[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 121
6. Amadori S, Suciu S, Selleslag D, Stasi R, Alimena G, Baila L, Rizzoli V, Borlenghi E, Gaidano G, Magro D, Torelli G, Muus P, Venditti A, Cacciola E, Lauria F, Vignetti M, de Witte T: Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. A phase II study of the EORTC and GIMEMA leukaemia groups (AML-19). Br J Haematol; 2010 May;149(3):376-82
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] Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. A phase II study of the EORTC and GIMEMA leukaemia groups (AML-19).
  • This study compared two schedules of low-dose gemtuzumab ozogamicin (GO) as induction monotherapy for untreated acute myeloid leukaemia in older patients unfit for intensive chemotherapy, to identify the more promising regimen for further study.
  • Primary endpoint was the rate of disease non-progression (DnP), defined as the proportion of patients either achieving a response or maintaining a stable disease following GO induction in each arm.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Humanized. Disease Progression. Drug Administration Schedule. Feasibility Studies. Female. Humans. Male. Middle Aged. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 May 15;97(10):3197-204 [11342449.001]
  • [Cites] Haematologica. 2009 Jan;94(1):10-6 [19118375.001]
  • [Cites] Arch Intern Med. 2002 Jul 22;162(14):1597-603 [12123403.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] JAMA. 2003 May 21;289(19):2554-9 [12759327.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):478-90 [1999719.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3678-84 [10339474.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1768-73 [16079891.001]
  • [Cites] Ann Oncol. 2006 Feb;17(2):281-5 [16373393.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] Leukemia. 2007 Jan;21(1):66-71 [17051246.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1114-24 [17315155.001]
  • [Cites] BMJ. 2007 Apr 14;334(7597):756-7 [17431231.001]
  • [Cites] Clin Adv Hematol Oncol. 2007 Mar;5(3):185-7 [17519879.001]
  • [Cites] Cancer Treat Rev. 2008 Feb;34(1):49-60 [17942233.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • (PMID = 20230405.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / U10 CA011488-33
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 93NS566KF7 / gemtuzumab
  • [Other-IDs] NLM/ NIHMS189126; NLM/ PMC2864316
  •  go-up   go-down


7. Nowicki M, Ostalska-Nowicka D, Miśkowiak B: Prognostic significance of Ki67-negative blast cell clone in the high risk group of children treated for acute myeloid leukaemia. Folia Histochem Cytobiol; 2006;44(1):49-52
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] Prognostic significance of Ki67-negative blast cell clone in the high risk group of children treated for acute myeloid leukaemia.
  • The aim of this study was to demonstrate the value of immunocytochemical staining of Ki67 antigen expression in blast cells of children with acute myeloid leukemia (AML) and to evaluate its correlation with treatment failure.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16584092.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
  •  go-up   go-down


8. Ley TJ, Mardis ER, Ding L, Fulton B, McLellan MD, Chen K, Dooling D, Dunford-Shore BH, McGrath S, Hickenbotham M, Cook L, Abbott R, Larson DE, Koboldt DC, Pohl C, Smith S, Hawkins A, Abbott S, Locke D, Hillier LW, Miner T, Fulton L, Magrini V, Wylie T, Glasscock J, Conyers J, Sander N, Shi X, Osborne JR, Minx P, Gordon D, Chinwalla A, Zhao Y, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson M, Baty J, Ivanovich J, Heath S, Shannon WD, Nagarajan R, Walter MJ, Link DC, Graubert TA, DiPersio JF, Wilson RK: DNA sequencing of a cytogenetically normal acute myeloid leukaemia genome. Nature; 2008 Nov 6;456(7218):66-72
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] DNA sequencing of a cytogenetically normal acute myeloid leukaemia genome.
  • Acute myeloid leukaemia is a highly malignant haematopoietic tumour that affects about 13,000 adults in the United States each year.
  • Here we present the results obtained from sequencing a typical acute myeloid leukaemia genome, and its matched normal counterpart obtained from the same patient's skin.
  • We discovered ten genes with acquired mutations; two were previously described mutations that are thought to contribute to tumour progression, and eight were new mutations present in virtually all tumour cells at presentation and relapse, the function of which is not yet known.


9. Szpecht D, Derwich K, Wachowiak J, Konatkowska B, Dworacki G: [Lineage switch - conversion of acute lymphoblastic leukaemia to acute myeloid leukaemia in 4 years old girl]. Med Wieku Rozwoj; 2008 Oct-Dec;12(4 Pt 2):1041-4
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Lineage switch - conversion of acute lymphoblastic leukaemia to acute myeloid leukaemia in 4 years old girl].
  • We report a case of a 4-year-old girl with diagnosed proB acute lymphoblastic leukaemia with co-expression CD33 antigen, treated according to Acute Lymphoblastic Leukaemia Intercontinental - Berlin Frankfurt Münster 2002 (ALL-IC BFM 2002) protocol for standard risk group.
  • The late isolated bone marrow relapse of acute myeloid leukaemia, type 7 was noted in our patient.
  • We recognized this case as a lineage switch acute lymphoblastic leukaemia to acute myeloid leukaemia.
  • In spite of Ida Flag regimen and following Acute Myeloid Leukaemia - Berlin Frankfurt Münster 2004 (AML-BFM 2004) protocol were administered, the clinical and haematological remission was not achieved and the patient died because of disease progression (circulatory and respiratory insufficiency).
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / therapeutic use. Cell Lineage. Cell Transformation, Neoplastic. Child, Preschool. Daunorubicin / therapeutic use. Disease Progression. Fatal Outcome. Female. Humans. Prednisone / therapeutic use. Remission Induction. Vincristine / therapeutic use

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19531823.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
  •  go-up   go-down


10. Keller G, Brassat U, Braig M, Heim D, Wege H, Brümmendorf TH: Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy. Hematol Oncol; 2009 Sep;27(3):123-9
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] Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy.
  • However, elevated telomerase activity has also been reported in the majority of solid tumours as well as in acute and chronic leukaemia.
  • Chronic myeloid leukaemia (CML) serves as a model disease to study telomere biology in clonal myeloproliferative disorders.
  • In addition, telomerase activity (TA) is already increased in CP CML and further upregulated with disease progression to accelerated phase and blast crisis (BC).
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Telomere / pathology
  • [MeSH-minor] Animals. Disease Progression. Humans

  • MedlinePlus Health Information. consumer health - Chronic 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
  • (PMID = 19569255.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  • [Number-of-references] 67
  •  go-up   go-down


11. Rigolin GM, Mauro E, Ciccone M, Fraulini C, Sofritti O, Castoldi G, Cuneo A: Neoplastic circulating endothelial-like cells in patients with acute myeloid leukaemia. Eur J Haematol; 2007 May;78(5):365-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoplastic circulating endothelial-like cells in patients with acute myeloid leukaemia.
  • In this report, we showed that, in seven acute myeloid leukaemia (AML) patients with known cytogenetic abnormalities, CEC levels were significantly increased in comparison with controls and that a significant proportion of these CECs carried the same chromosomal aberration as blast cells (20-78%, mean value 42.1% of CECs).
  • These findings suggest a possible direct contribution of AML-related CECs to tumour vasculogenesis and possibly to the spreading and progression of the disease.
  • [MeSH-major] Endothelium, Vascular / pathology. Leukemia, Myeloid / blood. Neoplastic Cells, Circulating
  • [MeSH-minor] Acute Disease. Humans. In Situ Hybridization, Fluorescence

