[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
Items 1 to 100 of about 180
1. Ogasawara T, Yasuyama M, Kawauchi K: Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). Am J Hematol; 2005 Jun;79(2):136-41
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
  • We describe a patient who developed myelodysplastic syndrome over 2 years after achieving complete remission of acute myeloid leukemia (AML).
  • The patient was treated in July 1998 with anthracycline, etoposide, and behenoyl cytarabine chemotherapy for AML (French-American-British classification, M2; World Health Organization classification, AML with maturation) and achieved complete remission.
  • The pancytopenia progressed rapidly, and he died 2 months after the diagnosis of MDS.
  • Therapy-related MDS and AML (t-MDS/t-AML) developing after treatment for acute leukemia is unusual; the primary leukemia associated with most cases of t-MDS/t-AML is acute promyelocytic leukemia (APL).
  • This unusual case suggests that AML excluding APL should be considered a primary hematologic malignancy for t-MDS/t-AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 5. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / chemically induced. Monosomy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics


2. 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
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [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.
  • However, APL and AML with maturation expressed comparable AQP9 levels, suggesting that AQP9 expression was related to granulocytic maturation.
  • [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 .
  • [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
  •  go-up   go-down


3. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • A 2-year-old domestic shorthair cat was presented to us with decreased activity and anorexia.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
  •  go-up   go-down


Advertisement
4. Saudemont A, Corm S, Wickham T, Hetuin D, Quesnel B: Induction of leukemia-specific CD8+ cytotoxic T cells with autologous myeloid leukemic cells maturated with a fiber-modified adenovirus encoding TNF-alpha. Mol Ther; 2005 Jun;11(6):950-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of leukemia-specific CD8+ cytotoxic T cells with autologous myeloid leukemic cells maturated with a fiber-modified adenovirus encoding TNF-alpha.
  • Acute myeloid leukemia (AML) cells can be differentiated into dendritic cells (DCs) using appropriate combinations of cytokines but generation of autologous antileukemic cytotoxic T cells using leukemic DCs remains difficult.
  • Transduction by adenoviral vectors has been reported to induce efficient maturation of monocyte-derived DCs but AML cells are generally resistant to adenoviral gene transfer.
  • In this study we tested the effects of adenoviral TNF-alpha gene transfer on maturation of AML cells using the fiber-modified AdTNF.F(pK7) adenovirus.
  • AdTNF.F(pK7) induced significantly greater maturation of AML cells into antigen-presenting cells (APC) than did recombinant TNF-alpha or control adenoviral vector.
  • Maturation of leukemic cells into APCs was mediated at least partially via a PI3K/mTOR pathway, as the inhibitors LY294002, wortmannin, and rapamycin inhibited the maturation effect induced by the AdTNF.F(pK7) adenovirus.
  • In addition, CD8+ T cells expanded with AdTNF.F(pK7)-transduced AML cells showed greater expansion and specific CD8+ CTL activity against autologous AML cells than T cells expanded by other means.
  • Thus, fiber-modified adenoviral vectors encoding TNF-alpha are able to maturate AML cells into APCs with high efficacy and reproducibility, providing a useful tool to generate efficiently specific CD8+ CTLs against leukemic disease.
  • [MeSH-major] Adenoviridae / genetics. Cytotoxicity, Immunologic / immunology. Leukemia, Myeloid / immunology. T-Lymphocytes, Cytotoxic / immunology. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Acute Disease. Antigen-Presenting Cells / immunology. Capsid Proteins / genetics. Cell Differentiation. Coculture Techniques. Humans. Phenotype. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. Protein Kinase Inhibitors / pharmacology. Protein Kinases / physiology. Signal Transduction. TOR Serine-Threonine Kinases. Transduction, Genetic

  • 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
  • (PMID = 15922966.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / Protein Kinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 0 / hexon capsid protein, Adenovirus; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
  •  go-up   go-down


5. Kim H, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ: [A Case of Acute Myeloid Leukemia with Masked t(8;21).]. Korean J Lab Med; 2006 Oct;26(5):338-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A Case of Acute Myeloid Leukemia with Masked t(8;21).].
  • We report a case that revealed the characteristics of acute myeloblastic leukemia with maturation (AML-M2) on the morphology of the bone marrow biopsy and 45,X,-Y in conventional cytogenetic study, but was confirmed to have a typical AML1/ETO translocation by molecular studies using reverse transcriptase polymerase chain reaction and fluorescence in situ hybridization.
  • In case typical morphologic features compatible with recurrent cytogenetic abnormalities are shown, molecular studies in addition to conventional cytogenetic study might be required to confirm the diagnosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18156748.001).
  • [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)
  •  go-up   go-down


6. Chen W, Konoplev S, Medeiros LJ, Koeppen H, Leventaki V, Vadhan-Raj S, Jones D, Kantarjian HM, Falini B, Bueso-Ramos CE: Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation. Cancer; 2009 Dec 1;115(23):5481-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation.
  • BACKGROUND: A small subset of patients with acute myeloid leukemia (AML) have cuplike nuclei.
  • METHODS: The authors searched for patients who had AML with cuplike nuclei at their institution over a 10-year interval.
  • The relevant data were reviewed, and the results were compared with a control group of patients who had AML without cuplike nuclei.
  • RESULTS: In total, 22 patients who had AML with cuplike nuclei were identified and were classified as AML without maturation (French-American-British classification M1) (AML M1).
  • Compared with the control group (AML M1), patients who had AML with cuplike nuclei were associated significantly with fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) (86% vs 38%, respectively; P = .002); nucleophosmin 1 (NPM1) mutations (86% vs 19%; P < .0001); both mutations (77% vs 14%; P < .0001); normal karyotype (86% vs 40%; P = .003); bone marrow blast count (90% vs 84%; P = .016); myeloperoxidase positivity (95% vs 30% blasts; P = .001); higher D-dimer levels (>5000 ng/mL vs 569 ng/mL; P = .001); and the absence of CD7 (91% vs 52%; P = .007), CD34 (82% vs 5%; P < .0001), and human leukocyte antigen, D-related (59% vs 10%; P = .001).
  • The positive predictive value of recognizing AML with cuplike nuclei for FLT3-ITD, NPM1, and both mutations was 81%, 86%, and 77%, respectively.
  • CONCLUSIONS: Cuplike nuclei in AML were highly associated with the presence of NPM1 and FLT3-ITD mutations and with several clinicopathologic and immunophenotypic features.
  • Recognition of the distinctive morphologic features of AML with cuplike nuclei may be helpful in streamlining the workup of these neoplasms.

  • 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] (c) 2009 American Cancer Society.
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Leuk Lymphoma. 2008 May;49(5):852-63 [18452067.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Leuk Lymphoma. 2002 Aug;43(8):1541-7 [12400596.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1266-72 [12481006.001]
  • [Cites] Leukemia. 2003 Apr;17(4):707-15 [12682628.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] Am J Clin Pathol. 2004 Sep;122(3):348-58 [15362364.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1591-8 [15343344.001]
  • [Cites] Blood. 1994 Jul 1;84(1):244-55 [7517211.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Int J Hematol. 2005 Aug;82(2):85-92 [16146837.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1783-4 [16926303.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2052-4; author reply 2054; discussion 2055-6 [17637816.001]
  • [Cites] Haematologica. 2008 Feb;93(2):283-6 [18223289.001]
  • [Cites] Haematologica. 2008 Mar;93(3):439-42 [18268276.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • (PMID = 19672946.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA 100632-04
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS140671; NLM/ PMC3378048
  •  go-up   go-down


7. Chang WR, Park IJ, Lee HW, Park JS, Kim HC, Kim HJ, Han JH, Cho SR: [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts]. Korean J Lab Med; 2009 Oct;29(5):390-5
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts].
  • Many AML-associated chromosomal abnormalities, such as t(8;21), t(15;17), inv(16), t(9;11), t(9;22) and t(6;9) are well known.
  • The chromosomal aberration of t(16;21)(p11;q22) in AML is rare and it is known to be associated with poor prognosis, young age (median age, 22 yr), and involvement of various subtypes of the French-American-British classification.
  • We report here 2 AML patients with t(16;21)(p11;q22), proved by conventional cytogenetics and/or reverse transcription (RT)-PCR.
  • One patient was a 24 yr-old male with acute myelomonocytic leukemia.
  • Although he received allogeneic peripheral blood stem cell transplantation after the first remission, he died 9 months after the initial diagnosis due to relapse of the disease and graft-versus-host disease.
  • The other patient was a 72 yr-old male with acute myeloid leukemia without maturation.
  • We suggest that the presence of t(16;21)(p11;q22) and/or TLS/FUS-ERG fusion transcripts has to be considered in cases of AML with erythrophagocytosis.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Graft vs Host Disease / diagnosis. Humans. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19893346.001).
  • [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)
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
  •  go-up   go-down


8. Tirado CA, Chena W, Valdez FJ, Henderson S, Smart RL, Doolittle J, Garcia R, Patel S, Holdridge S, Chastain C, Auchus M, Collins RH: A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation. J Assoc Genet Technol; 2009;35(3):88-92
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation.
  • The t(8;21)/RUNX1-RUNX1T1 is found in ~5 percent of cases of acute myeloid leukemia (AML) and in 10 percent of the prior AML with maturation (M2) category of the French-American-British (FAB) classification.
  • While AML with t(8;21) is considered a distinct entity with a favorable prognosis, the clinical consequence of variant translocations is less well defined.
  • In this report we described a 45 year-old male patient having a diagnosis of AML-M2 with morphologic and immunophenotypic features suggestive of t(8;21).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19738329.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


9. Jang JH, Yoo EH, Kim HJ, Kim DH, Jung CW, Kim SH: Acute myeloid leukemia with del(X)(p21) and cryptic RUNX1/RUNX1T1 from ins(8;21)(q22;q22q22) revealed by atypical FISH signals. Ann Clin Lab Sci; 2010;40(1):80-4
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia with del(X)(p21) and cryptic RUNX1/RUNX1T1 from ins(8;21)(q22;q22q22) revealed by atypical FISH signals.
  • A 57-yr-old woman was diagnosed with acute myeloid leukemia (AML) with maturation, based on morphological and cytochemical/immunophenotypic findings on bone marrow studies.
  • In addition to the cryptic RUNX1/RUNX1T1 rearrangement, this is the first report of partial deletion of an X chromosome as an additional cytogenetic aberration in AML with RUNX1/RUNX1T1.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, X / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20124335.001).
  • [ISSN] 1550-8080
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


10. Ohnishi H, Yoshino H, Yoneyama R, Ishii M, Watanabe T, Bessho F: Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation. Pediatr Hematol Oncol; 2008 Apr-May;25(3):165-70
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation.
  • The authors report a rare case of acute myeloid leukemia (AML) M1 with faggot formation in mature neutrophils and metamyelocytes.
  • Although Auer rods in mature neutrophils are occasionally experienced, they are usually found in AML M2, M3, or M4 cases, but not in M1 cases.
  • In addition, faggot formation in mature neutrophils, as seen in this case, is considered to be particularly unusual because most previously reported cases tended to show simple Auer rods except for AML M3 cases.
  • [MeSH-major] Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neutrophils / pathology. Trisomy / pathology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18432498.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


11. Villa O, Salido M, Pérez-Vila ME, Ferrer A, Arenillas L, Pedro C, Espinet B, Corzo C, Serrano S, Woessner S, Florensa L, Solé F: Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Aug;185(1):32-6
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia.
  • We report three cases of acute myeloid leukemia without maturation [AML-M1 subtype according to the French-American-British classification (FAB)] with the presence of MYC oncogene amplification in form of double minutes (dmin) or homogeneously staining region (hsr).
  • [MeSH-major] Cell Nucleus / pathology. Genes, myc. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18656691.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin
  •  go-up   go-down


12. Ressel A, Trümper L, Bäsecke J: [Occlusion of the femoral arteries in de novo AML]. Med Klin (Munich); 2007 May 15;102(5):388-92
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Occlusion of the femoral arteries in de novo AML].
  • [Transliterated title] Femoralarterienverschluss bei De-novo-AML.
  • BACKGROUND: Leukemic emboli in acute (AML) and chronic myelocytic leukemia (CML) are associated with hyperleukocytosis (>100,000/microl leukocytes) and most frequently detected at autopsy.
  • CASE REPORT: A 53-year-old woman was admitted with hyperleukocytosis and acute pain in her right leg.
  • An occlusion of the right femoral arteries as the presenting symptom of a de novo AML (FAB M1/WHO: AML without maturation) with hyperleukocytosis was diagnosed.
  • CONCLUSION: Leukemic emboli of large vessels are uncommon in leukemia with hyperleukocytosis.
  • Leukemic emboli mainly occur in AML and CML in blast crisis and are rare in acute (ALL) and chronic lymphocytic leukemia (CLL).
  • [MeSH-major] Arterial Occlusive Diseases / etiology. Femoral Artery. Leukemia, Myeloid, Acute / diagnosis. Neoplastic Cells, Circulating
  • [MeSH-minor] Angiography. Blood Coagulation Tests. Diagnosis, Differential. Female. Granulocyte Precursor Cells / pathology. Humans. Leukocyte Count. Leukocytosis / diagnosis. Leukocytosis / pathology. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17497090.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


13. Guo C, Inghirami G, Ibrahim S, Sen F: Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia. Arch Pathol Lab Med; 2006 Jul;130(7):1075-6
Hazardous Substances Data Bank. MELPHALAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia.
  • Therapy-related acute myeloid leukemias arise as a result of cytotoxic chemotherapy and/or radiation therapy.
  • The most common types of acute myeloid leukemia arising in this setting are acute myeloid leukemia with maturation, and lesser numbers of acute myelomonocytic leukemia, acute monocytic leukemia, acute erythroleukemia, or acute megakaryocytic leukemia.
  • We present a patient with multiple myeloma who was treated with melphalan and 4 years later developed acute erythroid leukemia.
  • The morphologic diagnosis of pure erythroid leukemia developing in the setting of multiple myeloma may be challenging.
  • [MeSH-major] Epistaxis / complications. Leukemia, Erythroblastic, Acute / complications. Multiple Myeloma / complications. Muscle Weakness / complications
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antineoplastic Agents, Alkylating / adverse effects. Humans. Leukemia, Myeloid. Male. Melphalan / adverse effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16831041.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
  •  go-up   go-down


14. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The PI3K p110δ isoform is highly expressed in cells of hematopoietic origin and plays a key role in B cell maturation and function.
  • In vitro studies of 0.1 to 10 μM CAL-101 showed inhibition of pAKT expression and/or apoptotic effects against primary chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) cells and against a range of leukemia and lymphoma cell lines.
  • Disease specific cohort expansion will occur at the maximally tolerated dose, and patients with AML will be added.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961357.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Wong KF, Yuen HL, Siu LL, Pang A, Kwong YL: t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia. Hum Pathol; 2008 Nov;39(11):1702-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia.
  • A Chinese girl presented with generalized papular rash and monocytic leukemia 19 days after birth.
  • Cytogenetic analysis showed t(8;16)(p11.2;p13.3) as the sole chromosomal abnormality.
  • Spontaneous regression of the leukemia was observed after 2 months, although the t(8;16) translocation persisted cytogenetically.
  • This was followed 7 months later by the development of acute myeloid leukemia with maturation and cytogenetic evolution with extra chromosomes 4 and 8.
  • Molecular study showed that the reciprocal MYST3 and CREBBP gene fusion characteristic of t(8;16) translocation persisted throughout the clinical course, even during spontaneous regression of the neonatal leukemia, and after chemotherapy-induced remission of the subsequent acute myeloid leukemia.
  • The possible role of MYST3 and CREBBP gene fusion in the pathogenesis of the leukemia is discussed.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18657848.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  •  go-up   go-down


16. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • The deletion was identified at initial diagnosis in one patient and at relapse in the other two.
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • The prognosis is poor, with survival similar to other AML cases with unfavorable cytogenetic changes.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

  • 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
  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
  •  go-up   go-down


17. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

  • Genetics Home Reference. consumer health - acute promyelocytic leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  •  go-up   go-down


18. Vardiman JW: The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasms. Chem Biol Interact; 2010 Mar 19;184(1-2):16-20
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasms.
  • The World Health Organization (WHO) classification of myeloid and lymphoid neoplasms utilizes morphology, immunophenotype, genetics and clinical features to define disease entities of clinical significance.
  • In general, the classification stratifies neoplasms according to their lineage (myeloid, lymphoid, histiocytic/dendritic) and distinguishes neoplasms of precursor cells from those comprised of functionally mature cells.
  • Five major subgroups of myeloid neoplasms are recognized based mainly on their degree of maturation and biologic properties: myeloproliferative neoplasms (MPNs) which are comprised primarily of mature cells with effective proliferation; myeloid (and lymphoid) neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB and FGFR1, defined largely by the finding of significant eosinophilia and specific genetic abnormalities; myelodysplastic/myeloproliferative neoplasms (MDS/MPN), comprised mainly of mature cells with both effective and ineffective proliferation of various lineages; myelodysplastic syndromes (MDS), in which immature and mature cells are found with abnormal, dysplastic and ineffective maturation, and acute myeloid leukemia (AML), comprised of precursor cells with impaired maturation.
  • Genetic abnormalities play an important role as diagnostic criteria for further sub-classification of some myeloid neoplasms, particularly of AML.
  • Although therapy-related MDS and AML (t-MDS/AML) often have genetic defects identical to those found in de novo AML and de novo MDS, they are classified separately from de novo AML and MDS in order to emphasize their unique clinical and biologic properties.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Lymphoma / classification. Myelodysplastic Syndromes / classification. Myelodysplastic-Myeloproliferative Diseases / classification. Myeloproliferative Disorders / classification


19. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • Conventional cytogenetic studies have shown a complex cytogenetic abnormality, notably and surprisingly, a t(8;21)(q22;q22) translocation.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


