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
acute mixed lineage leukaemia 2005:2010[pubdate] *count=100
167 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
acute mixed lineage leukaemia
' expands to
2 meanings
. Choose the one you intended:
Concept C0023464: acute biphenotypic leukemia disorder;
details
Concept C2826025: mixed phenotype acute leukemia morphologic abnormality;
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 167
1.
Strick R, Zhang Y, Emmanuel N, Strissel PL:
Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
Hum Genet
; 2006 Jun;119(5):479-95
[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]
Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and
acute
leukemias
.
The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of
acute
lymphocytic leukemia
.
Chromosome 11q23 translocations in
acute
myeloid and lymphoid leukemia
cells demonstrate
myeloid lymphoid leukemia
(MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
Therapy-related
leukemia
is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
In this report, using
cell
lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
Although MLL2 was expressed in all
cell
lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with
leukemia
.
[MeSH-major]
Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics.
Leukemia
/ genetics.
Leukemia
/ metabolism. Translocation, Genetic
[MeSH-minor]
Acute
Disease
.
Cell
Line, Tumor. Cells, Cultured. Chronic
Disease
. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic
MedlinePlus Health Information.
consumer health - Leukemia
.
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
[Cites]
Biochemistry. 1997 May 20;36(20):5934-9
[
9166762.001
]
[Cites]
Cell. 1985 May;41(1):127-32
[
2986841.001
]
[Cites]
Gene. 2002 May 29;291(1-2):251-7
[
12095698.001
]
[Cites]
EMBO J. 1990 Apr;9(4):1319-27
[
2323342.001
]
[Cites]
Science. 1994 Jan 28;263(5146):515-8
[
8290959.001
]
[Cites]
Curr Biol. 2000 Jul 27-Aug 10;10(15):923-6
[
10959840.001
]
[Cites]
Leukemia. 1996 Feb;10(2):372-7
[
8637251.001
]
[Cites]
J Cell Biochem. 2001;82(2):299-309
[
11527155.001
]
[Cites]
Genomics. 1995 May 1;27(1):67-82
[
7665185.001
]
[Cites]
Annu Rev Biochem. 1989;58:351-75
[
2549853.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9
[
8016145.001
]
[Cites]
Oncogene. 1989 May;4(5):559-67
[
2657572.001
]
[Cites]
Oncogene. 1990 Nov;5(11):1669-73
[
2267134.001
]
[Cites]
Oncogene. 2001 May 24;20(23):2900-7
[
11420702.001
]
[Cites]
J Cell Biol. 2001 Dec 10;155(6):899-910
[
11739403.001
]
[Cites]
Genes Chromosomes Cancer. 2002 Apr;33(4):331-45
[
11921269.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5
[
10758153.001
]
[Cites]
EMBO J. 2002 Oct 1;21(19):5269-80
[
12356743.001
]
[Cites]
Genes Chromosomes Cancer. 2001 Oct;32(2):144-54
[
11550282.001
]
[Cites]
Genes Chromosomes Cancer. 2003 Apr;36(4):393-401
[
12619163.001
]
[Cites]
Proc Natl Acad Sci U S A. 1988 Apr;85(7):2076-80
[
2832845.001
]
[Cites]
Nucleic Acids Res. 1997 Feb 1;25(3):511-7
[
9016589.001
]
[Cites]
Cancer Res. 1999 Jul 15;59(14 ):3357-62
[
10416593.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 14;98 (17 ):9802-7
[
11493704.001
]
[Cites]
Oncogene. 1998 Dec 3;17(22):2921-31
[
9879998.001
]
[Cites]
J Cell Sci. 2004 Sep 1;117(Pt 19):4583-90
[
15331666.001
]
[Cites]
Nucleic Acids Res. 1988 Jun 24;16(12):5533-56
[
2838820.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 Jul;86(14):5497-501
[
2546156.001
]
[Cites]
Cell. 1995 Dec 29;83(7):1137-48
[
8548801.001
]
[Cites]
J Cell Biochem Suppl. 2000;Suppl 35:3-22
[
11389527.001
]
[Cites]
Hum Mol Genet. 1998 May;7(5):767-76
[
9536079.001
]
[Cites]
Hum Mol Genet. 2000 Jul 1;9(11):1671-9
[
10861294.001
]
[Cites]
Mol Cell Biol. 1991 Oct;11(10):4973-84
[
1656219.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14535-40
[
10588740.001
]
[Cites]
Cell Mol Life Sci. 2002 Feb;59(2):373-85
[
11915950.001
]
[Cites]
Mol Cell Biol. 1997 Jul;17(7):4070-9
[
9199342.001
]
[Cites]
Biochem J. 1994 Nov 1;303 ( Pt 3):681-95
[
7980433.001
]
[Cites]
Blood. 1996 Apr 1;87(7):2649-58
[
8639880.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 May 15;90(10 ):4631-5
[
8506309.001
]
[Cites]
Hum Mol Genet. 2002 Jun 1;11(12):1391-7
[
12023981.001
]
[Cites]
J Biol Chem. 2002 Jun 14;277(24):21458-67
[
11940566.001
]
[Cites]
Hum Mutat. 2003 Sep;22(3):229-44
[
12938088.001
]
[Cites]
Cell. 1992 Nov 13;71(4):701-8
[
1423625.001
]
[Cites]
Oncogene. 1998 Dec 10;17 (23 ):3035-44
[
9881706.001
]
[Cites]
Genomics. 1999 Jul 15;59(2):187-92
[
10409430.001
]
[Cites]
Leuk Res. 2002 Aug;26(8):713-20
[
12191565.001
]
[Cites]
Br J Haematol. 1999 Apr;105(1):256-64
[
10233389.001
]
[Cites]
Blood. 2000 Feb 1;95(3):738-43
[
10648381.001
]
[Cites]
Oncogene. 1999 Dec 23;18(56):7975-84
[
10637508.001
]
[Cites]
Cancer Res. 1995 Jan 1;55(1):34-8
[
7805037.001
]
[Cites]
Cancer Res. 1996 Apr 15;56(8):1855-62
[
8620504.001
]
[Cites]
Blood. 1996 Mar 1;87(5):1912-22
[
8634439.001
]
[Cites]
Nature. 2001 Sep 27;413(6854):435-8
[
11574892.001
]
[Cites]
Cancer Lett. 2003 Apr 10;193(1):1-9
[
12691817.001
]
[Cites]
Leukemia. 1997 Sep;11(9):1571-4
[
9305614.001
]
[Cites]
Chromosoma. 1996 Aug;105(2):122-33
[
8753702.001
]
[Cites]
Leukemia. 1999 Dec;13(12):2107-13
[
10602437.001
]
[Cites]
Cancer Res. 1993 Oct 1;53(19):4489-92
[
8402620.001
]
[Cites]
Mol Cell Biol. 1999 Apr;19(4):2986-97
[
10082566.001
]
[Cites]
Hum Genet. 2003 Jul;113(1):80-91
[
12665971.001
]
[Cites]
Blood. 1998 Nov 15;92(10):3793-803
[
9808573.001
]
[Cites]
Genomics. 1998 Jan 15;47(2):217-29
[
9479494.001
]
[Cites]
Blood. 2001 Dec 15;98(13):3778-83
[
11739186.001
]
[Cites]
Genes Dev. 2001 Dec 15;15(24):3237-42
[
11751629.001
]
[Cites]
Genes Chromosomes Cancer. 2002 Sep;35(1):92-6
[
12203795.001
]
[Cites]
Cancer Res. 2001 Jun 1;61(11):4550-5
[
11389089.001
]
[Cites]
Blood. 1990 Aug 1;76(3):597-601
[
2198962.001
]
[Cites]
Genetics. 2002 Apr;160(4):1363-73
[
11973293.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9882-7
[
12114534.001
]
[Cites]
Genes Chromosomes Cancer. 2004 Nov;41(3):257-65
[
15334549.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4411-3
[
10781030.001
]
[Cites]
FASEB J. 2004 Jan;18(1):173-5
[
14630694.001
]
[Cites]
Genes Chromosomes Cancer. 2002 Apr;33(4):362-78
[
11921271.001
]
[Cites]
Mol Pharmacol. 1998 Jul;54(1):78-85
[
9658192.001
]
[Cites]
Cancer Res. 2004 Apr 15;64(8):2656-62
[
15087374.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):3070-5
[
11867721.001
]
[Cites]
Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72
[
10595755.001
]
[Cites]
Chromosoma. 1991 Feb;100(2):97-102
[
1849068.001
]
[Cites]
Leukemia. 1998 Mar;12(3):346-52
[
9529129.001
]
[Cites]
Leukemia. 1995 Aug;9(8):1305-12
[
7643617.001
]
(PMID = 16572268.001).
[ISSN]
0340-6717
[Journal-full-title]
Human genetics
[ISO-abbreviation]
Hum. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
Germany
[Chemical-registry-number]
0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
2.
Zhao XF, Gojo I, York T, Ning Y, Baer MR:
Diagnosis of biphenotypic acute leukemia: a paradigmatic approach.
Int J Clin Exp Pathol
; 2009;3(1):75-86
[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]
Diagnosis
of
biphenotypic
acute
leukemia
: a paradigmatic approach.
Biphenotypic
acute
leukemia
(BAL), or
acute
leukemia
with a single population of blasts coexpressing markers of two different lineages, is a rare clinical entity.
To define BAL, a scoring system was proposed by the European Group of Immunological Markers for
Leukemias
(EGIL) in 1995.
However, increasing evidence suggests that this system has limitations, as acknowledged by the 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic
and Lymphoid
Tissues.
We propose a new paradigmatic approach to defining BAL based on recent clinical studies of BAL and advances in immunologic marker definition and cytogenetics, and applied our new approach to 8 cases of "BAL" among a cohort of 742 new
acute
leukemias
in our Cancer Center.
By our new criteria, 6 cases were reclassified as
acute
lymphoblastic leukemia
(ALL), while only 2 were still classified as BAL.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
[MeSH-minor]
Adolescent. Adult. Aged, 80 and over. Antigens, Neoplasm / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Child. Female. Humans. Immunophenotyping. Male. Middle Aged.
Phenotype
. Retrospective Studies. World Health Organization. Young Adult
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Arch Pathol Lab Med. 2001 Jul;125(7):948-50
[
11419984.001
]
[Cites]
Am J Clin Pathol. 1998 Feb;109(2):211-20
[
9583894.001
]
[Cites]
Am J Hematol. 2001 Oct;68(2):69-74
[
11559944.001
]
[Cites]
Exp Hematol. 2002 Mar;30(3):205-11
[
11882357.001
]
[Cites]
Br J Haematol. 2003 Dec;123(5):842-9
[
14632775.001
]
[Cites]
Cancer Res. 2004 Oct 15;64(20):7399-404
[
15492262.001
]
[Cites]
Nature. 1975 Dec 4;258(5534):454-6
[
1059878.001
]
[Cites]
Br J Haematol. 1976 Aug;33(4):451-8
[
188440.001
]
[Cites]
Blood. 1981 Sep;58(3):648-52
[
6973348.001
]
[Cites]
Blood. 1983 Apr;61(4):718-25
[
6572534.001
]
[Cites]
Blood. 1983 Jun;61(6):1138-45
[
6404327.001
]
[Cites]
Hum Pathol. 1998 May;29(5):498-504
[
9596274.001
]
[Cites]
Am J Hematol. 1998 Jul;58(3):241-3
[
9662278.001
]
[Cites]
Cytometry. 1998 Aug 15;34(4):198-202
[
9725460.001
]
[Cites]
Haematologica. 1999 Aug;84(8):699-706
[
10457405.001
]
[Cites]
Cancer. 2004 Dec 15;101(12):2788-801
[
15481055.001
]
[Cites]
Exp Mol Pathol. 2005 Aug;79(1):39-41
[
16005710.001
]
[Cites]
Cancer Genet Cytogenet. 2005 Nov;163(1):62-7
[
16271957.001
]
[Cites]
Blood. 2007 May 1;109(9):3697-705
[
17218387.001
]
[Cites]
Exp Mol Pathol. 2007 Aug;83(1):138-41
[
17434163.001
]
[Cites]
Br J Haematol. 2007 Jul;138(2):213-6
[
17593028.001
]
[Cites]
Exp Mol Pathol. 2007 Dec;83(3):471-3
[
17963747.001
]
[Cites]
Trends Biochem Sci. 2008 Feb;33(2):51-7
[
18201888.001
]
[Cites]
Int J Hematol. 2008 Mar;87(2):132-6
[
18288568.001
]
[Cites]
Leuk Lymphoma. 2008 Apr;49(4):700-9
[
18398737.001
]
[Cites]
Cancer Genet Cytogenet. 2008 Aug;185(1):28-31
[
18656690.001
]
[Cites]
Blood. 2009 May 21;113(21):5083-9
[
19131545.001
]
[Cites]
J Biol Chem. 2000 Mar 24;275(12):8633-40
[
10722703.001
]
[Cites]
Am J Clin Pathol. 2000 Jun;113(6):823-30
[
10874883.001
]
[Cites]
J Chin Med Assoc. 2007 Jul;70(7):269-73
[
17631462.001
]
[Cites]
Leukemia. 2007 Nov;21(11):2264-70
[
17611554.001
]
[Cites]
Pathology. 1986 Jan;18(1):99-110
[
3014425.001
]
[Cites]
EMBO J. 1988 Nov;7(11):3457-64
[
2463161.001
]
[Cites]
Leukemia. 1989 Mar;3(3):170-81
[
2465463.001
]
[Cites]
Br J Haematol. 1990 Jun;75(2):202-7
[
2372506.001
]
[Cites]
Blood. 1990 Aug 15;76(4):808-13
[
2166608.001
]
[Cites]
Blood. 1992 Jul 15;80(2):470-7
[
1378322.001
]
[Cites]
J Immunol. 1992 Oct 1;149(7):2281-5
[
1382094.001
]
[Cites]
Leukemia. 1993 Apr;7(4):489-98
[
7681917.001
]
[Cites]
Blood. 1993 Aug 1;82(3):853-7
[
8338949.001
]
[Cites]
J Exp Med. 1993 Sep 1;178(3):1049-55
[
7688784.001
]
[Cites]
Blood. 1993 Sep 1;82(5):1599-607
[
8395912.001
]
[Cites]
J Pathol. 1993 Oct;171(2):99-104
[
7506772.001
]
[Cites]
Am J Clin Pathol. 1994 Mar;101(3):296-9
[
7510927.001
]
[Cites]
Br J Haematol. 1994 Jun;87(2):273-81
[
7947267.001
]
[Cites]
Leukemia. 1995 Oct;9(10):1783-6
[
7564526.001
]
[Cites]
Am J Clin Pathol. 1996 Jun;105(6):761-8
[
8659452.001
]
[Cites]
Am J Clin Pathol. 1996 Aug;106(2):185-91
[
8712171.001
]
[Cites]
Br J Haematol. 1997 Oct;99(1):101-6
[
9359509.001
]
[Cites]
Br J Haematol. 1998 Jan;100(1):147-55
[
9450804.001
]
[Cites]
Am J Clin Pathol. 2001 Jul;116(1):25-33
[
11447748.001
]
(PMID = 19918331.001).
[ISSN]
1936-2625
[Journal-full-title]
International journal of clinical and experimental pathology
[ISO-abbreviation]
Int J Clin Exp Pathol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
[Other-IDs]
NLM/ PMC2776262
[Keywords]
NOTNLM ; ALL / AML / Biphenotypic acute leukemia / EGIL / classification
3.
Dixon N, Kishnani PS, Zimmerman S:
Clinical manifestations of hematologic and oncologic disorders in patients with Down syndrome.
Am J Med Genet C Semin Med Genet
; 2006 Aug 15;142C(3):149-57
[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.
Increased erythrocyte mean corpuscular volume (MCV) is frequently found among DS infants and remains elevated throughout life in two-thirds of patients, making interpretation of red
cell
indices for
diagnosis
of nutritional anemias or bone marrow failure disorders more challenging.
Transient myeloproliferative
disorder
(TMD) associated with pancytopenia, hepatosplenomegaly, and circulating immature WBCs, is found almost exclusively in DS infants with an incidence of approximately 10%.
Despite the high rate of spontaneous regression, TMD can be a preleukemic
disorder
in 20-30% of children with DS.
There is an increased risk of
leukemia
with an equal incidence of
lymphoid and myeloid leukemia
.
Acute
megakaryocytic
leukemia
(AMKL) subtype is the most common form of
acute
myeloid leukemia
(AML) in this setting, and is uncommon in children without DS.
Children with DS
and leukemia
are more sensitive to some chemotherapeutic agents such as methotrexate than other children which requires careful monitoring for toxicity.
Although the risk for
leukemia
is higher in individuals with DS, these patients have a lower risk of developing solid tumors, with the exception of germ
cell
tumors, and perhaps retinoblastoma and lymphoma.
[MeSH-major]
Down Syndrome / complications. Hematologic Diseases /
diagnosis
. Hematologic Diseases / etiology. Neoplasms /
diagnosis
. Neoplasms / etiology
[MeSH-minor]
Child. Female. Humans. Infant.
Leukemia
/
diagnosis
.
Leukemia
/ etiology. Male. Myeloproliferative Disorders /
diagnosis
. Myeloproliferative Disorders / etiology
Genetic Alliance.
consumer health - Down Syndrome
.
MedlinePlus Health Information.
consumer health - Blood Disorders
.
MedlinePlus Health Information.
consumer health - Cancer in Children
.
MedlinePlus Health Information.
consumer health - Down Syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17048354.001).
[ISSN]
1552-4868
[Journal-full-title]
American journal of medical genetics. Part C, Seminars in medical genetics
[ISO-abbreviation]
Am J Med Genet C Semin Med Genet
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 2T32 CA 09307
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
72
Advertisement
4.
Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI:
Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
Am J Hematol
; 2007 Jan;82(1):69-72
[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]
Acute
myeloid leukemia
with T-
cell
receptor gamma gene rearrangement occurring in a patient with chronic
lymphocytic leukemia
: a case report.
The association of chronic
lymphocytic leukemia
(CLL) and
acute
leukemia
, either
lymphoid
or
myeloid
is a rare event.
Our review of the medical literature revealed only 6 cases of CLL transformation to
acute
myeloid leukemia
(AML) (M0, M1 and M2) with no other associated malignancy.
We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-
cell
receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
[MeSH-major]
Gene Rearrangement, gamma-Chain T-
Cell
Antigen Receptor.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasms, Second Primary / genetics
Genetic Alliance.
consumer health - Chronic Lymphocytic Leukemia
.
Genetic Alliance.
consumer health - Chronic Myeloid Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Genetic Alliance.
consumer health - Leukemia, T-cell, chronic
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
CYTARABINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16947317.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
[Number-of-references]
22
5.
Scolnik MP, Aranguren PN, Cuello MT, Palacios MF, Sanjurjo J, Giunta M, Bracco MM, Acevedo S:
Biphenotypic acute leukemia with t(15;17).
Leuk Lymphoma
; 2005 Apr;46(4):607-10
[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]
Biphenotypic
acute
leukemia
with t(15;17).
Biphenotypic
acute
leukemias
(BAL) represent 5% of all
acute
leukemias
.
Immunophenotype revealed the compromise of
myeloid and
B-
lymphoid
lineages.
This report describes a BAL case with an unfrequent cytogenetic
abnormality
, and highlights the importance of correlating the results of multiple diagnostic methods in order to establish a correct
diagnosis and
treatment in BAL patients.
[MeSH-major]
Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics.
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
. Child. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Female. Flow Cytometry / methods. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual /
diagnosis
. Neoplasm, Residual / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Trisomy
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16019491.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
6.
Yin B, Delwel R, Valk PJ, Wallace MR, Loh ML, Shannon KM, Largaespada DA:
A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene.
Blood
; 2009 Jan 29;113(5):1075-85
[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.
NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic
leukemia
, an aggressive myeloproliferative
disorder
of childhood.
However, evidence suggests that Nf1 loss alone does not cause
leukemia
.
We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause
acute
leukemia
.
One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of
leukemia
of either
myeloid
or
lymphoid
lineage
in mice when expressed in Nf1-deficient bone marrow.
Importantly, Bcl11a is expressed in human chronic myelomonocytic
leukemia and
juvenile myelomonocytic
leukemia
samples.
These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis,
and a
therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of
leukemia
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
Addgene Non-profit plasmid repository.
clones/clone libraries - Get Article's Plasmids - Addgene
(subscription/membership/fee required).
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Leukemia. 2007 May;21(5):1093-7
[
17301810.001
]
[Cites]
Blood. 2007 May 15;109(10):4392-8
[
17284535.001
]
[Cites]
Science. 2000 Mar 10;287(5459):1804-8
[
10710306.001
]
[Cites]
Exp Hematol. 2007 Jun;35(6):908-19
[
17533045.001
]
[Cites]
Bioinformatics. 2007 Jul 1;23(13):i133-41
[
17646289.001
]
[Cites]
Biotechniques. 2007 Jul;43(1):79-84
[
17695256.001
]
[Cites]
Oncogene. 2007 Aug 30;26(40):5840-50
[
17369851.001
]
[Cites]
Mol Cell Biol. 2000 May;20(9):3178-86
[
10757802.001
]
[Cites]
Leuk Res. 2000 Jul;24(7):601-10
[
10867136.001
]
[Cites]
Genomics. 2000 Dec 15;70(3):387-91
[
11161790.001
]
[Cites]
Exp Hematol. 2001 Mar;29(3):278-85
[
11274754.001
]
[Cites]
Genes Dev. 2001 Apr 1;15(7):859-76
[
11297510.001
]
[Cites]
Semin Cancer Biol. 2001 Jun;11(3):191-200
[
11407944.001
]
[Cites]
Nature. 2001 Aug 9;412(6847):647-51
[
11493923.001
]
[Cites]
J Virol. 2001 Oct;75(19):9427-34
[
11533205.001
]
[Cites]
J Clin Invest. 2001 Sep;108(5):709-15
[
11544276.001
]
[Cites]
Cell. 2001 Oct 19;107(2):137-48
[
11672522.001
]
[Cites]
Blood. 2001 Dec 1;98(12):3274-82
[
11719364.001
]
[Cites]
Blood. 2001 Dec 1;98(12):3413-20
[
11719382.001
]
[Cites]
Blood. 2002 Jan 15;99(2):627-33
[
11781247.001
]
[Cites]
Blood. 2002 Feb 15;99(4):1474-7
[
11830502.001
]
[Cites]
EMBO J. 2002 May 15;21(10):2383-96
[
12006491.001
]
[Cites]
Oncogene. 2002 Jul 25;21(32):4978-82
[
12118376.001
]
[Cites]
Exp Hematol. 2002 Nov;30(11):1263-72
[
12423679.001
]
[Cites]
Oncogene. 2002 Dec 5;21(55):8486-97
[
12466968.001
]
[Cites]
J Virol. 2003 Jan;77(2):1059-68
[
12502821.001
]
[Cites]
Mol Cell Biol. 2003 Apr;23(8):2859-70
[
12665584.001
]
[Cites]
Blood. 2003 Apr 15;101(8):3188-97
[
12515727.001
]
[Cites]
Nat Immunol. 2003 Jun;4(6):525-32
[
12717432.001
]
[Cites]
Oncogene. 2003 Jul 17;22(29):4581-5
[
12881715.001
]
[Cites]
Curr Opin Neurol. 2004 Apr;17(2):101-5
[
15021234.001
]
[Cites]
N Engl J Med. 2004 Apr 15;350(16):1617-28
[
15084694.001
]
[Cites]
Blood. 2004 Jun 1;103(11):4243-50
[
14982883.001
]
[Cites]
J Virol. 1982 May;42(2):379-88
[
6283161.001
]
[Cites]
Nature. 1990 Mar 15;344(6263):251-3
[
2179728.001
]
[Cites]
Mol Cell Biol. 1990 Sep;10(9):4658-66
[
2167436.001
]
[Cites]
Cell. 1990 Nov 16;63(4):843-9
[
2121370.001
]
[Cites]
Cell. 1992 Apr 17;69(2):265-73
[
1568246.001
]
[Cites]
Nature. 1992 Apr 23;356(6371):713-5
[
1570015.001
]
[Cites]
Mol Cell Biol. 1993 Jan;13(1):351-7
[
8093327.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Jun 15;90(12):5539-43
[
8516298.001
]
[Cites]
Cell. 1993 Sep 10;74(5):833-43
[
8104101.001
]
[Cites]
Genes Dev. 1994 May 1;8(9):1019-29
[
7926784.001
]
[Cites]
Br J Cancer. 1994 Nov;70(5):969-72
[
7947106.001
]
[Cites]
J Virol. 1995 Aug;69(8):5095-102
[
7609078.001
]
[Cites]
Blood. 1995 Dec 15;86(12):4603-11
[
8541551.001
]
[Cites]
Nat Genet. 1996 Feb;12(2):137-43
[
8563750.001
]
[Cites]
Nat Genet. 1996 Feb;12(2):149-53
[
8563752.001
]
[Cites]
Blood. 1996 Nov 15;88(10):3710-9
[
8916935.001
]
[Cites]
Cell. 1997 Mar 7;88(5):593-602
[
9054499.001
]
[Cites]
Science. 1997 May 2;276(5313):795-8
[
9115204.001
]
[Cites]
Brain Res. 1997 Jun 6;759(1):149-52
[
9219873.001
]
[Cites]
Nucleic Acids Res. 1997 Sep 1;25(17):3389-402
[
9254694.001
]
[Cites]
Nature. 2004 Dec 2;432(7017):635-9
[
15577913.001
]
[Cites]
Arch Biochem Biophys. 2005 Feb 15;434(2):316-25
[
15639232.001
]
[Cites]
Int J Cancer. 2005 May 1;114(5):683-95
[
15609309.001
]
[Cites]
Fam Cancer. 2005;4(4):323-33
[
16341812.001
]
[Cites]
Leukemia. 2006 Jan;20(1):151-4
[
16307021.001
]
[Cites]
Exp Hematol. 2006 May;34(5):631-41
[
16647569.001
]
[Cites]
Genes Dev. 2006 Aug 1;20(15):2024-9
[
16882980.001
]
[Cites]
Nat Rev Cancer. 2006 Sep;6(9):663-73
[
16915296.001
]
[Cites]
Leukemia. 2006 Oct;20(10):1880-2
[
16871282.001
]
[Cites]
J Immunol. 2007 Feb 15;178(4):2527-34
[
17277161.001
]
[Cites]
Blood. 2007 Feb 15;109(4):1687-91
[
17090653.001
]
[Cites]
Biochem Biophys Res Commun. 2007 Apr 6;355(2):538-42
[
17306224.001
]
[Cites]
Nat Genet. 2007 Apr;39(4):476-85
[
17369827.001
]
[Cites]
Br J Haematol. 2007 May;137(3):252-61
[
17408467.001
]
(PMID = 18948576.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221
[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 / BCL11A protein, human; 0 / Bcl11a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neurofibromin 1; 0 / Nuclear Proteins
[Other-IDs]
NLM/ PMC2635073
7.