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17391308.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  •  go-up   go-down


12. Ngo N, Lampert IA, Naresh KN: Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia. Br J Haematol; 2008 Feb;140(3):279-86
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia.
  • Acute myeloid leukaemia (AML) with multilineage dysplasia (MD) is one of the four main categories of AML in the World Health Organization (WHO) classification.
  • With respect to conforming to the WHO definition of AML, documentation of an increased proportion of immature myeloid cells was possible on morphology and counting of immature cells following immunostaining with CD34, CD117 or HLA-DR antibodies.
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / analysis. Biomarkers / analysis. Biopsy / methods. Bone Marrow Examination / methods. Cytogenetics. Disease Progression. Erythroblasts / pathology. Female. Humans. Immunohistochemistry. Immunophenotyping. Male. Megakaryocytes / pathology. Middle Aged. Myeloid Cells / pathology. Proto-Oncogene Proteins c-kit / analysis

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17973948.001).
  • [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 / Antigens, CD34; 0 / Biomarkers; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


13. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


1
Advertisement
4. Krauze E, Brzezińska-Wcisło L, Kamińska-Winciorek G, Wygledowska-Kania M, Sygula E: Pyoderma gangrenosum coexisting with acute myelogenous leukaemia. J Eur Acad Dermatol Venereol; 2005 Sep;19(5):589-92
MedlinePlus Health Information. consumer health - Leg Injuries and Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pyoderma gangrenosum coexisting with acute myelogenous leukaemia.
  • The aim of the study was to report a 26-year-old male patient with pyoderma gangrenosum coexisting with acute myelogenous leukaemia.
  • On the clinical and biochemical picture, the diagnosis of pyoderma gangrenosum within acute myelogenous leukaemia was made.
  • Although chemotherapy leukaemia was performed, the patient died after 4 months of the confirmation of the acute myelogenous leukaemia diagnosis.
  • [MeSH-major] Leg Ulcer / etiology. Leg Ulcer / therapy. Leukemia, Myeloid, Acute / complications. Pyoderma Gangrenosum / etiology. Pyoderma Gangrenosum / therapy
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Blood Transfusion. Combined Modality Therapy. Disease Progression. Fatal Outcome. Humans. Male. Risk Assessment. Severity of Illness Index

  • Genetic Alliance. consumer health - Pyoderma gangrenosum.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16164714.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents
  •  go-up   go-down


15. Goulden N, Virgo P, Grimwade D: Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now. Br J Haematol; 2006 Aug;134(3):273-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now.
  • The continued improvement in the prognosis of childhood acute myeloid leukaemia (AML) has been paralleled by the use of increasingly intensive therapy.
  • This annotation proposes that the introduction of protocols based on the measurement of minimal residual disease (MRD) holds the key to progression from an era of 'cure at all costs' to a more individualised approach.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Neoplasm, Residual / drug therapy. Patient Selection. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16848770.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
  •  go-up   go-down


21. Aref S, Osman E, Mansy S, Omer N, Azmy E, Goda T, El-Sherbiny M: Prognostic relevance of circulating matrix metalloproteinase-2 in acute myeloid leukaemia patients. Hematol Oncol; 2007 Sep;25(3):121-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic relevance of circulating matrix metalloproteinase-2 in acute myeloid leukaemia patients.
  • Matrix metalloproteinases (MMPs) were postulated to have important implication in progression and invasiveness of many malignant disorders.
  • On the other hand the biological role of MMP-2 in acute myeloid leukaemia (AML) is not fully clear.
  • [MeSH-major] Leukemia, Myeloid / blood. Matrix Metalloproteinase 2 / blood. Matrix Metalloproteinase 2 / cerebrospinal fluid
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Blast Crisis. Female. Hemoglobins / metabolism. Humans. Leukocyte Count. Male. Middle Aged. Platelet Count. Prognosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 John Wiley & Sons, Ltd.
  • (PMID = 17497745.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; EC 3.4.24.24 / Matrix Metalloproteinase 2
  •  go-up   go-down


22. Maserati E, Pressato B, Valli R, Minelli A, Sainati L, Patitucci F, Marletta C, Mastronuzzi A, Poli F, Lo Curto F, Locatelli F, Danesino C, Pasquali F: The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies. Br J Haematol; 2009 Apr;145(2):190-7
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] The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies.
  • (iii) the deletion del(20)(q11) involved the minimal region of deletion typical of myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML);.
  • [MeSH-major] Aging / genetics. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Human, Pair 20. Chromosomes, Human, Pair 7. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Humans. In Situ Hybridization, Fluorescence. Isochromosomes. Karyotyping. Male. Proteins / genetics. Young Adult


23. Gilby DC, Sung HY, Winship PR, Goodeve AC, Reilly JT, Kiss-Toth E: Tribbles-1 and -2 are tumour suppressors, down-regulated in human acute myeloid leukaemia. Immunol Lett; 2010 May 4;130(1-2):115-24
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tribbles-1 and -2 are tumour suppressors, down-regulated in human acute myeloid leukaemia.
  • Constitutive MAPK signalling is observed in approximately 50% of acute myeloid leukaemia (AML) cases.
  • Tribbles proteins (trb-1, trb-2 and trb-3) are potent negative regulators of MAPK pathways influencing apoptosis, differentiation and cell-cycle progression.
  • Myeloid cell proliferation and apoptosis were assayed in response to trb-1/trb-2 gene knockdown and overexpression, as well as a physical and functional interaction between trb and C/EBPalpha.
  • [MeSH-major] Down-Regulation. Intracellular Signaling Peptides and Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism. Protein-Serine-Threonine Kinases / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • (PMID = 20005259.001).
  • [ISSN] 1879-0542
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / TRIB1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.17 / TRIB2 protein, human
  •  go-up   go-down


24. Melo JV, Barnes DJ: Chronic myeloid leukaemia as a model of disease evolution in human cancer. Nat Rev Cancer; 2007 Jun;7(6):441-53
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] Chronic myeloid leukaemia as a model of disease evolution in human cancer.
  • Chronic myeloid leukaemia (CML) can be considered as a paradigm for neoplasias that evolve through a multi-step process.
  • If not cured at this stage, CML invariably progresses and transforms into an acute-type leukaemia undergoing a 'blast crisis'.
  • What mechanisms underlie this progression, and are they shared by other common cancers?
  • [MeSH-major] Blast Crisis. Disease Progression. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Models, Biological

  • 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 = 17522713.001).
  • [ISSN] 1474-175X
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 153
  •  go-up   go-down


25. Chevallier P, Hunault-Berger M, Larosa F, Dauriac C, Garand R, Harousseau JL: A phase II trial of high-dose imatinib mesylate for relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia: the AFR-15 trial. Leuk Res; 2009 Aug;33(8):1124-6
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] A phase II trial of high-dose imatinib mesylate for relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia: the AFR-15 trial.
  • This was a phase II investigation of high-dose imatinib in 15 adult patients with relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia (AML).
  • No clinical responses were reported with early death due to disease progression reported in 7 patients.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Genes, abl. Leukemia, Myeloid, Acute / drug therapy. Piperazines / administration & dosage. Proto-Oncogene Proteins c-kit. Pyrimidines / administration & dosage

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18990444.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