20. Abe T, Furukawa T, Masuko M, Sugimoto A, Okazuka K, Honma K, Fujimura T, Iguchi S, Nishi S, Ueno M, Nagahashi M, Watanabe G, Ajioka Y, Isahai N, Nagai K, Kazuyama Y, Aizawa Y: Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation. Int J Hematol; 2009 Oct;90(3):421-5
MedlinePlus Health Information. consumer health - Bleeding.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation.
  • We report a case of a 29-year-old male patient with a generalized adenovirus (AdV) infection after cord blood transplantation (CBT) for acute myelocytic leukemia with maturation at 2nd complete remission.
  • Molecular diagnosis using PCR-restriction fragment length polymorphism analysis demonstrated that AdV with the serotype 14 caused the cystitis.
  • [MeSH-major] Adenovirus Infections, Human / etiology. Cord Blood Stem Cell Transplantation / adverse effects. Cystitis / etiology. Hemorrhage / etiology. Leukemia, Myeloid, Acute / therapy

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19763745.001).
  • [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] United States
  •  go-up   go-down


21. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In spite of intensive chemotherapy, the patient died within a year of diagnosis.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology

  • Genetic Alliance. consumer health - Myeloid sarcoma.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20698144.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
  •  go-up   go-down


22. Miao YQ, Chen ZX, He J, Cen JN, Bao XJ, Qiu QC, Zhang DE, Yan M: [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jan;28(1):27-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype].
  • OBJECTIVE: To investigate the expression of AML1/ETO9a isoform in the acute myeloid leukemia (AML)-M2 patients.
  • METHODS: Expressions of AML1/ETO fusion gene and AML1/ETO9a isoform were detected by using reverse transcriptase-polymerase chain reaction (RT-PCR) in leukemia patients, MDS patients, leukemia cell lines and healthy subjects.
  • RESULT: In 30 newly diagnosed AML-M2 patients 15 were found to express AML1/ETO9a isoform, while the rest including 20 AML-M2CR, 18 other subtypes of AML, 5 chronic myelogenous leukemia (CML), 3 myelodysplastic syndromes (MDS), 3 leukemia cell lines (NB4, KG-1, K562) and 5 healthy subjects were AML1/ETO9a negative.
  • Among the 15 AML/ETO9a isoform expressing cases, 13 were demonstrated t(8;21) translocation and AML1/ETO expression.
  • CONCLUSION: Isoform AML1/ETO9a was correlated to AML/M2, and it may promote the development of leukemia in combination with the AML1/ETO fusion gene.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17649722.001).
  • [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
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
  •  go-up   go-down


23. Shen YM, Chao HY, Zhang R, Li WY, Feng YF, Zhu ZL, Xue YQ: [Detection of JAK2V617F mutation and its clinical significance in 80 patients with M2 acute myelogenous leukemia]. Zhonghua Zhong Liu Za Zhi; 2009 May;31(5):366-70
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of JAK2V617F mutation and its clinical significance in 80 patients with M2 acute myelogenous leukemia].
  • OBJECTIVE: To explore the prevalence and prognostic significance of JAK2V617F gene mutation in acute myelogenous leukemia M2 (AML-M2) patients.
  • RESULTS: Of 80 de novo AML-M2 patients, 6 at the time of first diagnosis and 1 at relapse were found to have JAK2V617F gene mutation (8.8%, 7/80).
  • Morphologically, the whole blood and bone marrow of the 7 AML-M2 patients with JAK2V617F gene mutation presented a picture of acute leukemia instead of myeloproliferative disorders.
  • Immunophenotypically, bone marrow samples showed myelogenous linage expression.
  • Complete remission was obtained in 4 of 5 AML-M2 patients with JAK2V617F mutation who received treatment, while one patient had no response to the treatment.
  • CONCLUSION: JAK2V617F gene mutation, as a type-1 mutation, might not be an initial event in the pathogenesis of acute myelogenous leukemia, and its presentation does not mean a poor prognosis in de novo AML patients.
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19799086.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


24. Han JS, Oh SY, Kim SH, Kwon HC, Hong SH, Han JY, Park KJ, Kim HJ: A case of pathologic splenic rupture as the initial manifestation of acute myeloid leukemia M2. Yonsei Med J; 2010 Jan;51(1):138-40
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of pathologic splenic rupture as the initial manifestation of acute myeloid leukemia M2.
  • A splenic rupture as the initial manifestation of acute myeloid leukemia is extremely rare.
  • In this study, we described a rare case of acute myeloid leukemia presenting principally as an acute abdomen due to a pathologic splenic rupture in a 35-year old male patient.
  • The oncologist should be aware of this rare initial presentation of acute myeloid leukemia (AML) M2, as the condition generally necessitates a prompt splenectomy.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Splenic Rupture / diagnosis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 2000 Jan 15;88(2):480-90 [10640983.001]
  • [Cites] J Assoc Physicians India. 2002 Nov;50:1435-7 [12583479.001]
  • [Cites] Ann Hematol. 2003 Apr;82(4):231-5 [12707726.001]
  • [Cites] Am J Hematol. 2007 May;82(5):405-8 [17133422.001]
  • [Cites] Bildgebung. 1994 Mar;61(1):37-9 [8193516.001]
  • [Cites] Ann Hematol. 1996 Dec;73(6):297-302 [9003161.001]
  • [Cites] Haematologica. 1998 Aug;83(8):760-1 [9793269.001]
  • [Cites] Jpn J Med. 1987 May;26(2):234-6 [3476781.001]
  • (PMID = 20046528.001).
  • [ISSN] 1976-2437
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2799964
  • [Keywords] NOTNLM ; Acute myeloid leukemia M2 / pathologic / splenic rupture
  •  go-up   go-down


25. Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z: Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2). Cancer Genet Cytogenet; 2009 Jan 15;188(2):95-8
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Acute myeloid leukemia with maturation (AML-M2 based on the French-American-British classification) is often accompanied by typical chromosomal changes such as t (8;21)(q22;q22).
  • The role of this complex variant translocation, as well as the possible formation mechanism, prognostic factors, and morphologic changes are discussed.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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
  • [RetractionIn] Cancer Genet Cytogenet. 2009 Jul;192(1):54 [19489159.001]
  • (PMID = 19100512.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


26. Patroglu T, Torun YA, Karakukcu M, Gorozen F: A case of Turner syndrome associated with acute myeloid leukemia (M2). J Pediatr Hematol Oncol; 2006 Oct;28(10):682-3
MedlinePlus Health Information. consumer health - Turner Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of Turner syndrome associated with acute myeloid leukemia (M2).
  • A 9-year-old girl was diagnosed as acute myeloid leukemia-M2 according to the French-American-British classification.
  • In addition, a diagnosis of Turner syndrome (TS) was made, on the basis of the presence of the chromosomal abnormality, ovarian failure, and abnormal physical features.
  • In particular, children with Down syndrome have increased risk of developing acute myeloblastic leukemia especially M7.
  • On the other hand, cases of myeloid leukemia that are complicated with TS are extremely rare.
  • This is the first report of TS with acute myeloid leukemia of M2 subtype and t (8;.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Turner Syndrome / genetics


27. Jiao B, Wu CF, Liang Y, Chen HM, Xiong SM, Chen B, Shi JY, Wang YY, Wang JH, Chen Y, Li JM, Gu LJ, Tang JY, Shen ZX, Gu BW, Zhao WL, Chen Z, Chen SJ: AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2. Leukemia; 2009 Sep;23(9):1598-604
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2.
  • AML1-ETO fusion gene is generated from chromosomal translocation t(8;21) mainly in acute myeloid leukemia M2 subtype (AML-M2).
  • Its spliced variant transcript, AML1-ETO9a, rapidly induces leukemia in murine model.
  • To evaluate its clinical significance, AML1-ETO9a expression was assessed in 118 patients with t(8;21) AML-M2, using qualitative and nested quantitative reverse transcriptase (RT)-PCR methods.
  • Taken together, these data suggest that AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19458628.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


28. de Oliveira FM, Tone LG, Simões BP, Falcão RP, Brassesco MS, Sakamoto-Hojo ET, dos Santos GA, Marinato AF, Jácomo RH, Rego EM: Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1. Cancer Genet Cytogenet; 2007 Jan 15;172(2):154-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1.
  • We report a case of acute myeloid leukemia (AML) subtype M2, with t(5;11)(q35;q13), in a 30-year-old man.
  • Conventional cytogenetic, spectral karyotyping, and fluorescence in situ hybridization (FISH) studies on bone marrow sample obtained at diagnosis revealed an abnormal karyotype in all cells examined.
  • Similar to the 11q23 region, 11q13 changes can be found in both myeloid and lymphoid neoplasias with different chromosomes serving as donors in translocations.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Cyclin D1 / biosynthesis. Cyclin D1 / genetics. Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Humans. Leukemia, Myelomonocytic, Acute. Male


29. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Iyer RR, Parikh EH, Shukla SN, Shah PM, Bakshi SR: A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21). Indian J Hum Genet; 2008 Jan;14(1):20-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21).
  • t(8;21)(q22;q22) is the most frequently observed karyotypic abnormality associated with acute myeloid leukemia (AML), specifically in FAB-M2.
  • Short-term unstimulated bone marrow (BM) and peripheral blood lymphocyte culture showed 47,XX, +4,t(8;21) in all metaphase plates; and interphase and metaphase results of AML-ETO fusion was positive and trisomy of 4 was confirmed with WCP probes.
  • Trisomy 4 in AML with t(8;21) is a rare numerical abnormality.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 1986 May;67(5):1328-32 [3697508.001]
  • [Cites] Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2007 Aug;24(4):369-72 [17680522.001]
  • [Cites] Leukemia. 2003 Apr;17(4):731-7 [12682630.001]
  • [Cites] Leuk Res. 1998 Oct;22(10):899-903 [9766750.001]
  • (PMID = 20300287.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2840780
  • [Keywords] NOTNLM ; Acute myeloid leukemia / cytogenetics / fluorescence in situ hybridization
  •  go-up   go-down


30. Udayakumar AM, Alkindi S, Pathare AV, Raeburn JA: Complex t(8;13;21)(q22;q14;q22)--a novel variant of t(8;21) in a patient with acute myeloid leukemia (AML-M2). Arch Med Res; 2008 Feb;39(2):252-6
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex t(8;13;21)(q22;q14;q22)--a novel variant of t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for about 3% of all t(8;21)(q22;q22) in acute myeloid leukemia (AML) patients.
  • We report a case of AML-M2 with t(8;13;21)(q22;q14;q22), not reported earlier.
  • Involvement of chromosome region 13q14 has never been reported earlier, although region 13q12 as a variant in AML with t(8;21) has been reported earlier.
  • [MeSH-major] Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18164974.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [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 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


31. Adhya AK, Varma N, Varma S: Acute myeloid leukemia (AML-M2) with mast cell hyperplasia of bone marrow: a report of three cases. Indian J Pathol Microbiol; 2007 Jul;50(3):655-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML-M2) with mast cell hyperplasia of bone marrow: a report of three cases.
  • Bone marrow mastocytosis, though infrequently documented in Indian patients, may be observed in association with many non mast cell hematological neoplasms, including acute myeloblastic leukemia (AML) and myelodysplastic syndromes (MDS).
  • We report three cases of acute myeloid leukemia with excess of mast cells in the bone marrow (BM) samples.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Mast Cells / pathology. Mastocytosis, Systemic / pathology


32. Shah N, Leaker MT, Teshima I, Baruchel S, Abdelhaleem M, Ye CC: Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 May;50(5):1052-3
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia.
  • A 3-year-old female was diagnosed with acute myeloid leukemia (AML-M2).
  • Cytogenetic analysis revealed a clone with trisomy 8 at diagnosis that was replaced by a clone containing a t(11;15) and del(20q) by the end of the second induction.
  • A new clone, characterized by a Philadelphia chromosome, with the minor BCR/ABL p190 transcript, emerged 14 months after diagnosis and remained to the end of disease course.
  • The late occurrence of the Philadelphia chromosome in AML has been documented rarely in adults.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Philadelphia Chromosome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • 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
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18213712.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


33. Bacher U, Schnittger S, Kern W, Trenn G, Weisser M, Haferlach T, Schoch C: Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22). Cancer Genet Cytogenet; 2006 Jul 15;168(2):172-4
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22).
  • We here report on an 48-year-old male patient with a primary diagnosis of acute myeloid leukemia (AML)-M2 with t(8;21)(q22;q22), who developed complete hematologic and molecular remission after induction chemotherapy.
  • Thirteen months later, he relapsed and showed an AML-M2 with t(3;21)(q26;q22).
  • Retrospectively, polymerase chain reaction (PCR) for AML1-EVI1 and EVI1 overexpression was performed on bone marrow and peripheral blood samples taken at diagnosis and during the first year after the first manifestation of AML to quantify the AML1-EVI1-positive clone.
  • In a bone marrow sample taken 25 days from diagnosis, PCR for AML1-EVI1 was negative, and EVI1 expression, as assessed by quantitative real-time PCR, was within the same range as that of healthy controls.
  • These data suggest that this patient developed a secondary therapy-related AML rather than a relapse.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16843110.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
  •  go-up   go-down


34. Anand M, Ghara N, Kumar R, Singh S, Sengar M, Panikar N, Raina V, Sharma A: Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia. Ann Hematol; 2005 Nov;84(12):767-70
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia.
  • Myeloperoxidase (MPO) cytochemical activity, recognized as a very important hallmark of myeloblasts, is generally negative in chronic myeloid leukemia (CML) blast crisis (BC).
  • Myeloperoxidase cytochemistry of peripheral blood blasts in 161 cases of CML, including 103 in chronic phase (CP) and 29 each in accelerated phase (AP) and BC, was assessed and compared with that of 30 cases of acute myeloid leukemia, AML-M2.
  • Compared with the strong MPO positivity, both in terms of intensity and proportion, in the AML-M2 cases, the positivity in the CML cases was generally weak and was seen in a small number of blasts (5-15%), except in one case of BC with 20% positive blasts.
  • This also explains why MPO cytochemistry, despite its high reputation as a myeloid-lineage marker, generally does not help in CML BC.
  • CML BC should therefore be considered as a possible diagnosis along with acute lymphoblastic leukemia, AML-M0, AML-M7, etc., in the setting of MPO-negative blasts.
  • Similarity between MPO expression pattern in CML, i.e., negative in blasts and positive in the more mature cells, and that during maturation of normal myeloid series of cells shows the deranged myelopoiesis of CML to be undisturbed at least with respect to MPO expression.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / biosynthesis. Peroxidase / biosynthesis
  • [MeSH-minor] Female. Gene Expression Regulation, Enzymologic. Histocytochemistry. Humans. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Leukocytes / enzymology. Leukocytes / pathology. Male. Predictive Value of Tests

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15990995.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 1.11.1.7 / Peroxidase
  •  go-up   go-down


35. Choi Y, Elagib KE, Goldfarb AN: AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein. Crit Rev Eukaryot Gene Expr; 2005;15(3):207-16
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein.
  • The chromosomal translocation t(8;21), generating the AML1-ETO fusion protein, is frequently associated with French-American-British (FAB) type M2 acute myeloid leukemia (AML).
  • Several mechanistic models for the role of AML1-ETO in leukemia development have emerged over the last decade.
  • Most of these models have emphasized the capacity of the fusion protein to redirect repressive cofactors, such as histone deacetylases (HDACs) and DNA methyltransferases (DNMTs), to RUNX target genes, thereby reversing the hematopoietic transcriptional program activated by wild-type RUNX1a phenomenon referred to collectively in this review as the "classical" corepressor model.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Animals. Cell Differentiation / genetics. Cells, Cultured. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Erythropoiesis / genetics. GATA1 Transcription Factor / physiology. Histone Deacetylases / genetics. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Signal Transduction / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16390317.001).
  • [ISSN] 1045-4403
  • [Journal-full-title] Critical reviews in eukaryotic gene expression
  • [ISO-abbreviation] Crit. Rev. Eukaryot. Gene Expr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins, Fusion; EC 3.5.1.98 / Histone Deacetylases
  • [Number-of-references] 58
  •  go-up   go-down


36. Christakis G, Perlorentzou S, Aslanidou M, Megalakaki A, Velegraki A: Fatal Blastoschizomyces capitatus sepsis in a neutropenic patient with acute myeloid leukemia: first documented case from Greece. Mycoses; 2005 May;48(3):216-20
Hazardous Substances Data Bank. AMPHOTERICIN B .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fatal Blastoschizomyces capitatus sepsis in a neutropenic patient with acute myeloid leukemia: first documented case from Greece.
  • Blastoschizomyces capitatus was isolated from peripheral blood cultures of a profoundly neutropenic patient with acute myeloid leukemia (M2 FAB).
  • [MeSH-major] Geotrichosis / microbiology. Geotrichum / isolation & purification. Leukemia, Myeloid, Acute / complications. Neutropenia / complications. Sepsis / microbiology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Sepsis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15842341.001).
  • [ISSN] 0933-7407
  • [Journal-full-title] Mycoses
  • [ISO-abbreviation] Mycoses
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
  •  go-up   go-down


37. Sawant RB, Rajadhyaksha SB: Plasma exchange for thrombotic thrombocytopenic purpura following hematopoietic stem cell transplantation. J Assoc Physicians India; 2005 Nov;53:981-3
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 17 years old female diagnosed with acute myeloid leukemia (AML)-M2 received an allogeneic haematopoietic stem cell transplant (HSCT) and was given graft versus host disease (GVHD) prophylaxis with methotrexate, cyclosporin-A (CsA) and methyl prednisolone.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid / surgery. Plasma Exchange. Purpura, Thrombotic Thrombocytopenic / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Female. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16515239.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  •  go-up   go-down