Buckley O, Reardon M:
A young male with bone pain.
Eur J Intern Med
; 2005 Sep;16(5):366-8
[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.
Bone marrow biopsy and peripheral blood film confirmed the
diagnosis
of an
acute
biphenotypic
leukaemia
.
This case report highlights the fact that bone pain associated with a normal peripheral blood count may be the presentation of an
acute
haematological
disorder
in both adults and children.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16137555.001).
[ISSN]
0953-6205
[Journal-full-title]
European journal of internal medicine
[ISO-abbreviation]
Eur. J. Intern. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
8.
Coche D, Bergues B, Harrivel V, Guillaume N:
[Biphenotypic acute leukaemia with Burkitt-like cytology].
Ann Biol Clin (Paris)
; 2009 Jul-Aug;67(4):437-40
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[
Biphenotypic
acute leukaemia
with Burkitt-like cytology].
[Transliterated title]
Leucémie aiguë biphénotypique avec aspect cytologique
de
type Burkitt.
Biphenotypic
acute leukaemia
(BAL) represents about 5% of adult
acute leukaemia
.
Based on a previously described scoring system, the European Group for Immunologic Classification of
Leukaemia
(EGIL) proposed a set of diagnostic criteria for BAL.
This scoring system is based on the number and degree of the specificity of several markers for
myeloid
or T/
B lymphoid
blasts.
Here, we report the case of a BAL with Burkitt-like cytology, corresponding to "the
acute
lymphoblastic
leukaemia
, Burkitt type" L3 for the FAB classification.
By flow cytometry, the blasts showed a positivity for
B lymphoid
cytoplasmic (CD79a and mu) and membrane (CD19, CD22, CD24, IgM) markers
AND a
positivity for the
myeloid
(CD13, CD33, CD65, CD15) markers.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ genetics
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 = 19654084.001).
[ISSN]
0003-3898
[Journal-full-title]
Annales de biologie clinique
[ISO-abbreviation]
Ann. Biol. Clin. (Paris)
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
9.
Murase K, Iyama S, Sato T, Takimoto R, Kobune M, Kato J:
[Therapeutic results in patients with biphenotypic acute leukemia at Sapporo Medical University Hospital].
Gan To Kagaku Ryoho
; 2010 Oct;37(10):2011-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Therapeutic results in patients with
biphenotypic
acute
leukemia
at Sapporo Medical University Hospital].
We reviewed the results of 6 patients with
biphenotypic
acute
leukemia
(BAL) which the diagnostic standard of the European Group for the Immunological Characterization of
Leukemia
(EGIL) at Sapporo Medical University Hospital between 2006 and 2008.
Among them, 4 were
B lymphoid and myeloid
, 2 were
T lymphoid and myeloid
, and one was T/
B lymphoid
.
Two of 4 patients did not attain complete remission, and two relapsed after first treatment with
acute
myeloblastic
leukemia
(AML) protocol.
On the other hand, two showed complete remission after the
acute
lymphoblastic leukemia
(ALL) protocol.
One of 4 patients survived who had been treated with hematopoietic stem
cell
transplantation as a post-remission therapy.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20948276.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
10.
Thavaraj V, Seth R:
Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate.
World J Pediatr
; 2008 May;4(2):145-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Prophylaxis of central nervous system
leukemia
: a case of chronic
myeloid leukemia
with
lymphoid
blast crisis treated with imatinib mesylate.
BACKGROUND: Chronic
myeloid leukemia
(CML) in blast crisis has a dismal prognosis.
METHODS: A child with CML in
lymphoid
blast crisis was diagnosed by complete hematological and bone marrow examination.
There was no central nervous system (CNS)
leukemia
at presentation.
Results of cerebrospinal fluid taken for cytopathology showed CNS
leukemia
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / prevention & control. Piperazines / administration & dosage. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Pyrimidines / administration & dosage
[MeSH-minor]
Anti-Inflammatory Agents / administration & dosage. Benzamides. Blood
Cell
Count. Chemoprevention / methods. Child. Clinical Protocols. Cytarabine / administration & dosage. Drug Therapy, Combination. Female. Humans. Hydrocortisone / administration & dosage. Imatinib Mesylate. Injections, Spinal. Methotrexate / therapeutic use. Remission Induction
Genetic Alliance.
consumer health - Chronic Myeloid Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
Hazardous Substances Data Bank.
HYDROCORTISONE
.
Hazardous Substances Data Bank.
METHOTREXATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Clin Cancer Res. 2003 Oct 15;9(13):4674-81
[
14581336.001
]
[Cites]
Blood. 1983 Jan;61(1):85-91
[
6571717.001
]
[Cites]
Ann Hematol. 2004 Jun;83(6):401-2
[
14673623.001
]
[Cites]
Am J Med. 1993 Jan;94(1):69-74
[
8420302.001
]
[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]
Blood. 2004 Nov 1;104(9):2655-60
[
15231574.001
]
[Cites]
FDA Consum. 2001 Jul-Aug;35(4):6
[
11692893.001
]
[Cites]
N Engl J Med. 2002 Feb 28;346(9):645-52
[
11870241.001
]
[Cites]
N Engl J Med. 1983 Oct 6;309(14):826-31
[
6412140.001
]
(PMID = 18661773.001).
[ISSN]
1708-8569
[Journal-full-title]
World journal of pediatrics : WJP
[ISO-abbreviation]
World J Pediatr
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
11.
Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX:
[Expression of PTEN mRNA in acute leukemia and its clinical significance].
Zhonghua Xue Ye Xue Za Zhi
; 2005 Aug;26(8):493-6
[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]
[Expression of PTEN mRNA in
acute
leukemia and
its clinical significance].
OBJECTIVE: To explore PTEN gene expression and its clinical significance in
acute
leukemia
.
METHODS: The expression levels of PTEN mRNA in 5
leukemia cell
lines, 87 patients with
acute
leukemias
(AL), including 59
acute
myeloid leukemia
(AML), 26
acute
lymphoblastic leukemia
(ALL), and 2
acute
hybrid leukemia
, 21 AL in complete remission (AL-CR), 31 chronic myelogenous
leukemia
(CML) and 14 normal controls were assayed by RT-PCR.
RESULTS: PTEN mRNA was detected in K562
cell
line, but not in Kasumi-1, HL-60, U937, Nalm-6
cell
lines.
The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood
cell
count of > or = 20 x 10(9)/L and chromosome
abnormality
).
[MeSH-major]
Leukemia
/ metabolism. PTEN Phosphohydrolase / metabolism
[MeSH-minor]
Cell
Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction
MedlinePlus Health Information.
consumer health - Leukemia
.
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 = 16383243.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
12.
Ara AI, Xia M, Ramani K, Mato JM, Lu SC:
S-adenosylmethionine inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation.
Hepatology
; 2008 May;47(5):1655-66
[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 previously showed that S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFalpha) expression in RAW (murine macrophage
cell
line) and Kupffer cells at the transcriptional level without affecting nuclear factor kappa B nuclear binding.
LPS increased the binding of histone methyltransferases Set1
and myeloid
/
lymphoid leukemia
to these promoters, which was unaffected by SAMe or MTA.
Exogenous SAMe is unstable and converts spontaneously to MTA, which is stable
and cell
-permeant.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Annu Rev Med. 1994;45:491-503
[
8198398.001
]
[Cites]
J Immunol. 1991 Sep 1;147(5):1694-700
[
1715367.001
]
[Cites]
Immunology. 1996 Dec;89(4):558-62
[
9014821.001
]
[Cites]
Biochem Biophys Res Commun. 1997 Jul 30;236(3):655-60
[
9245708.001
]
[Cites]
Am J Physiol. 1999 May;276(5 Pt 1):G1069-73
[
10329995.001
]
[Cites]
J Hepatol. 1999 Jun;30(6):1081-9
[
10406187.001
]
[Cites]
Biochem J. 1999 Aug 15;342 ( Pt 1):21-5
[
10432295.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8
[
15941828.001
]
[Cites]
J Biol Chem. 2005 Jul 1;280(26):24824-38
[
15870070.001
]
[Cites]
J Biol Chem. 2006 Jun 23;281(25):17180-8
[
16613853.001
]
[Cites]
Biochem J. 2007 Jan 1;401(1):87-96
[
16953798.001
]
[Cites]
Cell. 2007 Mar 9;128(5):889-900
[
17320163.001
]
[Cites]
Cell. 2007 Mar 23;128(6):1077-88
[
17320160.001
]
[Cites]
Hepatology. 2007 May;45(5):1306-12
[
17464973.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10835-40
[
17578910.001
]
[Cites]
Cell. 2007 Jul 13;130(1):77-88
[
17632057.001
]
[Cites]
Gastroenterology. 2007 Jul;133(1):207-18
[
17631143.001
]
[Cites]
Nature. 2001 Mar 1;410(6824):116-20
[
11242053.001
]
[Cites]
Science. 2001 Aug 10;293(5532):1074-80
[
11498575.001
]
[Cites]
Mol Cell Biol. 2001 Oct;21(20):7065-77
[
11564889.001
]
[Cites]
J Hepatol. 2001 Dec;35(6):692-9
[
11738094.001
]
[Cites]
Mol Cell. 2001 Dec;8(6):1207-17
[
11779497.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G256-65
[
12121871.001
]
[Cites]
J Clin Invest. 2002 Sep;110(5):643-50
[
12208865.001
]
[Cites]
Nature. 2002 Sep 26;419(6905):407-11
[
12353038.001
]
[Cites]
Mol Cell Biol. 2003 Jan;23(2):526-33
[
12509451.001
]
[Cites]
Nat Neurosci. 2004 Mar;7(3):229-35
[
14770186.001
]
[Cites]
Hepatology. 2004 Apr;39(4):1088-98
[
15057913.001
]
[Cites]
Cell. 2004 Jun 11;117(6):721-33
[
15186774.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2004 Aug;287(2):G352-62
[
15064230.001
]
[Cites]
J Virol. 2004 Nov;78(22):12308-19
[
15507618.001
]
[Cites]
Biochem Biophys Res Commun. 1981 May 29;100(2):523-31
[
6791639.001
]
[Cites]
Nucleic Acids Res. 1983 Mar 11;11(5):1475-89
[
6828386.001
]
[Cites]
J Exp Med. 1990 Jan 1;171(1):35-47
[
2104921.001
]
[Cites]
Mol Cell Biol. 1990 Apr;10(4):1498-506
[
2181276.001
]
[Cites]
Cell. 1995 May 19;81(4):641-50
[
7538909.001
]
(PMID = 18393372.001).
[ISSN]
1527-3350
[Journal-full-title]
Hepatology (Baltimore, Md.)
[ISO-abbreviation]
Hepatology
[Language]
ENG
[Grant]
United States / NIAAA NIH HHS / AA / T32 AA007578; None / None / / R01 AT001576-05; United States / NCCIH NIH HHS / AT / R01 AT001576-05; United States / NIAAA NIH HHS / AA / AA007578-07; United States / NIAAA NIH HHS / AA / AA12677; United States / NIDDK NIH HHS / DK / R01 DK051719-11; United States / NCCIH NIH HHS / AT / R01 AT001576; United States / NIDDK NIH HHS / DK / DK048522-139003; United States / NIDDK NIH HHS / DK / R01 DK051719; United States / NIAAA NIH HHS / AA / T32 AA07578; United States / NCCIH NIH HHS / AT / AT1576; United States / NIAAA NIH HHS / AA / T32 AA007578-07; United States / NIDDK NIH HHS / DK / DK48522; United States / NIAAA NIH HHS / AA / R01 AA013847; United States / NIAAA NIH HHS / AA / R01 AA012677; United States / NIDDK NIH HHS / DK / DK051719-11; United States / NIAAA NIH HHS / AA / R01 AA012677-05; United States / NIDDK NIH HHS / DK / DK51719; United States / NIAAA NIH HHS / AA / R01 AA013847-05; United States / NIDDK NIH HHS / DK / P30 DK048522; United States / NIAAA NIH HHS / AA / AA13847; United States / NIDDK NIH HHS / DK / P30 DK048522-139003; United States / NIAAA NIH HHS / AA / AA012677-05; United States / NIAAA NIH HHS / AA / AA013847-05
[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 / Chromatin; 0 / DNA Primers; 0 / Histones; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine
[Other-IDs]
NLM/ NIHMS49821; NLM/ PMC2408693
13.
Mohan AV, Ramnath VR, Patalas E, Attar EC:
Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report.
Cases J
; 2009;2:8217
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Non-specific interstitial pneumonia as the initial presentation of
biphenotypic
acute
leukemia
: a case report.
We present a 46-year-old woman with recent-onset rheumatologic illness who developed pulmonary symptoms as the presenting feature of
biphenotypic
acute leukaemia
.
Corticosteroid therapy resulted in resolution of both her pulmonary and rheumatologic symptoms, and her pulmonary symptoms did not recur following treatment of her
leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Leuk Lymphoma. 2002 Nov;43(11):2083-92
[
12533032.001
]
[Cites]
J Am Acad Dermatol. 2001 Mar;44(3):530-1
[
11209130.001
]
[Cites]
Am J Respir Crit Care Med. 2008 Jun 15;177(12):1338-47
[
18388353.001
]
[Cites]
Crit Rev Oncol Hematol. 2007 Aug;63(2):100-10
[
17391977.001
]
[Cites]
Intern Med. 2004 Aug;43(8):721-6
[
15468974.001
]
[Cites]
Semin Respir Crit Care Med. 2006 Dec;27(6):652-8
[
17195141.001
]
[Cites]
Respiration. 2005 Jan-Feb;72(1):39-45
[
15753633.001
]
[Cites]
Haematologica. 1997 Jan-Feb;82(1):64-6
[
9107085.001
]
[Cites]
Br J Haematol. 2007 Jul;138(2):213-6
[
17593028.001
]
(PMID = 19918465.001).
[ISSN]
1757-1626
[Journal-full-title]
Cases journal
[ISO-abbreviation]
Cases J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2769415
14.
Choi HW, Shin MG, Kim HJ, Lee IK, Yun JH, Kim HR, Kim YK, Yun HK, Cho D, Kee SJ, Shin JH, Suh SP, Ryang DW:
[Biphenotypic Acute Leukemia with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.].
Korean J Lab Med
; 2006 Aug;26(4):249-54
[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]
[
Biphenotypic
Acute
Leukemia
with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.].
Biphenotypic
acute
leukemia
(BAL) is a subtype of
leukemia
of ambiguous
lineage
in the World Health Organization classification system.
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 = 18156734.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
15.
Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN:
Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.
Cytometry B Clin Cytom
; 2009 May;76(3):199-205
[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]
Immunophenotypic profile of
acute
leukemia
: critical analysis and insights gained at a tertiary care center in India.
BACKGROUND: To analyze the spectrum of various types and subtypes of
acute
leukemia
.
METHODS: Two thousand five hundred and eleven consecutive new referral cases of
acute
leukemia
(AL) were evaluated based on WHO classification.
RESULTS: It included 1,471 cases (58%) of
acute
lymphoblastic leukemia
(ALL), 964 cases (38%) of
acute
myeloid leukemia
(AML), 45 cases (1.8%) of chronic myelogenous
leukemia
in blast crisis (CMLBC), 37 cases (1.5%) of
biphenotypic
acute
leukemia
(BAL), 1 case of Triphenotypic AL, and 2 cases of
acute
undifferentiated
leukemia
(AUL).
Common subtypes of ALL were B-
cell
ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).
T-
cell
ALL constituted 24% (351 cases) of ALL.
CMLBC was commonly of
myeloid
blast crisis subtype (40 cases).
CONCLUSION: B-
cell
ALL was the commonest subtype in children and AML in adults.
CD13 was most sensitive and CD117 most specific for determining
myeloid
lineage
.
A minimal primary panel of nine antibodies consisting of three
myeloid
markers (CD13, CD33, and CD117), B-
cell lymphoid
marker (CD19), T-
cell
marker (CD7), with CD45, CD10, CD34, and HLADR could assign
lineage
to 92% of AL.
Cytogenetics findings lead to a change in the diagnostic subtype of
myeloid
malignancy in 38 (1.5%) cases.
[MeSH-major]
Immunophenotyping.
Leukemia
/ immunology.
Leukemia
/ pathology
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
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
[Copyright]
(c) 2008 Clinical Cytometry Society.
(PMID = 18803279.001).
[ISSN]
1552-4957
[Journal-full-title]
Cytometry. Part B, Clinical cytometry
[ISO-abbreviation]
Cytometry B Clin Cytom
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
16.
Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX:
[Study on the clinical characteristics of adult biphenotypic acute leukaemia].
Zhonghua Xue Ye Xue Za Zhi
; 2009 Jan;30(1):18-21
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Study on the clinical characteristics of adult
biphenotypic
acute leukaemia
].
OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult
biphenotypic
acute leukaemia
(BAL).
The chemotherapy regimens were accordingly for
acute
lymphoblastic
leukaemia
(ALL),
acute
myeloid
leukaemia
(AML) or for both ALL and AML.
(1) The incidence of BAL in
acute
leukaemias
was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of
myeloid and B lymphoid
antigens were 81.5%, of
myeloid and T lymphoid
antigens 10.8%, of
myeloid
, B-
and T lymphoid
antigens 4.6%, and of
B and T lymphoid
antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.
(1) High white blood
cell
count and coexpression of
myeloid
/
B lymphoid
antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19563029.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
17.
Kakihana K, Ohashi K, Sakai F, Kamata N, Hosomi Y, Nishiwaki M, Yokoyama R, Kobayashi T, Yamashita T, Akiyama H, Sakamaki H:
Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation.
Int J Hematol
; 2009 Jan;89(1):118-22
[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]
Leukemic infiltration of the lung following allogeneic hematopoietic stem
cell
transplantation.
Pulmonary leukemic infiltration (PLI) is more common than generally recognized, but accurate antemortem
diagnosis
with pathological proof is rarely achieved.
We describe herein the clinical courses of two patients with PLI following hematopoietic stem
cell
transplantation (HSCT).
One case is a male patient with
acute
biphenotypic leukemia
, and the other is a female patient with myelodysplastic syndrome.
Moreover, the former case presented PLI as the initial manifestation of relapsed
leukemia and
the latter was accompanied with the fungal pneumonia.
High-resolution computed tomography (HRCT) of the chest at onset of PLI showed diffuse small nodular lesions along peribronchovascular bundle,
and diagnosis
of leukemic infiltration was made based on pathological findings obtained from transbronchial lung biopsy.
Thus, radiological and pathological corroborating assessment was important to reach the correct
diagnosis
.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation / adverse effects. Leukemic Infiltration /
diagnosis
. Lung Neoplasms / etiology
[MeSH-minor]
Adult. Female. Humans.
Leukemia
/ pathology. Lung / pathology. Male. Middle Aged. Myelodysplastic Syndromes /
diagnosis
. Myelodysplastic Syndromes / etiology. Opportunistic Infections. Transplantation, Homologous
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Haematol. 1998 Mar;100(4):680-7
[
9531334.001
]
[Cites]
Chest. 1990 Mar;97(3):674-8
[
2407452.001
]
[Cites]
Br J Haematol. 2003 Mar;120(6):1058-61
[
12648078.001
]
[Cites]
Bone Marrow Transplant. 1994;14 Suppl 4:S19-28
[
7728120.001
]
[Cites]
AJR Am J Roentgenol. 2000 Feb;174(2):517-21
[
10658733.001
]
[Cites]
Radiat Med. 2003 Jan-Feb;21(1):7-15
[
12801138.001
]
[Cites]
Clin Chest Med. 1990 Jun;11(2):323-32
[
2189666.001
]
[Cites]
Bone Marrow Transplant. 2001 Sep;28(5):425-34
[
11593314.001
]
[Cites]
Eur Radiol. 2002 Jan;12 (1):166-74
[
11868094.001
]
[Cites]
Semin Respir Crit Care Med. 2005 Oct;26(5):514-9
[
16267702.001
]
[Cites]
Bone Marrow Transplant. 2000 Jun;25(12):1263-8
[
10871731.001
]
[Cites]
Annu Rev Med. 1992;43:425-35
[
1580600.001
]
[Cites]
Bone Marrow Transplant. 2007 Sep;40(5):465-72
[
17618318.001
]
[Cites]
Chest. 1990 Nov;98(5):1233-9
[
2225971.001
]
[Cites]
Chest. 1996 Apr;109(4):1066-77
[
8635332.001
]
(PMID = 19093164.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
18.
Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY:
Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.
Haematologica
; 2009 Jul;94(7):919-27
[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]
Clinical and biological characteristics of adult
biphenotypic
acute
leukemia
in comparison with that of
acute
myeloid leukemia
and
acute
lymphoblastic leukemia
: a case series of a Chinese population.
BACKGROUND:
Biphenotypic
acute
leukemia
is a rare
disorder
that is difficult to diagnose.
It displays features of both
myeloid and lymphoid
lineage
.
There is still a lack of studies in
biphenotypic
acute
leukemia
in a Chinese population.
We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of
biphenotypic
acute
leukemia
in our hospital in over a seven year period.
DESIGN AND METHODS: We retrospectively analyzed 452 adult
acute
leukemia
patients diagnosed according to French-American-British (FAB) classification
and biphenotypic
acute
leukemia
diagnosed according to European Group for the Immunological Characterization of
Leukemias
(EGIL) classification, respectively.
Biological characteristics, response to treatment, and outcome were examined in
biphenotypic
acute
leukemia
patients and compared with that in
acute
myeloid leukemia
and
acute
lymphoblastic leukemia
patients with complete follow-up profiles diagnosed in the same period.
RESULTS: Of 452
acute
leukemia
patients, 21 cases (4.6%) were diagnosed as
biphenotypic
acute
leukemia
.
Among them, 14 (66.7%) were
B lymphoid and myeloid
, 5 (23.8%) were
T lymphoid and myeloid
, one (4.8%) was T/
B lymphoid
and one (4.8%) was trilineage differentiation.
When compared with
acute
myeloid leukemia
and
acute
lymphoblastic leukemia
, patients with
biphenotypic
acute
leukemia
showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).
In this cohort of patients with
biphenotypic
acute
leukemia
, t(9;22) was the most common
abnormality
in chromosome structure.
The median
disease
-free survival and overall survival in
biphenotypic
acute
leukemia
patients was five months and ten months, respectively, significantly shorter than those in
acute
myeloid leukemia
and
acute
lymphoblastic leukemia
patients (p<0.05).