26. Lu C, Hassan HT: Human stem cell factor-antibody [anti-SCF] enhances chemotherapy cytotoxicity in human CD34+ resistant myeloid leukaemia cells. Leuk Res; 2006 Mar;30(3):296-302
Hazardous Substances Data Bank. DAUNORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human stem cell factor-antibody [anti-SCF] enhances chemotherapy cytotoxicity in human CD34+ resistant myeloid leukaemia cells.
  • Acute myeloid leukaemia (AML) is a heterogenous malignant disease with diverse biological features in which disease progression at the level of CD34+ cells has a major impact on the resistance to chemotherapy and relapse.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD34. Antineoplastic Agents / pharmacology. Biomarkers, Tumor. Cytarabine / pharmacology. Daunorubicin / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Stem Cell Factor / antagonists & inhibitors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16112192.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; 0 / Receptors, Cytokine; 0 / Stem Cell Factor; 0 / bcl-2-Associated X Protein; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


27. Vener C, Soligo D, Berti E, Gianelli U, Servida F, Ceretti E, Caputo R, Passoni E, Lambertenghi Deliliers G: Indeterminate cell histiocytosis in association with later occurrence of acute myeloblastic leukaemia. Br J Dermatol; 2007 Jun;156(6):1357-61
MedlinePlus Health Information. consumer health - Skin Conditions.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Indeterminate cell histiocytosis in association with later occurrence of acute myeloblastic leukaemia.
  • We describe a 39-year-old man who developed diffuse ICH and, 6 years later, acute myeloblastic leukaemia (AML).
  • ICH has previously been reported in association with B-cell malignancy, but only one case has shown systemic progression.
  • [MeSH-major] Histiocytosis / pathology. Leukemia, Myeloid, Acute / pathology. Skin Diseases / pathology

  • Genetic Alliance. consumer health - Histiocytosis.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17459045.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


28. Vyas P, Roberts I: Down myeloid disorders: a paradigm for childhood preleukaemia and leukaemia and insights into normal megakaryopoiesis. Early Hum Dev; 2006 Dec;82(12):767-73
MedlinePlus Health Information. consumer health - Down Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down myeloid disorders: a paradigm for childhood preleukaemia and leukaemia and insights into normal megakaryopoiesis.
  • Newborns and children with Down Syndrome are predisposed to a range of blood disorders, which include acute lymphoblastic leukaemia and acute megakaryocytic leukaemia (AMKL).
  • Over the last four years there has been considerable progress in our understanding of DS AMKL.
  • In approximately 30% of TMD patients, additional as yet unidentified (epi)genetic mutations are required for progression to AMKL.
  • Thus, DS TMD and AMKL provide a unique model of childhood leukaemia where the preleukaemic and leukaemic phases are ascertainable and separable allowing distinct steps in leukaemogenesis to be studied individually.
  • These findings also have implications for the clinical management of DS TMD and AMKL specifically and also of childhood leukaemia more generally.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / physiopathology. Megakaryocytes / physiology. Thrombopoiesis / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17064858.001).
  • [ISSN] 0378-3782
  • [Journal-full-title] Early human development
  • [ISO-abbreviation] Early Hum. Dev.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 23
  •  go-up   go-down


29. Suzuki R, Onizuka M, Kojima M, Shimada M, Fukagawa S, Tsuboi K, Kobayashi H, Shintani A, Ogawa Y, Kawada H, Hotta T, Ando K: Preferential hypermethylation of the Dickkopf-1 promoter in core-binding factor leukaemia. Br J Haematol; 2007 Sep;138(5):624-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preferential hypermethylation of the Dickkopf-1 promoter in core-binding factor leukaemia.
  • Here, we investigated hypermethylation of the DKK1 promoter in patients with acute myeloid leukaemia (AML), especially core-binding factor (CBF) leukaemia.
  • DKK1 methylation was found in 14 (29.8%) patients, and more frequently in those with CBF leukaemia (6 of 12 patients), than in those with acute promyelocytic leukaemia (APL) (0 of 6 patients) (P = 0.03).
  • In contrast, Wnt inhibitory factor-1 methylation was found in APL (4 of 6 patients) but not in CBF leukaemia (0 of 12 patients) (P = 0.001).
  • Sequential analysis using four paired samples obtained at diagnosis and relapse suggested that DKK1 methylation was involved in the progression of leukaemia.
  • Therefore, DKK1 methylation may be involved in leukaemogenesis, especially in CBF leukaemia, and may be a useful prognostic marker in AML.
  • [MeSH-major] Biomarkers, Tumor / genetics. DNA Methylation. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow Cells / metabolism. Core Binding Factors / metabolism. DNA, Neoplasm / genetics. Disease Progression. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Prognosis. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Survival Analysis. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17686056.001).
  • [ISSN] 0007-1048
  • [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 / Biomarkers, Tumor; 0 / Core Binding Factors; 0 / DKK1 protein, human; 0 / DNA, Neoplasm; 0 / Intercellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins
  •  go-up   go-down


30. Drury NE, Ali A, Mussa S, Webb ST, Rege KP, Wallwork J: Acute leukaemoid reaction following cardiac surgery. J Cardiothorac Surg; 2007;2:3
MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute leukaemoid reaction following cardiac surgery.
  • Chronic myelomonocytic leukaemia is an atypical myeloproliferative disorder with a natural history of progression to acute myeloid leukaemia, a complex and poorly understood response by the bone marrow to stress.
  • We present a case of undiagnosed chronic myelomonocytic leukaemia who developed rapidly fatal multi-organ dysfunction following cardiac surgery due to an acute leukaemoid reaction.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemoid Reaction / etiology. Myocardial Revascularization / adverse effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cardiovasc Surg. 2000 Mar;8(2):149-52 [10737352.001]
  • [Cites] Ann Thorac Surg. 2002 Aug;74(2):384-9 [12173817.001]
  • [Cites] Ann Thorac Surg. 2003 Feb;75(2):S715-20 [12607717.001]
  • [Cites] Mayo Clin Proc. 2006 Apr;81(4):553-63 [16610578.001]
  • [Cites] Eur J Cardiothorac Surg. 2004 Apr;25(4):537-40 [15037268.001]
  • [Cites] Leuk Lymphoma. 2004 Jul;45(7):1311-8 [15359628.001]
  • [Cites] J Cardiothorac Vasc Anesth. 1993 Aug;7(4):455-7 [8400103.001]
  • [Cites] Jpn Heart J. 2003 May;44(3):435-9 [12825811.001]
  • (PMID = 17212818.001).
  • [ISSN] 1749-8090
  • [Journal-full-title] Journal of cardiothoracic surgery
  • [ISO-abbreviation] J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1774565
  • [General-notes] NLM/ Original DateCompleted: 20070802
  •  go-up   go-down


