001
]
[Cites]
Blood. 2004 Feb 15;103(4):1495-8
[
14576058.001
]
[Cites]
Cancer Chemother Pharmacol. 2001 Aug;48 Suppl 1:S77-8
[
11587372.001
]
[Cites]
Br J Haematol. 2003 Jan;120(1):145-53
[
12492591.001
]
[Cites]
Hematology Am Soc Hematol Educ Program. 2005;:183-7
[
16304378.001
]
[Cites]
Blood. 1991 Dec 1;78(11):2814-22
[
1835410.001
]
[Cites]
Clin Cancer Res. 2003 Oct 15;9(13):4674-81
[
14581336.001
]
[Cites]
J Clin Oncol. 2004 Jul 15;22(14):2816-25
[
15254049.001
]
[Cites]
Blood. 2005 May 1;105(9):3449-57
[
15657178.001
]
[Cites]
Biol Blood Marrow Transplant. 2003 Mar;9(3):206-12
[
12652472.001
]
[Cites]
J Clin Oncol. 2000 Feb;18(3):547-61
[
10653870.001
]
[Cites]
Bone Marrow Transplant. 2003 Apr;31(8):623-32
[
12692601.001
]
[Cites]
Hematology. 2004 Oct-Dec;9(5-6):369-76
[
15763976.001
]
[Cites]
Blood. 2005 Apr 1;105(7):2640-53
[
15618470.001
]
[Cites]
Hematol J. 2002;3(5):219-23
[
12391538.001
]
[Cites]
Blood. 2001 Mar 15;97(6):1572-7
[
11238093.001
]
[Cites]
Leukemia. 2002 Dec;16(12):2423-8
[
12454748.001
]
[Cites]
Blood. 2002 Sep 15;100(6):1965-71
[
12200353.001
]
[Cites]
Anticancer Drugs. 2005 Jul;16(6):631-4
[
15930891.001
]
[Cites]
Bone Marrow Transplant. 1998 Jan;21(2):153-8
[
9489632.001
]
[Cites]
Leukemia. 2002 Dec;16(12):2358-65
[
12454740.001
]
[Cites]
Nat Genet. 2004 May;36(5):453-61
[
15098032.001
]
[Cites]
Blood. 1997 Apr 1;89(7):2602-9
[
9116308.001
]
[Cites]
N Engl J Med. 2001 Apr 5;344(14):1038-42
[
11287973.001
]
[Cites]
Leuk Lymphoma. 2004 Apr;45(4):695-8
[
15160941.001
]
[Cites]
Haematologica. 2003 May;88(5):555-60
[
12745275.001
]
[Cites]
Blood. 2001 Apr 1;97(7):1999-2007
[
11264164.001
]
[Cites]
Bone Marrow Transplant. 2005 Nov;36(10):867-72
[
16113659.001
]
[Cites]
J Clin Oncol. 2006 Jan 20;24(3):460-6
[
16344315.001
]
[Cites]
Leuk Res. 2005 Dec;29(12):1381-6
[
15927253.001
]
[Cites]
Bone Marrow Transplant. 2005 Oct;36(7):565-74
[
15995714.001
]
[Cites]
Blood. 2002 Oct 1;100(7):2357-66
[
12239143.001
]
[Cites]
Haematologica. 2006 Apr;91(4):452-9
[
16585011.001
]
[Cites]
Bone Marrow Transplant. 2003 May;31(10):909-18
[
12748668.001
]
[Cites]
Blood. 2002 Mar 1;99(5):1860-2
[
11861307.001
]
[Cites]
Leukemia. 2003 Feb;17(2):290-7
[
12592325.001
]
[Cites]
Blood. 2004 Jun 15;103(12):4396-407
[
14551133.001
]
[Cites]
Leukemia. 2006 Mar;20(3):400-3
[
16437142.001
]
[Cites]
Blood. 2003 Jan 1;101(1):85-90
[
12393581.001
]
[Cites]
Bone Marrow Transplant. 2005 Jun;35(12):1141-8
[
15834433.001
]
[Cites]
Haematologica. 2005 Sep;90(9):1275-7
[
16154854.001
]
[Cites]
Br J Haematol. 2003 May;121(3):469-72
[
12716370.001
]
[Cites]
Haematologica. 2006 Mar;91(3):377-80
[
16531262.001
]
[Cites]
Blood. 2002 Mar 1;99(5):1536-43
[
11861265.001
]
[Cites]
Leukemia. 2005 Sep;19(9):1509-16
[
16034462.001
]
[Cites]
Blood. 2006 Aug 15;108(4):1421-3
[
16601247.001
]
(PMID = 16901395.001).
[ISSN]
1523-3790
[Journal-full-title]
Current oncology reports
[ISO-abbreviation]
Curr Oncol Rep
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
[Number-of-references]
61
61.
Pabst T, Mueller BU:
Transcriptional dysregulation during myeloid transformation in AML.
Oncogene
; 2007 Oct 15;26(47):6829-37
[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.
The current paradigm on leukemogenesis indicates that
leukemias
are propagated by leukemic stem cells.
This concept is based on genomic mutations or functional dysregulation of transcription factors in malignant cells of patients with
acute
myeloid
leukemia
(AML).
[MeSH-major]
Cell
Transformation, Neoplastic / genetics.
Cell
Transformation, Neoplastic / pathology.
Leukemia
, Myeloid / genetics.
Leukemia
, Myeloid / pathology. Myeloid Cells / pathology. Transcription, Genetic / physiology
[MeSH-minor]
Acute
Disease
. Animals. Humans
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 = 17934489.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
78
62.
Dou Y, Hess JL:
Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia.
Int J Hematol
; 2008 Jan;87(1):10-8
[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]
Mechanisms of transcriptional regulation by MLL and its disruption in
acute
leukemia
.
Fusion of the mixed lineage
leukemia
protein (MLL) to one of over 50 different translocation partners converts it into a potent leukemogenic oncoprotein.
The resulting fusion proteins transform primarily through upregulation
of A
-cluster Hox genes, including Hoxa9 and the Hox cofactor Meis1.
Considerable progress has been made in delineating the differences between normal Hox gene regulation by MLL and deregulated transcription in MLL-induced
leukemias
.
[MeSH-major]
Leukemia
/ genetics. Leukopoiesis / genetics. Myeloid-Lymphoid
Leukemia
Protein / genetics. Transcription, Genetic / genetics
[MeSH-minor]
Animals. DNA Methylation.
Disease
Models, Animal. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Homeodomain Proteins / physiology. Humans. Mice. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology
MedlinePlus Health Information.
consumer health - Leukemia
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 2004 Mar 1;103(5):1676-84
[
14604967.001
]
[Cites]
Blood. 2000 Dec 1;96(12):3887-93
[
11090074.001
]
[Cites]
Exp Hematol. 2002 Jan;30(1):49-57
[
11823037.001
]
[Cites]
J Cell Physiol. 1997 Nov;173(2):168-77
[
9365517.001
]
[Cites]
EMBO J. 2000 Sep 1;19(17 ):4655-64
[
10970858.001
]
[Cites]
Cancer Cell. 2003 Aug;4(2):99-110
[
12957285.001
]
[Cites]
Trends Mol Med. 2004 Oct;10(10):500-7
[
15464450.001
]
[Cites]
Blood. 2004 Dec 1;104(12):3679-87
[
15226186.001
]
[Cites]
Front Biosci. 2001 Aug 01;6:D866-76
[
11487466.001
]
[Cites]
Ann N Y Acad Sci. 2004 Apr;1014:189-98
[
15153434.001
]
[Cites]
J Clin Invest. 2005 Apr;115(4):919-29
[
15761502.001
]
[Cites]
Cell. 2005 Oct 21;123(2):207-18
[
16239140.001
]
[Cites]
Dev Cell. 2004 Mar;6(3):437-43
[
15030765.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6629-34
[
16618927.001
]
[Cites]
Br J Haematol. 2006 Nov;135(4):438-49
[
16965385.001
]
[Cites]
J Clin Oncol. 2006 Apr 10;24(11):1770-83
[
16603719.001
]
[Cites]
Blood. 2003 Sep 15;102(6):2198-204
[
12791658.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14028-33
[
16169901.001
]
[Cites]
Blood. 2006 Jul 1;108(1):297-304
[
16507773.001
]
[Cites]
Cell. 2003 Oct 31;115(3):293-303
[
14636557.001
]
[Cites]
Cell. 2006 Apr 21;125(2):315-26
[
16630819.001
]
[Cites]
Leuk Lymphoma. 2004 Mar;45(3):567-74
[
15160920.001
]
[Cites]
EMBO J. 2006 Oct 4;25(19):4503-12
[
16990798.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1107-17
[
12453418.001
]
[Cites]
Nature. 2006 Jul 6;442(7098):91-5
[
16728978.001
]
[Cites]
Stem Cells. 1996 May;14(3):281-91
[
8724694.001
]
[Cites]
Oncogene. 2005 Aug 18;24(35):5525-32
[
15856011.001
]
[Cites]
EMBO J. 2000 Mar 1;19(5):843-51
[
10698926.001
]
[Cites]
Blood. 2004 Jan 1;103(1):229-35
[
12946992.001
]
[Cites]
Blood. 1998 Jul 1;92(1):108-17
[
9639506.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1119-28
[
12453419.001
]
[Cites]
Genes Dev. 2003 Sep 15;17(18):2298-307
[
12952893.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jul 19;102(29):10094-8
[
16006523.001
]
[Cites]
Blood. 2003 Jan 15;101(2):633-9
[
12393557.001
]
[Cites]
Mol Cell Biol. 2002 Sep;22(18):6542-52
[
12192052.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):749-54
[
15640349.001
]
[Cites]
Nucleic Acids Res. 2002 Feb 15;30(4):958-65
[
11842107.001
]
[Cites]
Mol Cell Biol. 2004 Jul;24(13):5639-49
[
15199122.001
]
[Cites]
Mol Cell Biol. 2004 Jan;24(2):617-28
[
14701735.001
]
[Cites]
Mol Cell Biol. 2001 Aug;21(16):5678-87
[
11463848.001
]
[Cites]
Oncogene. 2001 Feb 15;20(7):874-8
[
11314021.001
]
[Cites]
Mol Cell Biol. 2001 Apr;21(7):2249-58
[
11259575.001
]
[Cites]
Leukemia. 2005 Nov;19(11):1948-57
[
16107895.001
]
[Cites]