CONCLUSIONS: The prognosis of
biphenotypic
acute
leukemia
patients is poor when compared with
de
novo
acute
myeloid leukemia
or
acute
lymphoblastic leukemia
.
Biphenotypic
acute
leukemia
patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma /
diagnosis
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Adult
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
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. 2000 Jun 20;97(13):7521-6
[
10861016.001
]
[Cites]
Zhonghua Xue Ye Xue Za Zhi. 2000 Jul;21(7):352-4
[
11877003.001
]
[Cites]
Nature. 2008 Apr 10;452(7188):768-72
[
18401412.001
]
[Cites]
Nat Rev Immunol. 2002 Feb;2(2):127-32
[
11910894.001
]
[Cites]
Blood. 2002 Sep 15;100(6):1965-71
[
12200353.001
]
[Cites]
Zhonghua Zhong Liu Za Zhi. 2002 Jul;24(4):375-7
[
12408768.001
]
[Cites]
Ann Intern Med. 1985 Oct;103(4):620-5
[
3862359.001
]
[Cites]
Blood. 1990 Aug 15;76(4):808-13
[
2166608.001
]
[Cites]
Ann Hematol. 1991 Feb;62(1):16-21
[
2031964.001
]
[Cites]
N Engl J Med. 1993 Sep 23;329(13):909-14
[
8361504.001
]
[Cites]
Leukemia. 1995 Oct;9(10):1783-6
[
7564526.001
]
[Cites]
Leukemia. 1996 Aug;10(8):1283-7
[
8709632.001
]
[Cites]
Haematologica. 1997 Jan-Feb;82(1):64-6
[
9107085.001
]
[Cites]
Blood. 1997 Oct 15;90(8):2863-92
[
9376567.001
]
[Cites]
Br J Haematol. 1998 Jan;100(1):147-55
[
9450804.001
]
[Cites]
Haematologica. 1999 Aug;84(8):699-706
[
10457405.001
]
[Cites]
Am J Hematol. 2005 Mar;78(3):173-80
[
15726601.001
]
[Cites]
Leukemia. 2006 Apr;20(4):620-6
[
16437134.001
]
[Cites]
Br J Haematol. 2007 Jul;138(2):213-6
[
17593028.001
]
[Cites]
Leukemia. 2007 Nov;21(11):2264-70
[
17611554.001
]
[Cites]
Int J Hematol. 2008 Mar;87(2):132-6
[
18288568.001
]
[Cites]
Leuk Lymphoma. 2008 Apr;49(4):700-9
[
18398737.001
]
[Cites]
Nature. 2008 Apr 10;452(7188):764-7
[
18401411.001
]
[CommentIn]
Haematologica. 2009 Dec;94(12):1778-80; author reply 1780
[
19996120.001
]
[CommentIn]
Haematologica. 2009 Jul;94(7):891-3
[
19570749.001
]
(PMID = 19454497.001).
[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 / Antigens, CD34
[Other-IDs]
NLM/ PMC2704302
19.
Carretta A, Ciriaco P, Melloni G, Bandiera A, Libretti L, Puglisi A, Giovanardi M, Zannini P:
Surgical treatment of multiple primary adenocarcinomas of the lung.
Thorac Cardiovasc Surg
; 2009 Feb;57(1):30-4
[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.
The aim of this study was to assess the results of surgical treatment of multiple primary adenocarcinomas of the lung (
MPAL
) analyzing the radiological and histological features.
METHODS: From 1988 to 2005, 26 patients underwent surgical treatment for
MPAL
at our department, for a total of 52 tumors.
RESULTS: Thirty-seven tumors were classified as solid, two as ground-glass opacities (GGO) and 13 as
mixed
solid/GGO tumors on the basis of CT scan evaluation.
CONCLUSIONS: Surgical treatment of
MPAL
is associated with favorable results.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19169994.001).
[ISSN]
0171-6425
[Journal-full-title]
The Thoracic and cardiovascular surgeon
[ISO-abbreviation]
Thorac Cardiovasc Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
20.
Daser A, Rabbitts TH:
The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis.
Semin Cancer Biol
; 2005 Jun;15(3):175-88
[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 versatile
mixed lineage leukaemia
gene MLL and its many associations in leukaemogenesis.
The marked association of abnormalities of chromosome 11 long arm, band q23, with human
leukaemia
led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1).
MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual
leukaemias
, leading to either
acute
myeloid
or
lymphoid
tumours (hence the name MLL for
mixed lineage leukaemia
).
The unusual
finding
that a single protein could be involved in both
myeloid and lymphoid
malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis.
[MeSH-major]
Cell
Transformation, Neoplastic / metabolism.
Cell
Transformation, Neoplastic / pathology.
Leukemia
/ metabolism.
Leukemia
/ pathology.
Myeloid
-
Lymphoid Leukemia
Protein / metabolism
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
(PMID = 15826832.001).
[ISSN]
1044-579X
[Journal-full-title]
Seminars in cancer biology
[ISO-abbreviation]
Semin. Cancer Biol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Number-of-references]
123
21.
Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY:
[Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].
Nan Fang Yi Ke Da Xue Xue Bao
; 2009 Mar;29(3):512-5
[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]
[Clinical characteristics and outcomes of 59 patients with
acute
lymphoblastic leukemia
positive for BCR/ABL].
OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive
acute
lymphoblastic leukemia
(BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.
METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the
diagnosis
of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.
The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem
cell
transplantation (allo-HSCT) (16 cases).
In patients with peripheral white blood
cell
(WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).
According to the FAB classification, 56 cases were divided into L1, L2
and biphenotypic
acute
leukemia
(BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).
In terms of immunophenotype grouping by EGIL, the patients with ALL,
myeloid
antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).
In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22)
abnormality
, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem
Cell
Transplantation. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
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 = 19304540.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
22.
Gozzetti A, Calabrese S, Raspadori D, Crupi R, Tassi M, Bocchia M, Fabbri A, Lauria F:
Concomitant t(4;11) and t(1;19) in a patient with biphenotypic acute leukemia.
Cancer Genet Cytogenet
; 2007 Aug;177(1):81-2
[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]
Concomitant t(4;11)
and t
(1;19) in a patient with
biphenotypic
acute
leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Banding. Fatal Outcome. Humans. Karyotyping. Male. Middle Aged.
Phenotype
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
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 = 17693199.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
23.
Cano F, Drynan LF, Pannell R, Rabbitts TH:
Leukaemia lineage specification caused by cell-specific Mll-Enl translocations.
Oncogene
; 2008 Mar 20;27(13):1945-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Leukaemia lineage
specification caused by
cell
-specific Mll-Enl translocations.
Chromosomal translocations involving the
Mixed
-
Lineage Leukaemia
(MLL) gene underlie many human
leukaemias and
MLL rearrangements are found in both
acute
myelogenous and
acute
lymphoblastic leukaemias
.
To assess the functionally relevant haematopoietic
cell
contexts for MLL fusions to be tumorigenic, we have generated different lines of mice in which
de
novo Mll-associated translocations occur.
Translocations between Mll and Enl cause
myeloid
neoplasias, initiating in stem cells or progenitors while no tumours arose when the translocation was restricted to the B-
cell
compartment.
Despite the absence of tumorigenesis, Mll-Enl translocations did occur and Mll-Enl fusion mRNA was expressed in B-
cell
-restricted translocators.
[MeSH-major]
B-Lymphocytes / pathology.
Cell
Lineage
.
Leukemia
/ genetics.
Myeloid
-
Lymphoid Leukemia
Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. T-Lymphocytes / pathology. Translocation, Genetic
[MeSH-minor]
Animals. Antigens, CD19 / genetics. Antigens, CD19 / physiology. Cells, Cultured. Histone-Lysine N-Methyltransferase. Integrases / metabolism. Mice.
Myeloid
Progenitor Cells / cytology.
Myeloid
Progenitor Cells / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / physiology.
Phenotype
. Recombination, Genetic. Stem Cells / cytology. Stem Cells / metabolism
MedlinePlus Health Information.
consumer health - Leukemia
.
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 = 17906700.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0600914; United Kingdom / Medical Research Council / / MC/ U105178807; United Kingdom / Medical Research Council / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD19; 0 / Mllt3 protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
24.
Schwartz CM, Cheng A, Mughal MR, Mattson MP, Yao PJ:
Clathrin assembly proteins AP180 and CALM in the embryonic rat brain.
J Comp Neurol
; 2010 Sep 15;518(18):3803-18
[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.
In this study, we focus on two closely related clathrin assembly proteins, AP180 and CALM (clathrin assembly
lymphoid myeloid leukemia
protein), in the developing embryonic rat brain.
[MeSH-minor]
Animals.
Cell
Line. Clathrin / metabolism. Clathrin-Coated Vesicles / metabolism. Female. Neurons / cytology. Neurons / metabolism. Pregnancy. Rats. Stem Cells / cytology. Stem Cells / metabolism
COS Scholar Universe.
author profiles
.
SciCrunch.
The Antibody Registry: Reagent: Antibodies
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Neurosci. 2008 Oct 8;28(41):10257-71
[
18842885.001
]
[Cites]
J Neurosci. 2009 Jun 10;29(23):7404-12
[
19515908.001
]
[Cites]
J Neurosci. 1995 Nov;15(11):7238-49
[
7472478.001
]
[Cites]
Genes Dev. 1995 Nov 1;9(21):2635-45
[
7590241.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 May 14;93(10):4804-9
[
8643484.001
]
[Cites]
J Biol Chem. 1997 Mar 7;272(10):6393-8
[
9045662.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13305-10
[
9371841.001
]
[Cites]
Science. 1998 Nov 6;282(5391):1145-7
[
9804556.001
]
[Cites]
Neuron. 1998 Dec;21(6):1465-75
[
9883738.001
]
[Cites]
Protein Sci. 1999 Feb;8(2):435-8
[
10048338.001
]
[Cites]
Mol Biol Cell. 1999 Jul;10(7):2343-60
[
10397769.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):8907-12
[
10430869.001
]
[Cites]
Mol Biol Cell. 1999 Aug;10(8):2687-702
[
10436022.001
]
[Cites]
J Comp Neurol. 2005 Jan 3;481(1):58-69
[
15558718.001
]
[Cites]
Dev Biol. 2005 Jun 15;282(2):467-79
[
15950611.001
]
[Cites]
Eur J Neurosci. 2005 Oct;22(8):1928-41
[
16262632.001
]
[Cites]
Traffic. 2005 Dec;6(12):1225-34
[
16262731.001
]
[Cites]
Stem Cells Dev. 2005 Oct;14(5):517-34
[
16305337.001
]
[Cites]
J Comp Neurol. 2006 Jan 10;494(2):368-79
[
16320245.001
]
[Cites]
Stem Cells. 2006 Apr;24(4):865-75
[
16357341.001
]
[Cites]
Neuroscience. 2006 Jul 7;140(3):1003-10
[
16600520.001
]
[Cites]
Curr Opin Cell Biol. 2006 Aug;18(4):416-21
[
16806881.001
]
[Cites]
Curr Opin Cell Biol. 2006 Aug;18(4):395-406
[
16806884.001
]
[Cites]
Nat Neurosci. 2009 Jun;12(6):735-44
[
19448628.001
]
[Cites]
J Comp Neurol. 2007 Jan 1;500(1):20-46
[
17099894.001
]
[Cites]
J Comp Neurol. 2007 Jun 10;502(5):673-82
[
17436285.001
]
[Cites]
J Comp Neurol. 2007 Sep 20;504(3):314-27
[
17640037.001
]
[Cites]
Neuron. 2003 Aug 28;39(5):749-65
[
12948443.001
]
[Cites]
Annu Rev Neurosci. 2003;26:701-28
[
14527272.001
]
[Cites]
Trends Cell Biol. 2004 Apr;14(4):167-74
[
15066634.001
]
[Cites]
J Biol Chem. 2004 Oct 29;279(44):46191-203
[
15292237.001
]
[Cites]
J Comp Neurol. 1981 Jun 1;198(4):677-716
[
7251936.001
]
[Cites]
Differentiation. 1983;25(2):193-203
[
6198232.001
]
[Cites]
J Neurosci. 1999 Dec 1;19(23):10201-12
[
10575017.001
]
[Cites]
Biotechniques. 2000 Feb;28(2):216-8
[
10683726.001
]
[Cites]
J Biol Chem. 2000 Mar 3;275(9):6479-89
[
10692452.001
]
[Cites]
Science. 2001 Feb 9;291(5506):1051-5
[
11161218.001
]
[Cites]
Cell. 2001 Feb 9;104(3):433-40
[
11239400.001
]
[Cites]
Science. 2002 Apr 19;296(5567):550-3
[
11910072.001
]
[Cites]
J Comp Neurol. 2002 May 27;447(2):152-62
[
11977118.001
]
[Cites]
Traffic. 2002 Aug;3(8):513-20
[
12121414.001
]
[Cites]
Neuromolecular Med. 2002;2(2):101-14
[
12428806.001
]
[Cites]
Cancer Res. 2003 May 1;63(9):2244-50
[
12727846.001
]
[Cites]
Cell. 2003 May 30;113(5):643-55
[
12787505.001
]
[Cites]
EMBO J. 2003 Jul 1;22(13):3254-66
[
12839988.001
]
[Cites]
Neuroscience. 2003;121(1):25-37
[
12946697.001
]
[Cites]
EMBO J. 1983;2(12):2355-61
[
6141938.001
]
[Cites]
Eur J Cell Biol. 1984 May;34(1):137-43
[
6428888.001
]
[Cites]
J Immunol. 1984 Oct;133(4):1710-5
[
6206131.001
]
[Cites]
Neurochem Pathol. 1985 Summer;3(2):119-38
[
2413405.001
]
[Cites]
J Neuropathol Exp Neurol. 1986 Nov;45(6):692-703
[
3534145.001
]
[Cites]
EMBO J. 1986 Dec 1;5(12):3143-9
[
3816757.001
]
[Cites]
Cell Motil Cytoskeleton. 1988;10(3):349-62
[
2460261.001
]
[Cites]
J Neurosci. 1989 Apr;9(4):1223-32
[
2564886.001
]
[Cites]
J Biol Chem. 1991 Mar 5;266(7):4401-8
[
1999423.001
]
[Cites]
J Neurosci. 1992 Jun;12(6):2130-43
[
1607932.001
]
[Cites]
Development. 1992 Sep;116(1):201-11
[
1483388.001
]
[Cites]
Mol Endocrinol. 1992 Dec;6(12):2129-35
[
1491694.001
]
[Cites]
EMBO J. 1993 Feb;12(2):667-75
[
8440257.001
]
[Cites]
J Biol Chem. 1993 Jun 15;268(17):12655-62
[
7685348.001
]
[Cites]
J Neurosci. 1994 Sep;14(9):5399-416
[
8083744.001
]
[Cites]
Nature. 2007 Aug 23;448(7156):883-8
[
17713526.001
]
[Cites]
Curr Opin Cell Biol. 2007 Aug;19(4):417-25
[
17631994.001
]
[Cites]
J Comp Neurol. 2008 Jan 1;506(1):16-29
[
17990269.001
]
[Cites]
Traffic. 2008 Mar;9(3):417-29
[
18182011.001
]
[Cites]
Stem Cells. 2008 Feb;26(2):412-21
[
18024420.001
]
(PMID = 20653035.001).
[ISSN]
1096-9861
[Journal-full-title]
The Journal of comparative neurology
[ISO-abbreviation]
J. Comp. Neurol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z99 AG999999
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Clathrin; 0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180
[Other-IDs]
NLM/ NIHMS215726; NLM/ PMC2909614
25.
Nishiuchi T, Ohnishi H, Kamada R, Kikuchi F, Shintani T, Waki F, Kitanaka A, Kubota Y, Tanaka T, Ishida T:
Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement.
Intern Med
; 2009;48(16):1437-41
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Acute
leukemia
of ambiguous
lineage
, biphenotype, without CD34, TdT or TCR-rearrangement.
Biphenotypic
acute
leukemia
(BAL) is a rare entity that comprises 0.5-3% of all
acute
leukemias and
probably arises from multipotent progenitor cells.
We report the case of a 41-year-old man with BAL having
myeloid and
T-
lymphoid
lineage
phenotypes.
This pattern is rarely encountered and suggests that the blast cells were possibly considered immature with aspects of differentiation indicating
myeloid
lineage
, rather than T-
lymphoid
lineage
.
[MeSH-major]
Antigens, CD34 / genetics.
Cell
Lineage
/ genetics. DNA Nucleotidylexotransferase / genetics. Gene Rearrangement / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Receptors, Antigen, T-
Cell
. Receptors, Antigen, T-
Cell
, alpha-beta / genetics. Receptors, Antigen, T-
Cell
, gamma-delta / genetics
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19687594.001).
[ISSN]
1349-7235
[Journal-full-title]
Internal medicine (Tokyo, Japan)
[ISO-abbreviation]
Intern. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.7.31 / DNA Nucleotidylexotransferase
26.
Allen MD, Grummitt CG, Hilcenko C, Min SY, Tonkin LM, Johnson CM, Freund SM, Bycroft M, Warren AJ:
Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase.
EMBO J
; 2006 Oct 04;25(19):4503-12
[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]
Solution structure of the nonmethyl-CpG-binding CXXC domain of the
leukaemia
-associated MLL histone methyltransferase.
The
mixed
-
lineage leukaemia
(MLL) CXXC domain selectively binds nonmethyl-CpG DNA, and is required for transformation by MLL fusion proteins that commonly arise from recurrent chromosomal translocations in infant and secondary treatment-related
acute
leukaemias
.
These data provide a template for the design of specifically targeted therapeutics for poor prognosis MLL-associated
leukaemias
.
[MeSH-major]
CpG Islands / genetics. Histone-Lysine N-Methyltransferase / chemistry.
Leukemia
/ metabolism.
Myeloid
-
Lymphoid Leukemia
Protein / chemistry. Neoplasm Proteins / chemistry
MedlinePlus Health Information.
consumer health - Leukemia
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nat Genet. 1997 Jul;16(3):256-9
[
9207790.001
]
[Cites]
Oncogene. 1999 Dec 23;18(56):7975-84
[
10637508.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14967-72
[
10611321.001
]
[Cites]
Oncogene. 1998 Jun 25;16(25):3233-41
[
9681821.001
]
[Cites]
Genes Chromosomes Cancer. 2001 Feb;30(2):175-80
[
11135434.001
]
[Cites]
Leukemia. 2001 Apr;15(4):595-600
[
11368362.001
]
[Cites]
Science. 2001 Aug 10;293(5532):1150-5
[
11498594.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10037-41
[
11517324.001
]
[Cites]
J Biol Chem. 2001 Nov 30;276(48):44669-76
[
11572867.001
]
[Cites]
J Biomol NMR. 2001 Oct;21(2):127-39
[
11727976.001
]
[Cites]
Nucleic Acids Res. 2002 Feb 15;30(4):958-65
[
11842107.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1107-17
[
12453418.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1119-28
[
12453419.001
]
[Cites]
Nucleic Acids Res. 2003 Jan 15;31(2):532-50
[
12527760.001
]
[Cites]
Genes Chromosomes Cancer. 2003 Jul;37(3):326-31
[
12759932.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8342-7
[
12829790.001
]
[Cites]
Cancer Genet Cytogenet. 2003 Aug;145(1):74-7
[
12885467.001
]
[Cites]
Genes Dev. 2003 Sep 15;17(18):2298-307
[
12952893.001
]
[Cites]
EMBO J. 2003 Oct 1;22(19):4910-21
[
14517231.001
]
[Cites]
Mol Cell Biol. 2004 Jan;24(2):617-28
[
14701735.001
]
[Cites]
Bioinformatics. 2004 Feb 12;20(3):426-7
[
14960472.001
]
[Cites]
Blood. 2004 Mar 1;103(5):1823-8
[
14615372.001
]
[Cites]
Dev Cell. 2004 Mar;6(3):437-43
[
15030765.001
]
[Cites]
Mol Cell Biol. 2004 Apr;24(8):3387-95
[
15060159.001
]
[Cites]
Blood. 2004 Apr 15;103(8):3192-9
[
15070702.001
]
[Cites]
J Mol Biol. 2004 Oct 15;343(2):339-60
[
15451665.001
]
[Cites]
Biopolymers. 1983 Dec;22(12):2577-637
[
6667333.001
]
[Cites]
Biochemistry. 1989 Sep 19;28(19):7510-6
[
2692701.001
]
[Cites]
Cell. 1992 Nov 13;71(4):691-700
[
1423624.001
]
[Cites]
Cell. 1992 Nov 13;71(4):701-8
[
1423625.001
]
[Cites]
Nat Genet. 1992 Oct;2(2):113-8
[
1303259.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7884-8
[
7689231.001
]
[Cites]
N Engl J Med. 1993 Sep 23;329(13):909-14
[
8361504.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8538-42
[
8378328.001
]
[Cites]
Biochemistry. 1994 Mar 29;33(12):3515-31
[
8142349.001
]
[Cites]
Curr Opin Cell Biol. 1994 Jun;6(3):380-9
[
7917329.001
]
[Cites]
J Magn Reson B. 1995 Jul;108(1):94-8
[
7627436.001
]
[Cites]
Curr Opin Genet Dev. 1995 Jun;5(3):309-14
[
7549424.001
]
[Cites]
Nature. 1995 Nov 30;378(6556):505-8
[
7477409.001
]
[Cites]
Trends Biochem Sci. 1995 Nov;20(11):478-80
[
8578593.001
]
[Cites]
Cancer Res. 1996 May 1;56(9):2171-7
[
8616868.001
]
[Cites]
J Med Chem. 1997 Sep 26;40(20):3144-50
[
9379433.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10632-6
[
9724755.001
]
[Cites]
Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21
[
9757107.001
]
[Cites]
J Biomol NMR. 1999 Mar;13(3):289-302
[
10212987.001
]
[Cites]
Genomics. 1999 Jul 15;59(2):187-92
[
10409430.001
]
[Cites]
Mol Cell Biol. 2004 Dec;24(23):10470-8
[
15542854.001
]
[Cites]
Curr Biol. 2004 Nov 23;14(22):2063-9
[
15556871.001
]
[Cites]
EMBO J. 2005 Jan 26;24(2):368-81
[
15635450.001
]
[Cites]
Semin Cancer Biol. 2005 Jun;15(3):175-88
[
15826832.001
]
[Cites]
Cell. 2005 Oct 21;123(2):207-18
[
16239140.001
]
[Cites]
J Biol Chem. 2005 Dec 16;280(50):41725-31
[
16253997.001
]
[Cites]
Nature. 2006 Feb 16;439(7078):811-6
[
16362057.001
]
[Cites]
Blood. 1998 Jul 1;92(1):108-17
[
9639506.001
]
[Cites]
Blood. 1997 Sep 1;90(5):1799-806
[
9292512.001
]
(PMID = 16990798.001).
[ISSN]
0261-4189
[Journal-full-title]
The EMBO journal
[ISO-abbreviation]
EMBO J.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / MC/ U105161083; United Kingdom / Medical Research Council / / MC/ U105459896
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Solutions; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 9007-49-2 / DNA; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Other-IDs]
NLM/ PMC1589984
27.
Nakada S, Katsuki Y, Imoto I, Yokoyama T, Nagasawa M, Inazawa J, Mizutani S:
Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations.
J Clin Invest
; 2006 Jan;116(1):80-9
[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.
Topoisomerase II (Topo II) inhibitors are
cell
cycle-specific DNA-damaging agents and often correlate with secondary
leukemia
with chromosomal translocations involving the
mixed
-
lineage
leukemia
/
myeloid lymphoid leukemia
(MLL) gene on chromosome 11 band q23 (11q23).
[MeSH-major]
Cell
Cycle / physiology. Chromosome Aberrations / chemically induced. Etoposide / pharmacology.
Myeloid
-
Lymphoid Leukemia
Protein / genetics. Translocation, Genetic
[MeSH-minor]
Bone Neoplasms.
Cell
Division.
Cell
Line.