38. Balamurugan S, Sugapriya D, Shanthi P, Thilaka V, Venkatadesilalu S, Pushpa V, Madhavan M: Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias. Indian J Hematol Blood Transfus; 2007 Dec;23(3-4):73-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias.
  • We have studied MDR1 expression and AgNORS in 41 cases of acute leukemia in children.
  • In this study, AgNOR counts in patients with acute lymphoblastic leukemia (ALL) L2 subtype (FAB classification) were significantly higher as compared to the ALL L1 subtype.
  • Similarly, mean AgNOR count in the acute myeloid Leukemia (AML) M2 subtype was significantly higher as compared to the ALL L1 subtype.
  • However, there was no correlation between AgNOR and treatment outcome or between AgNOR counts and MDR1 expression in any of the subtypes of acute leukemia included in this series.
  • In AML, MDR1 gene expression was found to be related to reduced remission induction rates and hence poorer prognosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Blood. 1992 Jan 15;79(2):295-8 [1346094.001]
  • [Cites] Blood. 1992 Jan 15;79(2):473-6 [1370388.001]
  • [Cites] Br J Haematol. 1991 Jan;77(1):50-3 [1671821.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1237-47 [8644864.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1202-10 [12663440.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1201-7 [15547738.001]
  • [Cites] J Pathol. 1989 Jul;158(3):185-8 [2475599.001]
  • [Cites] Br J Haematol. 1981 Apr;47(4):553-61 [6938236.001]
  • [Cites] Blood. 1993 May 1;81(9):2394-8 [8097634.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3480-1 [8507883.001]
  • [Cites] Leuk Lymphoma. 1995 Sep;19(1-2):135-40 [8574159.001]
  • [Cites] Cancer Lett. 1996 Nov 12;108(1):87-91 [8950214.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1673-80 [9324288.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1512-8 [9552060.001]
  • [Cites] Am J Hematol. 1999 Jun;61(2):149-52 [10367797.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):309-14 [11999562.001]
  • [Cites] Mol Cancer Res. 2004 Jun;2(6):339-47 [15235109.001]
  • [Cites] Best Pract Res Clin Haematol. 2004 Dec;17(4):641-51 [15494300.001]
  • (PMID = 23100919.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453125
  • [Keywords] NOTNLM ; Acute leukemia / AgNOR / Multidrug Resistance 1 / P-glycoprotein
  •  go-up   go-down


39. Liu X, Zhang Q, Zhang DE, Zhou C, Xing H, Tian Z, Rao Q, Wang M, Wang J: Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis. Leukemia; 2009 Apr;23(4):739-45
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis.
  • In this study, we found a higher expression level of AML1a in acute lymphoblastic leukemia and acute myeloid leukemia (AML)-M2 patients in comparison to the controls.
  • To investigate the role of AML1a in hematopoiesis and leukemogenesis in vivo, murine bone marrow mononuclear cells were transduced with AML1a and then transplanted into lethally irradiated mice, which developed lymphoblastic leukemia after transplantation.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Animals. Bone Marrow Cells / metabolism. Bone Marrow Transplantation. Case-Control Studies. Hematopoiesis. Humans. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Mice. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic. Protein Isoforms / genetics. Receptor, Macrophage Colony-Stimulating Factor / genetics. Transcription, Genetic. Transduction, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19151769.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Protein Isoforms; 0 / RUNX1 protein, human; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  •  go-up   go-down


40. Studzinski GP, Wang X, Ji Y, Wang Q, Zhang Y, Kutner A, Harrison JS: The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway. J Steroid Biochem Mol Biol; 2005 Oct;97(1-2):47-55
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway.
  • The evidence for the promising potential for derivatives of Vitamin D (deltanoids) in the treatment of myeloid leukemias is increasing, but currently is not matched by the understanding of the precise mechanisms by which these anti-neoplastic effects are achieved.
  • Unlike solid tumors in which growth retardation by deltanoids appears to result from inhibition of cell proliferation and the promotion of cell death by apoptosis, control of myeloid leukemia proliferation by deltanoids results from the induction of differentiation of the immature myelo-monocytic cells towards functional monocytic cells.
  • We present here the accumulating evidence that a pathway that is initiated by deltanoid activation of Vitamin D receptor (VDR) and leads to monocytic differentiation of human myeloblastic HL60 cells, includes the MEK-ERK and JNK mitogen-activated protein kinases (MAPKs), their positive and negative regulators and a downstream effector C/EBPbeta.
  • Importantly, in freshly obtained acute myeloid leukemia (AML)-M2 cells exposed to PRI-2191, a novel deltanoid with a modified side chain, upregulation of C/EBPbeta paralleled the induction of monocytic differentiation.
  • These data provide a basis for the hypothesis that deltanoid-induced upregulation of C/EBPbeta bypasses the block to granulocytic differentiation in myeloid leukemia cells by redirecting the cells to monocytic differentiation.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Vitamin D.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2004 Jan 1;64(1):370-7 [14729647.001]
  • [Cites] J Cell Physiol. 2004 Mar;198(3):333-42 [14755538.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):233-8 [15225777.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):365-70 [15225802.001]
  • [Cites] Exp Cell Res. 2004 Aug 15;298(2):339-58 [15265684.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5425-33 [15289351.001]
  • [Cites] Steroids. 2004 Sep;69(10):629-35 [15465107.001]
  • [Cites] Blood. 1979 Sep;54(3):713-33 [288488.001]
  • [Cites] J Biol Chem. 2000 Jun 9;275(23):17276-80 [10764733.001]
  • [Cites] Exp Cell Res. 2000 Aug 1;258(2):425-37 [10896794.001]
  • [Cites] J Cell Biochem. 2001;80(4):471-82 [11169731.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):963-9 [11221891.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] J Cell Sci. 2001 May;114(Pt 9):1609-12 [11309192.001]
  • [Cites] J Cell Biochem. 2001 Apr 2-27;82(1):68-77 [11400164.001]
  • [Cites] Exp Cell Res. 2001 Aug 15;268(2):294-300 [11478855.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 15;93(16):1224-33 [11504768.001]
  • [Cites] Biol Signals Recept. 2001 Nov-Dec;10(6):341-9 [11721090.001]
  • [Cites] Steroids. 2002 Aug;67(9):789-98 [12123791.001]
  • [Cites] Acta Biochim Pol. 2002;49(2):393-406 [12362981.001]
  • [Cites] Cell Cycle. 2002 Mar-Apr;1(2):103-10 [12429916.001]
  • [Cites] Cell Cycle. 2002 Nov-Dec;1(6):410-5 [12548017.001]
  • [Cites] J Cell Biochem. 2003 Mar 1;88(4):695-705 [12577303.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9402-6 [12522135.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1325-32 [12649194.001]
  • [Cites] J Cell Biochem. 2003 Aug 15;89(6):1087-101 [12898508.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52651-9 [14517214.001]
  • [Cites] Biochemistry. 1990 Jan 9;29(1):190-6 [2322540.001]
  • [Cites] J Biol Chem. 1990 Sep 15;265(26):15823-31 [2394750.001]
  • [Cites] J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):231-40 [1314073.001]
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27489-94 [7499206.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] J Natl Cancer Inst. 1997 Aug 20;89(16):1199-206 [9274914.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):12792-6 [9371754.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23242-8 [10438498.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):472-87 [15601867.001]
  • (PMID = 16046262.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA044722-15; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01 CA044722-15; United States / NCI NIH HHS / CA / R01 CA44722
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / Retinoblastoma Protein; 1406-16-2 / Vitamin D; EC 2.7.- / Protein Kinases; EC 2.7.1.- / KSR-1 protein kinase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS169830; NLM/ PMC2814418
  •  go-up   go-down


41. Licciulli S, Cambiaghi V, Scafetta G, Gruszka AM, Alcalay M: Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation. Leukemia; 2010 Feb;24(2):429-37
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation.
  • Terminal differentiation of blood cells requires the concerted action of a series of transcription factors that are expressed at specific stages of maturation and function in a cell-type and dosage-dependent manner.
  • Pirin (PIR) is a putative transcriptional regulator whose expression is silenced in cells bearing the acute myeloid leukemia-1 eight-twenty-one (AML1/ETO) and promyelocytic leukemia/retinoic acid receptor (PML/RAR) leukemogenic fusion proteins.
  • A role for PIR in myeloid differentiation has not to date been reported.
  • In this study we show that PIR expression is significantly repressed in a large proportion of acute myeloid leukemias (AMLs), regardless of subtype or underlying karyotypic abnormalities.
  • We show that PIR expression increases during in vitro myeloid differentiation of primary hematopoietic precursor cells, and that ablation of PIR in the U937 myelomonocytic cell line or in murine primary hematopoietic precursor cells results in impairment of terminal myeloid differentiation.
  • Our results suggest that PIR is required for terminal myeloid maturation, and its downregulation may contribute to the differentiation arrest associated with AML.
  • [MeSH-major] Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Differentiation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism


42. Martino V, Tonelli R, Montemurro L, Franzoni M, Marino F, Fazzina R, Pession A: Down-regulation of MLL-AF9, MLL and MYC expression is not obligatory for monocyte-macrophage maturation in AML-M5 cell lines carrying t(9;11)(p22;q23). Oncol Rep; 2006 Jan;15(1):207-11
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down-regulation of MLL-AF9, MLL and MYC expression is not obligatory for monocyte-macrophage maturation in AML-M5 cell lines carrying t(9;11)(p22;q23).
  • The MLL-AF9 oncogene originates from the translocation t(9;11)(p22;q23), which is mainly associated with monocytic acute myeloid leukaemia (AML-M5; FAB-classification).
  • In AML-M5 THP-1 cells carrying t(9;11) (p22;q23) and expressing MLL-AF9, we previously showed that MLL-AF9 expression is down-regulated during monocyte-macrophage maturation.
  • MLL fusion proteins (including MLL-AF9) deregulate MYC transactivation activity, and both presence and absence of MYC down-regulation have been reported during monocyte-macrophage maturation in THP-1 cells.
  • In the present study, we analyze the expression patterns of MLL-AF9, MLL wild-type and MYC after induction of monocyte-macrophage terminal differentiation in the AML-M5 cell lines, THP-1, THP-1-R, Mono-Mac-6 (MM6) and MOLM-13, all of which carry t(9;11)(p22;q23) and express MLL-AF9.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Macrophages / cytology. Monocytes / cytology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-myc / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16328057.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MYC protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-myc; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


43. van Binsbergen E, de Weerdt O, Buijs A: A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review. Cancer Genet Cytogenet; 2007 Jul 1;176(1):72-5
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review.
  • The t(2;11)(q37;q23) is a rare recurrent cytogenetic abnormality associated with de novo and therapy-related acute myeloid leukemia, resulting in a MLL-SEPT2 fusion gene.
  • We report on a case of therapy-related acute myeloid leukemia M2 showing a t(2;11)(q37;q23) and resulting in a new subtype of a MLL-SEPT2 chimeric transcript.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion. Phosphoric Monoester Hydrolases / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17574968.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
  • [Number-of-references] 9
  •  go-up   go-down


44. Kremser A, Dressig J, Grabrucker C, Liepert A, Kroell T, Scholl N, Schmid C, Tischer J, Kufner S, Salih H, Kolb HJ, Schmetzer H: Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods. J Immunother; 2010 Feb-Mar;33(2):185-99
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods.
  • Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
  • We studied the capability of 6 serum-free DC culture methods, chosen according to different mechanisms, to induce DC differentiation in 137 cases of AML and 52 cases of MDS.
  • The quality/quantity of DC generated was estimated by flow cytometry studying (co) expressions of "DC"antigens, costimulatory, maturation, and blast-antigens.
  • Comparing these methods on average 15% to 32% DC, depending on methods used, could be obtained from blast-containing mononuclear cells (MNC) in AML/MDS cases with a DC viability of more than 60%.
  • Average results of all culture methods tested were comparable, however not every given case of AML could be differentiated to DC with 1 selected method.
  • [MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20139775.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil
  •  go-up   go-down


45. Classen CF, Teigler-Schlegel A, Röttgers S, Reinhardt D, Döhner K, Debatin KM: AML bearing the translocation t(11;17)(q23;q21): involvement of MLL and a region close to RARA, with no differentiation response to retinoic acid. Ann Hematol; 2005 Nov;84(12):774-80
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML bearing the translocation t(11;17)(q23;q21): involvement of MLL and a region close to RARA, with no differentiation response to retinoic acid.
  • We describe a case of acute myeloid leukemia (AML) bearing the translocation t(11;17)(q23;q21).
  • The morphological phenotype represented a monoblastic leukemia, AML French-American-British (FAB) M5a.
  • Further analysis of the translocation revealed an involvement of the mixed-lineage leukemia (MLL) gene and a region closely proximal to the retinoic acid (RA) receptor alpha (RARA) gene.
  • Rearrangements of the MLL (11q23) gene in AML are usually related to the morphological phenotype FAB M5.
  • In acute promyelocytic leukemia, the translocation (15;17)(q22;q11-21) involving the RARA leads to a maturation arrest that can be overcome by RA, often inducing remission.
  • In other forms of AML, however, the effects of RA are limited and diverse.
  • To study whether RA might have a therapeutical potential in our case, we performed an in vitro analysis of RA effects on AML cells.
  • Our data indicate that in AML cells bearing the t(11;17)(q23;q21), a differentiation arrest that is overcome by RA is not present.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic. Tretinoin / pharmacology
  • [MeSH-minor] Antigens, CD38 / biosynthesis. Cell Death / drug effects. Cell Death / genetics. Child. Drug Screening Assays, Antitumor. Female. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / genetics. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Receptors, Retinoic Acid / therapeutic use. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16044313.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MLL protein, human; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5688UTC01R / Tretinoin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.2.2.5 / Antigens, CD38
  •  go-up   go-down


46. Secchiero P, Zerbinati C, Melloni E, Milani D, Campioni D, Fadda R, Tiribelli M, Zauli G: The MDM-2 antagonist nutlin-3 promotes the maturation of acute myeloid leukemic blasts. Neoplasia; 2007 Oct;9(10):853-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The MDM-2 antagonist nutlin-3 promotes the maturation of acute myeloid leukemic blasts.
  • The small-molecule inhibitor of murine double minute (MDM-2), Nutlin-3, induced variable apoptosis in primary acute myeloid leukemia (AML) blasts and promoted myeloid maturation of surviving cells, as demonstrated by analysis of CD11b and CD14 surface antigens and by morphologic examination.
  • Although the best-characterized activity of Nutlin-3 is activation of the p53 pathway, Nutlin-3 induced maturation also in one AML sample characterized by p53 deletion, as well as in the p53(-/-) human myeloblastic HL-60 cell line.
  • Taken together, these data disclose a novel, potentially relevant therapeutic role for Nutlin-3 in the treatment of both p53 wild-type and p53(-/-) AML, possibly in association with recombinant TRAIL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Imidazoles / pharmacology. Leukemia, Myeloid / drug therapy. Piperazines / pharmacology. Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Antigens, CD11b / drug effects. Antigens, CD11b / metabolism. Antigens, CD14 / drug effects. Antigens, CD14 / metabolism. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. E2F1 Transcription Factor / drug effects. E2F1 Transcription Factor / metabolism. Flow Cytometry. Humans. Immunoprecipitation. RNA, Small Interfering. Retinoblastoma Protein / biosynthesis. Retinoblastoma Protein / drug effects. TNF-Related Apoptosis-Inducing Ligand / drug effects. TNF-Related Apoptosis-Inducing Ligand / metabolism. Transfection. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / metabolism. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1983 Oct;80(19):5907-11 [6577459.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 May;77(5):2936-40 [6930676.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2230-7 [8161788.001]
  • [Cites] Semin Cell Biol. 1994 Apr;5(2):115-25 [8068884.001]
  • [Cites] Leuk Lymphoma. 1995 Mar;17(1-2):13-8 [7773150.001]
  • [Cites] J Leukoc Biol. 1995 Nov;58(5):547-55 [7595056.001]
  • [Cites] Cell Growth Differ. 1995 Nov;6(11):1405-13 [8562479.001]
  • [Cites] Br J Haematol. 1996 Jun;93(3):542-50 [8652371.001]
  • [Cites] J Immunol. 1998 Apr 15;160(8):3891-8 [9558095.001]
  • [Cites] Leuk Res. 1998 Feb;22(2):153-61 [9593472.001]
  • [Cites] J Biol Chem. 2004 Dec 17;279(51):53317-22 [15485814.001]
  • [Cites] EMBO J. 2005 Jan 12;24(1):160-9 [15577944.001]
  • [Cites] Curr Cancer Drug Targets. 2005 Feb;5(1):3-8 [15720184.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3150-9 [16014563.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3609-17 [16081689.001]
  • [Cites] Blood. 2006 May 15;107(10):4122-9 [16439677.001]
  • [Cites] Blood. 2006 May 15;107(10):4109-14 [16439685.001]
  • [Cites] Blood. 2006 Aug 1;108(3):993-1000 [16543464.001]
  • [Cites] Oncogene. 2007 May 24;26(24):3473-81 [17146434.001]
  • [Cites] J Exp Med. 1999 Dec 6;190(11):1583-94 [10587349.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(6):2186-97 [10688665.001]
  • [Cites] Blood. 2000 Jul 15;96(2):475-82 [10887108.001]
  • [Cites] Blood. 2001 Oct 1;98(7):2220-8 [11568010.001]
  • [Cites] Cell. 2002 May 3;109(3):335-46 [12015983.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2421-9 [12239152.001]
  • [Cites] Mol Cell Biol. 2003 May;23(10):3607-22 [12724419.001]
  • [Cites] Blood. 2004 Jan 15;103(2):517-22 [12969966.001]
  • [Cites] Mol Cancer Res. 2003 Dec;1(14):1001-8 [14707283.001]
  • [Cites] Science. 2004 Feb 6;303(5659):844-8 [14704432.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):458-67 [14713961.001]
  • [Cites] Carcinogenesis. 2004 Aug;25(8):1387-94 [15033903.001]
  • [Cites] Science. 1988 May 13;240(4854):889-95 [3283939.001]
  • (PMID = 17971905.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD14; 0 / Antineoplastic Agents; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Imidazoles; 0 / Piperazines; 0 / RNA, Small Interfering; 0 / Retinoblastoma Protein; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2040212
  • [Keywords] NOTNLM ; Acute myeloid leukemia / HL-60 cells / apoptosis / p53 pathway / surface antigens
  •  go-up   go-down