Nature. 2000 Apr 13;404(6779):782-7
[
10783894.001
]
[Cites]
Cancer Cell. 2003 Sep;4(3):197-207
[
14522254.001
]
[Cites]
Blood. 2007 Jun 1;109(11):4732-8
[
17327400.001
]
[Cites]
EMBO J. 1998 Jul 1;17(13):3714-25
[
9649441.001
]
[Cites]
Genes Dev. 2006 Sep 1;20(17):2397-409
[
16951254.001
]
[Cites]
Nat Cell Biol. 2006 Sep;8(9):1017-24
[
16921363.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10610-4
[
7938000.001
]
[Cites]
Science. 1996 Mar 29;271(5257):1873-6
[
8596958.001
]
[Cites]
Mol Cell Biol. 2003 Jan;23(1):186-94
[
12482972.001
]
[Cites]
Nat Struct Mol Biol. 2006 Aug;13(8):713-9
[
16878130.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14372-7
[
10588712.001
]
[Cites]
Immunity. 2006 May;24(5):611-22
[
16713978.001
]
[Cites]
Genes Dev. 2001 Feb 15;15(4):428-43
[
11230151.001
]
[Cites]
Cancer Res. 2007 Aug 1;67(15):7275-83
[
17671196.001
]
[Cites]
Genes Chromosomes Cancer. 2003 Jul;37(3):237-51
[
12759922.001
]
[Cites]
Blood. 2002 Jan 1;99(1):275-81
[
11756182.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14 ):8342-7
[
12829790.001
]
[Cites]
Mol Cell Biol. 1998 Jan;18(1):122-9
[
9418860.001
]
[Cites]
Oncogene. 2001 Sep 10;20(40):5695-707
[
11607819.001
]
[Cites]
Mol Cell Biol. 2001 May;21(10):3589-97
[
11313484.001
]
[Cites]
Blood. 1997 Sep 1;90(5):1799-806
[
9292512.001
]
[Cites]
Cell. 2005 Jun 17;121(6):873-85
[
15960975.001
]
[Cites]
Leukemia. 2004 Aug;18(8):1364-72
[
15269783.001
]
[Cites]
Oncogene. 2002 Jun 20;21(27):4247-56
[
12082612.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14765-70
[
16199523.001
]
[Cites]
Leukemia. 2004 Jan;18(1):92-102
[
14603337.001
]
[Cites]
Nat Genet. 1996 Feb;12(2):149-53
[
8563752.001
]
[Cites]
Nat Rev Mol Cell Biol. 2005 Nov;6(11):838-49
[
16261189.001
]
[Cites]
J Biomed Sci. 2002 May-Jun;9(3):234-45
[
12065898.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8
[
15941828.001
]
[Cites]
Mol Cell Biol. 1995 Oct;15(10):5434-43
[
7565694.001
]
[Cites]
Curr Top Microbiol Immunol. 2006;310:23-44
[
16909905.001
]
[Cites]
Hum Mol Genet. 2007 Jan 1;16(1):92-106
[
17135274.001
]
[Cites]
Cancer Cell. 2002 Mar;1(2):133-43
[
12086872.001
]
[Cites]
Nature. 1995 Nov 30;378(6556):505-8
[
7477409.001
]
[Cites]
Ann Hematol. 2006 Apr;85(4):244-9
[
16425025.001
]
[Cites]
Nat Genet. 2002 Jan;30(1):41-7
[
11731795.001
]
[Cites]
Eur J Cancer. 2004 Mar;40(5):707-21, discussion 722-4
[
15010072.001
]
[Cites]
Cancer Res. 1994 Aug 15;54(16):4277-80
[
8044771.001
]
[Cites]
J Clin Invest. 2006 Oct;116(10):2707-16
[
16981007.001
]
[Cites]
Curr Opin Hematol. 2005 Jan;12(1):7-13
[
15604885.001
]
[Cites]
Cell. 2005 Jun 17;121(6):859-72
[
15960974.001
]
[Cites]
Science. 1999 Oct 15;286(5439):531-7
[
10521349.001
]
[Cites]
Annu Rev Biochem. 2006;75:243-69
[
16756492.001
]
[Cites]
Mol Cell Biol. 2004 Dec;24(23):10470-8
[
15542854.001
]
[Cites]
Leuk Res. 2006 Nov;30(11):1453-6
[
16630659.001
]
(PMID = 18224408.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Japan
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Hoxa7 protein, mouse; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
63.
Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B:
Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
Blood
; 2008 Feb 1;111(3):1575-83
[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]
Cytogenetic features of
acute
lymphoblastic and myeloid
leukemias
in pediatric patients with Down syndrome: an iBFM-SG study.
Children with Down syndrome (DS) have a markedly increased risk of
acute
lymphoblastic
leukemia
(ALL) and
acute
myeloid
leukemia
(AML).
To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these
leukemias
, we analyzed 215 DS-ALLs and 189 DS-AMLs.
Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-
cell
precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
This series of DS
leukemias
-the largest to date-reveals that DS-ALL is a heterogeneous disorder that comprises both t(12;21) and HeH as well as DS-related abnormalities.
[MeSH-major]
Down Syndrome / complications. Down Syndrome / genetics.
Leukemia
, Myeloid,
Acute
/ complications.
Leukemia
, Myeloid,
Acute
/ genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / complications. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics
Genetic Alliance.
consumer health - Down Syndrome
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Down Syndrome
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17971484.001).
[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
64.
Kraicheva I, Bogomilova A, Tsacheva I, Momekov G, Troev K:
Synthesis, NMR characterization and in vitro antitumor evaluation of new aminophosphonic acid diesters.
Eur J Med Chem
; 2009 Aug;44(8):3363-7
[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.
The compounds were tested for antiproliferative effects against 4 human leukemic
cell
lines, namely LAMA-84, K-562 (chronic myeloid
leukemias
), HL-60 (
acute
promyelocyte
leukemia
) and HL-60/Dox (multi-drug-resistant sub-line, characterized by overexpression of MRP-1 (ABC-C1)) and were found to exert concentration-dependent cytotoxic effects.
A representative aminophosphonate compound was shown to induce oligonucleosomal DNA fragmentation which implies that the induction of
cell
death through apoptosis plays an important role for its cytotoxicity mode of action.
[MeSH-minor]
Animals.
Cell
Line, Tumor.
Cell
Survival / drug effects. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic / drug effects. Humans. Inhibitory Concentration 50. Magnetic Resonance Spectroscopy. Multidrug Resistance-Associated Proteins / metabolism
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19361895.001).
[ISSN]
1768-3254
[Journal-full-title]
European journal of medicinal chemistry
[ISO-abbreviation]
Eur J Med Chem
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / Organophosphonates; 0 / multidrug resistance-associated protein 1
65.
Boublikova L, Kalinova M, Ryan J, Quinn F, O'Marcaigh A, Smith O, Browne P, Stary J, McCann SR, Trka J, Lawler M:
Wilms' tumor gene 1 (WT1) expression in childhood acute lymphoblastic leukemia: a wide range of WT1 expression levels, its impact on prognosis and minimal residual disease monitoring.
Leukemia
; 2006 Feb;20(2):254-63
[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]
Wilms' tumor gene 1 (WT1) expression in childhood
acute
lymphoblastic
leukemia
: a wide range of WT1 expression levels, its impact on prognosis and minimal residual
disease
monitoring.
Wilms' tumor gene 1 (WT1) is overexpressed in the majority (70-90%) of
acute leukemias
and has been identified as an independent adverse prognostic factor, a convenient minimal residual
disease
(MRD) marker and potential therapeutic target in
acute
leukemia
.
We examined WT1 expression patterns in childhood
acute
lymphoblastic
leukemia
(ALL), where its clinical implication remains unclear.
In childhood B-
cell
precursor (BCP)-ALL, we detected a wide range of WT1 levels (5 logs) with a median WT1 expression close to that of normal BM.
[MeSH-major]
Gene Expression Regulation, Leukemic. Molecular Diagnostic Techniques / methods. Neoplasm, Residual / diagnosis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics. WT1 Proteins / genetics
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia, Childhood
.
Genetic Alliance.
consumer health - Wilms' tumor
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16341043.001).
[ISSN]
0887-6924
[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 / WT1 Proteins
66.
Godal R, Bachanova V, Gleason M, McCullar V, Yun GH, Cooley S, Verneris MR, McGlave PB, Miller JS:
Natural killer cell killing of acute myelogenous leukemia and acute lymphoblastic leukemia blasts by killer cell immunoglobulin-like receptor-negative natural killer cells after NKG2A and LIR-1 blockade.