31. Keith T, Araki Y, Ohyagi M, Hasegawa M, Yamamoto K, Kurata M, Nakagawa Y, Suzuki K, Kitagawa M: Regulation of angiogenesis in the bone marrow of myelodysplastic syndromes transforming to overt leukaemia. Br J Haematol; 2007 May;137(3):206-15
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] Regulation of angiogenesis in the bone marrow of myelodysplastic syndromes transforming to overt leukaemia.
  • To investigate the regulatory mechanisms of angiogenesis in the development of myelodysplastic syndromes (MDS) and its progression to overt leukaemia (OL), bone marrow samples from control, paired samples from MDS patients before and after transformation to OL (MDS --> OL) and de novo acute myeloid leukaemia (AML) were analysed.
  • Immunohistochemical staining showed a significant increase of bone marrow microvascular density (MVD) in MDS and de novo AML compared with controls.
  • Surprisingly, in MDS, MVD significantly decreased upon transformation to OL, which was also significantly lower than the MVD of de novo AML.
  • These findings indicate that the bone marrow microenvironment in MDS --> OL and de novo AML differs remarkably, suggesting the different efficacy of anti-angiogenic therapy between de novo AML and leukaemia secondary to MDS.
  • [MeSH-major] Bone Marrow / physiopathology. Leukemia / physiopathology. Myelodysplastic Syndromes / physiopathology. Neovascularization, Pathologic / physiopathology
  • [MeSH-minor] Aged. Angiopoietin-1 / analysis. Angiopoietin-2 / analysis. Disease Progression. Female. Fibroblast Growth Factor 2 / analysis. Hepatocyte Growth Factor / analysis. Humans. Immunohistochemistry / methods. Leukemia, Myeloid, Acute / physiopathology. Male. Microcirculation / physiopathology. Middle Aged. RNA, Messenger / analysis. Receptor, TIE-2 / analysis. Transforming Growth Factor beta / analysis. Tumor Necrosis Factor-alpha / analysis. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - 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 = 17408459.001).
  • [ISSN] 0007-1048
  • [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 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


32. Travaglino E, Comincini S, Benatti C, Azzalin A, Nano R, Rosti V, Ferretti L, Invernizzi R: Overexpression of the Doppel protein in acute myeloid leukaemias and myelodysplastic syndromes. Br J Haematol; 2005 Mar;128(6):877-84
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] Overexpression of the Doppel protein in acute myeloid leukaemias and myelodysplastic syndromes.
  • We investigated the expression patterns and distribution of Doppel (Dpl), the product of the prion-like gene PRND, in the leukaemic cell lines HL-60 and K562 and in bone marrow cells from 44 patients with acute myeloid leukaemia (AML) and 63 patients with myelodysplastic syndrome (MDS).
  • PRND expression was higher in advanced compared with early MDS (P = 0.01), but Dpl levels did not predict disease progression.
  • The molecular mechanism of the observed overexpression is unknown; however, the differential Dpl distribution in AML and MDS versus healthy subjects makes it a possible leukaemia-associated antigen that could be useful for diagnostic and therapeutic purposes.
  • [MeSH-major] Leukemia, Myeloid / metabolism. Myelodysplastic Syndromes / metabolism. Prions / metabolism
  • [MeSH-minor] Acute Disease. Aged. Antigens, CD34 / metabolism. Blotting, Western. Female. GPI-Linked Proteins. HL-60 Cells. Humans. Immunohistochemistry. Male. Middle Aged. Polymerase Chain Reaction / methods. RNA, Messenger / metabolism

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15755294.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions; 0 / RNA, Messenger
  •  go-up   go-down


33. Hoves S, Aigner M, Pfeiffer C, Laumer M, Obermann EC, Mackensen A: In situ analysis of the antigen-processing machinery in acute myeloid leukaemic blasts by tissue microarray. Leukemia; 2009 May;23(5):877-85
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] In situ analysis of the antigen-processing machinery in acute myeloid leukaemic blasts by tissue microarray.
  • Altered expression of major histocompatibility complex (MHC) class I molecules can be caused by defects in genes of the antigen-processing machinery (APM), and is often correlated to progression in solid tumours.
  • However, little is known about expression of the APM components in blasts from patients with acute myeloid leukaemia (AML).
  • By following disease progression in individual AML patients, we found severe downregulation of APM components in two out of four patients from initial diagnosis to relapse.
  • We conclude that downregulation of APM components may play a role in the failure of immuno-surveillance and may therefore contribute to relapse in acute leukaemia.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Cysteine Endopeptidases / metabolism. Histocompatibility Antigens Class I / metabolism. Leukemia, Myeloid, Acute / metabolism. Multienzyme Complexes / metabolism. beta 2-Microglobulin / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19148137.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histocompatibility Antigens Class I; 0 / Multienzyme Complexes; 0 / RNA, Messenger; 0 / TAP1 protein, human; 0 / beta 2-Microglobulin; 144416-78-4 / LMP-2 protein; 145892-13-3 / TAP2 protein, human; 82115-62-6 / Interferon-gamma; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.25.1 / LMP7 protein; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  •  go-up   go-down


34. Kobayashi H, Matsuyama T, Ueda M, Suzuki T, Ozaki K, Mori M, Nagai T, Muroi K, Ozawa K: Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome. Intern Med; 2009;48(18):1629-33
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] Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome.
  • OBJECTIVE: The progression of myelodysplastic syndrome to acute myeloid leukemia (MDS/AML) is generally incurable and its prognosis is extremely poor.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


35. Claxton DF, Ehmann C, Rybka W: Control of advanced and refractory acute myelogenous leukaemia with sirolimus-based non-myeloablative allogeneic stem cell transplantation. Br J Haematol; 2005 Jul;130(2):256-64
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Control of advanced and refractory acute myelogenous leukaemia with sirolimus-based non-myeloablative allogeneic stem cell transplantation.
  • A total of 23 patients with acute myelogenous leukaemia (AML) were treated, with a median age of 59 years (range: 28-72) at transplant.
  • Nine patients were in chemotherapy-refractory progression and seven were primarily refractory to induction therapy.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Immunosuppressive Agents / administration & dosage. Leukemia, Myeloid, Acute / therapy. Sirolimus / administration & dosage
  • [MeSH-minor] Adult. Aged. Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chronic Disease. Cyclophosphamide / administration & dosage. Disease Progression. Follow-Up Studies. Graft Survival. Graft vs Host Disease / prevention & control. Humans. Middle Aged. Survival Analysis. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029454.001).
  • [ISSN] 0007-1048
  • [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 / Antibiotics, Antineoplastic; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


36. Rodríguez Pérez A, López Carrizosa MC, Villalón Blanco L, Samper Ots PM, Ortiz Cruz E: Granulocytic sarcoma of the right humerus in a non-leukaemia patient. Clin Transl Oncol; 2008 Nov;10(11):758-60
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Granulocytic sarcoma of the right humerus in a non-leukaemia patient.
  • Granulocytic sarcoma (GS), an uncommon solid extramedullary tumour, should be considered even in the absence of leukaemia, as delay in diagnosis and treatment worsens the prognosis.
  • We present a GS (single humeral bone lesion) in a non-leukaemia patient, treated with intensive AML (Acute Myeloid Leukaemia) chemotherapy and sequential radiotherapy, in complete response 26 months after diagnosis, confirmed by histopathology and without leukaemia progression.
  • [MeSH-major] Bone Neoplasms / diagnosis. Humerus / pathology. Sarcoma, Myeloid / diagnosis

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 2002 Mar 15;94(6):1739-46 [11920536.001]
  • [Cites] Ann Intern Med. 1995 Sep 1;123(5):351-3 [7625623.001]
  • [Cites] Cancer. 1981 Sep 15;48(6):1426-37 [7023656.001]
  • [Cites] Med Clin (Barc). 1995 Mar 18;104(10):377-80 [7707732.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1100-3 [12764375.001]
  • [Cites] Leuk Lymphoma. 2006 Dec;47(12):2527-41 [17169797.001]
  • [Cites] Strahlenther Onkol. 2003 Mar;179(3):187-90 [12627262.001]
  • [Cites] Leuk Res. 2004 Nov;28(11):1165-9 [15380340.001]
  • [Cites] Orthopedics. 1999 Aug;22(8):773-5 [10465491.001]
  • (PMID = 19015073.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
  •  go-up   go-down