Cell
Line, Tumor. Chromosome Banding. Chromosomes, Human, Pair 11. Cloning, Molecular. G2 Phase. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Histone-Lysine N-Methyltransferase. Humans. Osteosarcoma
Coriell Cell Repositories.
culture/stock collections - Coriell Cell Repositories
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Mutat Res. 2000 Mar 3;466(1):9-15
[
10751720.001
]
[Cites]
J Biol Chem. 1996 Nov 15;271(46):29238-44
[
8910583.001
]
[Cites]
Br J Haematol. 2000 Apr;109(1):13-23
[
10848777.001
]
[Cites]
Leukemia. 2000 Jun;14(6):1014-7
[
10865966.001
]
[Cites]
Blood. 2000 Jul 1;96(1):24-33
[
10891426.001
]
[Cites]
Cancer Res. 2001 Mar 15;61(6):2542-6
[
11289128.001
]
[Cites]
Med Pediatr Oncol. 2001 May;36(5):525-35
[
11340607.001
]
[Cites]
Annu Rev Genet. 2001;35:673-745
[
11700297.001
]
[Cites]
Carcinogenesis. 2002 Jan;23(1):19-24
[
11756219.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):925-30
[
11805335.001
]
[Cites]
Mol Cell Biol. 2002 Feb;22(4):1049-59
[
11809797.001
]
[Cites]
Blood. 2002 Mar 15;99(6):1909-12
[
11877259.001
]
[Cites]
Genes Chromosomes Cancer. 2002 Apr;33(4):331-45
[
11921269.001
]
[Cites]
Genes Chromosomes Cancer. 2002 Apr;33(4):395-400
[
11921273.001
]
[Cites]
Lancet Oncol. 2002 Apr;3(4):235-43
[
12067686.001
]
[Cites]
Nat Genet. 2002 Sep;32(1):185-90
[
12195425.001
]
[Cites]
Nat Rev Cancer. 2003 Mar;3(3):155-68
[
12612651.001
]
[Cites]
Blood. 2003 May 1;101(9):3622-7
[
12511424.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5057-62
[
12679524.001
]
[Cites]
Curr Med Chem Anticancer Agents. 2003 Jul;3(4):271-90
[
12769773.001
]
[Cites]
J Clin Oncol. 2003 Jun 1;21(11):2123-37
[
12775738.001
]
[Cites]
Cancer Cell. 2003 May;3(5):449-58
[
12781363.001
]
[Cites]
Cancer Causes Control. 1996 Nov;7(6):581-90
[
8932918.001
]
[Cites]
Curr Opin Struct Biol. 1998 Feb;8(1):26-32
[
9519293.001
]
[Cites]
Leukemia. 1998 Mar;12(3):346-52
[
9529129.001
]
[Cites]
J Clin Oncol. 1999 Feb;17(2):569-77
[
10080601.001
]
[Cites]
EMBO J. 1999 Jul 1;18(13):3564-74
[
10393173.001
]
[Cites]
Oncologist. 1999;4(3):225-40
[
10394590.001
]
[Cites]
Nature. 2004 Nov 18;432(7015):316-23
[
15549093.001
]
[Cites]
Nature. 2004 Nov 18;432(7015):338-41
[
15549096.001
]
[Cites]
Mol Cell. 2004 Dec 22;16(6):991-1002
[
15610741.001
]
[Cites]
Mol Cell. 2004 Dec 22;16(6):1003-15
[
15610742.001
]
[Cites]
N Engl J Med. 2005 Apr 14;352(15):1529-38
[
15829534.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5
[
10758153.001
]
[Cites]
Cancer Cell. 2003 Aug;4(2):99-110
[
12957285.001
]
[Cites]
Blood. 2004 Jan 1;103(1):283-90
[
12969974.001
]
[Cites]
Science. 2004 Jan 2;303(5654):92-5
[
14704429.001
]
[Cites]
Nat Genet. 2004 Apr;36(4):331-4
[
15054488.001
]
[Cites]
Cancer Res. 1974 Aug;34(8):1788-93
[
4210356.001
]
[Cites]
J Cell Biol. 1975 Sep;66(3):521-30
[
1057547.001
]
[Cites]
J Biol Chem. 1984 Nov 10;259(21):13560-6
[
6092381.001
]
[Cites]
Mol Cell Biol. 1987 Sep;7(9):3119-23
[
2823120.001
]
[Cites]
Proc Natl Acad Sci U S A. 1988 Feb;85(4):1086-90
[
2829215.001
]
[Cites]
N Engl J Med. 1989 Jul 20;321(3):136-42
[
2787477.001
]
[Cites]
Cancer Res. 1993 Jul 1;53(13):2954-6
[
8319201.001
]
[Cites]
Lancet. 1993 Oct 2;342(8875):819-20
[
8104269.001
]
[Cites]
Blood. 1996 Mar 1;87(5):1912-22
[
8634439.001
]
[Cites]
Blood. 1996 Apr 1;87(7):2649-58
[
8639880.001
]
[Cites]
Cell. 1996 Jun 14;85(6):853-61
[
8681380.001
]
[ErratumIn]
J Clin Invest. 2006 Aug;116(8):2306-7
(PMID = 16357944.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
eng
[Publication-type]
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; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Other-IDs]
NLM/ PMC1312016
28.
Forissier S, Razanajaona D, Ay AS, Martel S, Bartholin L, Rimokh R:
AF10-dependent transcription is enhanced by its interaction with FLRG.
Biol Cell
; 2007 Oct;99(10):563-71
[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.
RESULTS: In order to analyse the function of the nuclear form of FLRG, we performed a yeast two-
hybrid
screen, in which we identified AF10 [ALL1 (
acute
lymphoblastic
leukaemia
) fused gene from chromosome 10], a translocation partner of the MLL (
mixed
-
lineage leukaemia
) oncogene in human
leukaemia
, as a FLRG-interacting protein.
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17868029.001).
[ISSN]
1768-322X
[Journal-full-title]
Biology of the cell
[ISO-abbreviation]
Biol. Cell
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Follistatin-Related Proteins; 0 / MLLT10 protein, human; 0 / Protein Isoforms; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors
29.
Rosenbluth MJ, Lam WA, Fletcher DA:
Force microscopy of nonadherent cells: a comparison of leukemia cell deformability.
Biophys J
; 2006 Apr 15;90(8):2994-3003
[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]
Force microscopy of nonadherent cells: a comparison of
leukemia cell
deformability.
We apply this technique to compare the deformability of human
myeloid and lymphoid leukemia
cells and neutrophils at low deformation rates, and we find that the cells are well described by an elastic model based on Hertzian mechanics.
Myeloid
(HL60) cells were measured to be a factor of 18 times stiffer than
lymphoid
(Jurkat) cells and six times stiffer than human neutrophils on average (E(infinity) = 855 +/- 670 Pa for HL60 cells, E(infinity) = 48 +/- 35 Pa for Jurkat cells, E(infinity) = 156 +/- 87 for neutrophils, mean +/- SD).
This work demonstrates a simple method for extending AFM mechanical property measurements to nonadherent cells and characterizes properties of human
leukemia
cells that may contribute to leukostasis, a complication associated with
acute
leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
/ pathology. Neutrophils / pathology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology
[MeSH-minor]
Acute
Disease
.
Cell
Adhesion.
Cell
Line, Tumor. Cells, Cultured. Elasticity. Humans. Micromanipulation. Microscopy, Atomic Force. Models, Biological. Viscosity
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
SciCrunch.
BioNumbers: The Database of Useful Biological Numbers: Data: Value observation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Baillieres Clin Haematol. 1987 Sep;1(3):725-46
[
3327563.001
]
[Cites]
Biophys J. 2005 Nov;89(5):3203-13
[
16113121.001
]
[Cites]
Biophys J. 1989 Jul;56(1):151-60
[
2752085.001
]
[Cites]
J Biomech Eng. 1990 Aug;112(3):269-76
[
2214708.001
]
[Cites]
J Biomech Eng. 1990 Aug;112(3):295-302
[
2214711.001
]
[Cites]
Blood. 1990 Dec 15;76(12):2606-12
[
2265253.001
]
[Cites]
Biophys J. 1991 Oct;60(4):856-66
[
1742456.001
]
[Cites]
Biorheology. 1991;28(6):557-67
[
1818744.001
]
[Cites]
Biophys J. 1992 Jun;61(6):1664-70
[
1617145.001
]
[Cites]
Ann Med. 1993 Feb;25(1):31-9
[
8435185.001
]
[Cites]
Biophys J. 1993 Nov;65(5):2078-88
[
8298037.001
]
[Cites]
Biophys J. 1994 Aug;67(2):696-705
[
7948682.001
]
[Cites]
Baillieres Clin Haematol. 1994 Jun;7(2):263-72
[
7803901.001
]
[Cites]
Biophys J. 1995 May;68(5):1678-80
[
7612810.001
]
[Cites]
Biophys J. 1996 Apr;70(4):2023-9
[
8785361.001
]
[Cites]
Biophys J. 1996 Jan;70(1):556-67
[
8770233.001
]
[Cites]
Biorheology. 1996 Jan-Feb;33(1):1-15
[
8869341.001
]
[Cites]
J Biomech. 2000 Jan;33(1):15-22
[
10609514.001
]
[Cites]
Biochem Biophys Res Commun. 2000 Mar 24;269(3):781-6
[
10720492.001
]
[Cites]
Phys Rev Lett. 2000 Jul 24;85(4):880-3
[
10991422.001
]
[Cites]
Biorheology. 2000;37(4):279-90
[
11145074.001
]
[Cites]
Biotechniques. 2001 Jun;30(6):1322-6, 1328, 1330-1
[
11414226.001
]
[Cites]
Biophys J. 2001 Dec;81(6):3166-77
[
11720983.001
]
[Cites]
Ther Apher. 2002 Feb;6(1):15-23
[
11886572.001
]
[Cites]
Biophys J. 2002 May;82(5):2798-810
[
11964265.001
]
[Cites]
Methods Cell Biol. 2002;68:67-90
[
12053741.001
]
[Cites]
J Biomech. 2002 Dec;35(12):1659-63
[
12445619.001
]
[Cites]
Blood. 1980 Nov;56(5):866-75
[
6775712.001
]
[Cites]
Virchows Arch B Cell Pathol Incl Mol Pathol. 1987;52(5):403-11
[
2883763.001
]
[Cites]
J Biomech Eng. 1988 Feb;110(1):27-36
[
3347021.001
]
[Cites]
Biophys J. 2003 Mar;84(3):2071-9
[
12609908.001
]
[Cites]
Biophys J. 2003 May;84(5):3389-413
[
12719267.001
]
[Cites]
J Cell Sci. 2003 Jun 15;116(Pt 12):2531-9
[
12734401.001
]
[Cites]
J Biomech Eng. 2003 Jun;125(3):323-33
[
12929236.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14618-22
[
14638939.001
]
[Cites]
Dis Markers. 2003-2004;19(2-3):139-54
[
15096710.001
]
[Cites]
J Clin Invest. 1973 Feb;52(2):350-8
[
4509637.001
]
[Cites]
Pediatr Clin North Am. 1997 Aug;44(4):809-30
[
9286286.001
]
[Cites]
Med Biol Eng Comput. 1998 Mar;36(2):246-50
[
9684470.001
]
[Cites]
Scanning. 1998 Aug;20(5):389-97
[
9737018.001
]
[Cites]
Br J Cancer. 1999 Jun;80(8):1156-61
[
10376966.001
]
[Cites]
J Biomech Eng. 1999 Oct;121(5):462-71
[
10529912.001
]
[Cites]
Diabetologia. 2004 Oct;47(10):1722-6
[
15517153.001
]
[Cites]
Biophys J. 2004 Dec;87(6):4246-58
[
15361412.001
]
[Cites]
Biophys J. 1988 Aug;54(2):331-6
[
3207829.001
]
(PMID = 16443660.001).
[ISSN]
0006-3495
[Journal-full-title]
Biophysical journal
[ISO-abbreviation]
Biophys. J.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1414579
30.
Takasaki H, Tachibana T, Tanaka M, Maruta A, Ishigatsubo Y, Kanamoari H:
[Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia].
Rinsho Ketsueki
; 2010 May;51(5):339-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Successful selection of chemotherapy based on
cell
surface antigens in a patient with
mixed
phenotype
acute
leukemia
].
The patient was diagnosed as having
mixed
phenotype
acute
leukemia
, T/
myeloid
, NOS, according to the WHO classification.
After initial treatment, residual leukemic cells with CD13, CD33 and MPO were detected by FCM; therefore, he received
re
-induction chemotherapy for AML, and achieved CR.
Acute
leukemia
of ambiguous
lineage
is a relatively rare subtype in
acute
leukemia and
standard chemotherapy has not been established.
[MeSH-major]
Antigens, Surface. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
/ drug therapy.
Leukemia
/ immunology
[MeSH-minor]
Acute
Disease
. Cyclophosphamide. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Treatment Outcome. Vincristine / administration & dosage
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
DAUNORUBICIN
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISOLONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20534955.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antigens, Surface; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin
31.
Marques-Salles Tde J, Barros JE, Soares-Ventura EM, Cartaxo Muniz MT, Santos N, Ferreira da Silva E, Silva ML, Liehr T, Mkrtchyan H:
Unusual childhood biphenotypic acute leukemia with a yet unreported t(3;13)(p25.1;q13).
Leuk Res
; 2010 Aug;34(8):e206-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Unusual childhood
biphenotypic
acute
leukemia
with a yet unreported t(3;13)(p25.1;q13).
[MeSH-major]
Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 3 / genetics. Killer Cells, Natural / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / pathology. Translocation, Genetic / genetics
[MeSH-minor]
Adolescent. Humans. Male.
Phenotype
. Prognosis
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
(PMID = 20338638.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
32.
Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ:
Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2005 Dec;13(6):943-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Comparison between CD19 and CD20 expression patterns on
acute
leukemic cells.
In order to provide the evidences for CD19 as a better antibody targeting molecule for B
lineage acute
leukemias
than CD20 through the multi-parameter flow-cytometry analysis of
leukemia
cells, the samples from 321 patients with
acute
leukemia
(AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B
lineage acute
lymphoblastic leukemia
(B
lineage
ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B
lineage
/
Myeloid
(B/My)
acute mixed lineage
leukemia
(AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
Both of the two antigens were negative in 29 patients with
acute
T lymphoblastic leukemia and
7 patients with T/My AMLL.
The positive rates of CD19 and CD20 in 152 patients with
acute
myeloid leukemia
(AML) were 7.2% and 2.0%, respectively.
The difference of the fluorescence intensity between the two antigens on the cells from each patient with B
lineage
ALL or B/My AMLL was statistically significant (t = 20.68, P < 0.001).
The specificity of CD19 and CD20 in
B lymphocytic
lineage
was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
It is concluded that CD19 continuously and steadily express on almost all subtypes of B
lineage
leukemic cells with homogeneous pattern while only a small number of
leukemias
express CD20.
These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-
lineage acute
leukemia
.
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - 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 = 16403255.001).
[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]
ENG
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD19; 0 / Antigens, CD20
33.
Hu XX, Gong SL, Song XM, Chen L, Qiu HY, Gao L, Wang JM:
[Report of a case of hybrid acute leukemia with t (12; 22) and literature review].
Zhonghua Xue Ye Xue Za Zhi
; 2006 May;27(5):331-4
[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]
[Report of a case of
hybrid
acute
leukemia
with t (12; 22) and literature review].
OBJECTIVE: To report
a hybrid
acute
leukemia
(HAL) patient with t (12;.
Leukemia
surface markers were detected by anti-biotin-biotin complex and monoclonal antibodies.
RESULTS: The clinical and hematological findings were compatible with the
diagnosis
of HAL.
Lymphoid and myeloid
markers were positive on the
leukemia
cells.
22) translocation is a rare chromosome
abnormality
in
leukemia
.
This translocation as a cytogenetic marker for poor-prognosis in
leukemia
needs to be further studied.
[MeSH-major]
Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 22 / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16875585.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
China
[Number-of-references]
20
34.
Jeha S, Kantarjian H:
Clofarabine for the treatment of acute lymphoblastic leukemia.
Expert Rev Anticancer Ther
; 2007 Feb;7(2):113-8
[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]
Clofarabine for the treatment of
acute
lymphoblastic leukemia
.
A marked improvement in the outcome of patients with
acute
lymphoblastic leukemia
has been achieved with chemotherapeutic agents developed between the 1950s and 1970s.
As the limits of optimizing the use of old drugs are reached, most adults with
acute
lymphoblastic leukemia
still succumb to their
disease and leukemia
remains the leading cause of nonaccidental death in children.
Clofarabine, a next-generation deoxyadenosine analog, has demonstrated significant activity in children and adults with refractory
lymphoid and myeloid leukemia
in early clinical trials and was granted approval for use in children with
acute
lymphoblastic leukemia
in second or higher relapse.
[MeSH-major]
Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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 = 17288522.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
[Number-of-references]
36
35.
Kinjo K, Sandoval S, Sakamoto KM, Shankar DB:
The role of CREB as a proto-oncogene in hematopoiesis.
Cell Cycle
; 2005 Sep;4(9):1134-5
[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.
Cyclic-AMP response element binding protein (CREB) is a transcription factor that functions in glucose homeostasis, growth-factor- dependent
cell
survival, proliferation and memory.
Data from our laboratory shows that a majority of patients with
acute
lymphoid and myeloid leukemia
overexpress CREB in the bone marrow.
CREB overexpression is associated with poor initial outcome of clinical
disease
in AML patients.
To study its role in hematopoiesis, we overexpressed CREB in
leukemia cell
lines and in mice.
CREB overexpression resulted in increased survival and proliferation of
myeloid
cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the
myeloid
lineage
.
CREB transgenic mice also develop myeloproliferative
disease
after one year.
Thus, CREB acts as a proto-oncogene to regulate hematopoiesis and contributes to the
leukemia phenotype
.
Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in
leukemia
in the future.
[MeSH-minor]
Animals. Bone Marrow Cells / metabolism.
Cell
Line, Tumor.
Cell
Proliferation.
Cell
Survival.
Cell
Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Glucose / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / metabolism. Humans.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Mice. Mice, Transgenic. Neoplasms / metabolism.
Phenotype
. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Proto-Oncogene Proteins / chemistry. Signal Transduction. Up-Regulation
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
GLUCOSE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16096372.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; IY9XDZ35W2 / Glucose
[Number-of-references]
18
36.
Ohe M, Hashino S:
[Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS].
Rinsho Ketsueki
; 2010 Apr;51(4):297-9
[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]
[Successful treatment with clarithromycin for
Mixed
phenotype
acute
leukemia
, T/
myeloid
, NOS].
The
diagnosis
was
Mixed
phenotype
acute
leukemia
, T/
myeloid
, NOS.
This clinical course suggests CAM is effective for this
leukemia
.
[MeSH-major]
Anti-Bacterial Agents / administration & dosage. Clarithromycin / administration & dosage.
Leukemia
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy
[MeSH-minor]
Acute
Disease
. Aged. Drug Synergism. Drug Therapy, Combination. Female. Humans. Pneumonia, Bacterial / complications. Pneumonia, Bacterial / drug therapy. Prednisolone / administration & dosage
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Antibiotics
.
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
PREDNISOLONE
.
Hazardous Substances Data Bank.
Clarithromycin
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20467229.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Anti-Bacterial Agents; 9PHQ9Y1OLM / Prednisolone; H1250JIK0A / Clarithromycin
37.
Shi M, Cui F, Li B, Li SY, Ma HJ:
Mixed phenotype acute leukaemia with giant inclusions.
Br J Haematol
; 2010 Apr;149(1):2
[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]
Mixed
phenotype
acute leukaemia
with giant inclusions.
[MeSH-major]
Inclusion Bodies / ultrastructure.
Leukemia
,
Biphenotypic
,
Acute
/ pathology
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20015299.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
38.
Suh B, Song J, Kim J, Park TS, Choi JR:
Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia.
Korean J Lab Med
; 2010 Jun;30(3):218-23
[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]
Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous
leukemia
.
BACKGROUND: Although the pericentric inversion of chromosome 9, inv(9)(p11q13), is generally considered a normal variation, it is also associated with solid tumors and several hematologic malignancies such as
biphenotypic
acute
leukemia
, ALL, AML, and myeloproliferative neoplasms.
The purpose of this retrospective study was to investigate the frequency and clinical features of CML patients with concomitant inv(9)
and t
(9;22)(q34;q11.2) variation at our institution.
METHODS: We reviewed the bone marrow chromosome database entries between October 2006 and December 2008 to identify patients with concomitant inv(9)
and t
(9;22) variations.
RESULTS: Among the 51 CML patients, 4 (7.8%) had concomitant inv(9)
and t
(9;22) variations.
[MeSH-major]
Asian Continental Ancestry Group / genetics. Chromosome Inversion. Chromosomes, Human, Pair 9.
Leukemia
,
Myeloid
,
Acute
/ 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 = 20603579.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
39.
Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S:
Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
J Clin Exp Hematop
; 2010;50(1):51-8
[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]
Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with
de
novo
mixed
-
lineage
leukemia
.
We report a case of
acute mixed
-
lineage
leukemia
, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
The
diagnosis
was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-
lineage
antigens
and myeloid
antigens accompanied by clonal rearrangements of IgH gene.
Add (11q23)
abnormality
was found in sideline karyotypes as well as the stemline
abnormality
of dic(17;20) (p11;q11).
[MeSH-major]
Gene Amplification.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20505276.001).
[ISSN]
1880-9952
[Journal-full-title]
Journal of clinical and experimental hematopathology : JCEH
[ISO-abbreviation]
J Clin Exp Hematop
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
40.
Yamamoto K, Sada A, Kawano Y, Katayama Y, Shimoyama M, Matsui T:
Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement.
Cancer Genet Cytogenet
; 2010 Sep;201(2):122-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Therapy-related,
mixed
phenotype
acute
leukemia
with t(1;21)(p36;q22) and RUNX1 rearrangement.
We describe here a new case of therapy-related
acute
leukemia
with t(1;21)(p36;q22).
Immunophenotypic analyses revealed that blasts were positive for CD19, CD79a, and cytCD22, as well as MPO, CD13, and CD33, fulfilling the diagnostic criteria of
mixed
phenotype
acute
leukemia
, B/
myeloid
.
The patient died of
disease
progression after 10 months.
Thus,
acute
leukemia
with t(1;21) and RUNX1 rearrangement could be associated with B/
myeloid
mixed
phenotype
as well as previous topoisomerase II inhibitor therapy and poor prognoses.
[MeSH-major]
Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasms, Second Primary / genetics
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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
[Copyright]
2010 Elsevier Inc. All rights reserved.
(PMID = 20682397.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
41.
Serefhanoglu S, Buyukasik Y, Goker H, Sayinalp N, Ozcebe OI:
Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series.
J Natl Med Assoc
; 2009 Mar;101(3):270-2
[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]
Biphenotypic
acute
leukemia
treated with
acute
myeloid leukemia
regimens: a case series.
This study retrospectively analyzed 8 cases of
biphenotypic
acute
leukemia
(BAL) in respect of morphology, immune
phenotype
, karyotype, and clinical manifestations.
Six patients had
myeloid
plus
T lymphoid
, and 2 cases had
myeloid
plus B-
lymphoid
immune phenotypic markers.
Because selection of an antileukemic chemotherapy regimen for
acute
leukemia
is largely based on whether a case is classified as
myeloid
or
lymphoid
, the presence of markers for both lineages may have important implications for treatment.
All of our patients were treated with regimens designed for
acute
myeloid leukemia
(AML).
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy
[MeSH-minor]
Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Biomarkers. Case-Control Studies. Cytarabine / therapeutic use. Female. Humans. Idarubicin / therapeutic use. Immunophenotyping.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ physiopathology. Male. Middle Aged. Mitoxantrone / therapeutic use. Retrospective Studies
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
NOVANTRONE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19331261.001).
[ISSN]
1943-4693
[Journal-full-title]
Journal of the National Medical Association
[ISO-abbreviation]
J Natl Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Biomarkers; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
42.
Shildkrot Y, Onciu M, Hoehn ME, Wilson MW:
Mixed-phenotype acute leukemia relapse in the iris.
J AAPOS
; 2010 Oct;14(5):453-4
[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]
Mixed
-
phenotype
acute
leukemia
relapse in the iris.
Mixed
-
phenotype
acute
leukemia
is a rare condition with no previously reported intraocular involvement.
We present clinical, radiologic, and cytologic findings of leukemic intraocular relapse in a 23-month-old girl, with
lineage
switch presenting as conjunctivitis after allogeneic bone marrow transplantation.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 American Association for Pediatric Ophthalmology and Strabismus. Published by Mosby, Inc. All rights reserved.
(PMID = 20863726.001).
[ISSN]
1528-3933
[Journal-full-title]
Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus
[ISO-abbreviation]
J AAPOS
[Language]
ENG
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
43.
Michaud J, Simpson KM, Escher R, Buchet-Poyau K, Beissbarth T, Carmichael C, Ritchie ME, Schütz F, Cannon P, Liu M, Shen X, Ito Y, Raskind WH, Horwitz MS, Osato M, Turner DR, Speed TP, Kavallaris M, Smyth GK, Scott HS:
Integrative analysis of RUNX1 downstream pathways and target genes.
BMC Genomics
; 2008 Jul 31;9:363
[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.
BACKGROUND: The RUNX1 transcription factor gene is frequently mutated in sporadic
myeloid and lymphoid leukemia
through translocation, point mutation or amplification.