47. Nguyen S, Beziat V, Dhedin N, Kuentz M, Vernant JP, Debre P, Vieillard V: HLA-E upregulation on IFN-gamma-activated AML blasts impairs CD94/NKG2A-dependent NK cytolysis after haplo-mismatched hematopoietic SCT. Bone Marrow Transplant; 2009 May;43(9):693-9
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-E upregulation on IFN-gamma-activated AML blasts impairs CD94/NKG2A-dependent NK cytolysis after haplo-mismatched hematopoietic SCT.
  • Natural killer (NK) cells generated after haploidentical hematopoietic SCT in patients with AML are characterized by specific phenotypic features and impaired functioning that may affect transplantation outcome.
  • We show that IFN-gamma produced by immature CD56(bright) NK cells upregulates cell surface expression of HLA-E on AML blasts and that this upregulation protects leukemic cells from NK-mediated cell lysis through the mediation of CD94/NKG2A, an inhibitory receptor overexpressed on NK cells after haploidentical SCT.
  • This implies that maturation of NK cells is the key to improved immune responses and transplantation outcome.
  • [MeSH-major] HLA Antigens / genetics. Hematopoietic Stem Cell Transplantation. Histocompatibility Antigens Class I / genetics. Interferon-gamma / pharmacology. Interferon-gamma / physiology. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / pathology. NK Cell Lectin-Like Receptor Subfamily C / immunology. NK Cell Lectin-Like Receptor Subfamily D / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19011664.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-E antigen; 0 / Histocompatibility Antigens Class I; 0 / KLRC1 protein, human; 0 / KLRD1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily C; 0 / NK Cell Lectin-Like Receptor Subfamily D; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


48. Schanz J, Weiss B, Henrich D, Bohrer MH, Uppenkamp M: [30 year-old patient with multiple pelvic lesions and fecal incontinence]. Internist (Berl); 2009 Sep;50(9):1155, 1157-60
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The results of a bone marrow aspiration showed acute myeloid leukemia M2 with translocation t(8,21) associated with granulocytic sarcoma.
  • [MeSH-major] Fecal Incontinence / prevention & control. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Pelvic Neoplasms / diagnosis. Pelvic Neoplasms / surgery. Stem Cell Transplantation

  • Genetic Alliance. consumer health - Incontinence.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hematol J. 2004;5(1):84-9 [14745436.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):466-75 [9053467.001]
  • [Cites] Cancer. 1981 Sep 15;48(6):1426-37 [7023656.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2480-9 [16735702.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3767-75 [10577848.001]
  • [Cites] Neurosurgery. 1997 Jun;40(6):1283-7 [9179903.001]
  • [Cites] Blood. 2002 May 15;99(10):3517-23 [11986202.001]
  • [Cites] N Engl J Med. 1998 Apr 2;338(14):969 [9521985.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1643-8 [9269784.001]
  • [Cites] Int J Hematol. 2005 Oct;82(3):210-4 [16207593.001]
  • [Cites] J Clin Oncol. 1993 Apr;11(4):690-7 [8478662.001]
  • [Cites] Bone Marrow Transplant. 2005 Apr;35(8):767-73 [15735660.001]
  • [Cites] Arch Pathol Lab Med. 2006 Jun;130(6):862-6 [16740041.001]
  • [Cites] J Korean Med Sci. 2006 Aug;21(4):745-8 [16891824.001]
  • [Cites] Clin Neurol Neurosurg. 1991;93(4):341-4 [1665771.001]
  • (PMID = 19585093.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


49. Nishizawa M, Hirayama F, Matsuyama N, Tada K, Kaneko H, Watanabe M, Miura Y, Tsudo M: [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate]. Rinsho Ketsueki; 2009 Jan;50(1):16-22
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate].
  • We report a fatal case of transfusion-related acute lung injury (TRALI) with anti-leukocyte antibodies detected both in the patient's serum and in the causative red cell concentrate (RC-M.A.P).
  • A 41-year-old Japanese woman diagnosed as having acute myeloid leukemia (AML, M2) developed TRALI caused by RC-M.A.P 15 days after the start of induction therapy for AML.
  • [MeSH-major] Acute Lung Injury / etiology. Autoantibodies / blood. Erythrocyte Transfusion / adverse effects. HLA Antigens / immunology. Leukemia, Myeloid, Acute / therapy. Leukocytes / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19225224.001).
  • [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 / Autoantibodies; 0 / HLA Antigens
  •  go-up   go-down


50. Vundinti BR, Kerketta L, Madkaikar M, Jijina F, Ghosh K: Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22. Indian J Cancer; 2008 Jan-Mar;45(1):30-2
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22.
  • The t(8;21)(q22;q22) is one of the most frequent chromosomal abnormality associated with acute myeloid leukemia (AML) M2 sub type.
  • We report a case of AML-M2 with t(X;8;21)(p22;q22;q22) associated with loss of Y chromosome.
  • The patient did not respond to therapy and follow-up of cytogenetics revealed same chromosome abnormality.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18453738.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


51. Wang XB, Liu J, Wu JS, Sun ZM, Huang SA: [Effects of soluble secreted by acute myeloid leukemia cells on differentiation, maturation, apoptosis, and functions of dendritic cells]. Ai Zheng; 2007 Feb;26(2):142-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of soluble secreted by acute myeloid leukemia cells on differentiation, maturation, apoptosis, and functions of dendritic cells].
  • This study was to investigate the effects of soluble factors secreted by acute myeloid leukemia (AML) cells on the differentiation, maturation, apoptosis, and functions of DCs derived from normal mononuclear cells.
  • METHODS: Mononuclear cells were cultured with interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF), in the presence or absence of 24-hour culture supernatants from fresh primary AML cells, to generate immature DCs.
  • The maturation of DCs was induced by cytokines IL-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), and prostaglandin-2 (PGE-2).
  • RESULTS: AML cell supernatant-treated DCs showed significantly lower expression of co-stimulatory molecules CD80 and CD86, and reduced response to cytokines IL-1beta, IL-6, TNF-alpha, and PGE-2.
  • The apoptosis rate was significantly lower in AML cell supernatant-treated DCs than in control DCs [(29.4+/-9.5)% vs. (15.1+/-4.2)%, P<0.01].
  • The allostimulatory effects of AML cell supernatant-treated DCs on CD4+ and CD8+ T cells were significantly lower than those of normal mature DCs [PF: (1.8+/-0.5)% vs. (5.2+/-1.6)% for CD4+ T cells, (2.1+/-0.6)% vs. (6.5+/-2.0)% for CD8+ T cells, P<0.01].
  • CONCLUSION: Soluble factors derived from AML cells could inhibit development and functions of DCs.
  • [MeSH-major] Apoptosis. Cell Differentiation. Dendritic Cells. Leukemia, Myeloid, Acute / immunology

  • 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
  • (PMID = 17298742.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / Culture Media; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down


52. Gozzini A, Santini V: Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts. Ann Hematol; 2005 Dec;84 Suppl 1:54-60
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts.
  • In leukemic cells, hypermethylation of CpG islands in the promoter region of genes critical for cell cycle and maturation is frequent, and DNMTs were found to be overexpressed, findings paralleled by evidence of transcriptional repression of downstream genes.
  • Therefore, the combination of HDAC and DNMT inhibitors has been considered to be a possible therapeutic approach to restore normal gene expression in acute myeloid leukemia (AML) and other diseases.
  • Thus, treatment of AML with HDAC inhibitors such as D1 and DNMT inhibitors such as decitabine might have clinical benefit for patients, especially these presenting subtypes of AML, like AML1/ETO, in which the leukemogenic mechanism involves corepressor protein complexes containing HDAC and DNMT.
  • [MeSH-major] Azacitidine / analogs & derivatives. Butyrates / pharmacology. DNA Modification Methylases / antagonists & inhibitors. Histone Deacetylase Inhibitors. Leukemia, Myeloid, Acute / genetics. Mannose / analogs & derivatives

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16228241.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Butyrates; 0 / Histone Deacetylase Inhibitors; 0 / O-n-butanoyl-2,3-O-isopropylidenemannofuranoside; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine; PHA4727WTP / Mannose
  •  go-up   go-down


53. Suárez L, Vidriales MB, Moreno MJ, López A, García-Laraña J, Pérez-López C, Tormo M, Lavilla E, López-Berges MC, de Santiago M, San Miguel JF, Orfao A, PETHEMA Cooperative Group: Differences in anti-apoptotic and multidrug resistance phenotypes in elderly and young acute myeloid leukemia patients are related to the maturation of blast cells. Haematologica; 2005 Jan;90(1):54-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in anti-apoptotic and multidrug resistance phenotypes in elderly and young acute myeloid leukemia patients are related to the maturation of blast cells.
  • BACKGROUND AND OBJECTIVES: Elderly patients with acute myeloid leukemia (AML) have a less favorable outcome, which has been related, among other factors, to multidrug resistance (MDR) phenotypes.
  • DESIGN AND METHODS: Freshly obtained erythrocyte-lysed bone marrow samples from 150 elderly patients (> 65 years) with de novo AML and 30 younger AML patients were analyzed using a 4-color immunofluorescence technique for quantitative expression of proteins associated with apoptosis (bcl-2, bax, APO2.7) and MDR (P-gp, MRP, LRP) in 3 blast cell subpopulations, defined according to their maturation stage.
  • RESULTS: Although a homogeneous CD34+ blast cell population was more frequent in the elderly patients, (25% vs 7%, p=0.02), no statistically significant differences were detected between the two age groups in the expression of either apoptosis- or MDR-associated proteins, except for slightly higher quantities of LRP protein in the more immature CD34+ blast cell subset in the elderly AML cases (p=0.04).
  • In addition, higher P-gp levels were found in CD34+ blast cells than in CD34-- ones in elderly AML patients.
  • INTERPRETATION AND CONCLUSIONS: In summary, our results suggest that the higher resistance to chemotherapy observed in elderly AML patients could be related to a higher incidence of cases with a CD34+ homogeneous blast cell population, since these blast cells frequently display a more pronounced anti-apoptotic and MDR1 phenotype.
  • [MeSH-major] Apoptosis / drug effects. Blast Crisis / pathology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Antigens, CD34. Drug Resistance, Multiple. Female. Genes, MDR / genetics. Genes, MDR / physiology. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Haematologica. 2005 Jan;90(1):3 [15644303.001]
  • (PMID = 15642669.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34
  •  go-up   go-down


54. Manola KN, Georgakakos VN, Margaritis D, Stavropoulou C, Panos C, Kotsianidis I, Pantelias GE, Sambani C: Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer. Cancer Genet Cytogenet; 2008 Jan 1;180(1):37-42
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer.
  • We describe a case of treatment-induced acute myeloid leukemia M2 after breast cancer with a rare reciprocal t(12;12)(p13;q13) as a secondary cytogenetic abnormality in addition to the t(11;19)(q23;p13.1).
  • To the best of our knowledge, our patient represents the first report of the rare t(12;12)(p13;q13) described in treatment-induced leukemia and the possible formation of a new fusion gene.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms / drug therapy. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18068531.001).
  • [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 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  •  go-up   go-down


55. Chen WL, Hsu YJ, Tsai WC, Tsao YT: An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen. J Natl Med Assoc; 2008 Aug;100(8):957-9
MedlinePlus Health Information. consumer health - Fever.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen.
  • Differential diagnosis of a focal splenic lesion in the context of acute leukemia is quite challenging.
  • The results of hematological work-up were consistent with acute myeloblastic leukemia (M2, French-American-British classification).
  • Being susceptible to infection in this leukemic patient with severe neutropenia, a diagnosis of splenic abscess was straightforward, plausibly supported by the radiographic findings.
  • Histological sections from ultrasound-guided percutaneous core-needle biopsy of the spleen confirmed the diagnosis of myeloid sarcoma.
  • However, delayed leukemia-targeted therapy, unfortunately, resulted in catastrophic mortality.
  • It should be addressed that, even with the advent of modern imaging modalities, there can be a diagnostic pitfall when managing solitary splenic lesion in acute leukemic patients without histological examination.
  • [MeSH-major] Fever / etiology. Leukemia, Myeloid, Acute / diagnosis. Neutropenia / etiology. Sarcoma, Myeloid / diagnosis. Splenic Neoplasms / diagnosis
  • [MeSH-minor] Biopsy, Needle. Diagnosis, Differential. Diagnostic Errors. Fatal Outcome. Female. Humans. Middle Aged. Spleen / pathology. Tomography, X-Ray Computed


56. Khalil SH: Molecular hematology. Qualitative to quantitative techniques. Saudi Med J; 2005 Oct;26(10):1516-22
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Section of Hematology, Department of Pathology and Laboratory Medicine at King Faisal Specialist Hospital and Research Center has shared this experience during the last 10 years with more than 6,546 samples submitted for the analysis of different gene rearrangements, fusion gene transcripts and gene mutations including Ig heavy chain gene rearrangement for B-cell malignancies, T-cell receptor gamma chain gene rearrangement for T-cell malignancies, BCR/ABL-P210 and P190 fusion gene transcripts, for chronic myeloid leukemia and Philadelphia positive acute lymphoblastic leukemia, PML/RARalpha fusion gene for promyelocytic leukemia, AML1/ETO for acute myeloid leukemia AML-M2 with t8;21, CBFB/MYH11 for AML M4E0 with inv 16, BCL-2 for follicular lymphoma, and BCL-1 for mantle cell lymphoma.
  • Hence, most molecular assays are qualitative in nature, quantitative assays are deemed necessary in the monitoring and follow-up of minimal residual disease in leukemia and lymphoma, and proved in our experience to serve as an essential tool to confirm complete remission CR post-chemotherapy and bone marrow transplantation, and to detect signs of early relapse for proper clinical intervention.
  • [MeSH-major] Hematologic Neoplasms / diagnosis. Molecular Biology / methods

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16228048.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Saudi Arabia
  • [Number-of-references] 36
  •  go-up   go-down


57. Hauer J, Tosi S, Schuster FR, Harbott J, Kolb HJ, Borkhardt A: Graft versus leukemia effect after haploidentical HSCT in a MLL-negative infant AML with HLXB9/ETV6 rearrangement. Pediatr Blood Cancer; 2008 Apr;50(4):921-3
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Graft versus leukemia effect after haploidentical HSCT in a MLL-negative infant AML with HLXB9/ETV6 rearrangement.
  • Recently published data show an extremely poor survival of infants with AML and HLXB9/ETV6 rearrangement which is the fusion, resulting from the translocation t(7;12)(q36;p13).
  • Herein, we report the clinical course of an 8-month-old patient with acute myeloid leukemia, M2 subtype and with a HLXB9/TEL rearrangement.
  • This case reinforces the potential benefit of a graft-versus-leukemia effect in the haploidentical setting even in chemoresistant myeloid leukemias with poor-prognosis molecular features.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / therapy. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17960638.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / Transcription Factors
  •  go-up   go-down


58. Mitina O, Warmuth M, Krause G, Hallek M, Obermeier A: Src family tyrosine kinases phosphorylate Flt3 on juxtamembrane tyrosines and interfere with receptor maturation in a kinase-dependent manner. Ann Hematol; 2007 Nov;86(11):777-85
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Src family tyrosine kinases phosphorylate Flt3 on juxtamembrane tyrosines and interfere with receptor maturation in a kinase-dependent manner.
  • Due to frequent mutations in the Flt3 gene in patients with acute myeloid leukemia (AML), Flt3 is regarded as a potential therapeutic target, but the underlying mechanisms are still poorly understood.
  • Employing sets of wt and mutant Flt3 and Hck, we analyzed protein binding as well as Flt3 phosphorylation and maturation in HEK-293 cells cotransfected with expression constructs encoding both binding partners.
  • As apparent from the distribution of mature and hypoglycosylated Flt3, SFKs interfered with Flt3 maturation in a kinase-dependent manner.
  • Together, these findings show a complex role of SFKs in Flt3 signaling and reveal a new function of SFKs in the maturation of RTKs.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17668209.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / HCK protein, human; EC 2.7.10.2 / Proto-Oncogene Proteins c-hck; EC 2.7.10.2 / src-Family Kinases
  •  go-up   go-down


59. Nowbakht P, Ionescu MC, Rohner A, Kalberer CP, Rossy E, Mori L, Cosman D, De Libero G, Wodnar-Filipowicz A: Ligands for natural killer cell-activating receptors are expressed upon the maturation of normal myelomonocytic cells but at low levels in acute myeloid leukemias. Blood; 2005 May 1;105(9):3615-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligands for natural killer cell-activating receptors are expressed upon the maturation of normal myelomonocytic cells but at low levels in acute myeloid leukemias.
  • Here, we have studied the role of NKG2D and natural cytotoxicity receptors (NCRs) in the recognition of human leukemia.
  • Analysis of UL16-binding protein-1 (ULBP1), ULBP2, and ULBP3 ligands for NKG2D and of potential ligands for NKp30, NKp44, and NKp46 in healthy hematopoietic cells demonstrated the ligand-negative phenotype of bone marrow-derived CD34(+) progenitor cells and the acquisition of cell-surface ligands during the course of myeloid differentiation.
  • In acute myeloid leukemia (AML), leukemic blasts from approximately 80% of patients expressed very low levels of ULBPs and NCR-specific ligands.
  • Treatment with differentiation-promoting myeloid growth factors, together with interferon-gamma, upregulated cell-surface levels of ULBP1 and putative NCR ligands on AML blasts, conferring an increased sensitivity to NK cell-mediated lysis.
  • We conclude that the ligand-negative/low phenotype in AML is a consequence of cell maturation arrest on malignant transformation and that defective expression of ligands for the activating NKG2D and NCR receptors may compromise leukemia recognition by NK cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / immunology. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Monocytes / pathology. Receptors, Immunologic / genetics
  • [MeSH-minor] Acute Disease. Case-Control Studies. Cell Differentiation. Humans. Ligands. Myeloid Cells / pathology. NK Cell Lectin-Like Receptor Subfamily K. Natural Cytotoxicity Triggering Receptor 1. Natural Cytotoxicity Triggering Receptor 2. Natural Cytotoxicity Triggering Receptor 3. Receptors, Natural Killer Cell

  • 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 = 15657183.001).
  • [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 / KLRK1 protein, human; 0 / Ligands; 0 / NCR1 protein, human; 0 / NCR2 protein, human; 0 / NCR3 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Natural Cytotoxicity Triggering Receptor 1; 0 / Natural Cytotoxicity Triggering Receptor 2; 0 / Natural Cytotoxicity Triggering Receptor 3; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell
  •  go-up   go-down


60. Abdul-Nabi AM, Yassin ER, Varghese N, Deshmukh H, Yaseen NR: In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML. PLoS One; 2010 Aug 27;5(8):e12464
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML.
  • Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation.
  • Here we compare the in vitro effects of representatives of 4 major groups of AML fusion oncogenes on primary human CD34+ cells.
  • They both caused erythroid hyperplasia and a clear block in erythroid and myeloid maturation.
  • On the other hand, AML1-ETO and PML-RARA had only modest effects on myeloid and erythroid differentiation.
  • These data show that differences among AML fusion oncogenes can be recapitulated in vitro using primary human CD34+ cells and that early gene expression profiling in these cells can reveal potential drug targets in AML.