37. Caudill JS, Sternberg AJ, Li CY, Tefferi A, Lasho TL, Steensma DP: C-terminal nucleophosmin mutations are uncommon in chronic myeloid disorders. Br J Haematol; 2006 Jun;133(6):638-41
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] C-terminal nucleophosmin mutations are uncommon in chronic myeloid disorders.
  • C-terminal somatic mutations in nucleophosmin (NPM), a nucleolar shuttling protein that binds p53 and p19(Arf), were recently described in karyotypically normal acute myeloid leukaemia (AML).
  • We analysed primary marrow samples from 150 patients with various chronic myeloid disorders for mutations in the NPM1 gene encoding NPM.
  • NPM1 mutations (tetranucleotide duplication) were detected in three patients, all of whom had chronic myelomonocytic leukaemia (CMML) and a short (<1 year) survival, with rapid progression to overt AML.
  • In conclusion, C-terminal NPM mutations are uncommon in chronic myeloid neoplasia, but if present may represent an evolving leukaemic clone.
  • [MeSH-major] Bone Marrow Diseases / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Base Sequence. Cell Transformation, Neoplastic / genetics. Chronic Disease. DNA Mutational Analysis / methods. DNA, Neoplasm / genetics. Disease Progression. Humans. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Prognosis

  • MedlinePlus Health Information. consumer health - Bone Marrow Diseases.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16704439.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  •  go-up   go-down


38. Teramoto H, Miwa H, Patel V, Letwin N, Castellone MD, Imai N, Shikami M, Imamura A, Gutkind JS, Nitta M, Lee NH: Gene expression changes in a patient presenting nonleukaemic nasal granulocytic sarcoma to acute myelogenous leukaemia using 40 K cDNA microarray. Clin Lab Haematol; 2006 Aug;28(4):262-6
MedlinePlus Health Information. consumer health - Nasal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression changes in a patient presenting nonleukaemic nasal granulocytic sarcoma to acute myelogenous leukaemia using 40 K cDNA microarray.
  • This is a case report of granulocytic sarcoma occurring as a nasal lesion prior to the onset of acute myelogenous leukaemia (AML).
  • To understand this case in more detail, we used 40,000 human cDNA microarray to identify the gene expression patterns of nonleukaemic stage bone marrow (BM), AML stage BM and AML stage peripheral blood cells and subsequently define the molecular basis of this disease progression.
  • Of significance, we have tracked the expression profile of BM samples during the course of nonleukaemic to leukaemic progression, and identified a number of genes that may account for the growth potential of leukaemia cells and indicate poor prognosis of this case.
  • [MeSH-major] Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Nose Neoplasms / genetics. Sarcoma, Myeloid / genetics
  • [MeSH-minor] Aged, 80 and over. Disease Progression. Down-Regulation / genetics. Fatal Outcome. Female. Humans. Oligonucleotide Array Sequence Analysis / methods. Up-Regulation / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16898967.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


39. Rosenberg PS, Alter BP, Link DC, Stein S, Rodger E, Bolyard AA, Aprikyan AA, Bonilla MA, Dror Y, Kannourakis G, Newburger PE, Boxer LA, Dale DC: Neutrophil elastase mutations and risk of leukaemia in severe congenital neutropenia. Br J Haematol; 2008 Jan;140(2):210-3
SciCrunch. Clinical Genomic Database: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neutrophil elastase mutations and risk of leukaemia in severe congenital neutropenia.
  • Severe congenital neutropenia (SCN) is a heterogeneous bone marrow failure syndrome predisposing to myelodysplastic syndrome and acute myeloid leukaemia (MDS/AML).

  • Genetics Home Reference. consumer health - severe congenital neutropenia.
  • Genetics Home Reference. consumer health - ELANE gene.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2000 Oct 1;96(7):2317-22 [11001877.001]
  • [Cites] Am J Hematol. 2003 Feb;72(2):82-93 [12555210.001]
  • [Cites] Br J Haematol. 2003 Feb;120(4):685-90 [12588357.001]
  • [Cites] Blood Rev. 2003 Dec;17(4):209-16 [14556775.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4119-25 [14962902.001]
  • [Cites] Pediatr Blood Cancer. 2007 Oct 15;49(5):609-14 [17584878.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4628-35 [16497969.001]
  • [Cites] Nat Genet. 2007 Jan;39(1):86-92 [17187068.001]
  • [Cites] J Natl Cancer Inst. 2007 Feb 7;99(3):183-6 [17284707.001]
  • [Cites] Blood. 2007 Mar 1;109(5):1817-24 [17053055.001]
  • [Cites] Blood. 1993 May 15;81(10):2496-502 [8490166.001]
  • (PMID = 18028488.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01DK54369; United States / NIAID NIH HHS / AI / K08 AI049392; United States / NIDDK NIH HHS / DK / R01 DK054369; United States / Intramural NIH HHS / / Z99 CA999999; United States / NIDDK NIH HHS / DK / R01 DK054369-09; United States / NIAID NIH HHS / AI / 1R24AI049392; United States / NIDDK NIH HHS / DK / DK054369-09
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.4.21.37 / Leukocyte Elastase
  • [Other-IDs] NLM/ NIHMS306469; NLM/ PMC3143022
  •  go-up   go-down


40. Martinelli G, Iacobucci I, Papayannidis C, Soverini S: New targets for Ph+ leukaemia therapy. Best Pract Res Clin Haematol; 2009 Sep;22(3):445-54
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] New targets for Ph+ leukaemia therapy.
  • The outcome for adults with Philadelphia chromosome (Ph+) leukaemias (chronic myeloid leukaemia (CML) and acute lymphoblastic leukaemia (ALL)) has been dramatically improved with the use of tyrosine kinase inhibitors (TKIs), but progression and/or relapse are still present in the majority of patients.
  • Some emerging aurora kinase inhibitors, such as VX-680, PHA-739358, MK-0457 and AS703569, and Smo1 and Hedgehog (Hh) inhibitors promise clinical efficacy against the Bcr-Ab T315I mutant form and leukaemia stem cells, respectively.
  • [MeSH-major] Drug Delivery Systems / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

  • MedlinePlus Health Information. consumer health - Chronic 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
  • (PMID = 19959093.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 88
  •  go-up   go-down


41. Krivtsov AV, Twomey D, Feng Z, Stubbs MC, Wang Y, Faber J, Levine JE, Wang J, Hahn WC, Gilliland DG, Golub TR, Armstrong SA: Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9. Nature; 2006 Aug 17;442(7104):818-22
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] Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9.
  • Here we show that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme.
  • The LSC were capable of transferring leukaemia to secondary recipient mice when only four cells were transferred, and possessed an immunophenotype and global gene expression profile very similar to that of normal granulocyte macrophage progenitors.
  • LSC can thus be generated from committed progenitors without widespread reprogramming of gene expression, and a leukaemia self-renewal-associated signature is activated in the process.
  • Our findings define progression from normal progenitor to cancer stem cell, and suggest that targeting a self-renewal programme expressed in an abnormal context may be possible.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. Cell Line. Cell Lineage. Granulocytes / cytology. Granulocytes / pathology. Humans. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Leukemia, Myelomonocytic, Acute / pathology. Macrophages / cytology. Macrophages / pathology. Mice. Neoplasm Transplantation. Survival Rate