Biol Blood Marrow Transplant
; 2010 May;16(5):612-21
[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]
Natural killer
cell
killing of
acute
myelogenous
leukemia
and
acute
lymphoblastic
leukemia
blasts by killer
cell
immunoglobulin-like receptor-negative natural killer cells after NKG2A and LIR-1 blockade.
Although the study of natural killer (NK)
cell
alloreactivity has been dominated by studies of killer
cell
immunoglobulin-like receptors (KIRs), we hypothesized that NKG2A and LIR-1, present on 53% +/- 13% and 36% +/- 18% of normal NK cells, respectively, play roles in the NK
cell
killing of primary
leukemia
targets.
KIR(-) cells, which compose nearly half of the circulating NK
cell
population, exhibit tolerance to primary
leukemia
targets, suggesting signaling through other inhibitory receptors.
Both
acute
myelogenous
leukemia
and
acute
lymphoblastic
leukemia
targets were rendered susceptible to lysis by fresh resting KIR(-) NK cells when inhibitory receptor-major histocompatibility class I interactions were blocked by pan-HLA antibodies, demonstrating that these cells are functionally competent.
Blockade
of a
single inhibitory receptor resulted in slightly increased killing, whereas combined LIR-1 and NKG2A blockade consistently resulted in increased NK
cell
cytotoxicity.
Together these results suggest that alloreactivity
of a
significant fraction of KIR(-) NK cells is mediated by NKG2A and LIR-1.
Thus strategies to interrupt NKG2A and LIR-1 in combination with anti-KIR blockade hold promise for exploiting NK
cell
therapy in
acute leukemias
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Adult
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Guide to Pharmacology.
gene/protein/disease-specific - CD159a - data and references
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
[Cites]
Blood. 2009 Apr 16;113(16):3875-84
[
19179302.001
]
[Cites]
Blood. 2008 Oct 15;112(8):3488-99
[
18645039.001
]
[Cites]
Semin Immunol. 2000 Apr;12(2):109-19
[
10764619.001
]
[Cites]
Cytometry. 2000 Dec 1;41(4):289-97
[
11084614.001
]
[Cites]
Hum Immunol. 2000 Nov;61(11):1177-95
[
11137224.001
]
[Cites]
Int Immunol. 2001 Feb;13(2):193-201
[
11157852.001
]
[Cites]
J Immunol. 2001 Apr 15;166(8):5018-26
[
11290782.001
]
[Cites]
Science. 2002 Mar 15;295(5562):2097-100
[
11896281.001
]
[Cites]
Hum Immunol. 2003 Mar;64(3):315-26
[
12590976.001
]
[Cites]
Leuk Res. 2003 Jul;27(7):643-8
[
12681364.001
]
[Cites]
Blood. 2003 May 1;101(9):3730-40
[
12511415.001
]
[Cites]
Blood. 2003 Aug 1;102(3):814-9
[
12689936.001
]
[Cites]
J Immunol Methods. 2003 Oct 1;281(1-2):65-78
[
14580882.001
]
[Cites]
Nat Med. 2003 Nov;9(11):1377-82
[
14528297.001
]
[Cites]
J Immunol. 2004 Jan 1;172(1):644-50
[
14688377.001
]
[Cites]
Eur J Immunol. 2004 Feb;34(2):455-60
[
14768050.001
]
[Cites]
J Immunol. 1997 Jun 15;158(12):5736-43
[
9190923.001
]
[Cites]
Immunity. 1997 Aug;7(2):273-82
[
9285411.001
]
[Cites]
J Exp Med. 1997 Dec 1;186(11):1809-18
[
9382880.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5199-204
[
9560253.001
]
[Cites]
Eur J Immunol. 1999 Jan;29(1):277-83
[
9933109.001
]
[Cites]
Int Immunol. 1999 Jan;11(1):29-35
[
10050671.001
]
[Cites]
Int Immunol. 1999 May;11(5):803-11
[
10330285.001
]
[Cites]
Mol Immunol. 2005 Feb;42(4):531-4
[
15607809.001
]
[Cites]
Blood. 2005 Mar 1;105(5):2066-73
[
15536144.001
]
[Cites]
Nat Rev Immunol. 2005 Mar;5(3):201-14
[
15719024.001
]
[Cites]
Immunity. 2005 Mar;22(3):295-304
[
15780987.001
]
[Cites]
Blood. 2005 May 15;105(10):4135-42
[
15687235.001
]
[Cites]
Blood. 2005 Jun 15;105(12):4878-84
[
15731175.001
]
[Cites]
Nature. 2005 Aug 4;436(7051):709-13
[
16079848.001
]
[Cites]
Blood. 2005 Dec 15;106(13):4370-6
[
16131567.001
]
[Cites]
Blood. 2006 Apr 15;107(8):3205-11
[
16373664.001
]
[Cites]
J Exp Med. 2006 Apr 17;203(4):1033-43
[
16606675.001
]
[Cites]
Nat Rev Immunol. 2006 Jul;6(7):520-31
[
16799471.001
]
[Cites]
Biol Blood Marrow Transplant. 2006 Aug;12(8):876-84
[
16864058.001
]
[Cites]
Immunity. 2006 Aug;25(2):331-42
[
16901727.001
]
[Cites]
Blood. 2007 Jun 1;109(11):5058-61
[
17317850.001
]
[Cites]
Clin Immunol. 2007 Jun;123(3):272-80
[
17446137.001
]
[Cites]
Curr Protoc Cell Biol. 2004 Feb;Chapter 18:Unit 18.8
[
18228448.001
]
[Cites]
Nat Rev Immunol. 2008 Apr;8(4):259-68
[
18340344.001
]
[Cites]
Exp Hematol. 2008 May;36(5):598-608
[
18295962.001
]
[Cites]
J Cell Mol Med. 2008 Jun;12(3):889-98
[
18494931.001
]
[Cites]
Trends Immunol. 2008 Jul;29(7):313-21
[
18538632.001
]
[Cites]
Blood. 2008 Aug 1;112(3):461-9
[
18650461.001
]
[Cites]
Blood. 2008 Sep 15;112(6):2369-80
[
18583565.001
]
[Cites]
Blood. 2009 Sep 24;114(13):2667-77
[
19553639.001
]
(PMID = 20139023.001).
[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
[Grant]
United States / NCI NIH HHS / CA / P01-CA-111412; United States / NCI NIH HHS / CA / CA111412-01A1; United States / NCI NIH HHS / CA / P01 CA065493; United States / NCI NIH HHS / CA / CA065493-110010; United States / NCI NIH HHS / CA / P01 CA111412-01A1; United States / NCI NIH HHS / CA / P01 CA065493-110010; United States / NCI NIH HHS / CA / P01-CA-65493; United States / NCI NIH HHS / CA / P01 CA111412
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies; 0 / Antigens, CD; 0 / Histocompatibility Antigens Class I; 0 / KLRC1 protein, human; 0 / LILRB1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily C; 0 / Receptors, Immunologic; 0 / Receptors, KIR
[Other-IDs]
NLM/ NIHMS177123; NLM/ PMC2854246
67.
O'Neil J, Look AT:
Mechanisms of transcription factor deregulation in lymphoid cell transformation.
Oncogene
; 2007 Oct 15;26(47):6838-49
[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]
Mechanisms of transcription factor deregulation in lymphoid
cell
transformation.
The most frequent targets of genetic alterations in human lymphoid
leukemias
are transcription factor genes with essential functions in blood
cell
development.
TAL1, LYL1, HOX11 and other transcription factors essential for normal hematopoiesis are often misexpressed in the thymus in T-
cell acute
lymphoblastic
leukemia
(T-ALL), leading to differentiation arrest and
cell
transformation.
The NOTCH1 gene, which is essential for key embryonic
cell
-fate decisions in multicellular organisms, was found to be activated by mutation in a large percentage of T-ALL patients.
[MeSH-major]
Cell
Transformation, Neoplastic / metabolism.
Cell
Transformation, Neoplastic / pathology. Lymphocyte Subsets / metabolism. Lymphocyte Subsets / pathology. Transcription Factors / genetics
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 = 17934490.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA109901
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Transcription Factors
[Number-of-references]
170
68.
Vempati S, Reindl C, Kaza SK, Kern R, Malamoussi T, Dugas M, Mellert G, Schnittger S, Hiddemann W, Spiekermann K:
Arginine 595 is duplicated in patients with acute leukemias carrying internal tandem duplications of FLT3 and modulates its transforming potential.
Blood
; 2007 Jul 15;110(2):686-94
[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]
Arginine 595 is duplicated in patients with
acute leukemias
carrying internal tandem duplications of FLT3 and modulates its transforming potential.
FLT3-internal tandem duplications (FLT3-ITDs) comprise a heterogeneous group of mutations in patients with
acute leukemias
that are prognostically important.
To characterize the mechanism of transformation by FLT3-ITDs, we sequenced the juxtamembrane region (JM) of FLT3 from 284 patients with
acute leukemias
.
[MeSH-major]
Arginine.
Leukemia
/ genetics. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Amino Acid Substitution.
Cell
Transformation, Neoplastic / genetics. Female. Gene Duplication. Humans. Male. Middle Aged. Mutagenesis. Sequence Deletion
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
(L)-ARGININE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
SciCrunch.
OMIM: Data: Gene Annotation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17387224.001).
[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]
94ZLA3W45F / Arginine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
69.