It is also responsible for a familial platelet
disorder
with predisposition to
acute
myeloid leukemia
(FPD-AML).
The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of
leukemia
.
We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to
leukemia
.
1)
cell
lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFbeta, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays.
A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair
cell
proliferation, microtubule dynamics and possibly genetic stability.
CONCLUSION: This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system
and leukemia
.
The biological pathways and target genes controlled by RUNX1 will have considerable importance in
disease
progression in both familial and sporadic
leukemia
as well as therapeutic implications.
COS Scholar Universe.
author profiles
.
Bern Open Repository and Information System.
Free Full text from BORIS
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Genome Res. 2003 Aug;13(8):1828-37
[
12902378.001
]
[Cites]
Chem Biol. 2003 Jul;10(7):597-607
[
12890533.001
]
[Cites]
Methods. 2003 Dec;31(4):265-73
[
14597310.001
]
[Cites]
J Clin Invest. 2003 Dec;112(11):1751-61
[
14660751.001
]
[Cites]
Mol Endocrinol. 2003 Dec;17(12):2448-60
[
14500759.001
]
[Cites]
Nat Rev Cancer. 2004 Apr;4(4):253-65
[
15057285.001
]
[Cites]
J Biol Chem. 2004 Apr 9;279(15):15678-87
[
14747476.001
]
[Cites]
N Engl J Med. 2004 Apr 15;350(16):1617-28
[
15084694.001
]
[Cites]
Oncogene. 2004 May 24;23(24):4211-9
[
15156175.001
]
[Cites]
Oncogene. 2004 May 24;23(24):4284-96
[
15156185.001
]
[Cites]
Nat Rev Mol Cell Biol. 2004 Jun;5(6):481-92
[
15173827.001
]
[Cites]
Bioinformatics. 2004 Jun 12;20(9):1464-5
[
14962934.001
]
[Cites]
J Virol. 1990 Oct;64(10):4808-19
[
2168969.001
]
[Cites]
Mol Cell Biol. 1993 Jun;13(6):3324-39
[
8497254.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6859-63
[
8341710.001
]
[Cites]
J Immunol. 1993 Oct 15;151(8):4306-14
[
8409403.001
]
[Cites]
Cell. 1994 Aug 26;78(4):635-44
[
8069912.001
]
[Cites]
IARC Sci Publ. 1997;(142):159-84
[
9354918.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4584-8
[
9539781.001
]
[Cites]
Oncogene. 1998 Nov 5;17(18):2287-93
[
9811459.001
]
[Cites]
Blood. 1999 Mar 15;93(6):1817-24
[
10068652.001
]
[Cites]
Development. 1999 Jun;126(11):2563-75
[
10226014.001
]
[Cites]
Nat Genet. 1999 Oct;23(2):144-6
[
10508507.001
]
[Cites]
Nat Genet. 1999 Oct;23(2):166-75
[
10508512.001
]
[Cites]
Int J Cancer. 2005 Jan 10;113(2):221-8
[
15386419.001
]
[Cites]
Bull Cancer. 2004 May;91(5):E81-112
[
15568225.001
]
[Cites]
Cancer Res. 2004 Dec 15;64(24):8846-53
[
15604243.001
]
[Cites]
Br J Haematol. 2005 Feb;128(3):318-23
[
15667533.001
]
[Cites]
Oncogene. 2005 Feb 10;24(7):1129-37
[
15592512.001
]
[Cites]
J Biol Chem. 2000 Feb 4;275(5):3438-45
[
10652337.001
]
[Cites]
Gene. 2000 Mar 21;245(2):223-35
[
10717473.001
]
[Cites]
Oncogene. 2000 Jul 13;19(30):3434-8
[
10918600.001
]
[Cites]
Blood. 2000 Aug 15;96(4):1366-73
[
10942379.001
]
[Cites]
Genomics. 2000 Aug 15;68(1):71-9
[
10950928.001
]
[Cites]
Nat Genet. 2000 Sep;26(1):103-5
[
10973259.001
]
[Cites]
Blood. 2000 Sep 15;96(6):2108-15
[
10979955.001
]
[Cites]
EMBO J. 2001 Feb 15;20(4):723-33
[
11179217.001
]
[Cites]
Gene. 2001 Jan 10;262(1-2):23-33
[
11179664.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403
[
11526243.001
]
[Cites]
Mech Dev. 2001 Dec;109(2):413-7
[
11731260.001
]
[Cites]
Blood. 2002 Feb 15;99(4):1364-72
[
11830488.001
]
[Cites]
Leukemia. 2002 Apr;16(4):658-68
[
11960347.001
]
[Cites]
Cell Mol Life Sci. 2002 Aug;59(8):1406-12
[
12363043.001
]
[Cites]
Leukemia. 2003 Jan;17(1):9-16
[
12529654.001
]
[Cites]
Nucleic Acids Res. 2003 Feb 15;31(4):e15
[
12582260.001
]
[Cites]
Cancer Invest. 2003;21(1):105-36
[
12643014.001
]
[Cites]
J Cell Physiol. 2003 Aug;196(2):301-11
[
12811823.001
]
[Cites]
Cell. 1996 Jan 26;84(2):321-30
[
8565077.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9
[
8622955.001
]
[Cites]
Oncogene. 1997 Aug 7;15(6):677-83
[
9264408.001
]
[Cites]
Oncogene. 1997 Sep;15(11):1315-27
[
9315100.001
]
[Cites]
Curr Opin Drug Discov Devel. 2005 Mar;8(2):262-9
[
15782549.001
]
[Cites]
Bioinformatics. 2005 May 1;21(9):2067-75
[
15657102.001
]
[Cites]
Nucleic Acids Res. 2005;33(10):3154-64
[
15933209.001
]
[Cites]
BMC Bioinformatics. 2005;6:144
[
15941488.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13544-9
[
16174746.001
]
[Cites]
Mutat Res. 2005 Oct 15;578(1-2):333-70
[
16084534.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50
[
16199517.001
]
[Cites]
BMC Bioinformatics. 2007;8:242
[
17612399.001
]
[Cites]
Exp Cell Res. 2003 Oct 15;290(1):93-107
[
14516791.001
]
(PMID = 18671852.001).
[ISSN]
1471-2164
[Journal-full-title]
BMC genomics
[ISO-abbreviation]
BMC Genomics
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK058161; United States / NHLBI NIH HHS / HL / R01 HL079507; United States / NIDDK NIH HHS / DK / DK58161; United States / NHLBI NIH HHS / HL / HL079507
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse
[Other-IDs]
NLM/ PMC2529319
44.
Kim MK, Mun YC, Seong CM, Chung WS, Huh J:
[Variant Philadelphia chromosome identified by interphase fluorescence in situ hybridization (FISH) without evidence on G-banded karyotyping and metaphase FISH].
Korean J Lab Med
; 2010 Dec;30(6):711-7
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
A 52-year-old man was diagnosed with
acute
leukemia
of
mixed
phenotype
.
[MeSH-minor]
Adult. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Humans. Interphase. Karyotyping.
Leukemia
/
diagnosis
.
Leukemia
/ genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive /
diagnosis
.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Metaphase. Middle Aged.
Phenotype
. Translocation, Genetic
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21157160.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
kor
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Korea (South)
45.
Liu H, Yu H, Jia HY, Zhang W, Guo CJ:
[Detection of FLT3 gene mutation in hematologic malignancies and its clinical significance].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Aug;15(4):709-13
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
To study the FLT3 gene expression and its internal tandem duplication in hematologic malignancies and its clinical significance, polymerase chain reaction (PCR) and DNA sequencing were used to detect the FLT3/ITD mutation in blast cells of bone marrow from 86 patients with hematologic malignancies, including 32 cases of
acute
myeoloid
leukemia
(AML), 18 cases of
acute
lymphoblastic leukemia
(ALL), 2 cases of
acute
hybrid leukemia
(AHL), 12 cases of myelodysplastic syndromes (MDS), 10 cases of chronic myelogenous
leukemia
(CML), 3 cases of non-Hodgkin's lymphoma (NHL) and 9 cases of multiple myeloma (MM).
FLT3/ITD was associated with a higher peripheral blood white
cell
count (p < 0.01), higher percentage of bone marrow blast cells (p < 0.01) and lower complete mission rate.
FLT3/ITD mutation is associated with higher peripheral blood white
cell
count, higher percentage of bone marrow blast cells and lower complete remission rate, FIT3/IID gene mutation may be used to predict prognosis of patients with AML.
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 = 17708788.001).
[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
[Publication-country]
China
[Chemical-registry-number]
EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
46.
Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ:
The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression.
Proc Natl Acad Sci U S A
; 2005 Sep 27;102(39):14028-33
[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.
MLL, involved in many chromosomal translocations associated with
acute
myeloid and lymphoid leukemia
, has >50 known partner genes with which it is able to form in-frame fusions.
Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated
leukemia
.
To this end, we developed inducible MLL-AF4 fusion
cell
lines in different backgrounds.
Overexpression of MLL-AF4 does not lead to increased proliferation in either
cell
line, but rather,
cell
growth was slowed compared with similar
cell
lines inducibly expressing truncated MLL.
We found that in the MLL-AF4-induced
cell
lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.
Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9
leukemia cell
lines.
Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background
cell
type, MLL-AF4 inhibits or activates CDKN1B expression.
This
finding
may have implications in terms of
leukemia
stem
cell
resistance to chemotherapy in MLL-AF4
leukemias
.
COS Scholar Universe.
author profiles
.
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]
Cell. 1994 Jul 15;78(1):67-74
[
8033213.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):749-54
[
15640349.001
]
[Cites]
J Biol Chem. 1995 Mar 10;270(10):4971-4
[
7890601.001
]
[Cites]
Mol Carcinog. 1999 Nov;26(3):172-9
[
10559792.001
]
[Cites]
Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72
[
10595755.001
]
[Cites]
Curr Opin Oncol. 2000 Jan;12(1):3-12
[
10687723.001
]
[Cites]
Oncogene. 2000 Jul 6;19(29):3290-8
[
10918585.001
]
[Cites]
EMBO J. 2000 Sep 1;19(17):4655-64
[
10970858.001
]
[Cites]
Am J Physiol Cell Physiol. 2000 Oct;279(4):C1045-57
[
11003585.001
]
[Cites]
Blood. 2000 Oct 15;96(8):2746-54
[
11023508.001
]
[Cites]
Nat Med. 2000 Nov;6(11):1235-40
[
11062534.001
]
[Cites]
J Immunol. 2001 Jan 1;166(1):304-12
[
11123306.001
]
[Cites]
Oncogene. 2001 Oct 4;20(45):6524-30
[
11641776.001
]
[Cites]
Nucleic Acids Res. 2002 Feb 15;30(4):958-65
[
11842107.001
]
[Cites]
Mol Cell Biol. 2002 May;22(9):3014-23
[
11940659.001
]
[Cites]
Oncogene. 2002 May 13;21(21):3403-13
[
12032778.001
]
[Cites]
Blood. 2002 Jun 15;99(12):4629-31
[
12036898.001
]
[Cites]
Curr Opin Hematol. 2002 Jul;9(4):282-7
[
12042701.001
]
[Cites]
Oncogene. 2002 May 9;21(20):3199-206
[
12082635.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8342-7
[
12829790.001
]
[Cites]
Cancer Cell. 2003 Aug;4(2):99-110
[
12957285.001
]
[Cites]
Leukemia. 2004 Jan;18(1):92-102
[
14603337.001
]
[Cites]
Mol Cell Biol. 2004 Jan;24(2):617-28
[
14701735.001
]
[Cites]
Cell. 2004 Jan 23;116(2):221-34
[
14744433.001
]
[Cites]
Leukemia. 2004 Jun;18(6):1064-71
[
14990976.001
]
[Cites]
Oncogene. 2004 Sep 20;23(43):7178-87
[
15378078.001
]
[Cites]
Blood. 1987 Jul;70(1):192-9
[
3496132.001
]
[Cites]
Cell. 1994 Jul 15;78(1):59-66
[
8033212.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11293-8
[
12151601.001
]
[Cites]
Blood. 2002 Nov 15;100(10):3710-8
[
12393701.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1107-17
[
12453418.001
]
[Cites]
Mol Cell. 2002 Nov;10(5):1119-28
[
12453419.001
]
[Cites]
Oncogene. 2003 Jun 5;22(23):3655-68
[
12789274.001
]
[Cites]
Nature. 1995 Nov 30;378(6556):505-8
[
7477409.001
]
[Cites]
Blood. 1996 Apr 1;87(7):2870-7
[
8639906.001
]
[Cites]
Cell. 1996 May 31;85(5):721-32
[
8646780.001
]
[Cites]
Cell. 1996 May 31;85(5):733-44
[
8646781.001
]
[Cites]
Nat Med. 1997 Feb;3(2):227-30
[
9018244.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6380-5
[
9177226.001
]
[Cites]
FEBS Lett. 1997 Jul 7;411(1):1-6
[
9247132.001
]
[Cites]
EMBO J. 1997 Jul 16;16(14):4226-37
[
9250666.001
]
[Cites]
Cancer Res. 1998 Jan 1;58(1):114-22
[
9426067.001
]
[Cites]
Leukemia. 1998 May;12(5):779-87
[
9593281.001
]
[Cites]
Leukemia. 1998 Jul;12(7):1119-27
[
9665199.001
]
[Cites]
Blood. 1999 Sep 15;94(6):2056-64
[
10477735.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10610-4
[
7938000.001
]
(PMID = 16169901.001).
[ISSN]
0027-8424
[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
[Grant]
United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269
[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 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Other-IDs]
NLM/ PMC1236570
47.
Papenhausen PR, Griffin S, Tepperberg J:
Oncogene amplification in transforming myelodysplasia.
Exp Mol Pathol
; 2005 Oct;79(2):168-75
[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 MLL gene, located within band 11q23, has been shown to be involved in translocations with a large variety of reciprocal sites in both
lymphoid and myeloid leukemia
and has also been shown to undergo submicroscopic self-fusion/partial duplication.
The frequency and clinical correlations of MLL gene amplification in
leukemia
will need careful follow-up, since the frequently cryptic amplification described in these cases may not generally provoke confirmatory FISH studies.
A common cytogenetic profile of 5 q-, -17/17 p-, -18/18 q-,
and a
missing or abnormal chromosome 11, may help direct appropriate follow-up studies.
Both genes also show a high degree of diversity of pathogenic mechanisms of
leukemia
evolution, including numerous reciprocal fusion genes in transformation to either AML or ALL and gain of function amplification.
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged.
Myeloid
-
Lymphoid Leukemia
Protein. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Proto-Oncogene Proteins / genetics
MedlinePlus Health Information.
consumer health - Neural Tube Defects
.
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 = 16026782.001).
[ISSN]
0014-4800
[Journal-full-title]
Experimental and molecular pathology
[ISO-abbreviation]
Exp. Mol. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
48.
Costantini AS, Benvenuti A, Vineis P, Kriebel D, Tumino R, Ramazzotti V, Rodella S, Stagnaro E, Crosignani P, Amadori D, Mirabelli D, Sommani L, Belletti I, Troschel L, Romeo L, Miceli G, Tozzi GA, Mendico I, Maltoni SA, Miligi L:
Risk of leukemia and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study.
Am J Ind Med
; 2008 Nov;51(11):803-11
[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]
Risk of
leukemia and
multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study.
BACKGROUND: While there is a general consensus about the ability of benzene to induce
acute
myeloid leukemia
(AML), its effects on chronic
lymphoid leukemia
and multiple myeloma (MM) are still under debate.
We conducted a population-based case-control study to evaluate the association between exposure to organic solvents and risk of
myeloid and lymphoid leukemia
and MM.
METHODS: Five hundred eighty-six cases of
leukemia
(and 1,278 population controls), 263 cases of MM (and 1,100 population controls) were collected.
There were elevated point estimates for the associations between medium/high benzene exposure and chronic lymphatic
leukemia
(OR = 1.8, 95% CI = 0.9-3.9) and MM (OR = 1.9, 95% CI = 0.9-3.9).
Risks of chronic lymphatic
leukemia
were somewhat elevated, albeit with wide confidence intervals, from medium/high exposure to xylene and toluene as well.
Our results support the association between benzene, xylene, and toluene and chronic lymphatic
leukemia and
between benzene and MM with longer latencies than have been observed for AML in other studies.
[MeSH-major]
Benzene / adverse effects.
Leukemia
,
Lymphoid
/ chemically induced. Multiple Myeloma / chemically induced. Occupational Exposure / adverse effects. Solvents / adverse effects
Genetic Alliance.
consumer health - Multiple myeloma
.
MedlinePlus Health Information.
consumer health - Acute Lymphocytic Leukemia
.
MedlinePlus Health Information.
consumer health - Chronic Lymphocytic Leukemia
.
MedlinePlus Health Information.
consumer health - Multiple Myeloma
.
MedlinePlus Health Information.
consumer health - Occupational Health
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
Hazardous Substances Data Bank.
TOLUENE
.
Hazardous Substances Data Bank.
BENZENE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2008 Wiley-Liss, Inc.
(PMID = 18651579.001).
[ISSN]
1097-0274
[Journal-full-title]
American journal of industrial medicine
[ISO-abbreviation]
Am. J. Ind. Med.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA51086
[Publication-type]
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 / Solvents; 0 / Xylenes; 3FPU23BG52 / Toluene; J64922108F / Benzene
49.
Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E:
CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes.
Leukemia
; 2005 Nov;19(11):1948-57
[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 t(10;11)(p13;q14-21) is found in T-ALL and
acute
myeloid leukemia
and fuses CALM (Clathrin-Assembly protein-like
Lymphoid
-
Myeloid
leukaemia
gene) to AF10.
Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to
mixed lineage
leukemia
-translocated
acute
leukemias
(MLL-t AL).
We propose to define a HOXA+
leukemia
group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
[MeSH-major]
Homeodomain Proteins / biosynthesis.
Leukemia
-Lymphoma, Adult T-
Cell
/ genetics.
Leukemia
-Lymphoma, Adult T-
Cell
/ physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
[MeSH-minor]
Adolescent. Adult.
Cell
Proliferation.
Cell
Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation
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 = 16107895.001).
[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 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
50.
Lee JC, Yang S, Zou Y, Joseph L:
Erythroid/B-cell biphenotypic acute leukemia first case report.
Leukemia
; 2009 Oct;23(10):1920-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Erythroid/B-
cell biphenotypic
acute
leukemia
first case report.
[MeSH-major]
B-Lymphocytes / pathology. Erythroid Cells / pathology.
Leukemia
,
Biphenotypic
,
Acute
/ pathology
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19458630.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD
51.
Basecke J, Whelan JT, Griesinger F, Bertrand FE:
The MLL partial tandem duplication in acute myeloid leukaemia.
Br J Haematol
; 2006 Nov;135(4):438-49
[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]
The MLL partial tandem duplication in
acute
myeloid
leukaemia
.
Mixed lineage leukaemia
gene-partial tandem duplications (MLL-PTD) characterise
acute
myeloid
leukaemia
(AML) with trisomy 11 and AML with a normal karyotype.
[MeSH-major]
Gene Duplication.
Leukemia
,
Myeloid
/ genetics.
Myeloid
-
Lymphoid Leukemia
Protein / genetics. Tandem Repeat Sequences
[MeSH-minor]
Acute
Disease
.
Cell
Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 11 / genetics. DNA, Neoplasm / genetics. Genetic Predisposition to
Disease
. Histone-Lysine N-Methyltransferase. Humans. Prognosis. Trisomy
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16965385.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Number-of-references]
81
52.
Van Etten RA:
Aberrant cytokine signaling in leukemia.
Oncogene
; 2007 Oct 15;26(47):6738-49
[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]
Aberrant cytokine signaling in
leukemia
.
Abnormalities of cytokine and growth factor signaling pathways are characteristic of all forms of
leukemia
:
lymphoid and myeloid
,
acute
and chronic.
In this review, our current knowledge of leukemic
cell
cytokine signaling will be summarized, and some speculations on the significance and implications of these insights will be advanced.
A better understanding of aberrant cytokine signaling in
leukemia
should provide additional targets for the rational therapy of these diseases.
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 = 17934482.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA090576; United States / NCI NIH HHS / CA / R01 CA105043; United States / NCI NIH HHS / CA / CA090576; United States / NCI NIH HHS / CA / CA105043
[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 / Cytokines
[Number-of-references]
139
[Other-IDs]
NLM/ NIHMS579951; NLM/ PMC4344827
53.
Kozlov I, Beason K, Yu C, Hughson M:
CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity.
Cancer Genet Cytogenet
; 2005 Nov;163(1):62-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
CD79a expression in
acute
myeloid leukemia
t(8;21) and the importance of cytogenetics in the
diagnosis
of
leukemias
with immunophenotypic ambiguity.
Acute
leukemias
that express antigens associated with more than one
lineage
have been classified as
acute
lymphocytic leukemia
with
myeloid
markers,
acute
myeloid leukemia
with
lymphoid
markers, or
biphenotypic
acute
leukemia
(BAL).
CD79a functions in and has a high degree of specificity for B-
cell
differentiation.
It has only recently begun to be reported in
biphenotypic
acute
leukemias
.
Cases of
acute
leukemia
submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to
leukemia and
lymphoma panels.
The immunophenotyping met proposed scoring criteria for
a diagnosis
of BAL.
Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-
cell
differentiation, represented the aberrant presence of
a B
-
cell
antigen in
leukemias
of distinct
myeloid
linage.
It is doubtful that, in this setting, CD79a expression should be considered a manifestation of
lineage
ambiguity.
[MeSH-major]
Antigens, CD79 / genetics. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8.
Leukemia
,
Myeloid
/ genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease
. Adult. Antigens, CD / genetics. Antigens, CD / immunology. B-Lymphocytes / immunology. Blast Crisis. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. T-Lymphocytes / immunology
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CYTARABINE
.
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
[CommentIn]
Cancer Genet Cytogenet. 2007 Apr 1;174(1):76-7
[
17350472.001
]
(PMID = 16271957.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD79; 04079A1RDZ / Cytarabine
54.
Miyazawa Y, Irisawa H, Matsushima T, Mitsui T, Uchiumi H, Saitohi T, Handa H, Karasawa M, Murakami H, Tsukamoto N, Nojima Y:
[Reversible posterior leukoencephalopathy syndrome probably caused by L-asparaginase].
Rinsho Ketsueki
; 2006 Jun;47(6):531-5
[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.
A 46-year-old male with refractory
biphenotypic
acute
leukemia
was treated with doxorubicin (days 1-3, 15-17), vincristine (days 1, 8, 15, 22), prednisolone (days 1-28), and L-asparaginase (L-ASP: days 15-28) as reinduction therapy.
[MeSH-major]
Asparaginase / adverse effects. Brain / pathology. Brain Diseases / chemically induced. Brain Diseases /
diagnosis
[MeSH-minor]
Acute
Disease
. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Doxorubicin / administration & dosage. Humans. Hypertension / chemically induced.
Leukemia
/ drug therapy. Male. Middle Aged. Prednisolone / administration & dosage. Seizures / chemically induced. Vincristine / administration & dosage
MedlinePlus Health Information.
consumer health - Brain Diseases
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
PREDNISOLONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16862982.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase
55.
Owaidah TM, Al Beihany A, Iqbal MA, Elkum N, Roberts GT:
Cytogenetics, molecular and ultrastructural characteristics of biphenotypic acute leukemia identified by the EGIL scoring system.
Leukemia
; 2006 Apr;20(4):620-6
[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]
Cytogenetics, molecular and ultrastructural characteristics of
biphenotypic
acute
leukemia
identified by the EGIL scoring system.
Biphenotypic
acute
leukemia
(BAL) is a rare, difficult to diagnose entity.
Its identification is important for risk stratification in
acute
leukemia
(AL).
The scoring proposal of the European Group for the Classification of
Acute
Leukemia
(EGIL) is useful for this purpose, but its performance against objective benchmarks is unclear.
Mixed
, small and large blast cells predominated, with FAB M2 and L1 constituting the majority.
All patients were positive for
myeloid
(M) markers and either
B cell
(B) (17 or 74%) or
T cell
(T) (8 or 34%) markers with two exceptional patients demonstrating trilineage
phenotype
.
In six (26%) patients
myeloid
lineage
commitment was also demonstrable by electron cytochemistry.
Abnormal findings were present in 19 (83%) patients by cytogenetics/FISH/molecular analysis as follows: t(9;22) (17%); MLL gene rearrangement (26%); deletion(6q) (13%); 12p11.2 (9%); numerical abnormalities (13%), and three (13%) new, previously unreported translocations t(X;6)(p22.3;q21); t(2;6)(q37;p21.3);
and t
(8;14)(p21;q32).
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human / genetics. Cytogenetic Analysis / methods.
Leukemia
/
diagnosis
.