42. Rujkijyanont P, Beyene J, Wei K, Khan F, Dror Y: Leukaemia-related gene expression in bone marrow cells from patients with the preleukaemic disorder Shwachman-Diamond syndrome. Br J Haematol; 2007 Jun;137(6):537-44
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] Leukaemia-related gene expression in bone marrow cells from patients with the preleukaemic disorder Shwachman-Diamond syndrome.
  • Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure disorder with cytopenia and a high propensity for myelodysplastic syndrome (MDS) and leukaemia, particularly acute myeloid leukaemia.
  • In accordance to the multi-hit theory of carcinogenesis, it is likely that several molecular and cellular hits occur before MDS/leukaemia become apparent.
  • Among 154 known leukaemia-related genes, several oncogenes were found to be upregulated, including LARG, TAL1 and MLL, and of several tumour suppressor genes were downregulated, including DLEU1, RUNX1, FANCD2 and DKC1.
  • We conclude that SDS marrow mononuclear cells exhibit abnormal gene expression patterns, which might result in continuous stimulation favouring evolution or progression of malignant clones.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / genetics. Male. Reverse Transcriptase Polymerase Chain Reaction. Syndrome


43. Kalff A, Shortt J, Farr J, McLennan R, Lui A, Scott J, Spencer A: Laboratory tumor lysis syndrome complicating LBH589 therapy in a patient with acute myeloid leukaemia. Haematologica; 2008 Jan;93(1):e16-7
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] Laboratory tumor lysis syndrome complicating LBH589 therapy in a patient with acute myeloid leukaemia.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Tumor Lysis Syndrome / etiology
  • [MeSH-minor] Disease Progression. Electrolytes / metabolism. Fatal Outcome. Humans. Indoles. Male. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18166770.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Electrolytes; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Indoles; 9647FM7Y3Z / panobinostat
  •  go-up   go-down


44. Bortul R, Tazzari PL, Billi AM, Tabellini G, Mantovani I, Cappellini A, Grafone T, Martinelli G, Conte R, Martelli AM: Deguelin, A PI3K/AKT inhibitor, enhances chemosensitivity of leukaemia cells with an active PI3K/AKT pathway. Br J Haematol; 2005 Jun;129(5):677-86
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] Deguelin, A PI3K/AKT inhibitor, enhances chemosensitivity of leukaemia cells with an active PI3K/AKT pathway.
  • We investigated whether or not deguelin could enhance the sensitivity to chemotherapeutic drugs of human U937 leukaemia cells and acute myeloid leukaemia (AML) blasts with an activated PI3K/Akt network.
  • Deguelin (10 nmol/l) induced S phase arrest with interference of progression to G2/M, and at 100 nmol/l significantly increased apoptotic cell death of U937.
  • At 10-100 nmol/l concentrations, deguelin downregulated Akt phosphorylation of leukaemia cells and markedly increased sensitivity of U937 cells to etoposide or cytarabine.
  • Overall, our results indicate that deguelin might be used in the future for increasing sensitivity to therapeutic treatments of leukaemia cells with an active PI3K/Akt signalling network.
  • [MeSH-major] Leukemia / drug therapy. Leukemia / enzymology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Rotenone / analogs & derivatives. Rotenone / therapeutic use
  • [MeSH-minor] Acute Disease. Antigens, CD34 / immunology. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Cell Line, Tumor. Cells, Cultured. Cytarabine / therapeutic use. Drug Resistance, Neoplasm / drug effects. Erythropoietin / pharmacology. Etoposide / therapeutic use. HL-60 Cells. Humans. Leukemia, Myeloid / drug therapy. Signal Transduction / drug effects. Stem Cell Factor / pharmacology. Stem Cells / drug effects. Stem Cells / immunology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. ROTENONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15916691.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Stem Cell Factor; 03L9OT429T / Rotenone; 04079A1RDZ / Cytarabine; 11096-26-7 / Erythropoietin; 6PLQ3CP4P3 / Etoposide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; K5Z93K66IE / deguelin
  •  go-up   go-down


45. Li H, Diao YT, Li HQ, Ma Q, Cui J, Zhou YZ, Li D: The association between serum levels of oxLDL-lgG and oxLDL-lgM autoantibody with adult acute myeloblastic leukaemia. Lipids Health Dis; 2010;9:11
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] The association between serum levels of oxLDL-lgG and oxLDL-lgM autoantibody with adult acute myeloblastic leukaemia.
  • AIM: To evaluate the relationship between serum antibodies against ox-LDL levels and adult acute myeloblastic leukemia (AML).
  • Future studies need to confirm the hypothesis whether they related to the development and progression of adult AML.
  • [MeSH-major] Autoantibodies / immunology. Immunoglobulin G / blood. Immunoglobulin M / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / immunology. Lipoproteins, LDL / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Disease Progression. Enzyme-Linked Immunosorbent Assay / methods. Female. Humans. Male. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arterioscler Thromb Vasc Biol. 2000 Jan;20(1):204-9 [10634819.001]
  • [Cites] Prog Lipid Res. 2003 Jul;42(4):318-43 [12689622.001]
  • [Cites] Circulation. 2003 Oct 28;108(17):2107-12 [14530200.001]
  • [Cites] Bratisl Lek Listy. 1990 Jan;91(1):70-6 [2322871.001]
  • [Cites] Clin Immunol. 2010 Jan;134(1):55-65 [19427818.001]
  • [Cites] Br J Cancer. 2006 Jan 16;94(1):156-60 [16404369.001]
  • [Cites] Clin Immunol. 2008 Jun;127(3):394-400 [18533284.001]
  • [Cites] Arch Med Res. 2008 Nov;39(8):760-7 [18996289.001]
  • [Cites] Nihon Koshu Eisei Zasshi. 1994 May;41(5):393-403 [8049507.001]
  • (PMID = 20113525.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lipoproteins, LDL; 0 / oxidized low density lipoprotein
  • [Other-IDs] NLM/ PMC2834680
  •  go-up   go-down


46. Kumar L, Gangadharan VP, Rao DR, Saikia T, Shah S, Malhotra H, Bapsy PP, Singh K, Rao R: Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India. Natl Med J India; 2005 Mar-Apr;18(2):66-70
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India.
  • BACKGROUND: Compared to hydroxyurea, treatment with interferon-alpha (IFN-alpha) is known to prolong survival in patients with chronic phase of chronic myelogenous leukaemia (CML) and was considered as first-line therapy till recently.
  • Nineteen patients had progression (blast crisis n=15, accelerated phase n=4) while on treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Natl Med J India. 2005 May-Jun;18(3):130
  • (PMID = 15981440.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b
  •  go-up   go-down