Takenokuchi M, Nakamachi Y, Yoneda K, Joo K, Kawano S, Tatsumi E, Saigo K, Kumagai S:
Quantitative detection of PML-RARalpha fusion transcript by real-time PCR with a single primer pair.
J Clin Lab Anal
; 2009;23(4):223-30
[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.
Quantitative detection of minimal residual
disease
has prognostic
value
for some
leukemias
.
Acute
promyelocytic
leukemia
(APL) is characterized by the specific PML-RARalpha fusion gene from t(15;17).
[MeSH-major]
Leukemia
, Promyelocytic,
Acute
/ genetics. Oncogene Proteins, Fusion / genetics. Receptors, Retinoic Acid / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
[MeSH-minor]
Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology.
Cell
Line, Tumor. DNA Primers / genetics. Humans. Prognosis. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Neoplasm / analysis. Reproducibility of Results
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19623654.001).
[ISSN]
1098-2825
[Journal-full-title]
Journal of clinical laboratory analysis
[ISO-abbreviation]
J. Clin. Lab. Anal.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / RNA, Neoplasm; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
70.
Zeng Z, Sarbassov dos D, Samudio IJ, Yee KW, Munsell MF, Ellen Jackson C, Giles FJ, Sabatini DM, Andreeff M, Konopleva M:
Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML.
Blood
; 2007 Apr 15;109(8):3509-12
[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.
We investigated the molecular effects of mTOR inhibition by the rapamycin derivatives (RDs) temsirolimus (CCI-779) and everolimus (RAD001) in
acute
myeloid
leukemia
(AML) cells.
Our study provides the first evidence that rapamycin derivatives inhibit AKT signaling in primary AML cells both in vitro and in vivo, and supports the therapeutic potential of mTOR inhibition strategies in
leukemias
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
SIROLIMUS
.
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 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
.
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
[Cites]
Eur J Haematol. 2000 Aug;65(2):109-13
[
10966170.001
]
[Cites]
Blood. 2002 Jan 1;99(1):326-35
[
11756188.001
]
[Cites]
Cancer Cell. 2002 Jul;2(1):81-91
[
12150827.001
]
[Cites]
Cell. 2002 Jul 26;110(2):177-89
[
12150926.001
]
[Cites]
Cancer. 2004 Feb 15;100(4):657-66
[
14770419.001
]
[Cites]
Cancer. 2004 Apr 15;100(8):1578-89
[
15073843.001
]
[Cites]
Clin Cancer Res. 2006 Sep 1;12(17):5165-73
[
16951235.001
]
[Cites]
Nat Med. 2004 Jun;10(6):594-601
[
15156201.001
]
[Cites]
Science. 2005 Feb 18;307(5712):1098-101
[
15718470.001
]
[Cites]
Curr Opin Genet Dev. 2006 Feb;16(1):78-84
[
16359855.001
]
[Cites]
Cancer Res. 2006 Feb 1;66(3):1500-8
[
16452206.001
]
[Cites]
Cell. 2006 Feb 10;124(3):471-84
[
16469695.001
]
[Cites]
Mol Cell. 2006 Apr 21;22(2):159-68
[
16603397.001
]
[Cites]
Nat Rev Cancer. 2004 May;4(5):335-48
[
15122205.001
]
(PMID = 17179228.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA 55164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA 49639; United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA055164
[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 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / Cyclin D; 0 / Cyclins; 0 / Glucose Transporter Type 1; 0 / Immunosuppressive Agents; 0 / Protein Kinase Inhibitors; 0 / Proteins; 0 / RICTOR protein, human; 0 / RNA, Messenger; 0 / RPTOR protein, human; 0 / SLC2A1 protein, human; 624KN6GM2T / temsirolimus; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
[Other-IDs]
NLM/ PMC1852241
71.
Hassanein NM, Alcancia F, Perkinson KR, Buckley PJ, Lagoo AS:
Distinct expression patterns of CD123 and CD34 on normal bone marrow B-cell precursors ("hematogones") and B lymphoblastic leukemia blasts.
Am J Clin Pathol
; 2009 Oct;132(4):573-80
[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.
[Title]
Distinct expression patterns of CD123 and CD34 on normal bone marrow B-
cell
precursors ("hematogones") and B lymphoblastic
leukemia
blasts.
We compared the expression of CD123, the alpha chain of the interleukin-3 receptor, on normal B-
cell
precursors in bone marrow ("hematogones") from 75 specimens and on leukemic blasts in 45 newly diagnosed B-
acute
lymphoblastic
leukemias
(B-ALL) cases.
[MeSH-major]
Antigens, CD34 / genetics. Interleukin-3 Receptor alpha Subunit / genetics. Precursor B-
Cell
Lymphoblastic
Leukemia
-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
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 = 19762535.001).
[ISSN]
1943-7722
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD34; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit
72.
Chu SH, Small D:
Mechanisms of resistance to FLT3 inhibitors.
Drug Resist Updat
; 2009 Feb-Apr;12(1-2):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.
The success of the small molecule tyrosine kinase receptor inhibitor (TKI) imatinib mesylate (Gleevec) in the treatment of chronic myeloid
leukemia
(CML) constitutes an eminent paradigm shift advocating the rational design of cancer therapeutics specifically targeting the transformation events that drive tumorigenicity.
In
acute
myeloid
leukemias
(AMLs), the most frequent identified transforming events are activating mutations in the FLT3 receptor tyrosine kinase that constitutively activate survival and proliferation pathways.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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 = 19162530.001).
[ISSN]
1532-2084
[Journal-full-title]
Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
[ISO-abbreviation]
Drug Resist. Updat.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA090668; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Scotland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
[Number-of-references]
119
[Other-IDs]
NLM/ NIHMS787037; NLM/ PMC4891941
73.
Bartynski WS, Zeigler ZR, Shadduck RK, Lister J:
Variable incidence of cyclosporine and FK-506 neurotoxicity in hematopoeitic malignancies and marrow conditions after allogeneic bone marrow transplantation.
Neurocrit Care
; 2005;3(1):33-45
[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.
INTRODUCTION: This study examines whether malignant
disease
under treatment influences the incidence of cyclosporine or FK-506 neurotoxicity after myeloablative conditioning and allogeneic bone marrow transplantation (allo-BMT).
Underlying malignancy necessitating allo-BMT included
leukemias
(67%), lymphoma (10%), myelodysplastic syndrome (10%), and multiple myeloma (MM).
Frequency of neurotoxicity by
disease
was compared.
Other diseases demonstrated intermediate incidence, including
acute leukemias
(10%), myelodysplastic syndrome (6.4%), and chronic myelogenous
leukemia
(4.9%).
The variable susceptibility to the development of neurotoxicity in this population may depend on the interaction of host vasculature with
disease
specific factors.