  • MedlinePlus Health Information. consumer health - Acute Myeloid 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
  • [Cites] Blood. 2002 Jan 1;99(1):15-23 [11756147.001]
  • [Cites] Cancer Res. 2009 Feb 1;69(3):1109-16 [19155294.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):331-45 [11921269.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3475-95 [12032783.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10008-13 [12105272.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):149-58 [12696063.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1857-65 [12750176.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2395-402 [12805060.001]
  • [Cites] Mol Cancer Res. 2003 Dec;1(14):1001-8 [14707283.001]
  • [Cites] Science. 2004 Feb 6;303(5659):844-8 [14704432.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1238-45 [15152269.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 May;87(9):3584-8 [2333304.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Cell. 1998 Mar 20;92(6):713-23 [9529248.001]
  • [Cites] Cell. 1998 Mar 20;92(6):725-34 [9529249.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4016-21 [15731354.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1189-98 [15878973.001]
  • [Cites] Oncogene. 2005 Aug 29;24(37):5693-700 [16123802.001]
  • [Cites] Trends Cell Biol. 2005 Sep;15(9):494-501 [16084092.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3150-9 [16014563.001]
  • [Cites] Leukemia. 2006 Feb;20(2):218-23 [16341046.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 24;103(4):1030-5 [16418266.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Feb;7(2):131-42 [16493418.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):2990-6 [16540647.001]
  • [Cites] Leukemia. 2006 Apr;20(4):696-706 [16467868.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6628-37 [16818636.001]
  • [Cites] Blood. 2006 Jul 15;108(2):685-96 [16597596.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1690-7 [16670269.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11781-91 [17178874.001]
  • [Cites] Curr Opin Hematol. 2007 Mar;14(2):85-9 [17255784.001]
  • [Cites] Science. 2007 Apr 27;316(5824):600-4 [17463288.001]
  • [Cites] Cancer Lett. 2007 Jun 28;251(2):179-86 [17125917.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1531-7 [10942402.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Leukemia. 2001 Nov;15(11):1689-95 [11681408.001]
  • [Cites] Clin Cancer Res. 1998 Dec;4(12):3051-62 [9865920.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(6):1063-70 [17468032.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1638-47 [17554387.001]
  • [Cites] J Interferon Cytokine Res. 2007 Jul;27(7):543-52 [17651015.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2190-9 [17975013.001]
  • [Cites] Semin Cell Dev Biol. 2008 Jun;19(3):294-308 [18343170.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]
  • [Cites] Oncogene. 2008 Jun 19;27(27):3765-79 [18264136.001]
  • [Cites] Arch Pathol Lab Med. 2008 Nov;132(11):1835-7 [18976025.001]
  • [Cites] Methods Mol Biol. 2009;538:263-85 [19277588.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2009;49:223-41 [18834305.001]
  • [Cites] Cell. 2009 May 15;137(4):609-22 [19450511.001]
  • [Cites] Haematologica. 2009 Jul;94(7):984-93 [19535349.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1303-10 [19225539.001]
  • [Cites] Blood. 2010 Jul 8;116(1):71-80 [20404136.001]
  • [Cites] Leukemia. 2002 Feb;16(2):186-95 [11840284.001]
  • (PMID = 20805992.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL082549; United States / NCI NIH HHS / CA / T32CA009547; United States / NCI NIH HHS / CA / T32 CA009547; United States / NHLBI NIH HHS / HL / K02 HL084179; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / P30CA91842; United States / NHLBI NIH HHS / HL / R01HL082549; United States / NHLBI NIH HHS / HL / K02HL084179
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2929205
  •  go-up   go-down


61. Gilles L, Guièze R, Bluteau D, Cordette-Lagarde V, Lacout C, Favier R, Larbret F, Debili N, Vainchenker W, Raslova H: P19INK4D links endomitotic arrest and megakaryocyte maturation and is regulated by AML-1. Blood; 2008 Apr 15;111(8):4081-91
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P19INK4D links endomitotic arrest and megakaryocyte maturation and is regulated by AML-1.
  • Chromatin immunoprecipitation assays performed in human MKs revealed that AML-1 binds in vivo the p19(INK4D) promoter.
  • Moreover, AML-1 inhibition led to the p19(INK4D) down-regulation in human MKs.

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18276842.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Platelet Glycoprotein GPIb-IX Complex; 0 / Platelet Membrane Glycoprotein IIb
  •  go-up   go-down


62. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The cytochemical profile of blasts was in concordance with immunophenotype, particularly in more differentiated AML subtypes, M3, M4 and M5.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
  •  go-up   go-down


63. Zhou J, Meng R, Sui XH, Meng L, Yang BF: Effects of arsenic trioxide administration styles on leukocytosis. Chin Med Sci J; 2006 Jun;21(2):111-4
Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Three kinds of leukemia cells, NB4, K562, and acute promyelocytic leukemia (APL) cells, were cultured in the media with constant concentration and varying concentrations of As2O3 respectively for 24 hours.
  • RESULTS: The apoptosis rates of NB4, K562, and APL leukemia cells in the media with constant As2O3 concentration were 56.6% +/- 2.4%, 27.6% +/- 3.1%, and 52.2% +/- 2.8%, respectively, which were significantly higher than those with changing As2O3 concentration (23.2% +/- 2.1%, 11.0% +/- 2.5%, and 21.0% +/- 2.5%, respectively, P < 0.01).
  • The apoptosis rates of APL, M2 type acute myeloid leukemia (AML-M2), and chronic myeloid leukemia (CML) patients in the trial group (28.5% +/- 1.9%, 9.5% +/- 0.6%, and 12.5% +/- 1.8%) were also significantly higher than those in control group (8.5% +/- 2.2%, 2.

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16845799.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


64. Veyret C, Levy C, Chollet P, Merrouche Y, Roche H, Kerbrat P, Fumoleau P, Fargeot P, Clavere P, Chevallier B: Inflammatory breast cancer outcome with epirubicin-based induction and maintenance chemotherapy: ten-year results from the French Adjuvant Study Group GETIS 02 Trial. Cancer; 2006 Dec 1;107(11):2535-44
Hazardous Substances Data Bank. EPIRUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammatory breast cancer outcome with epirubicin-based induction and maintenance chemotherapy: ten-year results from the French Adjuvant Study Group GETIS 02 Trial.
  • In the lenograstim group, 1 patient developed acute myeloblastic leukemia M2, and 1 patient developed myelodysplastic syndrome.
  • CONCLUSIONS: FEC-HD induction chemotherapy followed by FEC 75 maintenance regimen had moderate and acute long-term toxicities and lead to high DFS and OS rates in patients with IBC.

  • Genetic Alliance. consumer health - Inflammatory breast cancer.
  • Genetic Alliance. consumer health - TEN.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17054108.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Placebos; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 6WS4C399GB / lenograstim; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; FEC protocol
  •  go-up   go-down


65. Haferlach T, Kohlmann A, Schnittger S, Dugas M, Hiddemann W, Kern W, Schoch C: AML M3 and AML M3 variant each have a distinct gene expression signature but also share patterns different from other genetically defined AML subtypes. Genes Chromosomes Cancer; 2005 Jun;43(2):113-27
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML M3 and AML M3 variant each have a distinct gene expression signature but also share patterns different from other genetically defined AML subtypes.
  • Acute promyelocytic leukemia (APL) with t(15;17) appears in two phenotypes: AML M3, with abnormal promyelocytes showing heavy granulation and bundles of Auer rods, and AML M3 variant (M3v), with non- or hypogranular cytoplasm and a bilobed nucleus.
  • We investigated the global gene expression profiles of 35 APL patients (19 AML M3, 16 AML M3v) by using high-density DNA-oligonucleotide microarrays.
  • Furthermore, a supervised pairwise comparison between M3 and M3v revealed differential expression of genes that encode for biological functions and pathways such as granulation and maturation of hematologic cells, explaining morphologic and clinical differences.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Promyelocytic, Acute / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15751046.001).
  • [ISSN] 1045-2257
  • [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
  •  go-up   go-down


66. Schnittger S, Haferlach C, Ulke M, Alpermann T, Kern W, Haferlach T: IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status. Blood; 2010 Dec 16;116(25):5486-96
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status.
  • Mutations in the IDH1 gene at position R132 coding for the enzyme cytosolic isocitrate dehydrogenase are known in glioma and have recently been detected also in acute myeloid leukemia (AML).
  • To further clarify the role of this mutation in AML, we have analyzed IDH1R132 in 1414 AML patients.
  • IDH1-mutated cases more often had AML without maturation/French-American-British M1 (P < .001), an immature immunophenotype, and female sex (8.7% vs 4.7% in male, P = .003) compared with IDH1wt cases.
  • In conclusion, these data show that IDH1R132 may significantly add information regarding characterization and prognostication in AML.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20805365.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
  •  go-up   go-down


67. Roosild TP, Castronovo S, Choe S: Structure of anti-FLAG M2 Fab domain and its use in the stabilization of engineered membrane proteins. Acta Crystallogr Sect F Struct Biol Cryst Commun; 2006 Sep 1;62(Pt 9):835-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structure of anti-FLAG M2 Fab domain and its use in the stabilization of engineered membrane proteins.
  • Here, the stabilization of a detergent-solubilized K(+) channel protein, KvPae, by engineering a FLAG-binding epitope into a known loop region of the protein and creating a complex with Fab fragments from commercially available anti-FLAG M2 monoclonal antibodies is reported.
  • Although well diffracting crystals of the complex have not yet been obtained, during the course of crystallization trials the structure of the anti-FLAG M2 Fab domain was solved to 1.86 A resolution.
  • Thus, the use of antibody fragments for improving the stability of target proteins can be rapidly applied to the study of membrane-protein structure by placing the short DKYD motif within a predicted peripheral loop of that protein and utilizing commercially available anti-FLAG M2 antibody fragments.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol Methods. 1994 Jan 3;167(1-2):279-87 [7508479.001]
  • [Cites] Science. 1993 Oct 29;262(5134):734-8 [8235592.001]
  • [Cites] Nat Struct Biol. 1995 Oct;2(10):842-6 [7552705.001]
  • [Cites] J Bioenerg Biomembr. 1996 Feb;28(1):13-27 [8786233.001]
  • [Cites] J Mol Graph. 1996 Feb;14(1):51-5, 29-32 [8744573.001]
  • [Cites] Structure. 1995 Dec 15;3(12):1291-3 [8747455.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14532-5 [8962086.001]
  • [Cites] Curr Opin Struct Biol. 1997 Oct;7(5):697-701 [9345629.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):28576-82 [9786848.001]
  • [Cites] Protein Sci. 2005 Mar;14(3):836-40 [15689517.001]
  • [Cites] Science. 2005 Feb 25;307(5713):1317-21 [15731457.001]
  • [Cites] Protein Eng Des Sel. 2005 Feb;18(2):79-84 [15788421.001]
  • [Cites] J Struct Funct Genomics. 2005;6(2-3):171-5 [16211515.001]
  • [Cites] Structure. 2000 Jun 15;8(6):669-84 [10873857.001]
  • [Cites] Biochemistry. 2001 Jun 5;40(22):6636-45 [11380258.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):43-8 [11689936.001]
  • [Cites] J Mol Biol. 2002 Feb 8;316(1):1-6 [11829498.001]
  • [Cites] J Mol Biol. 2002 Apr 19;318(1):135-47 [12054774.001]
  • [Cites] Curr Opin Struct Biol. 2002 Aug;12(4):503-8 [12163074.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2002 Oct;58(Pt 10 Pt 1):1715-21 [12351893.001]
  • [Cites] Protein Sci. 2003 Feb;12(2):337-48 [12538897.001]
  • [Cites] Nat Biotechnol. 2003 Feb;21(2):171-6 [12524549.001]
  • [Cites] Science. 2003 Apr 4;300(5616):108-12 [12649487.001]
  • [Cites] Nature. 2003 May 1;423(6935):33-41 [12721618.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1828-33 [14766985.001]
  • [Cites] FEBS Lett. 2004 Apr 30;564(3):340-8 [15111119.001]
  • [Cites] J Mol Biol. 2004 Oct 22;343(3):747-58 [15465059.001]
  • [Cites] Biotechniques. 1994 Oct;17(4):754-61 [7530459.001]
  • (PMID = 16946459.001).
  • [ISSN] 1744-3091
  • [Journal-full-title] Acta crystallographica. Section F, Structural biology and crystallization communications
  • [ISO-abbreviation] Acta Crystallogr. Sect. F Struct. Biol. Cryst. Commun.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 2G60
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM074821; United States / NIGMS NIH HHS / GM / GM6653; United States / NIGMS NIH HHS / GM / GM74821
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Immunoglobulin Fab Fragments; 0 / Oligopeptides; 0 / Peptides; 98849-88-8 / FLAG peptide
  • [Other-IDs] NLM/ PMC2242885
  •  go-up   go-down


68. Obara H, Nishimura S, Hayashi N, Numagami Y, Inoue T, Kubo K, Kaimori M, Nishijima M: [Intracranial granulocytic sarcoma in a patient with acute myeloid leukemia]. No To Shinkei; 2006 Sep;58(9):797-801
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intracranial granulocytic sarcoma in a patient with acute myeloid leukemia].
  • Granulocytic sarcoma (GS) is extramedullary tumor composed of immature leukemic cells.
  • GS is presenting usually as a complication during the course of hematologic neoplasm, such as acute myeloblastic leukemia as well as myeloproliferative and myelodysplastic syndrome.
  • We report a 41-year-old man with acute leukemia type M7, who developed GS in the right occipital lobe after complete remission was achieved.
  • The majority of reported cases of GS in acute myeloid leukemia were M2 FAB classification and have chromosome translocation.
  • Our patient was M7 FAB classification, not have specific chromosome translocation.
  • GS occurrence in AML: M7 patient was extremely rare.
  • This is the first case report of AML: M7 with GS in the central nervous system.
  • [MeSH-major] Brain Neoplasms / complications. Leukemia, Myeloid, Acute / complications. Neoplasms, Multiple Primary / pathology. Occipital Lobe. Sarcoma, Myeloid / complications


69. Wagner M, Schmelz K, Wuchter C, Ludwig WD, Dörken B, Tamm I: In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia. Int J Cancer; 2006 Sep 15;119(6):1291-7
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia.
  • To determine the expression and prognostic role of survivin in acute myeloid leukemia (AML), we investigated the mRNA expression pattern of survivin and of the splice variants survivin-2B and survivin-DeltaEx3 in adult (n = 74) and children (n = 31) with de novo AML using RT-PCR.
  • Survivin was the predominant transcript variant in AML cells, whereas significantly lower levels of survivin-2B and survivin-DeltaEx3 were observed (p < or = 0.0001).
  • Neither expression of survivin nor of any splice variant correlated with maturation stage (FAB subtypes, immunophenotype) or cytogenetic risk groups.
  • For AML cases treated according to AMLCG92 (adult) and AML-BFM93 (children) protocols, respectively, expression patterns were correlated with clinical data: in adult AML (n = 51), low expression of survivin-2B correlated with a better overall survival (p = 0.05; mean survival time 19 months vs. 9 months) and a better eventfree survival (p < or = 0.01; 27 months vs. 10 months).
  • In childhood AML (n = 31), high survivin-DeltaEx3 expression was associated with a shorter overall survival (p < or = 0.05; 24 months vs. 43 months).
  • We conclude that certain survivin splice variants have potential prognostic impact for long-term therapy outcome in adult as well as childhood de novo AML.
  • [MeSH-major] Alternative Splicing. Leukemia, Myeloid / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Apoptosis. Case-Control Studies. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Disease-Free Survival. Female. Humans. Immunophenotyping. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16619249.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [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 / DNA, Neoplasm; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down


70. Bae SY, Kim JS, Ryeu BJ, Lee KN, Lee CK, Kim YK, Lim CS, Cho Y, Choi CW, Ryu SW, Yoon SY: Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases. Cancer Genet Cytogenet; 2010 May;199(1):31-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases.
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for approximately 3% of all t(8;21)(q22;q22) found in patients with acute myeloid leukemia (AML).
  • The clinicopathologic features of AML with the variant t(8;21) have not been well established.
  • We report three cases of AML with variants of t(8;21) characterized, respectively, by derivative 8 with the interstitial inverted insertion of 21q and concurrent monosomy 21, t(8;18;21)(p22;q11.3;q22), and t(2;21;8)(q11.2;q22;q22).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20417866.001).
  • [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
  •  go-up   go-down