47. Bolufer P, Barragan E, Collado M, Cervera J, López JA, Sanz MA: Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression. Leuk Res; 2006 Dec;30(12):1471-91
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] Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression.
  • BACKGROUND: Recent studies have provided evidence that common genetic variations with low penetrance could account for a proportion of leukemia and could also influence disease outcome, although the results obtained are still controversial.
  • MATERIAL AND METHODS: We reviewed 54 recent reports focused on the contribution of genetic polymorphisms to the risk of developing leukemia and to disease progression.
  • RESULTS: There was a good agreement on the influence of NQO1*2 polymorphism and those of the enzymes involved in DNA repair with the increased risk of therapy-related leukemia/myelodysplastic syndrome.
  • Most studies found a strong association between the polymorphisms MTHFR, C677T or A1298C, and NQO1*2 or *3 and the risk of acute lymphoblastic leukemia (ALL).
  • In addition, most of the studies reported an association between GSTT1 deletions and an increased risk of de novo acute myeloid leukemia.
  • CONCLUSION: The reports reviewed support the hypothesis that several low-penetrance genes with multiplicative effects together with dietary effects, ambient exposition, and individual immune system responses, may account for the risk of leukaemia.
  • [MeSH-major] Enzymes / genetics. Leukemia / genetics. Polymorphism, Genetic
  • [MeSH-minor] Animals. DNA Repair / genetics. Disease Progression. Folic Acid / metabolism. Genetic Variation. Humans. Risk Factors

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. FOLIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Res. 2007 Apr;31(4):569-70 [17118446.001]
  • (PMID = 17023046.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzymes; 935E97BOY8 / Folic Acid
  • [Number-of-references] 112
  •  go-up   go-down


48. Jädersten M, Hellström-Lindberg E: Myelodysplastic syndromes: biology and treatment. J Intern Med; 2009 Mar;265(3):307-28
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This review focuses on low-risk MDS, for which chronic anaemia and eventual progression to acute myeloid leukaemia are the main concerns.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Blood Transfusion. Chromosomes, Human, Pair 5 / genetics. Disease Progression. Erythropoietin / therapeutic use. Female. Humans. Immunosuppressive Agents / therapeutic use. Iron Chelating Agents / therapeutic use. Male. Recombinant Proteins. Sequence Deletion. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use. World Health Organization


49. Teachey DT, Grupp SA, Brown VI: Mammalian target of rapamycin inhibitors and their potential role in therapy in leukaemia and other haematological malignancies. Br J Haematol; 2009 Jun;145(5):569-80
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] Mammalian target of rapamycin inhibitors and their potential role in therapy in leukaemia and other haematological malignancies.
  • The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that functions as a key regulator of cell growth, protein synthesis, and cell-cycle progression through interactions with a number of signalling pathways, including PI3K/AKT, ras, TCL1, and BCR/ABL.
  • Promising early clinical data suggests activity of mTOR inhibitors in a number of haematological diseases, including acute lymphoblastic leukaemia, chronic myeloid leukaemia, mantle cell lymphoma, anaplastic large cell lymphoma, and lymphoproliferative disorders.
  • This review describes the rationale for using mTOR inhibitors in a variety of haematological diseases with a focus on their use in leukaemia.
  • [MeSH-minor] Autoimmune Diseases / drug therapy. Autoimmune Diseases / metabolism. Humans. Leukemia / drug therapy. Leukemia / metabolism. Lymphoproliferative Disorders / drug therapy. Lymphoproliferative Disorders / metabolism. Signal Transduction / drug effects. TOR Serine-Threonine Kinases

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10314-9 [11504908.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10031-3 [11526226.001]
  • [Cites] Eur J Cancer. 2001 Nov;37(16):2121-8 [11597394.001]
  • [Cites] Clin Nephrol. 2002 Jul;58(1):77-8 [12141412.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):5027-34 [12208757.001]
  • [Cites] Oncogene. 2002 Sep 26;21(43):6587-97 [12242656.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3741-8 [12393602.001]
  • [Cites] Blood. 2003 Jan 1;101(1):278-85 [12393642.001]
  • [Cites] Transplantation. 2003 May 27;75(10):1710-7 [12777861.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Cancer Biol Ther. 2003 May-Jun;2(3):222-32 [12878853.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5716-22 [14522890.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15113-8 [14657335.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2737-46 [14576155.001]
  • [Cites] Cancer Treat Rev. 2004 Feb;30(1):37-51 [14766125.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3130-5 [14976243.001]
  • [Cites] Blood. 2004 May 15;103(10):3905-14 [14764536.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4268-75 [14976048.001]
  • [Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]
  • [Cites] Oncogene. 2004 Jul 29;23(34):5781-91 [15208671.001]
  • [Cites] Cell. 1993 May 7;73(3):487-97 [8343202.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4181-7 [15304393.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4188-93 [15319277.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):11-9 [15621776.001]
  • [Cites] Nat Genet. 2005 Jan;37(1):19-24 [15624019.001]
  • [Cites] Am J Pathol. 2006 Dec;169(6):2171-80 [17148679.001]
  • [Cites] Lab Invest. 2007 Jan;87(1):29-39 [17075574.001]
  • [Cites] Leukemia. 2007 Feb;21(2):333-9 [17136116.001]
  • [Cites] Dev Cell. 2007 Apr;12(4):487-502 [17419990.001]
  • [Cites] Nephrol Dial Transplant. 2007 May;22 Suppl 1:i27-35 [17456616.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4287-94 [17483341.001]
  • [Cites] Cancer. 2007 Sep 15;110(6):1178-86 [17701954.001]
  • [Cites] Lupus. 2007;16(10):775-81 [17895299.001]
  • [Cites] Trends Biochem Sci. 2005 Jan;30(1):35-42 [15653324.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1717-23 [15486067.001]
  • [Cites] J Pathol. 2005 Mar;205(4):498-506 [15714459.001]
  • [Cites] Br J Pharmacol. 2005 Mar;144(6):791-800 [15778701.001]
  • [Cites] FASEB J. 2005 Jun;19(8):960-2 [15784722.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1400-6 [15878982.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1801-7 [15886325.001]
  • [Cites] Haematologica. 2005 Oct;90(10):1433-4 [16219581.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2153-8 [16193082.001]
  • [Cites] Cell Cycle. 2005 Nov;4(11):1540-9 [16205124.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4261-8 [16150937.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):915-20 [16424025.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1149-55 [16195324.001]
  • [Cites] Cell. 2006 Feb 10;124(3):471-84 [16469695.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2305-13 [16489035.001]
  • [Cites] Drugs. 2006;66(4):547-70 [16597167.001]
  • [Cites] Blood. 2006 May 15;107(10):4053-62 [16418332.001]
  • [Cites] Nature. 2006 May 25;441(7092):424-30 [16724053.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6589-97 [16818631.001]
  • [Cites] Nat Rev Drug Discov. 2006 Aug;5(8):671-88 [16883305.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1668-76 [16645163.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5165-73 [16951235.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1965-71 [16757690.001]
  • [Cites] Br J Haematol. 2006 Sep;134(5):475-84 [16856892.001]
  • [Cites] Mol Cancer Ther. 2006 Oct;5(10):2522-30 [17041096.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):331-42 [17010674.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9963-70 [17942929.001]
  • [Cites] Blood. 2008 Jan 1;111(1):285-91 [17855629.001]
  • [Cites] Curr Treat Options Oncol. 2007 Aug;8(4):265-76 [18097642.001]
  • [Cites] Eur J Clin Invest. 2008 Jan;38(1):43-52 [18173550.001]
  • [Cites] Leukemia. 2008 Jan;22(1):147-60 [17928881.001]
  • [Cites] Leuk Lymphoma. 2008 Feb;49(2):359-61 [18231928.001]
  • [Cites] Pediatr Blood Cancer. 2008 Apr;50(4):799-805 [17635004.001]
  • [Cites] Blood. 2008 Mar 15;111(6):2962-72 [18332230.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1017-29 [18358929.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2384-90 [18381446.001]
  • [Cites] Transpl Int. 2008 Jun;21(6):605-8 [18282244.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2756-62 [18451242.001]
  • [Cites] Leuk Res. 2008 Sep;32(9):1417-23 [18395253.001]
  • [Cites] Autophagy. 2008 Jul;4(5):707-9 [18469512.001]
  • [Cites] Immunol Rev. 2008 Jun;223:371-90 [18613848.001]
  • [Cites] Ann Rheum Dis. 2008 Aug;67(8):1090-5 [18037627.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):508-14 [18543327.001]
  • [Cites] Blood. 2008 Sep 1;112(5):2020-3 [18544682.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3038-50 [18704194.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1698-706 [18548104.001]
  • [Cites] Hum Mol Genet. 2008 Oct 1;17(19):2934-48 [18614546.001]
  • [Cites] Clin Lymphoma Myeloma. 2008 Aug;8 Suppl 4:S137-43 [18952544.001]
  • [Cites] Hematol Oncol Clin North Am. 2008 Oct;22(5):807-23, vii [18954738.001]
  • [Cites] Hematol Oncol Clin North Am. 2008 Oct;22(5):953-63, ix [18954745.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2091-6 [18685609.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Dec;8(8):647-65 [19075588.001]
  • [Cites] Curr Med Chem. 2008;15(29):3036-51 [19075651.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2159-68 [18784743.001]
  • [Cites] Immunol Res. 2008;42(1-3):84-105 [18716718.001]
  • [Cites] Ann Hematol. 2009 Mar;88(3):221-7 [18704419.001]
  • [Cites] Leuk Res. 2009 Mar;33(3):450-9 [18783828.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1723-9 [19064730.001]
  • [Cites] Blood. 2009 Feb 26;113(9):1875-91 [18812465.001]
  • [Cites] Br J Haematol. 2009 Apr;145(1):101-6 [19208097.001]
  • [Cites] Clin Cancer Res. 2006 Nov 15;12(22):6826-35 [17121904.001]
  • [Cites] Semin Hematol. 2000 Jan;37(1):102-9 [10676915.001]
  • [Cites] Cell. 2000 Oct 13;103(2):253-62 [11057898.001]
  • [Cites] Pediatr Clin North Am. 2000 Dec;47(6):1291-310 [11130997.001]
  • (PMID = 19344392.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA104882; United States / NCI NIH HHS / CA / 1K08 CA1 04882-01A1; United States / NCI NIH HHS / CA / R01 CA102646; United States / NCI NIH HHS / CA / CA 1116660; United States / NCI NIH HHS / CA / K08 CA104882-01A1; United States / NCI NIH HHS / CA / CA 102646
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Number-of-references] 104
  • [Other-IDs] NLM/ NIHMS139949; NLM/ PMC2784662
  •  go-up   go-down