[MeSH-minor]
Graft vs Host
Disease
/ diagnosis. Graft vs Host
Disease
/ diagnostic imaging. Graft vs Host
Disease
/ epidemiology. Graft vs Host
Disease
/ prevention & control. Humans. Ischemic Preconditioning. Magnetic Resonance Imaging. Retrospective Studies. Tomography, X-Ray Computed
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Bone Marrow Transplantation
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
CYCLOSPORIN A
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Obstet Gynecol. 1990 Sep;163(3):1049-54; discussion 1054-5
[
2403130.001
]
[Cites]
Cancer Res. 1988 Feb 15;48(4):1035-41
[
3422181.001
]
[Cites]
Bone Marrow Transplant. 2003 Jan;31(2):73-8
[
12621486.001
]
[Cites]
Neurology. 1987 Jun;37(6):1072-6
[
3587633.001
]
[Cites]
Lancet. 1984 Nov 17;2(8412):1116-20
[
6150182.001
]
[Cites]
Transfus Apher Sci. 2002 Aug;27(1):3-12
[
12201469.001
]
[Cites]
Lancet. 1985 Jan 26;1(8422):219-20
[
2857289.001
]
[Cites]
J Biol Chem. 1995 Jun 2;270(22):13333-40
[
7768934.001
]
[Cites]
J Neurosurg. 1995 Jun;82(6):1068-70
[
7760181.001
]
[Cites]
Cytokine. 2000 Aug;12(8):1225-7
[
10930300.001
]
[Cites]
Transplant Proc. 1991 Jun;23(3):1902-5
[
1712133.001
]
[Cites]
Am J Kidney Dis. 2000 Oct;36(4):844-50
[
11007689.001
]
[Cites]
N Engl J Med. 1984 Feb 23;310(8):527
[
6363932.001
]
[Cites]
Bone Marrow Transplant. 1990 Aug;6(2):147-9
[
2207451.001
]
[Cites]
Blood. 1991 Apr 15;77(8):1837-44
[
2015407.001
]
[Cites]
Transplantation. 1985 Jan;39(1):110
[
2981442.001
]
[Cites]
Am J Kidney Dis. 1999 Sep;34(3):556-9
[
10469868.001
]
[Cites]
J Lab Clin Med. 1997 Jun;129(6):584-91
[
9178724.001
]
[Cites]
Eur J Haematol. 1997 Oct;59(4):254-62
[
9338624.001
]
[Cites]
Transplantation. 1990 Jan;49(1):215-6
[
2301014.001
]
[Cites]
AJNR Am J Neuroradiol. 1996 Feb;17(2):337-44
[
8938308.001
]
[Cites]
Bone Marrow Transplant. 1998 May;21(9):887-92
[
9613780.001
]
[Cites]
Ann Hematol. 1998 Feb;76(2):61-5
[
9540759.001
]
[Cites]
FASEB J. 1993 Apr 1;7(6):523-32
[
8472891.001
]
[Cites]
N Engl J Med. 1987 Oct 1;317(14):861-6
[
3306386.001
]
[Cites]
Radiology. 2001 Jun;219(3):756-65
[
11376265.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6192-6
[
1631107.001
]
[Cites]
Lancet. 1982 Apr 17;1(8277):906
[
6122119.001
]
[Cites]
Blood. 1989 May 15;73(7):2018-24
[
2496776.001
]
[Cites]
Transplantation. 1984 Jul;38(1):34-7
[
6377609.001
]
[Cites]
Brain. 2002 Nov;125(Pt 11):2549-57
[
12390979.001
]
[Cites]
J Clin Neuroophthalmol. 1988 Dec;8(4):215-20
[
2977135.001
]
[Cites]
N Engl J Med. 1975 Apr 24;292(17):895-902
[
235092.001
]
[Cites]
J Comput Assist Tomogr. 1988 Nov-Dec;12(6):1078-81
[
3183120.001
]
[Cites]
AJNR Am J Neuroradiol. 2002 Jun-Jul;23(6):1038-48
[
12063238.001
]
[Cites]
J Infect Dis. 1999 Feb;179(2):484-8
[
9878035.001
]
[Cites]
N Engl J Med. 1990 Sep 13;323(11):748-50
[
2388672.001
]
[Cites]
Blood. 1997 Oct 15;90(8):3204-13
[
9376604.001
]
[Cites]
Lancet. 1982 Nov 27;2(8309):1216-7
[
6128517.001
]
[Cites]
J Clin Oncol. 1996 Feb;14(2):579-85
[
8636774.001
]
[Cites]
Bone Marrow Transplant. 2002 Jun;29(12):973-8
[
12098065.001
]
[Cites]
Bone Marrow Transplant. 2002 Dec;30(11):709-15
[
12439692.001
]
[Cites]
AJNR Am J Neuroradiol. 1993 Jul-Aug;14(4):1014-6
[
8352140.001
]
[Cites]
Bone Marrow Transplant. 1993 Mar;11(3):205-8
[
8467284.001
]
[Cites]
Bone Marrow Transplant. 1995 Jan;15(1):99-104
[
7742764.001
]
[Cites]
Bone Marrow Transplant. 1999 Jul;24(1):29-34
[
10435731.001
]
[Cites]
Lancet. 1990 Jan 6;335(8680):11-5
[
1967328.001
]
[Cites]
Leukemia. 2001 Jul;15(7):1089-91
[
11455978.001
]
[Cites]
Blood. 1999 Apr 15;93(8):2738-47
[
10194454.001
]
[Cites]
Brain Res. 1986 Mar 12;368(1):24-9
[
3485464.001
]
[Cites]
Science. 1996 Apr 5;272(5258):60-6
[
8600538.001
]
[Cites]
J Neurol Neurosurg Psychiatry. 1988 Nov;51(11):1434-7
[
3069960.001
]
[Cites]
Bone Marrow Transplant. 1991 May;7(5):405-9
[
2070153.001
]
[Cites]
Blood. 1995 Aug 1;86(3):890-9
[
7620183.001
]
[Cites]
AJNR Am J Neuroradiol. 1998 Apr;19(4):601-8; discussion 609-10
[
9576643.001
]
[Cites]
N Engl J Med. 1990 Sep 13;323(11):693-9
[
2388667.001
]
[Cites]
Bone Marrow Transplant. 1996 May;17 Suppl 3:S1-3
[
8769689.001
]
[Cites]
J Clin Apher. 1991;6(1):16-20
[
2045377.001
]
[Cites]
Blood. 1994 Sep 15;84(6):2036-43
[
8081005.001
]
[Cites]
Br Med J (Clin Res Ed). 1985 Jan 12;290(6462):139-40
[
3917716.001
]
[Cites]
AJNR Am J Neuroradiol. 2001 Nov-Dec;22(10 ):1901-14
[
11733324.001
]
[Cites]
Blood. 1998 May 15;91(10):3527-61
[
9572988.001
]
[Cites]
Bone Marrow Transplant. 1998 Aug;22(4):351-7
[
9722070.001
]
[Cites]
Blood. 1990 Feb 1;75(3):555-62
[
2297567.001
]
[Cites]
FASEB J. 1992 May;6(8):2591-9
[
1592209.001
]
[Cites]
AJNR Am J Neuroradiol. 1998 Mar;19(3):415-7
[
9541291.001
]
[Cites]
Blood. 1992 Dec 15;80(12):2964-8
[
1467511.001
]
[Cites]
Transplantation. 1984 Oct;38(4):341-3
[
6388059.001
]
[Cites]
AJNR Am J Neuroradiol. 1991 Jul-Aug;12(4):651-9
[
1882738.001
]
[Cites]
Blood. 1996 Oct 1;88(7):2787-93
[
8839877.001
]
[Cites]
J Comput Assist Tomogr. 1997 Nov-Dec;21(6):872-80
[
9386275.001
]
[Cites]
Lancet. 1988 Oct 15;2(8616):901
[
2902336.001
]
[Cites]
Cytokine. 2001 Nov 7;16(3):79-86
[
11741345.001
]
[Cites]
Nature. 1992 Oct 29;359(6398):843-5
[
1279431.001
]
[Cites]
Lancet. 1982 Nov 27;2(8309):1217
[
6128518.001
]
[Cites]
Lancet. 1984 Jan 7;1(8367):52
[
6140379.001
]
[Cites]
Blood. 1999 Jan 1;93(1):55-65
[
9864146.001
]
[Cites]
J Clin Invest. 1999 Aug;104(3):317-25
[
10430613.001
]
[Cites]
Thromb Haemost. 1997 Mar;77(3):585-90
[
9066014.001
]
[Cites]
J Clin Oncol. 1995 Jun;13(6):1312-22
[
7751876.001
]
[Cites]
J Bone Miner Res. 2002 Nov;17(11):1921-5
[
12412796.001
]
[Cites]
QJM. 1994 Dec;87(12):741-5
[
7532091.001
]
[Cites]
Blood. 1990 Feb 15;75(4):1011-6
[
2405918.001
]
[Cites]
J Allergy Clin Immunol. 2000 Jul;106(1 Pt 2):S40-4
[
10887332.001
]
[Cites]
Blood. 1990 Nov 1;76(9):1867-71
[
2224134.001
]
[Cites]
Bone Marrow Transplant. 2002 Oct;30(7):441-6
[
12368956.001
]
[Cites]
Transplantation. 1987 Dec;44(6):778-83
[
3321587.001
]
[Cites]
Lancet. 1982 Oct 9;2(8302):829-30
[
6126705.001
]
[Cites]
Am J Hematol. 1998 Dec;59(4):279-87
[
9840908.001
]
[Cites]
Lancet. 1985 Jan 26;1(8422):219
[
2857288.001
]
[Cites]
Br J Haematol. 2000 Jun;109(3):652-7
[
10886219.001
]
[Cites]
Am J Obstet Gynecol. 1998 Nov;179(5):1359-75
[
9822529.001
]
[Cites]
Brain Behav Evol. 1988;32(2):65-75
[
2902898.001
]
[Cites]
J Clin Oncol. 1992 Nov;10(11):1690-5
[
1403052.001
]
[Cites]
Neurology. 1998 Nov;51(5):1369-76
[
9818862.001
]
[Cites]
Am J Hematol. 1996 Dec;53(4):213-20
[
8948657.001
]
[Cites]
Lancet. 1985 Aug 3;2(8449):280-1
[
2862458.001
]
[Cites]
Transplantation. 1985 Mar;39(3):286-9
[
3919480.001
]
[Cites]
Kidney Int. 1998 Jun;53(6):1810-26
[
9607219.001
]
[Cites]
J Biol Chem. 1998 Jun 12;273(24):15099-103
[
9614120.001
]
[Cites]
J Immunol. 1990 Nov 1;145(9):2902-7
[
2120340.001
]
[Cites]
AJNR Am J Neuroradiol. 2004 Feb;25(2):261-9
[
14970028.001
]
[Cites]
Leukemia. 2003 Jun;17(6):1150-6
[
12764383.001
]
[Cites]
N Engl J Med. 1996 Feb 22;334(8):494-500
[
8559202.001
]
[Cites]
Bone Marrow Transplant. 1999 Nov;24(9):1005-7
[
10556960.001
]
[Cites]
J Allergy Clin Immunol. 2000 Jul;106(1 Pt 2):S45-50
[
10887333.001
]
[Cites]
N Engl J Med. 1988 Mar 24;318(12):788-9
[
3347234.001
]
[Cites]
AJR Am J Roentgenol. 1995 Sep;165(3):627-31
[
7645483.001
]
[Cites]
Springer Semin Immunopathol. 1994;16(1):23-37
[
7997943.001
]
[Cites]
Bone Marrow Transplant. 1997 Sep;20(5):369-74
[
9339751.001
]
[Cites]
Cell. 1991 Dec 20;67(6):1033-6
[
1760836.001
]
[Cites]
J Clin Oncol. 1993 Dec;11(12):2342-50
[
8246023.001
]
[Cites]
Bone Marrow Transplant. 1991 Nov;8(5):393-401
[
1768975.001
]
[Cites]
Blood. 1994 Aug 15;84(4):1050-5
[
8049425.001
]
[Cites]
Bone Marrow Transplant. 1998 Jun;21(12):1263-6
[
9674861.001
]
[Cites]
Lab Invest. 1986 Oct;55(4):455-62
[
3531716.001
]
[Cites]
AJNR Am J Neuroradiol. 2001 Sep;22(8):1455-61
[
11559490.001
]
[Cites]
J Comput Assist Tomogr. 1990 Mar-Apr;14(2):262-6
[
2312856.001
]
[Cites]
Bone Marrow Transplant. 1995 Feb;15(2):247-53
[
7773214.001
]
[Cites]
J Hematother Stem Cell Res. 2000 Jun;9(3):299-306
[
10894351.001
]
[Cites]
Bone Marrow Transplant. 1999 Apr;23(7):675-80
[
10218843.001
]
[Cites]
Am J Med. 1979 Apr;66(4):611-20
[
35001.001
]
[Cites]
Br Med J (Clin Res Ed). 1984 Nov 17;289(6455):1347-8
[
6437543.001
]
[Cites]
Arch Neurol. 1984 Mar;41(3):329-30
[
6582812.001
]
[Cites]
Br J Haematol. 1987 May;66(1):45-7
[
3297128.001
]
[Cites]
Bone Marrow Transplant. 1998 Apr;21(7):705-9
[
9578311.001
]
[Cites]
J Appl Physiol (1985). 2000 Nov;89(5):1937-42
[
11053346.001
]
[Cites]
Bone Marrow Transplant. 1989 Sep;4(5):529-31
[
2790331.001
]
(PMID = 16159093.001).