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged.
Cell
Lineage
. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Female. Gene Rearrangement. Guidelines as Topic. Humans. In Situ Hybridization, Fluorescence / methods. In Vitro Techniques. Infant. Male.
Myeloid
-
Lymphoid Leukemia
Protein / genetics.
Phenotype
. Risk Factors. Sensitivity and Specificity
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16437134.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article
[Publication-country]
England
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
56.
Archangelo LF, Gläsner J, Krause A, Bohlander SK:
The novel CALM interactor CATS influences the subcellular localization of the leukemogenic fusion protein CALM/AF10.
Oncogene
; 2006 Jul 6;25(29):4099-109
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The Clathrin Assembly
Lymphoid Myeloid leukemia
gene (CALM or PICALM) was first identified as the fusion partner of AF10 in the t(10;11)(p13;q14) translocation, which is observed in
acute
myeloid leukemia
(AML),
acute
lymphoblastic leukemia
(ALL) and malignant lymphoma.
Using the N-terminal half of CALM as a bait in a yeast two-
hybrid
screen, a novel protein named CATS (CALM interacting protein expressed in thymus and spleen) was identified.
[MeSH-major]
Active Transport,
Cell
Nucleus. Carrier Proteins / metabolism.
Cell
Nucleolus / metabolism. Monomeric Clathrin Assembly Proteins / metabolism. Oncogene Proteins, Fusion / metabolism
[MeSH-minor]
3T3 Cells. Animals. Base Sequence.
Cell
Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 10 / metabolism. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 13 / metabolism. Gene Expression Regulation / genetics. Humans. Mice. Molecular Sequence Data. Organ Specificity. Protein Binding / genetics. Translocation, Genetic / genetics
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
SciCrunch.
HGNC: Data: Gene Annotation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16491119.001).
[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 / AF10-CALM fusion protein, human; 0 / Carrier Proteins; 0 / FAM64A protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human
57.
Hinrichsen L, Meyerholz A, Groos S, Ungewickell EJ:
Bending a membrane: how clathrin affects budding.
Proc Natl Acad Sci U S A
; 2006 Jun 6;103(23):8715-20
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
We have found that domains containing the adapter complex 2 (AP2)-coated vesicle adapter and the endocytic accessory proteins CALM (clathrin assembly
lymphoid myeloid leukemia
protein), epsin, and eps15/eps15R (EGF receptor pathway substrate 15-related) nevertheless persist at the plasma membrane.
[MeSH-major]
Cell
Membrane / metabolism.
Cell
Surface Extensions / metabolism. Clathrin / metabolism
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Nat Rev Mol Cell Biol. 2002 Aug;3(8):555-65
[
12154367.001
]
[Cites]
Nature. 2002 Sep 26;419(6905):361-6
[
12353027.001
]
[Cites]
Biophys J. 2003 Feb;84(2 Pt 1):842-53
[
12547768.001
]
[Cites]
Mol Biol Cell. 2003 Feb;14(2):516-28
[
12589051.001
]
[Cites]
J Cell Biol. 2003 Jul 7;162(1):113-24
[
12847086.001
]
[Cites]
J Cell Biol. 2003 Aug 18;162(4):693-701
[
12913109.001
]
[Cites]
J Cell Biol. 2003 Sep 1;162(5):909-18
[
12952941.001
]
[Cites]
EMBO J. 2003 Oct 1;22(19):4980-90
[
14517237.001
]
[Cites]
Annu Rev Cell Dev Biol. 2003;19:287-332
[
14570572.001
]
[Cites]
J Biol Chem. 2003 Nov 14;278(46):45160-70
[
12960147.001
]
[Cites]
Dev Cell. 2004 Jan;6(1):29-41
[
14723845.001
]
[Cites]
Science. 2004 Jan 23;303(5657):495-9
[
14645856.001
]
[Cites]
Curr Biol. 2004 Mar 23;14(6):R250-2
[
15043839.001
]
[Cites]
Mamm Genome. 2000 Nov;11(11):1006-15
[
11063258.001
]
[Cites]
Science. 2001 Feb 9;291(5506):1051-5
[
11161218.001
]
[Cites]
Traffic. 2000 Jul;1(7):545-52
[
11208142.001
]
[Cites]
Traffic. 2000 Jan;1(1):19-28
[
11208055.001
]
[Cites]
Traffic. 2001 Feb;2(2):138-47
[
11247304.001
]
[Cites]
J Cell Biol. 2001 Sep 17;154(6):1209-23
[
11564758.001
]
[Cites]
J Cell Biol. 2001 Oct 15;155(2):193-200
[
11604418.001
]
[Cites]
J Cell Biol. 2001 Oct 15;155(2):291-300
[
11604424.001
]
[Cites]
J Biol Chem. 2001 Dec 7;276(49):46230-6
[
11577110.001
]
[Cites]
J Biol Chem. 2002 Mar 8;277(10):8209-16
[
11756460.001
]
[Cites]
Nature. 2002 Mar 28;416(6879):451-5
[
11919637.001
]
[Cites]
J Biol Chem. 2002 May 31;277(22):19897-904
[
11889126.001
]
[Cites]
J Biol Chem. 2002 Jul 26;277(30):27433-41
[
12021271.001
]
[Cites]
Nat Rev Mol Cell Biol. 2006 Jan;7(1):9-19
[
16365634.001
]
[Cites]
Traffic. 2006 Mar;7(3):262-81
[
16497222.001
]
[Cites]
Dev Cell. 2006 Mar;10(3):329-42
[
16516836.001
]
[Cites]
EMBO J. 1988 Apr;7(4):919-29
[
3402440.001
]
[Cites]
J Biol Chem. 2004 Apr 16;279(16):16657-61
[
14985334.001
]
[Cites]
Trends Cell Biol. 2004 Jul;14(7):352-8
[
15246428.001
]
[Cites]
Cell. 2004 Sep 3;118(5):591-605
[
15339664.001
]
[Cites]
J Cell Biol. 1969 Jul;42(1):202-20
[
4182372.001
]
[Cites]
Cell. 1979 Feb;16(2):303-12
[
455437.001
]
[Cites]
J Cell Biol. 1980 Mar;84(3):560-83
[
6987244.001
]
[Cites]
J Cell Biol. 1981 Dec;91(3 Pt 1):790-7
[
7328122.001
]
[Cites]
J Cell Biol. 1985 Dec;101(6):2055-62
[
4066749.001
]
[Cites]
Eur J Cell Biol. 1986 Oct;42(1):35-44
[
3792341.001
]
[Cites]
EMBO J. 1986 Dec 1;5(12):3143-9
[
3816757.001
]
[Cites]
J Cell Biol. 1988 Sep;107(3):877-86
[
3417785.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 Dec;86(23):9289-93
[
2574457.001
]
[Cites]
J Biol Chem. 1991 Mar 5;266(7):4437-41
[
1900294.001
]
[Cites]
J Cell Biol. 1992 Nov;119(4):787-96
[
1358896.001
]
[Cites]
Biophys J. 1993 Jul;65(1):316-24
[
8369439.001
]
[Cites]
J Biol Chem. 1995 Mar 3;270(9):4933-42
[
7876268.001
]
[Cites]
J Biol Chem. 1995 Apr 28;270(17):10079-83
[
7730311.001
]
[Cites]
Biophys J. 1997 Feb;72(2 Pt 1):953-7
[
9017220.001
]
[Cites]
J Biol Chem. 1998 Jan 30;273(5):3003-12
[
9446614.001
]
[Cites]
Biophys J. 1998 Jun;74(6):2862-75
[
9635740.001
]
[Cites]
Curr Biol. 1998 Dec 17-31;8(25):1399-402
[
9889104.001
]
[Cites]
Mol Biol Cell. 1999 Apr;10(4):961-74
[
10198050.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6775-80
[
10359788.001
]
[Cites]
EMBO J. 2004 Nov 10;23(22):4371-83
[
15496985.001
]
[Cites]
Mol Biol Cell. 2005 Feb;16(2):964-75
[
15601897.001
]
[Cites]
J Biol Chem. 2005 Feb 18;280(7):6109-17
[
15533940.001
]
[Cites]
J Biol Chem. 2005 Feb 18;280(7):6101-8
[
15533941.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2760-5
[
15701692.001
]
[Cites]
Mol Biol Cell. 2005 Apr;16(4):1769-76
[
15689492.001
]
[Cites]
Biochim Biophys Acta. 2005 Jul 10;1744(3):415-37
[
15922462.001
]
[Cites]
Traffic. 2005 Dec;6(12):1225-34
[
16262731.001
]
[Cites]
Nature. 2005 Dec 1;438(7068):590-6
[
16319878.001
]
[Cites]
Dev Cell. 2005 Dec;9(6):791-804
[
16326391.001
]
[Cites]
Nat Cell Biol. 1999 May;1(1):33-9
[
10559861.001
]
(PMID = 16735469.001).
[ISSN]
0027-8424
[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 / Adaptor Protein Complex 2; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / epsin
[Other-IDs]
NLM/ PMC1482644
58.
Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Amare P, Arora B, Banavali SD, Nair CN:
Clinico-hematological profile in biphenotypic acute leukemia.
Indian J Cancer
; 2009 Apr-Jun;46(2):160-8
[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]
Clinico-hematological profile in
biphenotypic
acute
leukemia
.
BACKGROUND: We present a clinico-hematological profile and treatment outcome of
Biphenotypic
Acute
Leukemia
(BAL).
MATERIAL AND METHODS:
Diagnosis
was based on WHO classification, including clinical details, morphology, cytochemistry, immunophenotyping, and molecular genetics.
We included those cases, which fulfilled the European Group for the Immunological Characterization of
Acute
Leukemia
's (EGIL's) scoring system criteria for the
diagnosis
of BAL, as per recommendation of the WHO classification.
B-
Myeloid
(14 cases) followed by T-
Myeloid
BAL (13 cases) were the commonest subtypes.
Polymorphous population of blasts (16 cases) was commonly associated with T-
Myeloid
BAL (10 cases).
BCR ABL fusion positivity was a common cytogenetic
abnormality
(seven cases).
CONCLUSIONS: Pediatric BAL
and T
-
B lymphoid
BAL have a better prognosis.
BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic
myeloid leukemia
(CML) in blast crisis with
biphenotypic
expression and treated accordingly.
[MeSH-major]
Immunophenotyping.
Leukemia
,
Biphenotypic
,
Acute
/ blood.
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
[MeSH-minor]
Adolescent. Adult. Case-Control Studies. Child. Child, Preschool.
Disease
Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged.
Phenotype
. Retrospective Studies. Young Adult
Genetic Alliance.
consumer health - Acute Biphenotypic 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 = 19346652.001).
[ISSN]
0019-509X
[Journal-full-title]
Indian journal of cancer
[ISO-abbreviation]
Indian J Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
59.
Saitoh T, Matsushima T, Iriuchishima H, Yamane A, Irisawa H, Handa H, Tsukamoto N, Karasawa M, Nojima Y, Murakami H:
Presentation of extramedullary Philadelphia chromosome-positive biphenotypic acute leukemia as testicular mass: Response to imatinib-combined chemotherapy.
Leuk Lymphoma
; 2006 Dec;47(12):2667-9
[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]
Presentation of extramedullary Philadelphia chromosome-positive
biphenotypic
acute
leukemia
as testicular mass: Response to imatinib-combined chemotherapy.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive /
diagnosis
. Piperazines / pharmacology. Pyrimidines / pharmacology. Testicular Neoplasms /
diagnosis
[MeSH-minor]
Benzamides. Bone Marrow Cells / cytology. Flow Cytometry. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Stem
Cell
Transplantation. Transplantation, Homologous
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17169818.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
60.
Balgobind BV, Hollink IH, Reinhardt D, van Wering ER, de Graaf SS, Baruchel A, Stary J, Beverloo HB, de Greef GE, Pieters R, Zwaan CM, van den Heuvel-Eibrink MM:
Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique.
Eur J Cancer
; 2010 Jul;46(10):1892-9
[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]
Low frequency of MLL-partial tandem duplications in paediatric
acute
myeloid
leukaemia
using MLPA as a novel DNA screenings technique.
Mixed
-
lineage leukaemia
(MLL)-partial tandem duplications (PTDs) are found in 3-5% of adult
acute
myeloid
leukaemia
(AML), and are associated with poor prognosis.
[MeSH-major]
Gene Duplication. Genetic Testing / methods.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-
Lymphoid Leukemia
Protein / genetics. Tandem Repeat Sequences / genetics
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Genetic Testing
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright 2010 Elsevier Ltd. All rights reserved.
(PMID = 20233657.001).
[ISSN]
1879-0852
[Journal-full-title]
European journal of cancer (Oxford, England : 1990)
[ISO-abbreviation]
Eur. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
61.
Leung J, Pang A, Yuen WH, Kwong YL, Tse EW:
Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
Blood
; 2007 Jan 15;109(2):740-6
[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]
Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in
leukemia
cells.
Arsenic trioxide (As2O3) is highly efficacious in
acute
promyelocytic
leukemia
(APL).
In 10 of 11
myeloid and lymphoid leukemia
lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
Similarly, the chronic
myeloid leukemia
line K562 expressed low levels of AQP9 and was As2O3 insensitive.
Pretreatment of the
myeloid leukemia
line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other
acute
myeloid leukemias
(AMLs), which might explain their exquisite As2O3 sensitivity.
[MeSH-major]
Aquaporins / metabolism. Arsenicals / pharmacology.
Leukemia
,
Myeloid
/ metabolism.
Leukemia
, Promyelocytic,
Acute
/ drug therapy.
Leukemia
, Promyelocytic,
Acute
/ metabolism. Oxides / pharmacology
[MeSH-minor]
Acute
Disease
.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects
Hazardous Substances Data Bank.
ARSENIC TRIOXIDE
.
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16968895.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
62.
Han X, Bueso-Ramos CE:
Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias.
Am J Clin Pathol
; 2007 Apr;127(4):528-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Precursor T-
cell
acute
lymphoblastic leukemia
/
lymphoblastic
lymphoma and
acute
biphenotypic leukemias
.
Session 4 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop focused on case presentations of precursor T-
cell
acute
lymphoblastic leukemia
/
lymphoblastic
lymphoma (pre-T ALL/LBL) and
acute
biphenotypic leukemia
.
Acute
biphenotypic leukemias
are characterized by a single population of blasts that express
myeloid
, T- or B-
lineage
antigens in various combinations and account for fewer than 4% of all
acute
leukemias
.
An accurate
diagnosis
of pre-T ALL/LBL and
acute
biphenotypic leukemia
requires a multiparametric approach, including examination of
morphologic
features, immunophenotype, clinical characteristics, and cytogenetic and molecular findings.
[MeSH-major]
Biomarkers, Tumor / analysis.
Leukemia
,
Lymphoid
/
diagnosis
. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma /
diagnosis
[MeSH-minor]
Chromosome Aberrations.
Diagnosis
, Differential. Gene Expression Profiling. Humans. Immunohistochemistry
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Lymphoblastic lymphoma
.
MedlinePlus Health Information.
consumer health - Chronic Lymphocytic Leukemia
.
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 = 17369128.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Congresses
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
63.
Xavier MO, Oliveira Fde M, Almeida Vd, Prolla G, Severo LC:
Invasive Aspergillus flavus sinusitis: case report in a patient with biphenotypic acute leukemia.
Rev Inst Med Trop Sao Paulo
; 2009 Jan-Feb;51(1):57-8
[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]
Invasive Aspergillus flavus sinusitis: case report in a patient with
biphenotypic
acute
leukemia
.
Here we report a case of invasive pansinusitis with proptosis of the right eye caused by Aspergillus flavus in an immunocompromised patient with
acute
biphenotypic leukemia
without aggressive therapy response.
[MeSH-major]
Aspergillosis /
diagnosis
. Aspergillus flavus / isolation & purification. Immunocompromised Host.
Leukemia
,
Biphenotypic
,
Acute
/ immunology. Sinusitis / microbiology
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Aspergillosis
.
MedlinePlus Health Information.
consumer health - Sinusitis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19229393.001).
[ISSN]
1678-9946
[Journal-full-title]
Revista do Instituto de Medicina Tropical de São Paulo
[ISO-abbreviation]
Rev. Inst. Med. Trop. Sao Paulo
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Brazil
64.
Liu B, Li R, Wu HJ, Chen Y:
[Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Apr;15(2):421-4
[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]
[Clinical study on prognosis of
acute
leukemia
subtypes Ly + AML and My + ALL].
The purpose of this study was to investigate the prognosis of
acute
myelogenous
leukemia
(AML),
acute
lymphoblastic leukemia
(ALL),
lymphoid
antigen-positive
acute
myeloid leukemia
(Ly + AML),
myeloid
antigen-positive
acute
leukemia
(My + ALL)
and biphenotypic
acute
leukemia
(BAL).
Immunophenotyping was performed on medullary specimens of 197
acute
leukemia
(AL) patients by using three-color flow cytometry analysis and CD45/SSC gating.
The results showed that in Ly + AML, CD7 was the most common (53.8%) as compared to other
lymphoid
markers, however, in My + ALL CD13 was the most common (47.2%) as compared to other
myeloid
markers.
It is concluded that since Ly + AML has
lymphoid
markers, and the prognosis of Ly + AML is worse than AML, the clinical therapy for Ly + AML should contain both AML and ALL.
Though My + ALL had
myeloid
markers, no significant difference was found between My + ALL and ALL, it might be supposed that their therapy could be the same.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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 = 17493361.001).
[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
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Antigens, CD7; EC 3.4.11.2 / Antigens, CD13
65.
Alvarado Y, Welch MA, Swords R, Bruzzi J, Schlette E, Giles FJ:
Nelarabine activity in acute biphenotypic leukemia.
Leuk Res
; 2007 Nov;31(11):1600-3
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Nelarabine activity in
acute
biphenotypic leukemia
.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use.
Leukemia
/ drug therapy
[MeSH-minor]
Acute
Disease
. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Flow Cytometry. Humans. Middle Aged.
Phenotype
. Vincristine / administration & dosage
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Leukemia
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17512588.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Arabinonucleosides; 5J49Q6B70F / Vincristine; 60158CV180 / nelarabine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
66.
Asgarian Omran H, Shabani M, Shahrestani T, Sarafnejad A, Khoshnoodi J, Vossough P, Faranoush M, Sharifian RA, Jeddi-Tehrani M, Rabbani H, Shokri F:
Immunophenotypic subtyping of leukemic cells from Iranian patients with acute lymphoblastic leukaemia: association to disease outcome.
Iran J Immunol
; 2007 Mar;4(1):15-25
[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]
Immunophenotypic subtyping of leukemic cells from Iranian patients with
acute
lymphoblastic
leukaemia
: association to
disease
outcome.
BACKGROUND: Immunophenotypic characterization of the leukemic cells has been widely used as a tool for
diagnosis
, classification, stratification and prognosis of
leukaemia
.
OBJECTIVE: To investigate the immunophenotypic subtype profiles of Iranian patients with
acute
lymphoblastic leukemia
(ALL) and its association to
disease
outcome.
RESULTS: The samples were initially categorized into T-ALL (n=9), B-ALL (n=50) and
mixed lineage
(n=1) based on the expression patterns of CD3 and CD19 molecules.
B-ALL patients could further be classified into four subtypes, including Pro-B (n=7, 11.7%), Pre-
B I
(n=28, 46.7%), Pre-B II (n=13, 21.7%) and immature/mature B cells (n=2, 3.3%) on the basis of expression of CD10, CD19, CD20, HLA-DR and TdT.
Clinical manifestations and laboratory findings of the patients did not reveal association with immunophenotypic subtypes of ALL, with the exception of mediastinal mass and WBC count at the time of
diagnosis
which were found to be significantly higher in patients with T-ALL compared with B-ALL (p=0.001 and 0.014), respectively.
CONCLUSION: Our results indicate that overall the immunophenotypic profile of Iranian ALL patients is similar to previous reports and it might be used for monitoring of minimal residual
disease and
prognosis.
[MeSH-major]
Immunophenotyping.
Leukemia
, B-
Cell
/ immunology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / immunology
[MeSH-minor]
Adult. Child.
Disease
Progression. Humans. Iran / epidemiology. Predictive Value of Tests. Recurrence
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 = 17652839.001).
[ISSN]
1735-1383
[Journal-full-title]
Iranian journal of immunology : IJI
[ISO-abbreviation]
Iran J Immunol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Iran
67.
Liu Y, Tang SQ, Yang G, Feng C, Liu LZ, Lei Q:
[Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Oct;15(5):961-6
[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]
[Skin lesions and myelodysplastic syndrome as initial manifestations of
biphenotypic
acute
leukemia
].
The aim of this study was to investigate the clinical, pathological and biological features of
biphenotypic
acute
leukemia
.
The results showed that extramedullary skin lesions and myelodysplasia occurred before the onset of overt
disease
.
At the time of
diagnosis
, this case had more than 30% blasts in bone marrow with meningeal involvement.
Flow cytometry revealed the co-expression of
myeloid
antigens (cMPO, CD33 and CD117)
and T
-
lymphoid
antigens (cCD3, CD5, CD7, dual expression of CD4 and CD8).
All above-mentioned results led to the
diagnosis
of
biphenotypic
acute
leukemia
.
It is concluded that the
biphenotypic
acute
leukemia
is an uncommon type of
leukemia
which may be preceded by myelodysplastic syndrome and has aggressive clinical and biological behavior.
Immunophenotype, cytogenetics and molecular analysis can contribute to early
diagnosis
of BAL and evaluation of prognosis.
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
Genetic Alliance.
consumer health - Myelodysplastic syndromes
.
MedlinePlus Health Information.
consumer health - Leukemia
.
MedlinePlus Health Information.
consumer health - Myelodysplastic Syndromes
.
MedlinePlus Health Information.
consumer health - Skin Conditions
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17956670.001).
[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]
Case Reports; English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD43; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
68.
Kuroda N, Mizobuchi M, Shimamura Y, Daibata M, Miyoshi I, Ohara M, Hirouchi T, Mizuno K, Lee GH:
Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia.
APMIS
; 2006 Dec;114(12):908-11
[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]
Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of
acute
biphenotypic leukemia
.
A 47-year-old Japanese woman was diagnosed as having
acute
biphenotypic leukemia
with association of t(9;22)(q34;q11).
In conclusion, extensive intrahepatic involvement by neoplastic cells in adult
acute
biphenotypic leukemia
may cause the unusual "disorganized" hepatic fibrosis.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ pathology. Liver Cirrhosis / pathology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Cirrhosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17207092.001).
[ISSN]
0903-4641
[Journal-full-title]
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
[ISO-abbreviation]
APMIS
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Reticulin; 0 / Transforming Growth Factor beta1; 0 / platelet-derived growth factor BB; 9007-34-5 / Collagen
69.
Kong CT, Sham MH, So CW, Cheah KS, Chen SJ, Chan LC:
The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice.
Leukemia
; 2006 Oct;20(10):1829-39
[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 Mll-Een knockin fusion gene enhances proliferation of
myeloid
progenitors derived from mouse embryonic stem cells and causes
myeloid
leukaemia
in chimeric mice.
Rearrangement of the
mixed lineage leukaemia
(MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with
acute
myeloid
leukaemia
.
Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when Mll(Een/+) embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of
myeloid
progenitors with self-renewal property.
We also generated Mll(Een/+) chimeric mice, which developed
leukaemia
displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells.
Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the Mll(Een/+) chimeras revealed an accumulation of Mac-1+/Gr-1- immature
myeloid
cells
and a
reduction in normal B-
and T
-
cell
populations.
We observed differential regulation of Hox genes between
myeloid
cells derived from Mll(Een/+) ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the
disease
.
We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of
leukaemia
.
[MeSH-major]
Hematopoietic Stem Cells / pathology. Intracellular Signaling Peptides and Proteins / genetics.
Leukemia
,
Myeloid
/ genetics.
Leukemia
,
Myeloid
/ pathology.
Myeloid
Cells / pathology.
Myeloid
-
Lymphoid Leukemia
Protein / genetics
[MeSH-minor]
Amino Acid Sequence. Animals. Base Sequence.
Cell
Division / physiology. Chimera.
Disease
Models, Animal. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Genes, Homeobox / physiology. Humans. Infant. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Translocation, Genetic
MedlinePlus Health Information.
consumer health - Stem Cells
.
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
(PMID = 16888613.001).
[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 / Intracellular Signaling Peptides and Proteins; 0 / SH3GL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
70.
Royer-Bégyn M, Teira P, Deybach JC, Mas E, Mazereeuw-Hautier J:
[Porphyria cutanea tarda in a child undergoing bone marrow grafting].
Ann Dermatol Venereol
; 2010 Oct;137(10):640-4
[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.