71. Martino V, Bianchera A, Reia L, Bussolati O, Fazzina R, Marino F, Montemurro L, Tonelli R, Pession A, Gazzola GC, Sala R: Down-regulation of HOXA4, HOXA7, HOXA10, HOXA11 and MEIS1 during monocyte-macrophage differentiation in THP-1 cells. Mol Med Rep; 2009 Mar-Apr;2(2):241-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The translocation t(9;11)(p22;q23) generates the MLL-AF9 oncogene and is commonly associated with monocytic acute myeloid leukemia (AML-M5; FAB-classification).
  • We previously showed that the down-regulation of MLL-AF9 expression is not obligatory for monocyte-macrophage maturation in AML-M5 cells carrying t(9;11)(p22;q23).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21475819.001).
  • [ISSN] 1791-2997
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


72. Gu LJ, Tie LJ, Jiang LM, Chen J, Pan C, Dong L, Chen J, Xue HL, Tang JY, Wang YP, Ye H: [Relationship between immunological characteristics and prognosis in children with acute myeloid leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):241-5
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Relationship between immunological characteristics and prognosis in children with acute myeloid leukemia].
  • OBJECTIVE: The prognostic significance of immunophenotyping in acute myeloid leukemia (AML) has been controversial.
  • This study investigated the relationship of immunophenotypes with French-American-British (FAB) subtypes and chromosomal abnormalities and assessed the prognostic value of immunophenotyping in children with AML.
  • METHODS: From January 1998 to May 2003, 75 children with newly diagnosed AML were enrolled on protocol AML-XH-99.
  • According to the McAbs used, the patients were classified into five groups: panmyeloid antigens (CD13, CD33, and MPO), myeloid-lineage associated antigens (CD14, CD15), lineage-specific antigens (CD41, GlyA), progenitor-associated antigens (CD34, HLA-DR) and lymphoid-associated antigens (CD19, CD7).
  • The proportion of children with AML expressing one or more of the lymphoid-associated antigens was 24.3%.
  • Lymphoid-associated antigen CD19 was expressed by blast cells in most of FAB M2 patients.
  • The patients with acute promyelocytic leukemia were characterized by the absence of HLA-DR and lymphoid-associated antigens CD19 and CD7.
  • Multivariate analysis suggested immunophenotyping had no independent prognostic value in AML.
  • CONCLUSIONS: Immunophenotyping can not be used independently in the evaluation of risk classification in children with AML.
  • However, it is useful in the reorganization of special types of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology

  • 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
  • (PMID = 19374802.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


73. Li L, Piloto O, Nguyen HB, Greenberg K, Takamiya K, Racke F, Huso D, Small D: Knock-in of an internal tandem duplication mutation into murine FLT3 confers myeloproliferative disease in a mouse model. Blood; 2008 Apr 1;111(7):3849-58
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Constitutive activation of FMS-like tyrosine kinase 3 (FLT3) by internal tandem duplication (ITD) mutations is one of the most common molecular alterations known in acute myeloid leukemia (AML).
  • To investigate the role FLT3/ITD mutations play in the development of leukemia, we generated a FLT3/ITD knock-in mouse model by inserting an ITD mutation into the juxtamembrane domain of murine Flt3.
  • FLT3wt/ITD mice developed myeloproliferative disease, characterized by splenomegaly, leukocytosis, and myeloid hypercellularity, which progressed to mortality by 6 to 20 months.
  • No sign of acute leukemia was observed over the lifetime of these mice.
  • BM from FLT3wt/ITD mice showed enhanced potential to generate myeloid colonies in vitro.
  • In the long-term competitive repopulation assay, BM cells from FLT3wt/ITD mice outgrew the wild-type competitor cells and showed increased myeloid and reduced lymphoid expansion activity.
  • In summary, our data indicate that expression of FLT3/ITD mutations alone is capable of conferring normal hematopoietic stem/progenitor cells (HSPCs) with enhanced myeloid expansion.
  • It also appears to suppress B lymphoid maturation.
  • Additional cooperative events appear to be required to progress to acute leukemia.


74. Udayakumar AM, Pathare AV, Al-Kindi S, Khan H, Rehmen JU, Zia F, Al-Ghazaly A, Nusrut N, Khan MI, Wali YA, Al-Lamki Z, Dennison D, Raeburn JA: Cytogenetic, morphological, and immunophenotypic patterns in Omani patients with de novo acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):89-94
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic, morphological, and immunophenotypic patterns in Omani patients with de novo acute myeloid leukemia.
  • Chromosome aberrations observed at diagnosis are considered to be the most valuable prognostic factors in acute myeloid leukemia (AML).
  • There are only limited studies on the role of such variability in AML patients.
  • Here, we report the results of a cytogenetic study on 63 ethnic Omani patients with de novo AML: 18 children (<or=16 years) and 45 adults.
  • By sex, 41 were male and 22 female; median age at diagnosis was 25 years.
  • The morphological diagnosis was based on the French-American-British (FAB) WHO criteria.
  • Karyotypes with a sole abnormality accounted for 20 of 63 patients (32%).
  • Chromosome abnormalities were more common in patients with the FAB-M2 subtype (15 of 22; 68%), which was also the most frequent subtype observed (22 of 63; 35%).
  • Among the normal karyotypes (24 of 63; 38%), M2 subtype was the also most frequent (7 of 24; 29%), followed by M4 (4 of 24; 17%).
  • Our population differed morphologically, with the M2 subtype as most common, whereas M4 and M3 were more commonly in those reports.
  • [MeSH-major] Antigens, CD / metabolism. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Aberrations. Chromosomes, Human / ultrastructure. Ethnic Groups / genetics. Female. Fluorescent Antibody Technique. Humans. Immunophenotyping. Infant. Karyotyping. Male. Middle Aged. Oman / ethnology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17854660.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
  •  go-up   go-down


75. Harani MS, Adil SN, Shaikh MU, Kakepoto GN, Khurshid M: Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):26-9
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease.
  • The commonly used method for diagnosis and classification is based on FAB criteria using morphology and cytochemical stains.
  • The aim of present study is to determine the frequency of various sub types in acute myeloid leukemia using FAB criteria in our population.
  • This will aid in the correct diagnosis of acute leukemia and hence proper management of the patients.
  • The patients were diagnosed on the basis of bone marrow morphology using FAB classification.
  • AML-M4 was the predominant French-American-British (FAB) subtype (36.2%) followed by M2 (30.25%), M3 (10.4%), M1 (8.7%), M0 (7.7%), M5a (3.5%), M5b (2.5%) and M6 (0.8%).
  • CONCLUSIONS: The most common FAB subtype observed in our study was Acute myelomonocytic leukemia (M4) which is in accordance with studies reported from Saudia Arabia and a previous study reported from our institution.
  • However,other national and international studies have reported Myeloblastic Leukemia with maturation (M2) as the predominant subtype of AML.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Female. Hospitals, University. Humans. Infant. Male. Middle Aged. Pakistan

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15929522.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  •  go-up   go-down


76. Kharfan-Dabaja M, Ayala E, Lindner I, Cejas PJ, Bahlis NJ, Kolonias D, Carlson LM, Lee KP: Differentiation of acute and chronic myeloid leukemic blasts into the dendritic cell lineage: analysis of various differentiation-inducing signals. Cancer Immunol Immunother; 2005 Jan;54(1):25-36
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differentiation of acute and chronic myeloid leukemic blasts into the dendritic cell lineage: analysis of various differentiation-inducing signals.
  • PURPOSE: Ex vivo differentiation of myeloid leukemic blasts into dendritic cells (DCs) holds significant promise for use as cellular vaccines, as they may present a constellation of endogenously expressed known and unknown leukemia antigens to the immune system.
  • Although variety of stimuli can drive leukemia --> DC differentiation in vitro, these blast-derived DCs typically have aberrant characteristics compared with DCs generated from normal progenitors by the same stimuli.
  • It is not clear whether this is due to underlying leukemogenic mechanisms (e.g., specific oncogenes), genetic defects, stage of maturation arrest, defects in cytokine receptor expression or signal transduction pathways, or whether different stimuli themselves induce qualitatively dissimilar DC differentiation.
  • METHODS: To assess what factors may contribute to aberrant leukemic blast --> DC differentiation, we have examined how the same leukemic blasts (AML and CML) respond to different DC differentiation signals--including extracellular (the cytokine combination GM-CSF + TNF-alpha + IL-4) and intracellular (the protein kinase C agonist PMA, the calcium ionophore A23187, and the combination of PMA plus A23187) stimuli.
  • There were no clear differences in the responses relative to specific oncogene expression or stage of maturation arrest (AML vs CML).
  • CONCLUSIONS: Our findings suggest that signal transduction may play an important role in the aberrant DC differentiation of leukemic blasts, and demonstrate that direct activation of PKC together with intracellular calcium signaling may be an effective method for generating immunostimulatory leukemia-derived DCs.
  • [MeSH-major] Blast Crisis / metabolism. Dendritic Cells / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15693136.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA85208; United States / NCI NIH HHS / CA / CA95829
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Surface
  •  go-up   go-down


77. Van Driessche A, Van de Velde AL, Nijs G, Braeckman T, Stein B, De Vries JM, Berneman ZN, Van Tendeloo VF: Clinical-grade manufacturing of autologous mature mRNA-electroporated dendritic cells and safety testing in acute myeloid leukemia patients in a phase I dose-escalation clinical trial. Cytotherapy; 2009;11(5):653-68
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical-grade manufacturing of autologous mature mRNA-electroporated dendritic cells and safety testing in acute myeloid leukemia patients in a phase I dose-escalation clinical trial.
  • We report on a phase I dose-escalation trial using clinical-grade manufactured mature RNA-electroporated DC in acute myeloid leukemia (AML) patients.
  • To test product safety, increasing doses of DC were administered intradermally four times at 2-week intervals in 10 AML patients.
  • We also validated a simplified DC maturation protocol yielding a consistent phenotype, migration and allogeneic T-cell stimulatory capacity in AML patients in remission.
  • Despite a decreased cell recovery of mDC after a combination of mRNA electroporation and cryopreservation, successful vaccine preparations were obtained in all AML patients.
  • Intradermal injection of such DC vaccines in AML patients is safe.
  • [MeSH-major] Dendritic Cells / cytology. Electroporation. Immunotherapy, Adoptive / adverse effects. Immunotherapy, Adoptive / methods. Leukemia, Myeloid, Acute / therapy

  • 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
  • (PMID = 19530029.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / RNA, Messenger
  •  go-up   go-down


78. Satoh Y, Matsumura I, Tanaka H, Ezoe S, Fukushima K, Tokunaga M, Yasumi M, Shibayama H, Mizuki M, Era T, Okuda T, Kanakura Y: AML1/RUNX1 works as a negative regulator of c-Mpl in hematopoietic stem cells. J Biol Chem; 2008 Oct 31;283(44):30045-56
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Wild-type AML1 activated the c-mpl promoter through the proximal AML-binding site in luciferase assays using 293T and HeLa cells.
  • AML1dC dominant-negatively suppressed transcriptional activity of wild-type AML1.
  • Furthermore, we found that early hematopoietic cells that derived from AML1(+/-) ES cells expressed c-Mpl more intensely than those that developed from wild-type ES cells.
  • In contrast, AML1dC hardly affected c-Mpl expression and maturation of megakaryocytes.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 Jan;20(1):91-103 [10594012.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):651-6 [10617663.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1737-42 [10677527.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] Blood. 2000 Jul 1;96(1):288-96 [10891464.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2862-9 [11023523.001]
  • [Cites] Int J Hematol. 2001 Oct;74(3):245-51 [11721958.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):7184-96 [11742995.001]
  • [Cites] Oncogene. 1996 Jan 18;12(2):265-75 [8570204.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12359-63 [8901586.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 27;94(11):5697-702 [9159135.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1403-9 [9269757.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1605-9 [9324277.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1195-200 [9448308.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2985-90 [9531610.001]
  • [Cites] Blood. 1998 Jul 1;92(1):4-10 [9639492.001]
  • [Cites] Genes Dev. 1998 Jul 1;12(13):2048-60 [9649508.001]
  • [Cites] EMBO J. 1999 Mar 1;18(5):1367-77 [10064602.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1817-24 [10068652.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] J Biol Chem. 2004 Dec 31;279(53):55578-86 [15485843.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4664-70 [15741216.001]
  • [Cites] Blood. 2005 Jul 15;106(2):494-504 [15784726.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(24):10675-83 [16314494.001]
  • [Cites] Cancer Res. 2007 Feb 15;67(4):1853-8 [17308127.001]
  • [Cites] Circ Res. 2007 May 11;100(9):1292-9 [17413042.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 2007;17(4):271-80 [17725493.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] Immunity. 2002 May;16(5):661-72 [12049718.001]
  • [Cites] J Clin Invest. 2002 Aug;110(3):389-94 [12163458.001]
  • [Cites] Cell. 2002 Nov 27;111(5):621-33 [12464175.001]
  • [Cites] Blood. 2003 Jan 1;101(1):270-7 [12393465.001]
  • [Cites] Blood. 2003 Jan 15;101(2):673-80 [12393679.001]
  • [Cites] J Cell Biochem. 2003 May 1;89(1):9-18 [12682904.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4333-41 [12576332.001]
  • [Cites] Jpn J Clin Oncol. 2003 Apr;33(4):153-60 [12810828.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7731-6 [12796513.001]
  • [Cites] Nat Med. 2004 Mar;10(3):299-304 [14966519.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2316-24 [14615365.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15678-87 [14747476.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4284-96 [15156185.001]
  • [Cites] J Biol Chem. 2004 Jun 11;279(24):24986-93 [15067010.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Science. 1993 Feb 12;259(5097):968-71 [8438156.001]
  • [Cites] Blood. 1993 Jun 1;81(11):3022-6 [8499637.001]
  • [Cites] Blood. 1993 Jul 15;82(2):590-9 [8329714.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6336-45 [8413232.001]
  • [Cites] Blood. 1994 May 15;83(10):2851-9 [8180380.001]
  • [Cites] Nature. 1994 Jun 16;369(6481):568-71 [8202159.001]
  • [Cites] Blood. 1994 Aug 15;84(4):1243-8 [8049440.001]
  • [Cites] Science. 1994 Aug 19;265(5175):1098-101 [8066449.001]
  • [Cites] Mol Cell Biol. 1994 Dec;14(12):8085-95 [7969146.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4917-21 [7761424.001]
  • [Cites] Blood. 1995 Jul 15;86(2):607-16 [7605990.001]
  • [Cites] Mol Cell Biol. 2000 Jan;20(1):319-28 [10594034.001]
  • (PMID = 18687690.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Mpl protein, mouse; 0 / RUNX1 protein, human; 0 / Receptors, Thrombopoietin; 0 / Runx1 protein, mouse; 143641-95-6 / MPL protein, human
  • [Other-IDs] NLM/ PMC2662069
  •  go-up   go-down


79. Khanna-Gupta A: Sumoylation and the function of CCAAT enhancer binding protein alpha (C/EBP alpha). Blood Cells Mol Dis; 2008 Jul-Aug;41(1):77-81
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is expressed at high levels throughout myeloid differentiation and binds to the promoters of multiple myeloid-specific genes at different stages of myeloid maturation.
  • Mutations in C/EBP alpha are present in a subset of patients with AML presenting with a normal karyotype.
  • In this review, the functional implications of post-translational modification, particularly sumoylation, of C/EBP alpha in normal granulopoiesis and leukemia are considered.

  • 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. 1999 Oct 26;96(22):12350-5 [10535925.001]
  • [Cites] Mol Cell Biol. 1997 Dec;17(12):7353-61 [9372966.001]
  • [Cites] Cell. 2001 Oct 19;107(2):247-58 [11672531.001]
  • [Cites] Mol Cell. 2001 Oct;8(4):817-28 [11684017.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26293-9 [11978795.001]
  • [Cites] Biochem J. 2002 Aug 1;365(Pt 3):561-75 [12006103.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38037-44 [12161447.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9134-41 [12511558.001]
  • [Cites] Mol Cell. 2003 Apr;11(4):1043-54 [12718889.001]
  • [Cites] EMBO J. 2003 May 1;22(9):2047-59 [12727872.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):675-86 [14701740.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):611-7 [14992729.001]
  • [Cites] Genes Dev. 2004 Apr 15;18(8):912-25 [15107404.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 5;101(40):14373-8 [15388847.001]
  • [Cites] Genes Dev. 1992 Mar;6(3):439-53 [1547942.001]
  • [Cites] Science. 1995 Aug 25;269(5227):1108-12 [7652557.001]
  • [Cites] Genes Dev. 1996 Apr 1;10(7):804-15 [8846917.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3736-41 [9108047.001]
  • [Cites] Blood. 1997 Jul 15;90(2):489-519 [9226149.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):28545-8 [9786841.001]
  • [Cites] J Biol Chem. 1998 Nov 13;273(46):30057-60 [9804754.001]
  • [Cites] J Biol Chem. 1998 Nov 20;273(47):30843-6 [9812973.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):2936-45 [10082561.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(4):1325-38 [15684384.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(7):2688-97 [15767674.001]
  • [Cites] Curr Opin Hematol. 2006 Jan;13(1):7-14 [16319681.001]
  • [Cites] Dev Cell. 2005 Dec;9(6):769-79 [16326389.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] BMC Mol Biol. 2006;7:14 [16600022.001]
  • [Cites] J Biol Chem. 2006 Aug 4;281(31):21629-39 [16735515.001]
  • [Cites] Biochim Biophys Acta. 2006 Aug;1766(1):88-103 [16616425.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3560-3 [16873674.001]
  • [Cites] Trends Biochem Sci. 2007 Jun;32(6):286-95 [17499995.001]
  • [Cites] Folia Biol (Praha). 2007;53(3):97-108 [17580000.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3301-9 [17671234.001]
  • [Cites] Leukemia. 2001 Apr;15(4):688-9 [11368383.001]
  • (PMID = 18406180.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL063357-090008; United States / NHLBI NIH HHS / HL / P01 HL063357; United States / NHLBI NIH HHS / HL / P01 HL063357-090008; United States / NHLBI NIH HHS / HL / P01HL63357
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Small Ubiquitin-Related Modifier Proteins
  • [Number-of-references] 37
  • [Other-IDs] NLM/ NIHMS54847; NLM/ PMC2505045
  •  go-up   go-down