[ISSN]
1541-6933
[Journal-full-title]
Neurocritical care
[ISO-abbreviation]
Neurocrit Care
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide
74.
Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK:
Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
Blood Cells Mol Dis
; 2010 Oct 15;45(3):186-91
[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]
Backtracking RAS mutations in high hyperdiploid childhood
acute
lymphoblastic
leukemia
.
High hyperdiploidy is the single largest subtype of childhood
acute
lymphoblastic
leukemia
(ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
We screened for RAS mutations among 517
acute
childhood
leukemias
(including 437
lymphocytic
, of which 393 were B-
cell
subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of
leukemias
of other subtypes (P<0.0001).
While RAS mutations were previously associated with prior chemical exposures in childhood and adult
leukemias
, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the
leukemia
clone.
We posit a natural history for hyperdiploid
leukemia
in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic
cell
phenotype.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia, Childhood
.
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
[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
[Cites]
N Engl J Med. 2006 Oct 12;355(15):1572-82
[
17035650.001
]
[Cites]
Leuk Res. 2006 Sep;30(9):1085-9
[
16533526.001
]
[Cites]
Haematologica. 2007 Nov;92(11):1565-8
[
18024407.001
]
[Cites]
Cancer Res. 2008 Aug 15;68(16):6803-9
[
18701506.001
]
[Cites]
Leukemia. 2008 Sep;22(9):1692-7
[
18548099.001
]
[Cites]
Radiat Prot Dosimetry. 2008;132(2):212-9
[
18940823.001
]
[Cites]
Leukemia. 2010 May;24(5):924-31
[
20237506.001
]
[Cites]
Clin Chem. 2000 May;46(5):620-4
[
10794742.001
]
[Cites]
Blood. 2000 Jul 1;96(1):264-8
[
10891460.001
]
[Cites]
Blood. 2002 Apr 15;99(8):2992-6
[
11929791.001
]
[Cites]
Br J Cancer. 2002 May 6;86(9):1419-24
[
11986774.001
]
[Cites]
Blood. 2002 Jul 1;100(1):347-9
[
12070048.001
]
[Cites]
Environ Health Perspect. 2002 Sep;110(9):955-60
[
12204832.001
]
[Cites]
Genes Chromosomes Cancer. 2004 May;40(1):38-43
[
15034866.001
]
[Cites]
Leukemia. 2004 Apr;18(4):685-92
[
14990973.001
]
[Cites]
Blood. 2004 May 1;103(9):3544-6
[
14670924.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1230-5
[
15247135.001
]
[Cites]
Blood. 1992 Jul 1;80(1):203-8
[
1351763.001
]
[Cites]
Leukemia. 1993 Mar;7(3):349-60
[
8445941.001
]
[Cites]
Leukemia. 1996 Feb;10(2):213-24
[
8637229.001
]
[Cites]
Genes Chromosomes Cancer. 1996 May;16(1):40-5
[
9162196.001
]
[Cites]
Leukemia. 2005 Mar;19(3):415-9
[
15674422.001
]
[Cites]
Genes Chromosomes Cancer. 2005 Oct;44(2):113-22
[
15942938.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):578-81
[
16537719.001
]
[Cites]
Am J Epidemiol. 2006 Jun 15;163(12):1091-100
[
16597704.001
]
[Cites]
Genes Chromosomes Cancer. 2008 Jan;47(1):26-33
[
17910045.001
]
(PMID = 20688547.001).
[ISSN]
1096-0961
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
ENG
[Grant]
United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
[Other-IDs]
NLM/ NIHMS224426; NLM/ PMC2943008
75.
Inthal A, Krapf G, Beck D, Joas R, Kauer MO, Orel L, Fuka G, Mann G, Panzer-Grümayer ER:
Role of the erythropoietin receptor in ETV6/RUNX1-positive acute lymphoblastic leukemia.
Clin Cancer Res
; 2008 Nov 15;14(22):7196-204
[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]
Role of the erythropoietin receptor in ETV6/RUNX1-positive
acute
lymphoblastic
leukemia
.
PURPOSE: We explored the mechanisms leading to the distinct overexpression of EPOR as well as the effects of EPO signaling on ETV6/RUNX1-positive
acute
lymphoblastic
leukemias
.
EXPERIMENTAL DESIGN: ETV6/RUNX1-expressing model
cell
lines and leukemic cells were used for real-time PCR of EPOR expression.
Serum EPO levels and sequences of the EPOR (n = 53) as well as hemoglobin levels were taken from children with
acute
lymphoblastic
leukemia
enrolled in Austrian protocols.
Anemia, however, did not appear to influence EPOR expression on leukemic cells, although children with ETV6/RUNX1-positive
leukemias
had a lower median hemoglobin than controls.
Exposure to EPO increased proliferation and survival of ETV6/RUNX1-positive
leukemias
in vitro, whereas blocking its binding site did not alter
cell
survival.
CONCLUSIONS: Our data suggest that ETV6/RUNX1 leads to EPOR up-regulation and that activation by EPO might be of relevance to the biology of this
leukemia
subtype.
[MeSH-major]
Core Binding Factor Alpha 2 Subunit / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / metabolism. Receptors, Erythropoietin / metabolism. Signal Transduction / physiology
[MeSH-minor]
Animals. Antineoplastic Agents, Hormonal / pharmacology. Apoptosis / drug effects. Blotting, Western.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Child. Erythropoietin / metabolism. Flow Cytometry. Humans. Prednisone / pharmacology. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Hazardous Substances Data Bank.
PREDNISONE
.
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]
Science. 2008 Jan 18;319(5861):336-9
[
18202291.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8443-8
[
15155899.001
]
[Cites]
J Clin Lab Anal. 2000;14(6):271-3
[
11138608.001
]
[Cites]
Curr Opin Oncol. 2004 Nov;16(6):553-63
[
15627017.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19069-74
[
16354839.001
]
[Cites]
Clin Cancer Res. 2006 Aug 15;12(16):4845-50
[
16914570.001
]
[Cites]
Science. 2004 Oct 8;306(5694):269-71
[
15472075.001
]
[Cites]
Blood. 2002 Apr 15;99(8):3066-9
[
11929803.001
]
[Cites]
Int J Cancer. 2006 Dec 15;119(12):2870-7
[
17016825.001
]
[Cites]
Crit Rev Eukaryot Gene Expr. 2005;15(3):207-16
[
16390317.001
]
[Cites]
Oncogene. 2005 Jan 27;24(5):737-45
[
15580299.001
]
[Cites]
Clin Cancer Res. 2006 Jan 15;12(2):332-9
[
16428469.001
]
[Cites]
Biochim Biophys Acta. 2005 Apr 15;1740(1):17-28
[
15878737.001
]
[Cites]
Blood. 2004 May 15;103(10):3890-6
[
14726384.001
]
[Cites]
Oncogene. 2005 Nov 17;24(51):7579-91
[
16044150.001
]
[Cites]
Wien Klin Wochenschr. 2002 Feb 28;114(4):148-57
[
12060981.001
]
[Cites]
Cancer Res. 2002 Jul 15;62(14):3904-8
[
12124316.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8242-7
[
12048236.001
]
[Cites]
Oncogene. 2004 May 24;23(24):4275-83
[
15156184.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15166-71
[
17015828.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9
[
15650049.001
]
[Cites]
Leukemia. 2000 Dec;14(12):2193-4
[
11187910.001
]
[Cites]
Blood. 2004 Oct 15;104(8):2452-7
[
15217836.001
]
[Cites]
Lancet. 1999 Oct 30;354(9189):1499-503
[
10551495.001
]
[Cites]
Leukemia. 2006 Feb;20(2):381-3
[
16341038.001
]
[Cites]
Kidney Int. 2000 Jul;58(1):269-82
[
10886572.001
]
[Cites]
Blood. 1989 Aug 1;74(2):645-51
[
2752138.001
]
[Cites]
Blood. 2004 Feb 1;103(3):1043-9
[
14525776.001
]
[Cites]
Blood. 2007 Mar 15;109(6):2607-10
[
17095626.001
]
[Cites]
N Engl J Med. 2004 Apr 8;350(15):1535-48
[
15071128.001
]
[Cites]
Blood. 1997 Jun 15;89(12):4248-67
[
9192747.001
]
[Cites]
Br J Haematol. 2005 Sep;130(6):964-5
[
16156866.001
]
[Cites]
N Engl J Med. 2006 Jan 12;354(2):166-78
[
16407512.001
]
[Cites]
J Exp Med. 2004 Oct 4;200(7):871-82
[
15466621.001
]
[Cites]
Cancer Genet Cytogenet. 2001 Oct 15;130(2):93-104
[
11675129.001
]
[Cites]
Cancer. 2007 Aug 1;110(3):477-88
[
17582631.001
]
[Cites]
Leukemia. 2000 Dec;14(12):2205-22
[
11187912.001
]
[Cites]
Curr Drug Targets. 2007 Jun;8(6):703-14
[
17584026.001
]
[Cites]
Blood. 1998 Sep 1;92(5):1793-8
[
9716610.001
]
[Cites]
Nat Rev Cancer. 2005 Jul;5(7):543-55
[
15965494.001
]
[Cites]
Immunity. 2007 Apr;26(4):407-19
[
17433729.001
]
[Cites]
Leuk Res. 1998 Feb;22(2):145-51
[
9593471.001
]
[Cites]
Blood. 2006 Mar 1;107(5):1892-5
[
16249375.001
]
(PMID = 19010836.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
Austria / Austrian Science Fund FWF / / P 17551
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Erythropoietin; 0 / TEL-AML1 fusion protein; 11096-26-7 / Erythropoietin; VB0R961HZT / Prednisone
[Other-IDs]
NLM/ EMS32871; NLM/ PMC4194425
76.