[Transliterated title]
Porphyrie cutanée tardive chez un enfant greffé
de
moelle.
His past medical history revealed
acute
biphenotypic
leukaemia
with complete remission after allogeneic hematopoietic stem
cell
transplantation (unrelated donor).
Complications of bone marrow transplant comprised anaemia (treated by blood transfusions), primary cytomegalovirus (CMV) infection, pulmonary aspergillosis and
acute
digestive graft-versus-host
disease
.
The
diagnosis
of type I sporadic PCT was based on high levels of porphyria and normal erythrocytic uroporphyrinogen decarboxylase activity.
The causative role of bone marrow transplantation in the development of PCT could be related to several triggering factors: primary CMV infection, hepatotoxic drugs, blood transfusion and possible chronic hepatic graft-versus-host
disease
.
[MeSH-major]
Bone Marrow Transplantation / adverse effects. Hematopoietic Stem
Cell
Transplantation / adverse effects.
Leukemia
,
Biphenotypic
,
Acute
/ therapy. Porphyria Cutanea Tarda /
diagnosis
. Porphyria Cutanea Tarda / therapy
Genetic Alliance.
consumer health - Porphyria
.
Genetic Alliance.
consumer health - Porphyria cutanea tarda
.
MedlinePlus Health Information.
consumer health - Bone Marrow Transplantation
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 Elsevier Masson SAS. All rights reserved.
(PMID = 20932445.001).
[ISSN]
0151-9638
[Journal-full-title]
Annales de dermatologie et de vénéréologie
[ISO-abbreviation]
Ann Dermatol Venereol
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
71.
Matsumoto Y, Taki T, Fujimoto Y, Taniguchi K, Shimizu D, Shimura K, Uchiyama H, Kuroda J, Nomura K, Inaba T, Shimazaki C, Horiike S, Taniwaki M:
Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for diagnosis of T/myeloid biphenotypic acute leukemia and its clonal evolution.
Int J Hematol
; 2009 Apr;89(3):352-8
[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]
Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for
diagnosis
of T/
myeloid biphenotypic
acute
leukemia and
its clonal evolution.
Biphenotypic
acute
leukemia
co-expressing T-
lymphoid and myeloid
markers is rare, accounting for less than 1% of
acute
leukemias
.
Recurrence of monosomies 7p and/or 12p in T/
myeloid biphenotypic
acute
leukemia
has been reported.
We treated a patient with T/
myeloid biphenotypic
acute
leukemia
showing clonal chromosomal and genetic abnormalities including dic(7;12)(p11;p11) and Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication.
Cytogenetic analysis of both bone marrow and lymph node cells disclosed that the patient's lymph node
leukemia
cells had chromosomal abnormalities in addition to dic(7;12).
Our findings suggest that the
leukemia
cells of systemic lymphadenopathy had evolved as secondary cells from marrow
leukemia
cells.
The patient was successfully treated with induction chemotherapy for
acute
myeloid leukemia
followed by allogeneic bone marrow transplantation.
[MeSH-major]
Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Duplication.
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/ enzymology. fms-Like Tyrosine Kinase 3 / metabolism
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Surg Pathol. 1997 Sep;21(9):1037-46
[
9298880.001
]
[Cites]
Leukemia. 2000 Mar;14(3):522-4
[
10720156.001
]
[Cites]
Br J Haematol. 2003 Dec;123(5):842-9
[
14632775.001
]
[Cites]
Br J Haematol. 2004 Jun;125(6):814-5
[
15180872.001
]
[Cites]
Leukemia. 2006 Nov;20(11):2074-6
[
16990788.001
]
[Cites]
Leuk Lymphoma. 2008 Apr;49(4):700-9
[
18398737.001
]
[Cites]
Haematologica. 1997 Jan-Feb;82(1):64-6
[
9107085.001
]
[Cites]
Blood. 2005 Nov 15;106(10 ):3658-65
[
16076872.001
]
[Cites]
Leukemia. 1993 Jun;7(6):919-27
[
8501986.001
]
[Cites]
Endoscopy. 2002 Oct;34(10):808-13
[
12244503.001
]
[Cites]
Br J Haematol. 1998 Jan;100(1):147-55
[
9450804.001
]
[Cites]
Leukemia. 1996 Dec;10(12):1911-8
[
8946930.001
]
[Cites]
Haematologica. 1999 Aug;84(8):699-706
[
10457405.001
]
[Cites]
Leuk Res. 2006 Sep;30(9):1085-9
[
16533526.001
]
[Cites]
Leukemia. 1995 Oct;9(10):1783-6
[
7564526.001
]
[Cites]
Bone Marrow Transplant. 1995 Jun;15(6):825-8
[
7581076.001
]
[Cites]
Br J Haematol. 1999 Apr;105(1):155-62
[
10233379.001
]
[Cites]
Blood. 2006 May 1;107(9):3724-6
[
16368883.001
]
[Cites]
Leukemia. 1996 Aug;10(8):1283-7
[
8709632.001
]
[Cites]
Leukemia. 2006 Apr;20(4):620-6
[
16437134.001
]
[Cites]
Leukemia. 1997 Sep;11(9):1442-6
[
9305595.001
]
(PMID = 19308660.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
72.
Zheng C, Wu J, Liu X, Ding K, Cai X, Zhu W:
What is the optimal treatment for biphenotypic acute leukemia?
Haematologica
; 2009 Dec;94(12):1778-80; author reply 1780
[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]
What is the optimal treatment for
biphenotypic
acute
leukemia
?
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 1992 Oct 15;80(8):2066-73
[
1327288.001
]
[Cites]
Leukemia. 2003 Aug;17(8):1538-43
[
12886240.001
]
[Cites]
Blood. 1989 Nov 1;74(6):2096-102
[
2553160.001
]
[Cites]
Haematologica. 2009 Jul;94(7):919-27
[
19454497.001
]
[Cites]
Leukemia. 1995 Oct;9(10):1783-6
[
7564526.001
]
[Cites]
Leukemia. 2007 Nov;21(11):2264-70
[
17611554.001
]
[Cites]
Blood. 2009 May 21;113(21):5083-9
[
19131545.001
]
[CommentOn]
Haematologica. 2009 Jul;94(7):919-27
[
19454497.001
]
(PMID = 19996120.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comment; Letter
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD34; EC 1.11.1.7 / Peroxidase
[Other-IDs]
NLM/ PMC2791943
73.
Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B:
[Biphenotypic and bilineal acute leukemias].
Acta Med Croatica
; 2008 Oct;62(4):387-90
[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]
[
Biphenotypic and
bilineal
acute
leukemias
].
Human
acute
leukemias
(AL) are classified as
myeloid
or
lymphoid
according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
However, in the minority of cases leukemic cells express markers of more than one
lineage
, which has led to the introduction of a new subgroup of
acute
leukemias
termed
mixed
or
biphenotypic
acute
leukemias
(BAL).
In an effort to distinguish between BAL and those AL with aberrant expression of markers of other
lineage
, the European Group for the Immunological Characterization of
Acute
Leukemias
(EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for
myeloid
, B- and/or T-
lymphoid
lineage
, respectively.
The new WHO classification of hematologic tumors has adopted the EGIL criteria for BAL and introduced a new group of AL termed 'AL of ambiguous
lineage
'.
In addition to BAL in which a single
cell
population expresses both
myeloid and lymphoid
differentiation markers, this new group of
leukemias
also comprises cases that present with two separate blast populations (
acute
bilineal
leukemia
, aBLL).
In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare
disease
constituting 1%-2% of AL cases that contains B- or T-
lymphoid
along with
myeloid
blasts.
Chromosome abnormalities are frequent in both entities with a relatively high incidence of Philadelphia chromosome and rearrangements involving 11q23, especially in cases with B-
and myeloid
involvement.
Unfortunately, optimal therapy is not known, although regimens designed for
acute
lymphoblastic leukemia
may result in a better response rate.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19209464.001).
[ISSN]
1330-0164
[Journal-full-title]
Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
[ISO-abbreviation]
Acta Med Croatica
[Language]
hrv
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Croatia
[Number-of-references]
30
74.
Sárová I, Brezinová J, Zemanová Z, Izáková S, Lizcová L, Malinová E, Berková A, Cermák J, Maaloufová J, Nováková L, Michalová K:
Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia.
Cancer Genet Cytogenet
; 2010 Jun;199(2):121-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Cytogenetic manifestation of chromosome 11 duplication/amplification in
acute
myeloid leukemia
.
Gene amplification is a frequent genetic
abnormality
in solid tumors, and many oncogenes are activated in this way.
In
acute
myeloid leukemia
(AML), a frequent target of gene amplification is chromosome 11, particularly chromosome region 11q23, including the MLL (
myeloid
/
lymphoid leukemia
) gene.
[MeSH-major]
Chromosomes, Human, Pair 11 / genetics. Gene Amplification. Gene Duplication.
Leukemia
,
Myeloid
,
Acute
/ genetics. Trisomy
Genetic Alliance.
consumer health - Chromosome 11
.
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
[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
(PMID = 20471515.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
75.
Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF:
Clinical characteristics and outcome of children with biphenotypic acute leukemia.
Haematologica
; 2009 Dec;94(12):1682-90
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Clinical characteristics and outcome of children with
biphenotypic
acute
leukemia
.
BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of
biphenotypic
acute
leukemia
in children is limited.
DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with
biphenotypic
acute
leukemia
diagnosed and treated over an 8-year period.
According to the EGIL scoring system 24 (3.7%) of 633 patients with
acute
leukemia
were classified as having
biphenotypic
acute
leukemia
.
The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the
diagnosis
of
leukemia
of ambiguous
lineage
.
Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having
mixed
phenotype
acute
leukemia
.
The majority of the patients (58.3%) had
a B
-
lymphoid
/
myeloid phenotype
, followed by the T-
lymphoid
/
myeloid phenotype
.
The most frequent chromosomal
abnormality
involved the 14q32 locus.
Patients received therapy based on a treatment regimen for
acute
lymphocytic leukemia
regimen, which included
myeloid
-effective agents.
The survival of those patients who underwent hematopoietic stem
cell
transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
The outcome of the 11 patients who were retrospectively classified as having
mixed
phenotype
acute
leukemia
according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
CONCLUSIONS: An
acute
lymphocytic leukemia
type of induction therapy, using agents that are active against
lymphoid and myeloid leukemias
, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
Hematopoietic stem
cell
transplantation may not be necessary for all patients in first complete remission.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/ therapy
[MeSH-minor]
Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem
Cell
Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Clin Pathol. 2002 Mar;117(3):380-9
[
11888077.001
]
[Cites]
Pediatr Blood Cancer. 2009 Sep;53(3):444-52
[
19489056.001
]
[Cites]
Blood. 2004 Nov 1;104(9):2690-6
[
15251979.001
]
[Cites]
Am J Clin Pathol. 1990 Jul;94(1):54-8
[
1694392.001
]
[Cites]
Blood. 1990 Jul 1;76(1):150-6
[
2364166.001
]
[Cites]
Br J Haematol. 1990 Jun;75(2):202-7
[
2372506.001
]
[Cites]
Leukemia. 1993 Jun;7(6):919-27
[
8501986.001
]
[Cites]
J Clin Pathol. 1993 Oct;46(10):903-7
[
8227405.001
]
[Cites]
Leukemia. 1995 Oct;9(10):1783-6
[
7564526.001
]
[Cites]
Blood. 1997 Apr 1;89(7):2488-93
[
9116293.001
]
[Cites]
Haematologica. 1997 Jan-Feb;82(1):64-6
[
9107085.001
]
[Cites]
Br J Haematol. 1998 Jan;100(1):147-55
[
9450804.001
]
[Cites]
Blood. 1998 Aug 1;92(3):795-801
[
9680347.001
]
[Cites]
J Clin Oncol. 1998 Dec;16(12):3768-73
[
9850020.001
]
[Cites]
Haematologica. 1999 Aug;84(8):699-706
[
10457405.001
]
[Cites]
Leukemia. 2006 Apr;20(4):620-6
[
16437134.001
]
[Cites]
Br J Haematol. 2007 Jul;138(2):213-6
[
17593028.001
]
[Cites]
J Chin Med Assoc. 2007 Jul;70(7):269-73
[
17631462.001
]
[Cites]
Blood. 2009 May 21;113(21):5083-9
[
19131545.001
]
[Cites]
Br J Haematol. 2003 Dec;123(5):842-9
[
14632775.001
]
(PMID = 19713227.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD
[Other-IDs]
NLM/ PMC2791935
76.
Tsutsumi Y, Tanaka J, Minami H, Musashi M, Fukushima A, Ehira N, Kanamori H, Yamato H, Sasaki J, Funaki C, Hasegawa S, Obara S, Ogura N, Asaka M, Imamura M, Masauzi N:
Acute biphenotypic leukemia and an acquired X chromosome.
Cancer Genet Cytogenet
; 2005 Feb;157(1):94-5
[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]
Acute
biphenotypic leukemia
and an acquired X chromosome.
[MeSH-major]
Chromosomes, Human, X.
Leukemia
/ genetics. Sex Chromosome Aberrations
[MeSH-minor]
Acute
Disease
. Aged. Humans. Male
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15676158.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
77.
Georgy M, Yonescu R, Griffin CA, Batista DA:
Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.
Cancer Genet Cytogenet
; 2008 Aug;185(1):28-31
[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 mixed lineage
leukemia and a t
(6;14)(q25;q32) in two adults.
Acute mixed lineage
leukemia
(AMLL) is a rare form of
leukemia
in which both
myeloid and lymphoid
markers are present.
Few chromosome abnormalities have been identified associated with this form of
leukemia
.
A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with
acute
leukemia and
in three of these cases the
diagnosis
was
mixed lineage
.
[MeSH-major]
Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18656690.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
78.
Oka S, Yokote T, Akioka T, Hara S, Kobayashi K, Hirata Y, Hiraoka N, Tsuji M, Hanafusa T:
Trisomy 21 as the sole acquired karyotypic abnormality in biphenotypic acute leukemia.
Int J Hematol
; 2007 Apr;85(3):270-2
[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]
Trisomy 21 as the sole acquired karyotypic
abnormality
in
biphenotypic
acute
leukemia
.
[MeSH-major]
Chromosome Aberrations. Down Syndrome / blood. Down Syndrome / pathology.
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
/ classification.
Acute
Disease
/ therapy. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Humans. Male. Treatment Outcome. Vincristine / therapeutic use
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - Down Syndrome
.
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 1998 Jul 15;92(2):596-9
[
9657760.001
]
[Cites]
Br J Haematol. 2005 Feb;128(4):548-51
[
15686466.001
]
[Cites]
Ann Hematol. 2003 Apr;82(4):236-40
[
12707727.001
]
[Cites]
Blood. 1986 Jan;67(1):1-11
[
3079640.001
]
[Cites]
Leukemia. 1992 Mar;6(3):171-5
[
1533007.001
]
[Cites]
Blood. 1990 Aug 15;76(4):808-13
[
2166608.001
]
[Cites]
Leuk Res. 1999 Nov;23(11):1079-83
[
10576514.001
]
[Cites]
Am J Med Genet Suppl. 1990;7:262-6
[
2149959.001
]
[Cites]
Blood. 1983 Jun;61(6):1138-45
[
6404327.001
]
[Cites]
J Clin Oncol. 1998 Dec;16(12):3803-9
[
9850025.001
]
(PMID = 17483067.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
Japan
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
79.
Nakagawa Y, Hasegawa M, Kurata M, Yamamoto K, Abe S, Inoue M, Takemura T, Hirokawa K, Suzuki K, Kitagawa M:
Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).
Am J Hematol
; 2005 Mar;78(3):173-80
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression of IAP-family proteins in adult
acute mixed lineage
leukemia
(AMLL).
To determine the apoptosis-resistant mechanism in adult
acute mixed lineage
leukemia
(AMLL) with
biphenotypic
blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.
These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of
leukemia
.
[MeSH-major]
Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism.
Leukemia
,
Biphenotypic
,
Acute
/ metabolism. Proteins / metabolism
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins.
Leukemia
, Monocytic,
Acute
/ drug therapy.
Leukemia
, Monocytic,
Acute
/ metabolism.
Leukemia
, Monocytic,
Acute
/ pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15726601.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[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 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger
80.
Dimou J, Jithoo R, Tsui A, Morokoff AP:
Spinal cord compression as the initial presentation of acute biphenotypic leukaemia.
J Clin Neurosci
; 2009 Dec;16(12):1696-8
[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]
Spinal cord compression as the initial presentation of
acute
biphenotypic
leukaemia
.
Acute
biphenotypic
leukaemia
(BAL) is an uncommon haematological malignancy with features of
myeloid and lymphoid
origin and poor overall prognosis.
Histopathology confirmed the
diagnosis
of
acute
biphenotypic
(B/
myeloid
)
leukaemia
.
He succumbed to the
disease
three months post-
diagnosis
after failing induction chemotherapy.
While central nervous system involvement with
acute leukaemia
is well recognised, this is the first reported patient with spinal cord compression secondary to this
leukaemia
subtype.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ etiology. Spinal Cord Compression / complications
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19815414.001).
[ISSN]
1532-2653
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Scotland
[Chemical-registry-number]
0 / Antigens, CD79; EC 1.11.1.7 / Peroxidase
81.
Kim HR, Hong JH, Yoon CH, Lee SH, Park SH, Kim HY:
Arthritis preceding acute biphenotypic leukemia.
Clin Rheumatol
; 2006 May;25(3):380-1
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Arthritis preceding
acute
biphenotypic leukemia
.
[MeSH-major]
Arthritis / etiology.
Leukemia
/ complications
[MeSH-minor]
Acute
Disease
. Adult. Ankle / pathology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Pain / drug therapy.
Phenotype
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
Genetic Alliance.
consumer health - Arthritis
.
MedlinePlus Health Information.
consumer health - Arthritis
.
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Acta Haematol. 1999 Mar;101(1):1-6
[
10085431.001
]
[Cites]
Wiad Lek. 1998;51 Suppl 4:296-9
[
10731987.001
]
[Cites]
Semin Arthritis Rheum. 1994 Aug;24(1):48-56
[
7985037.001
]
(PMID = 16220224.001).
[ISSN]
0770-3198
[Journal-full-title]
Clinical rheumatology
[ISO-abbreviation]
Clin. Rheumatol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents
82.
Ramamoorthy SK, Pandita R, Prakash A, Ramaswamy NV, Al Bahar S:
Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice.
Acta Haematol
; 2007;118(3):141-5
[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]
Safety of imatinib in chronic
myeloid leukemia
in blastic crisis presenting as cholestatic jaundice.
Acute
leukemia
presenting as cholestatic jaundice is rare.
It can occur due to granulocytic sarcoma compressing the bile ducts in case of
acute
myeloid leukemia
.
We report a case of chronic
myeloid leukemia
in
lymphoid
blast
cell
crisis presenting with severe cholestatic jaundice due to diffuse infiltration of the liver sinusoids with lymphoblasts.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Jaundice, Obstructive / drug therapy.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Neoplasms / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
[MeSH-minor]
Adult. Benzamides.
Diagnosis
, Differential. Drug-Related Side Effects and Adverse Reactions. Humans. Imatinib Mesylate. Male
Genetic Alliance.
consumer health - Chronic Myeloid Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Liver Cancer
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
2007 S. Karger AG, Basel
(PMID = 17804901.001).
[ISSN]
1421-9662
[Journal-full-title]
Acta haematologica
[ISO-abbreviation]
Acta Haematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
83.
Mandal C, Dutta A, Mallick A, Chandra S, Misra L, Sangwan RS, Mandal C:
Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade.
Apoptosis
; 2008 Dec;13(12):1450-64
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of
lymphoid and myeloid
origin through mitochondrial death cascade.
Here we demonstrate how WA exhibits a strong growth-inhibitory effect on several human leukemic
cell
lines and on primary cells from patients with
lymphoblastic and myeloid leukemia
in a dose-dependent manner, showing no toxicity on normal human lymphocytes and primitive hematopoietic progenitor cells.
WA-mediated decrease in
cell
viability was observed through apoptosis as demonstrated by externalization of phosphatidylserine, a time-dependent increase in Bax/Bcl-2 ratio; loss of mitochondrial transmembrane potential, cytochrome c release, caspases 9 and 3 activation; and accumulation of cells in sub-G0 region based on DNA fragmentation.
WA caused increased levels of Bax in response to MAPK signaling, which resulted in the initiation of mitochondrial death cascade, and therefore it holds promise as a new, alternative, inexpensive chemotherapeutic agent for the treatment of patients with
leukemia
of both
lymphoid and myeloid
origin.
[MeSH-major]
Apoptosis / drug effects. Ergosterol / analogs & derivatives.
Leukemia
. MAP Kinase Signaling System / physiology. Mitochondria. Tumor Cells, Cultured / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism
[MeSH-minor]
Animals. Caspase Inhibitors. Caspases / metabolism.
Cell
Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Medicine, Traditional. Membrane Potential, Mitochondrial / drug effects. Mice. Molecular Structure. Plants, Medicinal / chemistry. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Withanolides. bcl-2-Associated X Protein / metabolism
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
ERGOSTEROL
.
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 = 18987975.001).
[ISSN]
1573-675X
[Journal-full-title]
Apoptosis : an international journal on programmed cell death
[ISO-abbreviation]
Apoptosis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Caspase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / Withanolides; 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; L6DO3QW4K5 / withaferin A; Z30RAY509F / Ergosterol
84.
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
.
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
.
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
[
16936318.001
]
[Cites]
Leukemia. 2007 Mar;21(3):588-90
[
17252016.001
]
[Cites]
Oncogene. 2007 Mar 1;26(10):1361-71
[
16983345.001
]
[Cites]
Nat Rev Cancer. 2007 Nov;7(11):823-33
[
17957188.001
]
[Cites]
Bioinformatics. 2007 Nov 1;23(21):2947-8
[
17846036.001
]
[Cites]
Methods Mol Biol. 2009;538:71-83
[
19277576.001
]
[Cites]
Int J Cancer. 2009 Jun 15;124(12):2893-8
[
19296537.001
]
[Cites]
Leukemia. 2009 Aug;23(8):1490-9
[
19262598.001
]
[Cites]
Blood. 2010 Apr 8;115(14):2835-44
[
20032505.001
]
[Cites]
Cancer Genet Cytogenet. 2000 Jun;119(2):94-101
[
10867142.001
]
[Cites]
Mol Cell Biol. 2000 Dec;20(23):9068-75
[
11074004.001
]
[Cites]
Cell Mol Life Sci. 2002 Feb;59(2):373-85
[
11915950.001
]
[Cites]
Oncogene. 2003 Mar 6;22(9):1400-10
[
12618766.001
]
[Cites]
Hum Mutat. 2003 Sep;22(3):229-44
[
12938088.001
]
[Cites]
Hum Mutat. 2003 Sep;22(3):245-51
[
12938089.001
]
[Cites]
J Exp Med. 1996 Mar 1;183(3):725-9
[
8642276.001
]
[Cites]
Cytogenet Cell Genet. 1997;79(3-4):237-40
[
9605863.001
]
[Cites]
Oncogene. 1998 Dec 10;17(23):3035-44
[
9881706.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):449-54
[
15626757.001
]
[Cites]
Nat Rev Cancer. 2005 Aug;5(8):615-25
[
16034368.001
]
(PMID = 20920256.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / CT45A1 protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Other-IDs]
NLM/ PMC2956734
85.
Jin ZX, Zhang SL, Wang XM, Bi SH, Xin M, Zhou JJ, Cui Q, Duan WX, Wang HB, Yi DH:
The myocardial protective effects of a moderate-potassium adenosine-lidocaine cardioplegia in pediatric cardiac surgery.
J Thorac Cardiovasc Surg
; 2008 Dec;136(6):1450-5
[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.
METHODS: One hundred thirty-four patients with congenital heart
disease
were randomly allocated to one of 3 groups according to the cardioplegia formula used: the high-potassium (HP) group (K(+), 20 mmol/L), 46 patients; the high-potassium adenosine-lidocaine (HPAL) group (K(+), 20 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients; and the moderate-potassium adenosine-lidocaine (
MPAL
) group (K(+), 10 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients.
RESULTS: At the end of cardiopulmonary bypass and modified ultrafiltration, the systolic and pulse pressures of the
MPAL
group were significantly increased compared with the respective values of the HP group.
At the time points of 1 to 12 hours after reperfusion, the levels of serum cardiac troponin I were significantly decreased in the
MPAL
group compared with those in the HP and HPAL groups.
CONCLUSIONS: The
MPAL
cardioplegia formula was associated with better myocardial protective effects.
MedlinePlus Health Information.
consumer health - Congenital Heart Defects
.
Hazardous Substances Data Bank.
LIDOCAINE
.
Hazardous Substances Data Bank.
Adenosine
.