80. Riccioni R, Pasquini L, Mariani G, Saulle E, Rossini A, Diverio D, Pelosi E, Vitale A, Chierichini A, Cedrone M, Foà R, Lo Coco F, Peschle C, Testa U: TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL. Haematologica; 2005 May;90(5):612-24
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL.
  • The present study was designed to evaluate the sensitivity to TRAIL-induced apoptosis in acute myeloblastic leukemias (AML).
  • DESIGN AND METHODS: TRAIL/TRAIL receptor (TRAIL-R) expression and sensitivity to TRAIL-mediated apoptosis were explored in 79 AML patients, including 17 patients with acute promyelocytic leukemia (APL).
  • RESULTS: In non-APL AML we observed frequent expression of TRAIL decoy receptors (TRAIL-R3 and TRAIL-R4), while TRAIL-R1 and TRAIL-R2 expression was restricted to AML exhibiting monocytic features.
  • Total leukemic blasts, as well as AML colony-forming units (AML-CFU), were invariably resistant to TRAIL-mediated apoptosis.
  • APL express membrane-bound TRAIL on their surface and exhibit a pattern of TRAIL-R expression similar to that observed in the other types of AML.
  • The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression.
  • We suggest that AML blasts, including APL blasts, are resistant to TRAIL-mediated apoptosis, a phenomenon seemingly related to the expression of TRAIL decoy receptors on these cells.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / physiology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Agents / pharmacology. Caspase 3 / analysis. Caspase 8 / analysis. Cell Differentiation / drug effects. Cell Membrane / metabolism. Cytarabine / pharmacology. Etoposide / pharmacology. Female. GPI-Linked Proteins. Granulocytes / drug effects. HL-60 Cells / pathology. Humans. Hydroxyurea / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Monocytes / drug effects. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. U937 Cells / drug effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15921376.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


81. Campioni D, Secchiero P, Corallini F, Melloni E, Capitani S, Lanza F, Zauli G: Evidence for a role of TNF-related apoptosis-inducing ligand (TRAIL) in the anemia of myelodysplastic syndromes. Am J Pathol; 2005 Feb;166(2):557-63
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We focused our study on the cytokine TRAIL (TNF-related apoptosis-inducing ligand), which has been shown to exhibit an anti-differentiation activity on erythroid maturation.
  • Immunocytochemical analysis of bone marrow mononuclear cells (BMMC) showed an increased expression of TRAIL in MDS patients with respect to acute myeloid leukemia (AML) patients and normal BM donors.
  • TRAIL expression was increased predominantly in myeloid precursors of granulocytic lineage and in a subset of monocytes and pro-erythroblasts.
  • On the other hand, TRAIL was detected less frequently in the culture supernatants of AML (4 of 33) and normal BMMC (0 of 22).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Apoptosis. Apoptosis Regulatory Proteins. Bone Marrow Cells / metabolism. Culture Media, Conditioned / pharmacology. Culture Media, Serum-Free / metabolism. Enzyme-Linked Immunosorbent Assay. Erythrocytes / metabolism. Female. Fetal Blood / metabolism. Flow Cytometry. Glycophorin / metabolism. Humans. Immunohistochemistry. Leukemia, Myeloid, Acute / blood. Leukocytes, Mononuclear / metabolism. Ligands. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand. Time Factors

  • Genetic Alliance. consumer health - Anemia.
  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Anemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leuk Lymphoma. 2000 Apr;37(3-4):405-14 [10752992.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4210-8 [15315976.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1388-92 [10942382.001]
  • [Cites] Exp Hematol. 2000 Aug;28(8):941-9 [10989195.001]
  • [Cites] Int J Hematol. 2000 Aug;72(2):131-3 [11039659.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3932-8 [11090080.001]
  • [Cites] Blood. 2001 Nov 15;98(10):3058-65 [11698291.001]
  • [Cites] Exp Hematol. 2001 Dec;29(12):1484-93 [11750108.001]
  • [Cites] Leukemia. 2002 Jan;16(1):67-73 [11840265.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1594-601 [11861273.001]
  • [Cites] Br J Haematol. 2002 Apr;117(1):119-26 [11918541.001]
  • [Cites] Leukemia. 2002 May;16(5):785-90 [11986938.001]
  • [Cites] Int J Hematol. 2002 Apr;75(3):289-97 [11999358.001]
  • [Cites] Leuk Res. 2002 Jul;26(7):687-8 [12008087.001]
  • [Cites] Cell Death Differ. 2003 Jan;10(1):66-75 [12655296.001]
  • [Cites] Cytokine. 2003 Dec 21;24(6):244-53 [14609566.001]
  • [Cites] Blood. 2004 Jan 15;103(2):517-22 [12969966.001]
  • [Cites] J Exp Med. 2004 Mar 15;199(6):785-95 [15007095.001]
  • [Cites] Blood. 1995 Jul 1;86(1):268-76 [7795232.001]
  • [Cites] Immunity. 1995 Dec;3(6):673-82 [8777713.001]
  • [Cites] Blood. 1996 Apr 1;87(7):3064 [8639933.001]
  • [Cites] J Biol Chem. 1996 May 31;271(22):12687-90 [8663110.001]
  • [Cites] Leukemia. 1997 Jun;11(6):839-45 [9177438.001]
  • [Cites] Br J Haematol. 1998 Oct;103(1):176-88 [9792306.001]
  • [Cites] Nat Med. 1999 Feb;5(2):157-63 [9930862.001]
  • [Cites] Int J Hematol. 1999 Apr;69(3):152-9 [10222652.001]
  • [Cites] N Engl J Med. 1999 May 27;340(21):1649-60 [10341278.001]
  • [Cites] J Clin Invest. 1999 Jul;104(2):155-62 [10411544.001]
  • [Cites] Nature. 1999 Sep 30;401(6752):489-93 [10519553.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3716-24 [10845902.001]
  • (PMID = 15681838.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Apoptosis Regulatory Proteins; 0 / Culture Media, Conditioned; 0 / Culture Media, Serum-Free; 0 / Glycophorin; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1602326
  •  go-up   go-down


82. Nebbioso A, Clarke N, Voltz E, Germain E, Ambrosino C, Bontempo P, Alvarez R, Schiavone EM, Ferrara F, Bresciani F, Weisz A, de Lera AR, Gronemeyer H, Altucci L: Tumor-selective action of HDAC inhibitors involves TRAIL induction in acute myeloid leukemia cells. Nat Med; 2005 Jan;11(1):77-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-selective action of HDAC inhibitors involves TRAIL induction in acute myeloid leukemia cells.
  • Inhibitors of histone deacetylases (HDACIs) induce proliferation arrest, maturation and apoptosis of cancer cells, but not normal cells, in vitro and in vivo, and are currently being tested in clinical trials.
  • We report that HDACIs induce, in addition to p21, expression of TRAIL (Apo2L, TNFSF10) by directly activating the TNFSF10 promoter, thereby triggering tumor-selective death signaling in acute myeloid leukemia (AML) cells and the blasts of individuals with AML.
  • HDACIs induced proliferation arrest, TRAIL-mediated apoptosis and suppression of AML blast clonogenicity irrespective of French-American-British (FAB) classification status, karyotype and immunophenotype.
  • [MeSH-major] Apoptosis / drug effects. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Membrane Glycoproteins / metabolism. Receptors, Cell Surface / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins. Humans. TNF-Related Apoptosis-Inducing Ligand. Tumor Suppressor Protein p53 / metabolism

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • Nature Publishing Group. commentaries/discussion - Highlights from Nature Reviews Cancer .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15619633.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


83. Chan WK, Cheung CC, Law HK, Lau YL, Chan GC: Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function. J Hematol Oncol; 2008;1:9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function.
  • BACKGROUND: Previous studies demonstrated Ganoderma lucidum polysaccharides (GL-PS), a form of bioactive beta-glucan can stimulate the maturation of monocyte-derived dendritic cells (DC).
  • The possible clinical impact of using this commonly used medicinal mushroom in patients with monocytic leukemia (AML-M4 and M5) deserved further investigation.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Dendritic Cells / immunology. Leukemia / immunology. Monocytes / immunology. Polysaccharides / immunology. Reishi / chemistry

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pediatr Hematol Oncol. 2000 Sep-Oct;22(5):412-6 [11037851.001]
  • [Cites] Leuk Res. 2006 Jul;30(7):841-8 [16423392.001]
  • [Cites] J Immunol. 2001 Nov 15;167(10):6021-30 [11698483.001]
  • [Cites] Blood. 2002 Jul 15;100(2):701-3 [12091369.001]
  • [Cites] Immunol Lett. 2002 Oct 1;83(3):163-9 [12095706.001]
  • [Cites] Pediatr Res. 2003 Jul;54(1):105-12 [12672905.001]
  • [Cites] J Altern Complement Med. 2003 Aug;9(4):491-7 [14499024.001]
  • [Cites] Oncol Rep. 2004 Sep;12(3):659-62 [15289852.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Oct 8;323(1):133-41 [15351712.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1983 Spring;5(1):65-71 [6859456.001]
  • [Cites] Anticancer Res. 1992 Jul-Aug;12(4):1211-5 [1503411.001]
  • [Cites] Crit Rev Immunol. 1999;19(1):65-96 [9987601.001]
  • [Cites] Acta Pharmacol Sin. 2004 Nov;25(11):1387-95 [15525457.001]
  • [Cites] J Immunol. 2004 Nov 15;173(10):5989-99 [15528333.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Aug 5;333(3):896-907 [15963458.001]
  • [Cites] J Leukoc Biol. 2005 Aug;78(2):533-43 [15894585.001]
  • [Cites] Br J Haematol. 2005 Sep;130(5):777-80 [16115136.001]
  • [Cites] J Altern Complement Med. 2005 Dec;11(6):1047-57 [16398597.001]
  • [Cites] Exp Mol Med. 2006 Feb 28;38(1):72-84 [16520555.001]
  • [Cites] J Altern Complement Med. 2001 Jun;7(3):281-7 [11439851.001]
  • (PMID = 18644156.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Polysaccharides; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2517069
  •  go-up   go-down


84. Gutiérrez NC, López-Pérez R, Hernández JM, Isidro I, González B, Delgado M, Fermiñán E, García JL, Vázquez L, González M, San Miguel JF: Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia. Leukemia; 2005 Mar;19(3):402-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia.
  • Bone marrow samples from 43 adult patients with de novo diagnosed acute myeloid leukemia (AML)--10 acute promyelocytic leukemias (APL) with t(15;17), four AML with inv(16), seven monocytic leukemias and 22 nonmonocytic leukemias--were analyzed using high-density oligonucleotide microarrays.
  • Hierarchical clustering analysis segregated APL, AML with inv(16), monocytic leukemias and the remaining AML into separate groups.
  • A set of only 21 genes was able to assign AML to one of these three classes: APL, inv(16) and other AML subtype without a specific translocation.
  • AML with inv(16) showed an upregulation of MYH11 and a downregulation of a gene encoding a core-binding factor protein, RUNX3.
  • Two major groups emerged from the remaining 22 AML: cluster A with 10 samples and cluster B with 12.
  • In the latter cluster, CD34 upregulation and serine proteases downregulation is consistent with a maturation arrest and lack of granulocytic differentiation.
  • [MeSH-major] Gene Expression Profiling / methods. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cluster Analysis. Female. Humans. Leukemia, Monocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. Phylogeny. Retrospective Studies


85. Gibson SE, Dong HY, Advani AS, Hsi ED: Expression of the B cell-associated transcription factors PAX5, OCT-2, and BOB.1 in acute myeloid leukemia: associations with B-cell antigen expression and myelomonocytic maturation. Am J Clin Pathol; 2006 Dec;126(6):916-24
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the B cell-associated transcription factors PAX5, OCT-2, and BOB.1 in acute myeloid leukemia: associations with B-cell antigen expression and myelomonocytic maturation.
  • The aberrant expression of the B-cell transcription factor PAX5 has been described in a subset of acute myeloid leukemia (AML) with t(8;21)(q22;q22) in association with B-cell antigen expression.
  • However, the expression of other B cell-associated transcription factors, particularly OCT-2 and its B cell-specific coactivator BOB.1, has not been described in AML.
  • In this study, expression of PAX5, OCT-2 and BOB.1 was evaluated by immunohistochemical staining of bone marrow samples from 83 cases of AML.
  • The expression patterns were correlated with t(8;21)(q22;q22), B cell-associated antigen expression, and AML subtype.
  • We confirmed the expression of PAX5 in AML with t(8;21)(q22;q22), but also demonstrated its expression in cases that express B-cell antigens but lack this translocation.
  • Although OCT-2 and BOB.1 were not associated with PAX5 expression, we report expression of OCT-2 in AML with myelomonocytic/monocytic maturation and BOB.1 in normal hematopoietic elements.
  • [MeSH-major] Antigens, CD / metabolism. B-Cell-Specific Activator Protein / metabolism. Leukemia, Myeloid / metabolism. Octamer Transcription Factor-2 / metabolism. Trans-Activators / metabolism
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Differentiation. Flow Cytometry. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Monocytes / metabolism. Monocytes / pathology. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Tissue Array Analysis

  • Genetic Alliance. consumer health - Acute Myelomonocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17074681.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Octamer Transcription Factor-2; 0 / PAX5 protein, human; 0 / POU2AF1 protein, human; 0 / Trans-Activators
  •  go-up   go-down


86. Nitta M, Hoshi A, Shinozaki T, Soeda S, Kawakami M, Kin H, Nakajima N, Hanai K, Kato S, Nomoto T, Usui Y, Terachi T: [Granulocytic sarcoma of the prostate]. Hinyokika Kiyo; 2010 Sep;56(9):521-5
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Granulocytic sarcoma of the prostate].
  • Histological examination revealed leukemia-like cells, and bone-marrow examination (aspiration) was performed to determine the location of the original lesion.
  • However, no leukemia-like cells or any other form of malignant cells were identified.
  • Clinical imaging confirmed the absence of any other lesions, and granulocytic sarcoma of the prostate was subsequently diagnosed.
  • Four months after initial presentation, the patient developed acute myeloid leukemia [M2 by French-American-British classification].
  • [MeSH-major] Prostatic Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Aged. Humans. Leukemia, Myeloid, Acute / etiology. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20940529.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


87. Imataki O, Ohnishi H, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Isolated extramedullary relapse presenting as autologous lymphocyte response. Am J Hematol; 2008 Jun;83(6):512-4
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Isolated EMR in the CNS is a relatively rare form of recurrent leukemia.
  • We report here a case of a 38-year-old man with inv(16) acute myeloid leukemia (AML, M2) who suffered a central nervous system (CNS) relapse after allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)-matched sibling donor.
  • His leukemia relapsed in the CNS 2.5 years after the allogeneic BMT.
  • Lumbar puncture revealed 780/muL white blood cells with 67.3% leukemia cells and 32.7% mature lymphocytes.
  • Fluorescent in situ hybridization (FISH) using a probe for the Y chromosome demonstrated that both leukemia cells and lymphocytes in the cerebrospinal fluid (CSF) were derived from the recipient, although the bone marrow cells were from the donor.
  • No leukemia cells with inv(16) were detected by FISH in the bone marrow.
  • This observation suggests that the CNS is a "sanctuary" site not only from chemotherapy but also from the graft-versus-leukemia effect.
  • The present case contributes to our understanding of the possibility of immunological escape phenomenon of recurrent leukemia cells in extramedullary sites.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Bone Marrow Transplantation / methods. Humans. Male. Recurrence. Sarcoma, Myeloid. Transplantation Chimera

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18306363.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


88. Kufner S, Zitzelsberger H, Kroell T, Pelka-Fleischer R, Salem A, de Valle F, Schweiger C, Nuessler V, Schmid C, Kolb HJ, Schmetzer HM: Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions. Scand J Immunol; 2005 Jul;62(1):86-98
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions.
  • Functional dendritic cells (DC) are professional antigen-presenting cells (APC) and can be generated in vitro from healthy as well as from leukaemic cells from acute myeloid leukemia (AML) patients giving rise to APC of leukaemic origin-presenting leukaemic antigens.
  • We describe the generation and characterization of DC from different mononuclear cell (MNC) fractions from 50 AML patients under different serum-free culture conditions, determine the optimal culture conditions and compare the results with that from 23 healthy donors.
  • In detail, we could show that AML-DC harvests were higher after 10-14 days culture (healthy DC: 7 days); total or adherent PB or BM-MNC fractions yield comparable DC counts, however, from magnetic cell sorting (MACS)-depleted MNC fractions or thawn MNC lower DC counts can be generated.
  • Whereas the addition of FL increases the DC harvest, the addition of autologous plasma in many cases has inhibitory influence on DC maturation.
  • Optimal harvest of vital and mature DC from AML samples was obtained with a granulocyte/macrophage-colony stimulating factor, interleukin-4, FL and tumour necrosis factor-alpha-containing serum-free Xvivo medium after 10-14 days of culture (36/26% DC; 38/64% vital DC; 46/51% mature DC were generated from AML/healthy MNC samples).
  • Surface marker profiles (e.g. costimulatory antigen expressing) of DC obtained from AML samples were comparable with that of healthy DC.
  • The leukaemic derivation of AML-DC was demonstrated by the persistence of the clonal cytogenetic aberration in the DC or by coexpression of leukaemic antigens on DC.
  • Autologous T-cell activation of leukaemia-derived DC was demonstrated in cases with AML.
  • We demonstrate that the generation of leukaemia-derived DC is feasable in AML under serum-free culture conditions giving rise to DC with comparable characteristics as healthy DC and offering an anti-leukaemia-directed immunotherapeutical vaccination strategy in AML.
  • [MeSH-major] Bone Marrow Cells / immunology. Cell Culture Techniques. Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Middle Aged. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / pharmacology. Vaccination / methods

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16091128.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Culture Media, Serum-Free; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down


89. Yamagami T, Porada CD, Pardini RS, Zanjani ED, Almeida-Porada G: Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line. Cancer Biol Ther; 2009 Feb;8(4):331-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line.
  • Acute myeloid leukemia (AML) is the most frequently diagnosed adulthood leukemia, yet current therapies offer a cure rate of less than 30%.
  • This may be due in part to the fact that the leukemia-initiating cells in AML reside within the rare and highly primitive CD34(+)CD38(-) hematopoietic stem/progenitor cell (HSC) population that are often resistant to chemotherapy.
  • In the present studies, we investigated DHA's effect on the primitive and undifferentiated AML cell line KG1a, to explore the potential of this fatty acid to serve as adjuvant therapy for AML.
  • Treatment of KG1a cells with DHA for 96 hours did not lead to maturation or cell cycle modification when compared to an untreated KG1a control (n = 4).
  • Since we also show that DHA does not have a detrimental effect on normal hematopoiesis our results suggest that DHA could potentially serve as an well-tolerated adjuvant in the treatment of AML patients.