Rizack T, Mega A, Legare R, Castillo J:
Management of hematological malignancies during pregnancy.
Am J Hematol
; 2009 Dec;84(12):830-41
[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.
The purpose of this review is to evaluate the limited existing data and make useful suggestions in the management of
acute
and chronic
leukemias
, Hodgkin and non-Hodgkin lymphomas, plasma
cell
myeloma, and other hematological malignancies, such as myelodysplastic syndromes and hairy
cell
leukemia
, during pregnancy.
[MeSH-minor]
Abnormalities, Drug-Induced / etiology. Abnormalities, Drug-Induced / prevention & control. Abortion, Induced. Adult. Antiemetics / therapeutic use. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents / contraindications. Antineoplastic Agents / therapeutic use. Cesarean Section. Clinical Protocols. Combined Modality Therapy.
Disease
Management. Female. Humans. Incidence. Infant, Newborn. Infant, Newborn, Diseases / chemically induced. Infant, Newborn, Diseases / prevention & control. Leukapheresis. Pregnancy. Pregnancy Outcome. Pregnancy Trimesters
Genetic Alliance.
consumer health - Pregnancy
.
MedlinePlus Health Information.
consumer health - Tumors and Pregnancy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
(c) 2009 Wiley-Liss, Inc.
(PMID = 19844988.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antiemetics; 0 / Antineoplastic Agents
[Number-of-references]
179
77.
Italiano A, Chambonniere ML, Attias R, Chibon F, Coindre JM, Pedeutour F:
Monosomy 7 and absence of 12q amplification in two cases of spindle cell liposarcomas.
Cancer Genet Cytogenet
; 2008 Jul 15;184(2):99-104
[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]
Monosomy 7 and absence of 12q amplification in two cases of spindle
cell
liposarcomas.
Spindle
cell
liposarcoma (SCL) is a rare malignant adipose tissue tumor presently regarded as a variant of well-differentiated liposarcoma (WDLPS).
It has been described in myelodysplastic syndromes and
acute
myeloid or lymphoblastic
leukemias
, as well as in several benign or malignant solid tumors.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18617058.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
78.
Burmeister T, Meyer C, Thiel G, Reinhardt R, Thiel E, Marschalek R:
A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32).
Blood Cells Mol Dis
; 2008 Sep-Oct;41(2):210-4
[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 MLL-KIAA0284 fusion gene in a patient with secondary
acute
myeloid
leukemia
and t(11;14)(q23;q32).
MLL aberrations are found in approximately 10% of
acute leukemias
.
More than 80 different MLL fusion genes have been cytogenetically described but a significant number of MLL fusion partners remain unidentified on the molecular
level
.
We describe here the case
of a
patient who developed secondary
acute
myeloid
leukemia
five years after the patient had received adjuvant radiochemotherapy because of breast cancer.
This therapy comprised 4 cycles epirubicin/cyclophosphamide, a mitoxantrone-based high-dose chemotherapy with autologous stem
cell
transplantation and a subsequent radiation.
[MeSH-major]
Leukemia
, Myeloid,
Acute
/ genetics. Myeloid-Lymphoid
Leukemia
Protein / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18640063.001).
[ISSN]
1096-0961
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
79.
Geddes M, Kangarloo SB, Naveed F, Quinlan D, Chaudhry MA, Stewart D, Savoie ML, Bahlis NJ, Brown C, Storek J, Andersson BS, Russell JA:
High busulfan exposure is associated with worse outcomes in a daily i.v. busulfan and fludarabine allogeneic transplant regimen.
Biol Blood Marrow Transplant
; 2008 Feb;14(2):220-8
[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.
Low plasma busulfan (Bu) area under the concentration-time curve (AUC) is associated with graft failure and relapsed
leukemias
, and high AUC with toxicities when Bu is used orally or i.v.
4 times daily combined with cyclophosphamide in myeloablative hematopoietic stem
cell
transplantation (SCT) conditioning regimens.
Total-body irradiation (TBI) 200 cGy x 2 was added for 51 patients with
acute leukemias
.
This effect was apparent in patients with standard-risk and high-risk
disease
, and persisted when potential confounders were considered (hazard ratio 3.2, 95% confidence interval 1.7-6.3).
[MeSH-major]
Busulfan / administration & dosage. Busulfan / pharmacokinetics. Hematopoietic Stem
Cell
Transplantation / methods. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
BUSULFAN
.
Hazardous Substances Data Bank.
VIDARABINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18215782.001).
[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]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
80.
Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW:
FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
Leuk Res
; 2008 Nov;32(11):1751-5
[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]
FBXW7 mutation in adult T-
cell
and B-
cell acute
lymphocytic
leukemias
.
Engineered FBXW7 null cells display
cell
cycle and chromosome stability defects.
Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-
cell acute
lymphocytic
leukemias
.
Prompted by these findings we have examined
acute
myeloid
leukemia
, non-Hodgkin's lymphoma, T-
cell acute
lymphocytic leukemia
, B-
cell acute
lymphocytic leukemia
and adult T-
cell
leukemia
DNA for mutations of the FBXW7 gene.
As expected, mutations were found in T-
cell acute
lymphocytic
leukemias
.
However mutations of FBXW7 were also found in four of 118 B-
cell acute
lymphocytic
leukemias
and one of 24 adult T-
cell
leukemia
samples.
These observations suggest that disruption of FBXW7 has a role in several forms
of lymphocytic
leukemias
and not exclusively T-
cell acute
lymphocytic leukemia
.
[MeSH-major]
Burkitt Lymphoma / genetics.
Cell
Cycle Proteins / genetics. F-Box Proteins / genetics.
Leukemia
-Lymphoma, Adult T-
Cell
/ genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics
COS Scholar Universe.
author profiles
.
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 = 18485478.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
81.
Erkeland SJ, Palande KK, Valkhof M, Gits J, Danen-van Oorschot A, Touw IP:
The gene encoding thioredoxin-interacting protein (TXNIP) is a frequent virus integration site in virus-induced mouse leukemia and is overexpressed in a subset of AML patients.
Leuk Res
; 2009 Oct;33(10):1367-71
[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 gene encoding thioredoxin-interacting protein (TXNIP) is a frequent virus integration site in virus-induced mouse
leukemia
and is overexpressed in a subset of AML patients.
In a screen for novel
disease
genes in murine
leukemia
virus (MLV)-induced mouse
leukemias
, we identified Txnip as a frequent target for proviral integration.
These findings suggest that deregulated TXNIP expression contributes to MLV-induced murine
leukemia
as well as human AML.
[MeSH-major]
Carrier Proteins / genetics. Gene Expression Regulation.
Leukemia
/ genetics.
Leukemia
, Experimental / genetics.
Leukemia
, Myeloid,
Acute
/ genetics. Thioredoxins / genetics. Virus Integration / genetics
[MeSH-minor]
Animals. Blast Crisis / genetics. Blast Crisis / pathology.
Cell
Line. DNA Primers. Genes, Reporter. Humans.
Leukemia
Virus, Murine / genetics. Mice. Polymerase Chain Reaction. Promoter Regions, Genetic
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Leuk Res. 2009 Oct;33(10):1297
[
19560202.001
]
(PMID = 19327827.001).
[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
[Chemical-registry-number]
0 / Carrier Proteins; 0 / DNA Primers; 0 / TXNIP protein, human; 0 / Txnip protein, mouse; 52500-60-4 / Thioredoxins
82.
Jourde-Chiche N, Dussol B, Daniel L:
[Kidney involvement in hematologic malignancies. Diagnostic approach].
Rev Med Interne
; 2010 Oct;31(10):685-96
[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.