Hazardous Substances Data Bank.
POTASSIUM, ELEMENTAL
.
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 = 19114188.001).
[ISSN]
1097-685X
[Journal-full-title]
The Journal of thoracic and cardiovascular surgery
[ISO-abbreviation]
J. Thorac. Cardiovasc. Surg.
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cardioplegic Solutions; 0 / Cardiotonic Agents; 98PI200987 / Lidocaine; K72T3FS567 / Adenosine; RWP5GA015D / Potassium
86.
Boatsman EE, Fu CH, Song SX, Moore TB:
Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
J Pediatr Hematol Oncol
; 2010 Mar;32(2):e57-60
[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]
Graft-versus-
leukemia
effect on infant
lymphoblastic leukemia
relapsed after sibling hematopoietic stem
cell
transplantation.
INTRODUCTION: Infant
acute
lymphoblastic leukemia
(ALL) is considered a high-risk entity.
By morphology, infant ALL is classified as
a lymphoid
lineage
leukemia
; however, its physiologic behavior has brought many to consider it a pathologic
hybrid
between
lymphoid leukemia and myeloid leukemias
.
As such, standard of care currently employs the use of chemotherapeutic agents used commonly in ALL protocols and agents typically reserved for the treatment of myelogenous
lineage
leukemias
.
The role of hematopoietic stem
cell
transplantation and graft-versus-
leukemia
effect in these patients has not been well studied.
CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-
cell lymphoblastic leukemia
was treated with protocol P9407 and matched sibling hematopoietic stem
cell
transplantation.
The sole antigraft-versus-host
disease
(GVHD) agent, cyclosporine, was discontinued.
He remains
disease
free more than 2 years posttransplant.
CONCLUSION: Traditionally, graft-versus-
leukemia
effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem
cell
transplantation (HSCT).
The effects of graft-versus-
leukemia
immunologic phenomenon in our patient with infant
acute
lymphoblastic leukemia
underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-
leukemia
effect may play a role in
disease
control in infant ALL after HSCT.
This suggests that other immunotherapeutic interventions in the context of relapse may offer potential clinical benefit in this
disease
.
[MeSH-major]
Graft vs
Leukemia
Effect. Hematopoietic Stem
Cell
Transplantation. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
Genetic Alliance.
consumer health - Transplantation
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20168246.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
87.
Di Croce L:
Chromatin modifying activity of leukaemia associated fusion proteins.
Hum Mol Genet
; 2005 Apr 15;14 Spec No 1:R77-84
[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]
Chromatin modifying activity of
leukaemia
associated fusion proteins.
The
leukaemias
, which are divided into chronic and
acute
forms, are malignant diseases of haematopoietic cells in which the proper balance between proliferation, differentiation and apoptosis is no longer operative.
Genes, such as those of
mixed
-
lineage leukaemia
, AML1 and retinoic acid receptor alpha, have been found to be aberrantly fused to different partners, which often encode transcription factors or other chromatin modifying enzymes, in numerous types of
acute
lymphoid and myeloid leukaemias
.
These chimeric fusion oncoproteins, generated by reciprocal chromosomal translocations, are responsible for chromatin alterations on target genes whose expression is critical to stem
cell
development or
lineage
specification in haematopoiesis.
[MeSH-major]
Chromatin / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic.
Leukemia
/ metabolism. Proto-Oncogene Proteins / metabolism. Receptors, Retinoic Acid / metabolism. Transcription Factors / metabolism
[MeSH-minor]
Amino Acid Sequence. Animals.
Cell
Differentiation. Core Binding Factor Alpha 2 Subunit. DNA Methylation. Epigenesis, Genetic. Gene Silencing. Hematopoiesis. Humans. Models, Biological. Molecular Sequence Data. Oncogene Proteins, Fusion / chemistry
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15809276.001).
[ISSN]
0964-6906
[Journal-full-title]
Human molecular genetics
[ISO-abbreviation]
Hum. Mol. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Chromatin; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / retinoic acid receptor alpha
[Number-of-references]
64
88.
Gluzman DF, Nadgornaya VA, Sklyarenko LM, Ivanovskaya TS, Poludnenko LY, Ukrainskaya NI:
Immunocytochemical markers in acute leukaemias diagnosis.
Exp Oncol
; 2010 Sep;32(3):195-9
[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]
Immunocytochemical markers in
acute
leukaemias diagnosis
.
The study included 1742 patients with
acute
myeloblastic
leukaemias
(AML) and
acute
lymphoblastic leukaemias
(ALL), Kyiv city residents and patients from 20 regions of Ukraine.
Bone marrow and blood smears were sent at
diagnosis
to Reference Center.
Immunocytochemical techniques (APAAP, LSAB) and broad panel of monoclonal antibodies (MoAbs) against
lineage
specific and differentiation antigens of leukocytes were employed for immunophenotyping of leukemic blast cells directly in blood and bone marrow smears.
Different types of AML were defined by the expression of the
cell
surface and cytoplasmic antigens.
Immunocytochemical study was required especially in diagnosing of AML with minimal differentiation,
acute
megakaryoblastic
leukaemia
,
acute
erythroid
leukaemia
and
acute
leukaemias
of ambiguous
lineage
.
Acute
lymphoblastic leukaemias
was broadly classified into B-
lineage
and T
-
lineage
ALL.
According to the degree of B-
lymphoid
differentiation of the blast cells four subtypes of B-
lineage
ALL were established.
T-
lineage
ALL observed in patients were also divided into four subtypes.
Immunocytochemical examination was required to diagnose AL of ambiguous
lineage
with no clear evidence of
lineage
differentiation (
acute
undifferentiated
leukaemia
) or those with blasts that express markers of more than one
lineage
(
mixed
phenotype
acute
leukaemias
).
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ immunology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / immunology
[MeSH-minor]
Acute
Disease
. Biomarkers, Tumor / immunology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocyte Subsets / immunology. Lymphocyte Subsets / pathology
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21403617.001).
[ISSN]
1812-9269
[Journal-full-title]
Experimental oncology
[ISO-abbreviation]
Exp. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Ukraine
[Chemical-registry-number]
0 / Biomarkers, Tumor
89.
Gibaud S, Zirar SB, Mutzenhardt P, Fries I, Astier A:
Melarsoprol-cyclodextrins inclusion complexes.
Int J Pharm
; 2005 Dec 8;306(1-2):107-21
[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.
Melarsoprol, a water-insoluble drug, is mainly used in the treatment of trypanosomiasis and has demonstrated an in vitro activity on
myeloid and lymphoid leukemia
derived
cell
lines.
However, the cytotoxic properties of melarsoprol on K562 and U937 human
leukemia cell
lines was not modified by complexation.
[MeSH-minor]
Cell
Line, Tumor.
Cell
Survival / drug effects. Drug Compounding. Drug Stability. Humans. Kinetics. Magnetic Resonance Spectroscopy. Molecular Structure. Solubility
HAL archives ouvertes.
Full text from
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16253447.001).
[ISSN]
0378-5173
[Journal-full-title]
International journal of pharmaceutics
[ISO-abbreviation]
Int J Pharm
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Cyclodextrins; ZF3786Q2E8 / Melarsoprol
90.
Lou Z, Zhang CC, Tirado CA, Slone T, Zheng J, Zaremba CM, Oliver D, Chen W:
Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.
Leuk Res
; 2010 Aug;34(8):1107-9
[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]
Infantile
mixed
phenotype
acute
leukemia
(bilineal
and biphenotypic
) with t(10;11)(p12;q23);MLL-MLLT10.
We report a case of a 6-month-old boy with a
mixed
phenotype
acute
leukemia
(
MPAL
), bilineal
and biphenotypic
immunophenotype (B-
lymphoid
lineage
and combined B-
lymphoid and
monocytic
lineage
) with t(10;11)(p12;q23);MLL-MLLT10.
He was treated with
acute
myeloid leukemia
protocol and in complete remission at 7-month follow-up.
To the best of our knowledge, this is the first reported MLL-MLLT10 rearranged case presenting as
MPAL
in an infant.
From a clinical practice standpoint, this case illustrates the importance of detection of MLL rearrangement due to its prognostic implication and the effectiveness of flow cytometry immunophenotyping in diagnosing
MPAL and
monitoring minimal residual
disease
.
[MeSH-major]
Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics.
Leukemia
, Monocytic,
Acute
/ genetics.
Myeloid
-
Lymphoid Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Translocation, Genetic / genetics
[MeSH-minor]
Flow Cytometry. Gene Rearrangement. Humans. Immunophenotyping. Infant. Karyotyping. Male. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Neoplasm, Residual / therapy.
Phenotype
. Prognosis. Remission Induction
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright (c) 2010 Elsevier Ltd. All rights reserved.
(PMID = 20299091.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
91.
Park AH, Muntz HR, Smith ME, Afify Z, Pysher T, Pavia A:
Pediatric invasive fungal rhinosinusitis in immunocompromised children with cancer.
Otolaryngol Head Neck Surg
; 2005 Sep;133(3):411-6
[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.
RESULTS: Seventeen consecutive pediatric immunocompromised patients with hematologic
and lymphoid
neoplasms underwent nasal endoscopy and biopsy for possible FS.
Eight patients had
acute
myelogenous
leukemia
(AML); 6 patients had
acute
lymphoblastic leukemia
(ALL); 1 patient had Burkitt's lymphoma, 1 patient had undifferentiated
leukemia
; and 1 patient had
biphenotypic
acute
leukemia
.
MedlinePlus Health Information.
consumer health - Cancer in Children
.
MedlinePlus Health Information.
consumer health - Fungal Infections
.
MedlinePlus Health Information.
consumer health - Sinusitis
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16143192.001).
[ISSN]
0194-5998
[Journal-full-title]
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
[ISO-abbreviation]
Otolaryngol Head Neck Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
92.
El-Ziny MA, Al-Tonbary YA, Salama OS, Bakr AA, Al-Marsafawy H, Elsharkawy AA:
Low turnover bone disease in Egyptian children with acute leukemia.
Hematology
; 2005 Aug;10(4):327-33
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Low turnover bone
disease
in Egyptian children with
acute
leukemia
.
The aim of this work was to study bone turnover markers, calcium homeostasis and bone mineral density (BMD) in children with
acute
leukemia
at
diagnosis
, after induction chemotherapy, and during maintenance therapy to delineate abnormalities present.
After evaluation of L2-L4 BMD using dual-energy X-ray absorptiometry in patients with
acute
myeloid and lymphoid leukemia
at presentation and after treatment, the results were compared to 352 healthy age- and sex-matched Egyptian controls.
Osteopenia was observed at
diagnosis and
during treatment in patients with
acute
leukemia
.
At
diagnosis
osteopenia was observed in 27 patients (62.8%): 10 (23.3%) had non severe osteopenia and 17 (39.5%) had severe osteopenia.
Parathyroid hormone (PTH) (pg/ml) levels demonstrated non significant differences between children with
acute
leukemia
at different stages of therapy and controls, while, 25 (OH) D3 (ng/ml) was significantly lower in
acute
leukemia
patients at different stages of therapy compared to controls (p<0.001).
Osteocalcin (ng/ml) is significantly lower in patients at different stages of the
disease
compared to controls (p<0.001) but there was no significant difference between patients at different stages of therapy.
Deoxy-pyridoline cross links showed non-significant difference between the different types of
acute
leukemia and
with controls.
Osteopenia is a significant problem in children with
acute
leukemia
at presentation and after chemotherapy.
Osteopenia in
acute
leukemia
appears to be of the low turnover type (decreased osteoblastic activity and decreased bone mineralization).
[MeSH-major]
Bone Density. Bone Diseases, Metabolic / blood. Bone Remodeling.
Leukemia
/ blood
[MeSH-minor]
Acute
Disease
. Adolescent. Child. Child, Preschool. Cholecalciferol / blood. Egypt. Humans. Infant. Male. Osteoblasts / metabolism. Osteocalcin / blood. Parathyroid Hormone / blood
MedlinePlus Health Information.
consumer health - Bone Density
.
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
Hazardous Substances Data Bank.
CHOLECALCIFEROL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16085546.001).
[ISSN]
1024-5332
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Parathyroid Hormone; 104982-03-8 / Osteocalcin; 1C6V77QF41 / Cholecalciferol
93.
Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B:
V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
Genes Chromosomes Cancer
; 2009 Aug;48(8):725-36
[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]
V(D)J targeting mistakes occur at low frequency in
acute
lymphoblastic leukemia
.
Translocations of proto-oncogenes to the B-
cell
or T-
cell
antigen receptor loci in
acute
T- or B-
cell leukemia
and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
[MeSH-major]
Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
[MeSH-minor]
Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-
Cell
Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-
Cell
/ genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19455608.001).
[ISSN]
1098-2264
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
94.
Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML:
Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
J Clin Pathol
; 2007 May;60(5):562-4
[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]
Therapy-related,
mixed
-
lineage leukaemia
translocation-positive, monoblastic
myeloid
sarcoma of the uterus.
Myeloid
sarcomas are tumour masses of
myeloid
leukaemic cells at extramedullary sites.
These tumours can, on occasion, occur without concurrent or antecedent
leukaemia
.
Myeloid
sarcomas have been described at unusual locations including the female genital tract.
An unusual case of therapy-related
acute
myeloid
leukaemia
(t-AML) presenting as isolated monoblastic
myeloid
sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a
mixed
-
lineage leukaemia
(MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these
myeloid
sarcomas can be useful for risk assessment and guiding definitive therapy.
Genetic Alliance.
consumer health - Myeloid sarcoma
.
MedlinePlus Health Information.
consumer health - Uterine Cancer
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Am J Clin Pathol. 2000 Nov;114(5):807-11
[
11068557.001
]
[Cites]
Leuk Lymphoma. 2001 Apr;41(3-4):255-76
[
11378539.001
]
[Cites]
Am J Pathol. 2002 Jun;160(6):1967-72
[
12057901.001
]
[Cites]
Leuk Lymphoma. 2002 Nov;43(11):2151-3
[
12533040.001
]
[Cites]
Int J Surg Pathol. 2003 Oct;11(4):271-82
[
14615822.001
]
[Cites]
Leukemia. 2005 Feb;19(2):183-90
[
15618964.001
]
[Cites]
Urology. 1986 Mar;27(3):268-70
[
3082059.001
]
[Cites]
Gynecol Oncol. 1992 Jul;46(1):128-37
[
1634133.001
]
[Cites]
Blood. 1993 Dec 15;82(12):3705-11
[
8260707.001
]
[Cites]
Am J Clin Pathol. 1995 Oct;104(4):431-43
[
7572794.001
]
[Cites]
Am J Surg Pathol. 1997 Oct;21(10):1156-65
[
9331287.001
]
[Cites]
Leuk Res. 2004 Nov;28(11):1165-9
[
15380340.001
]
(PMID = 17513515.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
[Publication-type]
Case Reports; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Other-IDs]
NLM/ PMC1994540
95.
Iacobucci I, Storlazzi CT, Cilloni D, Lonetti A, Ottaviani E, Soverini S, Astolfi A, Chiaretti S, Vitale A, Messa F, Impera L, Baldazzi C, D'Addabbo P, Papayannidis C, Lonoce A, Colarossi S, Vignetti M, Piccaluga PP, Paolini S, Russo D, Pane F, Saglio G, Baccarani M, Foà R, Martinelli G:
Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).
Blood
; 2009 Sep 3;114(10):2159-67
[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]
Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive
acute
lymphoblastic leukemia
patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto
Acute
Leukemia
Working Party (GIMEMA AL WP).
The BCR-ABL1 fusion gene defines the subgroup of
acute
lymphoblastic leukemia
(ALL) with the worst clinical prognosis.
The IKZF1 deletion also was identified in the progression of chronic
myeloid leukemia
to
lymphoid
blast crisis (66%) but never in
myeloid
blast crisis or chronic-phase chronic
myeloid leukemia
or in patients with
acute
myeloid leukemia
.
[MeSH-major]
Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Sequence Deletion
[MeSH-minor]
Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism.
Cell
Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / metabolism.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
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
[ErratumIn]
Blood. 2010 Sep 23;116(12):2196
(PMID = 19589926.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
96.
Pieters R, Schrappe M, De Lorenzo P, Hann I, De Rossi G, Felice M, Hovi L, LeBlanc T, Szczepanski T, Ferster A, Janka G, Rubnitz J, Silverman L, Stary J, Campbell M, Li CK, Mann G, Suppiah R, Biondi A, Vora A, Valsecchi MG:
A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial.
Lancet
; 2007 Jul 21;370(9583):240-50
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A treatment protocol for infants younger than 1 year with
acute
lymphoblastic
leukaemia
(Interfant-99): an observational study
and a
multicentre randomised trial.
BACKGROUND:
Acute
lymphoblastic
leukaemia
in infants younger than 1 year is rare, and infants with the
disease
have worse outcomes than do older children.
We initiated an international study to investigate the effects of a new
hybrid
treatment protocol with elements designed to treat both
acute
lymphoblastic
leukaemia
and
acute
myeloid
leukaemia
, and to identify any prognostic factors for outcome in infants.
Eligible patients were stratified for risk according to their peripheral blood response to a 7-day prednisone prophase, and then given
a hybrid
regimen based on the standard protocol for
acute
lymphoblastic
leukaemia
, with some elements designed for treatment of
acute
myeloid
leukaemia
.
The primary outcomes were event-free survival (EFS) for the initial cohort of patients
and disease
-free survival (DFS) for the patients randomly assigned to a treatment group.
FINDINGS: In the 482 enrolled patients who underwent
hybrid
treatment, 260 (58%) were in complete remission at a median follow-up of 38 (range 1-78) months, and EFS at 4 years was 47.0% (SE 2.6, 95% CI 41.9-52.1).
At a median follow-up of 42 (range 1-73) months, 60 patients in the treatment group and 57 controls were
disease
-free.
All types of rearrangements in the (
mixed lineage leukaemia
) MLL gene, very high white blood
cell
count, age of younger than 6 months,
and a
poor response to the prednisone prophase were independently associated with inferior outcomes.
INTERPRETATION: Patients treated with our
hybrid
protocol, and especially those who responded poorly to prednisone, had higher EFS than most reported outcomes for treatment of infant ALL.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
METHOTREXATE
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Lancet. 2007 Jul 21;370(9583):198-200
[
17658376.001
]
(PMID = 17658395.001).
[ISSN]
1474-547X
[Journal-full-title]
Lancet (London, England)
[ISO-abbreviation]
Lancet
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00015873; ISRCTN/ ISRCTN24251487
[Grant]
United Kingdom / Medical Research Council / / G0300130
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
04079A1RDZ / Cytarabine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
97.
Okada Y, Jiang Q, Lemieux M, Jeannotte L, Su L, Zhang Y:
Leukaemic transformation by CALM-AF10 involves upregulation of Hoxa5 by hDOT1L.
Nat Cell Biol
; 2006 Sep;8(9):1017-24
[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.
Chromosomal translocation is a common cause of
leukaemia
and the most common chromosome translocations found in
leukaemia
patients involve the
mixed lineage leukaemia
(MLL) gene.
AF10 is one of more than 30 MLL fusion partners in
leukaemia
.
In addition to MLL, AF10 has also been reported to fuse to CALM (clathrin-assembly protein-like
lymphoid
-
myeloid
) in patients with T-
cell
acute
lymphoblastic
leukaemia
(T-ALL) and
acute
myeloid
leukaemia
(AML).
Thus, our study establishes CALM-AF10 fusion as a cause of
leukaemia
and reveals that mistargeting of hDOT1L and upregulation of Hoxa5 through H3K79 methylation is the underlying mechanism behind
leukaemia
caused by CALM-AF10 fusion.
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
[ErratumIn]
Nat Cell Biol. 2006 Oct;8(10):1178
(PMID = 16921363.001).
[ISSN]
1465-7392
[Journal-full-title]
Nature cell biology
[ISO-abbreviation]
Nat. Cell Biol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / AI48407; United States / NIAID NIH HHS / AI / R56 AI048407; United States / NHLBI NIH HHS / HL / R21 HL072240; United States / NIAID NIH HHS / AI / R01 AI080432; United States / NIGMS NIH HHS / GM / R01 GM068804; United States / NIAID NIH HHS / AI / R01 AI077454; United States / NIGMS NIH HHS / GM / GM68804; United States / NHLBI NIH HHS / HL / HL72240; United States / NIAID NIH HHS / AI / R01 AI048407
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 0 / Hoxa5 protein, mouse; 0 / MLLT10 protein, human; 0 / Mllt10 protein, mouse; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Phosphoproteins; 0 / Transcription Factors; EC 2.1.1.- / DOT1L protein, human; EC 2.1.1.- / Methyltransferases
[Other-IDs]
NLM/ NIHMS684864; NLM/ PMC4425349
98.
Naghashpour M, Lancet J, Moscinski L, Zhang L:
Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.
Am J Hematol
; 2010 Jun;85(6):451-4
[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]
Mixed
phenotype
acute
leukemia
with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-
lymphoid
type: A first case report.
The majority of cases of
acute
leukemia
belong to a specific
lineage
origin, either
lymphoid
or
myeloid
, and therefore are classified as
acute
lymphoblastic leukemia
(ALL) or
acute
myelogenous
leukemia
(AML), based on
morphologic
features and cytochemical and immunophenotypic profile of the blast cells.
A minority of
acute
leukemias
however, show no clear evidence of differentiation along a single
lineage
.
These are now classified under
acute
leukemias
of ambiguous
lineage
by the most recent WHO classification and account for <4% of all cases of
acute
leukemia
[1].
They include
leukemias
with no
lineage
specific antigens (
acute
undifferentiated
leukemias
) and those with blasts that express antigens of more than one
lineage
to such degree that it is not possible to assign the
leukemia
to any one particular
lineage
with certainty (
mixed
phenotype
acute
leukemias
).
The latter can either be
leukemias
with two distinct populations of blasts, each expressing antigens of a different
lineage
(historically referred to as "bilineal"
leukemias
) or a single blast population expressing antigens of multiple lineages (historically referred to as "
biphenotypic
"
acute
leukemias
) [2].
Acute
leukemias
of ambiguous
lineage
may harbor a variety of genetic lesions.
Those with t(9;22)(q34;q11) or translocations associated with
mixed lineage
leukemias
(MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.
Co-expression of
myeloid and
B-
lymphoid
antigens is most common in
mixed
phenotype
acute
leukemia
(
MPAL
), followed by co-expression of
myeloid and
T-
lymphoid
antigens, accounting for 66-70% and 23-24% of MLLs, respectively.
Coexpression of B-
and T
-
lineage
associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].
The requirements for assigning more than one
lineage
to a single blast population has been established by current WHO classification [1].
[MeSH-major]
Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping.
Leukemia
/ classification.
Myeloid
-
Lymphoid Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease
. Adult. Antigens, CD / analysis. Bone Marrow / pathology.
Cell
Lineage
. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20513125.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
99.
Wang L, Lin D, Zhang X, Chen S, Wang M, Wang J:
Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients.
Leuk Res
; 2005 Dec;29(12):1393-8
[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]
Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese
acute
leukemia
patients.
Genomic aberrations of Fms-like tyrosine kinase 3 (FLT3), including internal tandem duplication (ITD) and point mutations, have been demonstrated in 25-30% of adults
acute
myeloid leukemia
(AML) and are markers of poor prognosis.
FLT3/ITD and D835 mutations were analyzed in 194 Chinese patients with
acute
leukemia and
myelodysplastic syndromes (MDS) by polymerase chain reaction (PCR).
However, neither aberrations was found in 25 patients with
acute
lymphoblastic leukemia
(ALL), 2
acute
hybrid leukemia
, 17 MDS and 7 chronic
myeloid leukemia
in blast crisis (CML-BC).
[MeSH-major]
Leukemia
/ genetics. Mutation, Missense. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Amino Acid Sequence. Asian Continental Ancestry Group / genetics. DNA Mutational Analysis. Female. Humans. Leukocytosis. Male. Middle Aged. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Prognosis. Remission Induction
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
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 = 15996732.001).
[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]
EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
100.
Dickson GJ, Lappin TR, Thompson A:
Complete array of HOX gene expression by RQ-PCR.
Methods Mol Biol
; 2009;538:369-93
[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.
Many of the chromosomal translocations associated with
acute
leukemias
involve HOX genes directly or some of their regulatory factors, e.g.,
mixed lineage leukaemia
(MLL), leading to inappropriate expression of certain subsets of the genes.
Defining the roles for HOX in hematopoiesis should help to elucidate the mechanisms of deregulation in
leukemia and
eventually identify targets for therapeutic intervention.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19277582.001).
[ISSN]
1064-3745
[Journal-full-title]
Methods in molecular biology (Clifton, N.J.)
[ISO-abbreviation]
Methods Mol. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Homeodomain Proteins