  • 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] Methods Mol Biol. 2007;407:177-208 [18453257.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4403-11 [10969785.001]
  • [Cites] Leuk Res. 1998 Mar;22(3):221-39 [9619914.001]
  • [Cites] Biosci Biotechnol Biochem. 2004 Nov;68(11):2415-7 [15564688.001]
  • [Cites] Ann N Y Acad Sci. 2004 Dec;1030:361-8 [15659818.001]
  • [Cites] Urol Oncol. 2005 Jan-Feb;23(1):36-48 [15885582.001]
  • [Cites] J Cell Physiol. 2005 Sep;204(3):881-8 [15795939.001]
  • [Cites] Nutr Cancer. 2005;52(2):121-9 [16201843.001]
  • [Cites] Leuk Res. 2006 Mar;30(3):296-302 [16112192.001]
  • [Cites] Bioorg Med Chem Lett. 2006 Jun 1;16(11):2974-7 [16563756.001]
  • [Cites] Biotechnol J. 2006 Apr;1(4):420-39 [16892270.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):3942-7 [10632323.001]
  • [Cites] Cytometry. 2000 Apr 15;42(2):83-94 [10797445.001]
  • [Cites] Mol Pharmacol. 2007 Dec;72(6):1545-56 [17878267.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4990-7 [12609832.001]
  • [Cites] Breast Cancer Res. 2004;6(4):R291-9 [15217495.001]
  • [Cites] Int J Oncol. 2004 Sep;25(3):737-44 [15289877.001]
  • [Cites] Int J Cancer. 2004 Nov 20;112(4):707-12 [15382055.001]
  • [Cites] Blood. 1983 Oct;62(4):709-21 [6192859.001]
  • [Cites] Biochem Pharmacol. 1993 May 5;45(9):1881-7 [8494547.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8707-11 [7690969.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3745-53 [7579341.001]
  • [Cites] Chem Biol Interact. 2006 Aug 25;162(2):140-8 [16857180.001]
  • [Cites] Nutr Cancer. 2007;58(2):178-87 [17640164.001]
  • [Cites] Toxicol In Vitro. 2007 Dec;21(8):1678-85 [17604596.001]
  • [Cites] Trends Mol Med. 2007 Nov;13(11):470-81 [17981087.001]
  • [CommentIn] Cancer Biol Ther. 2009 Feb;8(4):338-9 [19197147.001]
  • (PMID = 19197149.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070566; United States / NHLBI NIH HHS / HL / HL70566; United States / NHLBI NIH HHS / HL / R01 HL073737; United States / NHLBI NIH HHS / HL / HL052955-14A1; United States / NHLBI NIH HHS / HL / R01 HL052955; United States / NHLBI NIH HHS / HL / R01 HL052955-14A1; United States / NHLBI NIH HHS / HL / HL73737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / bcl-2-Associated X Protein; 25167-62-8 / Docosahexaenoic Acids; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS122907; NLM/ PMC3954154
  •  go-up   go-down


90. Houtenbos I, Santegoets S, Westers TM, Waisfisz Q, Kipriyanov S, Denkers F, Scheper RJ, de Gruijl TD, Ossenkoppele GJ, van de Loosdrecht AA: The novel bispecific diabody alphaCD40/alphaCD28 strengthens leukaemic dendritic cell-induced T-cell reactivity. Br J Haematol; 2008 Jun;142(2):273-83
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have recently shown the feasibility of generating fully functional DC from acute myeloid leukaemic (AML) blasts, but with varying expression levels of the important costimulatory molecule CD86.
  • To overcome this variability, we developed a novel bispecific diabody that simultaneously and agonistically targeted CD40 on AML-DC and CD28 on naïve T cells.
  • Beside optimization of CD28-mediated signalling, the resulting cellular cross-linking was also hypothesized to increase the strength and duration of T cell/AML-DC interactions, thus increasing T-cell responsiveness to AML antigens.
  • The alphaCD40/alphaCD28 diabody is capable of increasing T-cell proliferation induced by AML-DC as well as the induction of DC maturation.
  • Importantly, priming efficacy of tumour-specific cytotoxic T cells can also be improved by cross-linking AML-DC and T cells with the alphaCD40/alphaCD28 diabody.
  • We propose that the alphaCD40/alphaCD28-bispecific diabody can serve as a potent therapeutic tool to effectively augment anti-tumour T-cell responses elicited by AML-DC.
  • [MeSH-major] Antibodies, Bispecific / therapeutic use. Antigens, CD28 / immunology. Antigens, CD40 / immunology. Antigens, Neoplasm / immunology. Cancer Vaccines / immunology. Immunotherapy / methods. Leukemia, Myeloid, Acute / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18492117.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antigens, CD28; 0 / Antigens, CD40; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines
  •  go-up   go-down


91. Cleary ML: Regulating the leukaemia stem cell. Best Pract Res Clin Haematol; 2009 Dec;22(4):483-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulating the leukaemia stem cell.
  • Leukaemia stem cells (LSCs) are responsible for sustaining and propagating malignant disease, and, as such, are promising targets for therapy.
  • Studies of human LSCs have served an important role in defining the major tenets of the cancer stem cell model, which centre on the frequencies of cancer stem cells, their potential hierarchical organisation and their degree of maturation.
  • LSCs in acute myeloid leukaemia (AML) have recently been studied using mouse syngeneic models of leukaemia induced by MLL oncogenes.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Br J Haematol. 1999 Sep;106(3):614-26 [10468849.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Science. 2007 Jul 20;317(5836):337 [17641192.001]
  • [Cites] Cell Stem Cell. 2008 Apr 10;2(4):333-44 [18397753.001]
  • [Cites] Nat Genet. 2008 May;40(5):499-507 [18443585.001]
  • [Cites] Blood. 2008 Aug 1;112(3):568-75 [18523148.001]
  • [Cites] Cell Stem Cell. 2009 Feb 6;4(2):129-40 [19200802.001]
  • [Cites] Exp Hematol. 2000 Jun;28(6):660-71 [10880752.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10984-9 [10995463.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1849-56 [12738660.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Trends Mol Med. 2004 Oct;10(10):500-7 [15464450.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1166-73 [16234360.001]
  • (PMID = 19959097.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 16
  • [Other-IDs] NLM/ NIHMS157679; NLM/ PMC2802107
  •  go-up   go-down


92. Ayala RM, Martínez-López J, Albízua E, Diez A, Gilsanz F: Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia. Am J Hematol; 2009 Feb;84(2):79-86
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia.
  • The aim of this study was to evaluate the biological correlation and prognostic impact of Gata-1, Gata-2, EKLF, and c-MPL transcript level in a group of 41 acute myeloid leukemia (AML) patients.
  • Expression of c-MPL was associated with CD34+ AML and M2 FAB AML subtype.
  • A higher expression of EKLF was found in secondary AML versus primary AML.
  • Our study has identified expression of EKLF as a factor with a favorable impact on prognosis in AML.
  • [MeSH-major] GATA1 Transcription Factor / physiology. GATA2 Transcription Factor / physiology. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Receptors, Thrombopoietin / physiology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19097174.001).
  • [ISSN] 1096-8652
  • [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 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Receptors, Thrombopoietin; 0 / erythroid Kruppel-like factor; 143641-95-6 / MPL protein, human
  •  go-up   go-down


93. Tagliafico E, Tenedini E, Manfredini R, Grande A, Ferrari F, Roncaglia E, Bicciato S, Zini R, Salati S, Bianchi E, Gemelli C, Montanari M, Vignudelli T, Zanocco-Marani T, Parenti S, Paolucci P, Martinelli G, Piccaluga PP, Baccarani M, Specchia G, Torelli U, Ferrari S: Identification of a molecular signature predictive of sensitivity to differentiation induction in acute myeloid leukemia. Leukemia; 2006 Oct;20(10):1751-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a molecular signature predictive of sensitivity to differentiation induction in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) blasts are immature committed myeloid cells unable to spontaneously undergo terminal maturation, and characterized by heterogeneous sensitivity to natural differentiation inducers.
  • Here, we show a molecular signature predicting the resistance or sensitivity of six myeloid cell lines to differentiation induced in vitro with retinoic acid or vitamin D.
  • The identified signature was further validated by TaqMan assay for the prediction of response to an in vitro differentiation assay performed on 28 freshly isolated AML blast populations.
  • The TaqMan assay successfully predicts the in vitro resistance or responsiveness of AML blasts to differentiation inducers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Acute Disease. Cell Differentiation / drug effects. Cell Line, Tumor. Cluster Analysis. Databases, Factual. Gene Expression Regulation, Leukemic / drug effects. Humans. Meta-Analysis as Topic. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction. Vitamin D / pharmacology. Vitamins / pharmacology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16932344.001).
  • [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 / Antineoplastic Agents; 0 / Vitamins; 1406-16-2 / Vitamin D; 5688UTC01R / Tretinoin
  •  go-up   go-down


94. Putz G, Rosner A, Nuesslein I, Schmitz N, Buchholz F: AML1 deletion in adult mice causes splenomegaly and lymphomas. Oncogene; 2006 Feb 9;25(6):929-39
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AML1 is one of the most frequently mutated genes associated with human acute leukemia, suggesting that genetic alterations of the gene contribute to leukemogenesis.
  • AML1 was deleted in adult mice by inducing Cre activity to replicate AML1 deletions found in human MDS, familial platelet disorder and rare de novo human AML.
  • At a latency of 2 months after induction, the thymus was reduced in size and frequently populated by immature double negative thymocytes, indicating defective T-lymphocyte maturation, resulting in lymphatic diseases with 50% penetrance, including atypical hyperplasia and thymic lymphoma.
  • Mice also developed splenomegaly with an expansion of the myeloid compartment.


95. Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH: CEBPalpha mutations in childhood acute myeloid leukemia. Leukemia; 2005 Mar;19(3):410-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CEBPalpha mutations in childhood acute myeloid leukemia.
  • CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.
  • We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product.
  • CEBPalpha mutations were detected in seven patients, four had FAB M2, two M1 and one M4.
  • Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation


96. Malaise M, Steinbach D, Corbacioglu S: Clinical implications of c-Kit mutations in acute myelogenous leukemia. Curr Hematol Malig Rep; 2009 Apr;4(2):77-82
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical implications of c-Kit mutations in acute myelogenous leukemia.
  • This finding culminated in a two-class model integrating constitutive activating and maturation arrest-inducing mutations as key elements for the pathogenesis of acute myelogenous leukemia (AML).
  • c-Kit is expressed by myeloblasts in about 60% to 80% of patients, and the most frequently observed activating RTK mutations in AML (next to FLT3) are mutations or internal tandem duplications in c-Kit, with an overall incidence of 17%.
  • The identification of small-molecule tyrosine kinase inhibitors capable of blocking key kinase switches introduced a paradigm change in the treatment of diseases like gastrointestinal stromal tumors and chronic myelogenous leukemia.
  • Despite encouraging preclinical data, it appears that a complex clonal disease like AML will probably benefit from a synergistic approach of targeted drugs used (at least for now) in combination with conventional chemotherapy.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gene Expression Regulation, Leukemic. Humans. Prognosis. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / therapeutic use. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • 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 = 20425418.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Number-of-references] 53
  •  go-up   go-down


97. Mardis ER, Ding L, Dooling DJ, Larson DE, McLellan MD, Chen K, Koboldt DC, Fulton RS, Delehaunty KD, McGrath SD, Fulton LA, Locke DP, Magrini VJ, Abbott RM, Vickery TL, Reed JS, Robinson JS, Wylie T, Smith SM, Carmichael L, Eldred JM, Harris CC, Walker J, Peck JB, Du F, Dukes AF, Sanderson GE, Brummett AM, Clark E, McMichael JF, Meyer RJ, Schindler JK, Pohl CS, Wallis JW, Shi X, Lin L, Schmidt H, Tang Y, Haipek C, Wiechert ME, Ivy JV, Kalicki J, Elliott G, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson MA, Baty J, Heath S, Shannon WD, Nagarajan R, Link DC, Walter MJ, Graubert TA, DiPersio JF, Wilson RK, Ley TJ: Recurring mutations found by sequencing an acute myeloid leukemia genome. N Engl J Med; 2009 Sep 10;361(11):1058-66
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurring mutations found by sequencing an acute myeloid leukemia genome.
  • BACKGROUND: The full complement of DNA mutations that are responsible for the pathogenesis of acute myeloid leukemia (AML) is not yet known.
  • METHODS: We used massively parallel DNA sequencing to obtain a very high level of coverage (approximately 98%) of a primary, cytogenetically normal, de novo genome for AML with minimal maturation (AML-M1) and a matched normal skin genome.
  • Four of the 64 mutations occurred in at least 1 additional AML sample in 188 samples that were tested.
  • Mutations in NRAS and NPM1 had been identified previously in patients with AML, but two other mutations had not been identified.
  • One of these mutations, in the IDH1 gene, was present in 15 of 187 additional AML genomes tested and was strongly associated with normal cytogenetic status; it was present in 13 of 80 cytogenetically normal samples (16%).
  • The other was a nongenic mutation in a genomic region with regulatory potential and conservation in higher mammals; we detected it in one additional AML tumor.
  • The AML genome that we sequenced contains approximately 750 point mutations, of which only a small fraction are likely to be relevant to pathogenesis.
  • CONCLUSIONS: By comparing the sequences of tumor and skin genomes of a patient with AML-M1, we have identified recurring mutations that may be relevant for pathogenesis.


98. Kotru M, Batra M, Gomber S, Rusia U: Transient thrombocytosis with megathrombocytes in a case of acute myeloblastic leukemia. Indian J Pathol Microbiol; 2009 Jan-Mar;52(1):113-4
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transient thrombocytosis with megathrombocytes in a case of acute myeloblastic leukemia.
  • It is rarely seen in acute leukemia.
  • A 12-year-old girl with acute myeloblastic leukemia (FAB M2) in remission presented with pyoderma.
  • This case has been presented because thrombocytosis is rare in AML and its appearance calls for a close follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / pathology. Thrombocytosis / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19136802.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  •  go-up   go-down


99. Babusíková O, Zelezníková T, Kirschnerová G, Kankuri E: Hematogones in acute leukemia during and after therapy. Leuk Lymphoma; 2008 Oct;49(10):1935-44
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematogones in acute leukemia during and after therapy.
  • After each leukemia therapy phase, characteristics of normal regenerating B-cells may be reminiscent of and mistaken for a relapse.
  • We compared the incidence and phenotypic characteristics of hematogone stages in a total of 669 bone marrow aspirates from 107 patients with B-ALL, 97 patients of AML, and 27 patients with T-ALL at diagnosis, during, and after therapy.
  • The three individual physiological maturation phases of B-lymphocytes (hematogone stages 1, 2, and 3) were studied by four-color flow cytometry in the course of bone marrow regeneration in leukemia patients.
  • Multiple stages of hematogones were observed twice as frequently in B-ALL (73.8%) and T-ALL (69.2%) samples as in AML aspirates (34.1%).
  • The hematogones had an extremely high phenotypic stability unaffected by disease or therapy or by their coincidence with leukemia cells.
  • [MeSH-major] B-Lymphocytes / cytology. Bone Marrow / physiology. Leukemia / immunology. Leukemia, Myeloid, Acute / immunology. Regeneration
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow Examination. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Infant. Infant, Newborn. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Lymphoma. 2009 Apr;50(4):523-4 [19373647.001]
  • (PMID = 18452085.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


100. Florian S, Sonneck K, Hauswirth AW, Krauth MT, Schernthaner GH, Sperr WR, Valent P: Detection of molecular targets on the surface of CD34+/CD38-- stem cells in various myeloid malignancies. Leuk Lymphoma; 2006 Feb;47(2):207-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of molecular targets on the surface of CD34+/CD38-- stem cells in various myeloid malignancies.
  • Recent data suggest that myeloid neoplasms are organized hierarchically in terms of self-renewal and maturation of early progenitor cells, similar to normal myelopoiesis.
  • In acute myeloid leukemia (AML), the NOD/SCID mouse-repopulating leukemic stem cells usually co-express CD123 with CD34, but lack CD38.
  • In the present study, expression of target antigens on CD34+/CD38- cells was analysed by multi-color flow cytometry in patients with AML (n = 18), myelodysplastic syndromes (MDS, n = 6), chronic myeloid leukemia (CML, n = 8) and systemic mastocytosis (SM, n = 9).
  • Independent of the type of disease, the vast majority of these stem cells co-expressed aminopeptidase-N (CD13) and CD44 in all patients.
  • In conclusion, neoplastic stem cells in various myeloid neoplasms appear to express a similar phenotype including target antigens such as CD13, CD33 and CD44.
  • [MeSH-major] Antigens, CD34 / analysis. Antigens, CD38 / analysis. Leukemia, Myeloid / diagnosis. Mastocytosis, Systemic / diagnosis. Myelodysplastic Syndromes / diagnosis. Stem Cells / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Chronic Disease. Female. Flow Cytometry. Gene Expression Regulation, Leukemic / genetics. Humans. Immunophenotyping. Male. Middle Aged






Advertisement