Various mechanisms could be implicated: deposits of immunoglobulin fractions or crystals, renal infiltration by malignant cells, urinary tract obstruction, paraneoplastic or storage glomerulopathies… Diagnostic strategy relies on the clinical presentation:
acute
renal failure, chronic kidney
disease
, glomerular proteinuria with or without nephrotic syndrome, tubular proteinuria, hydroelectrolytic disorders.
We propose diagnostic strategies of renal involvement in myeloma, Waldenström's
disease
, high grade lymphomas and
acute leukemias
, low grade lymphomas and chronic
leukemias
.
The adverse effects of treatments (chemotherapy, radiotherapy, stem
cell
graft …) are not addressed in this review.
MedlinePlus Health Information.
consumer health - Kidney Diseases
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.
(PMID = 20483511.001).
[ISSN]
1768-3122
[Journal-full-title]
La Revue de medecine interne
[ISO-abbreviation]
Rev Med Interne
[Language]
FRE
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
83.
Miyazaki K, Yamasaki N, Oda H, Kuwata T, Kanno Y, Miyazaki M, Komeno Y, Kitaura J, Honda Z, Warming S, Jenkins NA, Copeland NG, Kitamura T, Nakamura T, Honda H:
Enhanced expression of p210BCR/ABL and aberrant expression of Zfp423/ZNF423 induce blast crisis of chronic myelogenous leukemia.
Blood
; 2009 May 7;113(19):4702-10
[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]
Enhanced expression of p210BCR/ABL and aberrant expression of Zfp423/ZNF423 induce blast crisis of chronic myelogenous
leukemia
.
Chronic myelogenous
leukemia
(CML) is a hematopoietic disorder originating from p210BCR/ABL-transformed stem cells, which begins as indolent chronic phase (CP) but progresses into fatal blast crisis (BC).
To investigate molecular mechanism(s) underlying
disease
evolution, CML-exhibiting p210BCR/ABL transgenic mice were crossed with BXH2 mice that transmit a replication-competent retrovirus.
Whereas nontransgenic mice in the BXH2 background exclusively developed
acute
myeloid
leukemia
, p210BCR/ABL transgenic littermates developed nonmyeloid
leukemias
, in which inverse polymerase chain reaction detected 2 common viral integration sites (CISs).
The other was the 5' noncoding region
of a
transcription factor, Zfp423, which induced aberrant Zfp423 expression.
(1) introduction of Zfp423 in p210BCR/ABL transgenic bone marrow (BM) cells increased colony-forming ability, (2) suppression of ZNF423 (human homologue of Zfp423) in ZNF423-expressing, p210BCR/ABL-positive hematopoietic cells retarded
cell
growth, (3) mice that received a transplant of BM cells transduced with Zfp423 and p210BCR/ABL developed
acute
leukemia
, and (4) expression of ZNF423 was found in human BCR/ABL-positive
cell
lines and CML BC samples.
[MeSH-major]
B-
Lymphocytes
/ pathology. Blast Crisis / genetics. DNA-Binding Proteins / physiology. Fusion Proteins, bcr-abl / physiology. Gene Expression Regulation, Leukemic.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics. Transcription Factors / physiology
[MeSH-minor]
Animals. Blotting, Northern. Blotting, Southern. Blotting, Western. Bone Marrow Transplantation.
Cell
Proliferation. Colony-Forming Units Assay. Female. Flow Cytometry. Gene Rearrangement. Humans. Male. Mice. Mice, Knockout. Phenotype. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Zinc Fingers
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
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
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19234145.001).
[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 / DNA-Binding Proteins; 0 / Ebfaz protein, mouse; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
84.
Eguchi-Ishimae M, Eguchi M, Ishii E, Knight D, Sadakane Y, Isoyama K, Yabe H, Mizutani S, Greaves M:
The association of a distinctive allele of NAD(P)H:quinone oxidoreductase with pediatric acute lymphoblastic leukemias with MLL fusion genes in Japan.
Haematologica
; 2005 Nov;90(11):1511-5
[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]
The association
of a
distinctive allele of NAD(P)H:quinone oxidoreductase with pediatric
acute
lymphoblastic
leukemias
with MLL fusion genes in Japan.
Previous studies in Caucasian populations have provided evidence that a loss of function allele at nt 609 (C609T, Pro187Ser) is associated with increased risk of infant
acute
lymphoblastic
leukemia
(ALL) with MLL-AF4 fusion genes.
DESIGN AND METHODS: We genotyped 103 infants (<18 months) with ALL or
acute
myeloid
leukemia
(AML) in Japan and 185 controls for the frequency of allelic variation at nt 609 and 465 in NQO1 using standardized polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology.
[MeSH-major]
Alleles. Asian Continental Ancestry Group / genetics. Myeloid-Lymphoid
Leukemia
Protein / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / genetics
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16266898.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
85.
Chen J, Jette C, Kanki JP, Aster JC, Look AT, Griffin JD:
NOTCH1-induced T-cell leukemia in transgenic zebrafish.
Leukemia
; 2007 Mar;21(3):462-71
[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]
NOTCH1-induced T-
cell
leukemia
in transgenic zebrafish.
Activating mutations in the NOTCH1 gene have been found in about 60% of patients with T-
cell acute
lymphoblastic
leukemia
(T-ALL).
In order to study the molecular mechanisms by which altered Notch signaling induces
leukemia
, a zebrafish model of human NOTCH1-induced T-
cell
leukemia
was generated.
Seven of sixteen mosaic fish developed a T-
cell
lymphoproliferative
disease
at about 5 months.
These neoplastic cells extensively invaded tissues throughout the fish and caused an aggressive and lethal
leukemia
when transplanted into irradiated recipient fish.
However, stable transgenic fish exhibited a longer latency for
leukemia onset
.
When the stable transgenic line was crossed with another line overexpressing the zebrafish bcl2 gene, the
leukemia onset
was dramatically accelerated, indicating synergy between the Notch pathway and the bcl2-mediated antiapoptotic pathway.
Reverse transcription-polymerase chain reaction analysis showed that Notch target genes such as her6 and her9 were highly expressed in NOTCH1-induced
leukemias
.
[MeSH-major]
Cell
Transformation, Neoplastic / genetics.
Leukemia
-Lymphoma, Adult T-
Cell
/ etiology. Proto-Oncogene Proteins c-bcl-2 / physiology. Receptor, Notch1 / physiology
[MeSH-minor]
Animals. Animals, Genetically Modified. Apoptosis. Basic Helix-Loop-Helix Transcription Factors / physiology. Female. Gamma Rays. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Gene Rearrangement, alpha-Chain T-
Cell
Antigen Receptor. Genes, bcl-2. Humans. Male. Mosaicism. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology. Neoplasm Transplantation. Oncogenes. Radiation Chimera. Radiation Tolerance. Recombinant Fusion Proteins / physiology. Signal Transduction. Time Factors. Zebrafish. Zebrafish Proteins / physiology
COS Scholar Universe.
author profiles
.
SciCrunch.
ZFIN: Data: Gene Expression
.
ZFIN.
ZFIN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17252014.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA-36167; United States / NCI NIH HHS / CA / CA-68484
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Her6 protein, zebrafish; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptor, Notch1; 0 / Recombinant Fusion Proteins; 0 / Zebrafish Proteins; 0 / her9 protein, zebrafish
86.
Passweg JR, Chalandon Y, Matthes T, Beris P, Aapro MS, Plan PA:
[Acute leukemias].
Rev Med Suisse
; 2008 May 21;4(158):1272-4, 1276-8
[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]
[
Acute leukemias
].
[MeSH-major]
Leukemia
, Myeloid,
Acute
/ diagnosis.
Leukemia
, Myeloid,
Acute
/ therapy. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / diagnosis. Precursor
Cell
Lymphoblastic
Leukemia
-Lymphoma / therapy
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18616210.001).
[ISSN]
1660-9379
[Journal-full-title]
Revue médicale suisse
[ISO-abbreviation]
Rev Med Suisse
[Language]
fre
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Number-of-references]
22
87.
Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR:
A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
BMC Cancer
; 2010;10:518
[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 spliced fusion of MLL with CT45A2 in a pediatric biphenotypic
acute
leukemia
.
BACKGROUND: Abnormalities of 11q23 involving the MLL gene are found in approximately 10% of human
leukemias
.
To date, nearly 100 different chromosome bands have been described in rearrangements involving 11q23 and 64 fusion genes have been cloned and characterized at the molecular
level
.
In this work we present the identification
of a
novel MLL fusion partner in a pediatric patient with
de
novo biphenotypic
acute
leukemia
.
METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric
acute
leukemia
.
RNA analysis revealed the presence
of a
novel MLL-CT45A2 fusion transcript in which the first 9 exons of the MLL gene were fused in-frame to exon 2 of the CT45A2 gene, resulting in a spliced MLL fusion transcript with an intact open reading frame.
CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with
de
novo biphenotypic
acute
leukemia
, as a result
of a
cryptic insertion of 11q23 in Xq26.3.
Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in
acute
leukemia
, future studies addressing its biologic relevance for leukemogenesis are warranted.
[MeSH-major]
Antigens, Neoplasm / genetics.
Leukemia
, Myeloid,
Acute
/ genetics. Myeloid-Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Proc Natl Acad Sci U S A. 2005 May 31;102(22):7940-5
[
15905330.001
]
[Cites]
Semin Cancer Biol. 2005 Jun;15(3):175-88
[
15826832.001
]
[Cites]
DNA Repair (Amst). 2006 Sep 8;5(9-10):1282-97
[
16893685.001
]
[Cites]
Nucleic Acids Res. 2006;34(15):4168-80