50. Kim HG, Kojima K, Swindle CS, Cotta CV, Huo Y, Reddy V, Klug CA: FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia. Blood; 2008 Feb 01;111(3):1567-74
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] FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.
  • The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML).
  • Compared with animals transplanted with only CBFbeta-SMMHC-expressing cells, FLT3-ITD further restricted early myeloid differentiation and promoted peripheralization of primitive myeloblasts as early as 2.5 weeks after transplantation.
  • FLT3-ITD also accelerated disease progression in all CBFbeta-SMMHC/FLT3-ITD-reconstituted animals, which died of a highly aggressive and transplantable AML within 3 to 5 months.
  • [MeSH-major] Chromosome Inversion / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Oncogene Proteins, Fusion / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Animals. Core Binding Factor beta Subunit / genetics. Core Binding Factor beta Subunit / metabolism. Disease Progression. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Lymphopoiesis. Mice. Mutation / genetics. Myelopoiesis. Smooth Muscle Myosins / genetics. Smooth Muscle Myosins / metabolism. Survival Rate

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Cancer Cell. 2006 Jan;9(1):57-68 [16413472.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12822-7 [10536006.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):723-33 [11179217.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Cancer Res. 2002 Apr 15;62(8):2232-5 [11956074.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Nat Struct Biol. 2002 Sep;9(9):674-9 [12172539.001]
  • [Cites] Blood. 2002 Dec 1;100(12):4154-61 [12393674.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):607-19 [12509458.001]
  • [Cites] Curr Opin Genet Dev. 2003 Feb;13(1):48-54 [12573435.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4342-6 [12560221.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 27;94(11):5697-702 [9159135.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11863-8 [9751756.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7432-43 [9819429.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7 Suppl):1789s-1793s [10197598.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):144-6 [10508507.001]
  • [Cites] Br J Haematol. 2005 Jan;128(1):18-34 [15606546.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):523-38 [12899708.001]
  • [Cites] Haematologica. 2004 Jan;89(1):106 [14754614.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4924-9 [15044690.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3200-7 [15070703.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4297-307 [15156186.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1213-25 [1827140.001]
  • [Cites] Virology. 1993 May;194(1):314-31 [8386878.001]
  • [Cites] Mol Cell Biol. 1993 Jun;13(6):3324-39 [8497254.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Blood. 1995 May 1;85(9):2289-302 [7727763.001]
  • [Cites] J Exp Med. 1996 Jan 1;183(1):187-94 [8551222.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1630-5 [8643682.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8508-11 [8710900.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12359-63 [8901586.001]
  • [Cites] Cell. 1996 Nov 15;87(4):687-96 [8929537.001]
  • [Cites] J Biol Chem. 2005 Dec 2;280(48):40097-103 [16199529.001]
  • (PMID = 17967943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK067186; United States / NCI NIH HHS / CA / R01 CA096798; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NCI NIH HHS / CA / R01CA96798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / Smooth Muscle Myosins
  • [Other-IDs] NLM/ PMC2214774
  •  go-up   go-down


51. Neukirchen J, Blum S, Kuendgen A, Strupp C, Aivado M, Haas R, Aul C, Gattermann N, Germing U: Platelet counts and haemorrhagic diathesis in patients with myelodysplastic syndromes. Eur J Haematol; 2009 Nov;83(5):477-82
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.
  • Platelets lower than 100 000/microL were associated with significantly shortened survival (P < 0.00005), because of an increased risk of progression to acute myeloid leukaemia (AML) (30% vs. 21%) (P < 0.02) and bleeding (16% vs. 8%) (P = 0.0005).
  • [MeSH-minor] Disease-Free Survival. Female. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Platelet Transfusion. Predictive Value of Tests. Registries. Retrospective Studies. Survival Rate. Thrombocytopenia / blood. Thrombocytopenia / complications. Thrombocytopenia / mortality. Thrombocytopenia / therapy


52. Suemitsu R, Fukuyama S, Ondo K, Ueda H: Resection of mediastinal granulocytic sarcoma triggered the rapid progression of acute myeloid leukemia. Ann Thorac Cardiovasc Surg; 2008 Jun;14(3):181-3
MedlinePlus Health Information. consumer health - Thymus Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resection of mediastinal granulocytic sarcoma triggered the rapid progression of acute myeloid leukemia.
  • We experienced a case of acute myeloid leukemia (AML) that took a rapid turn for the worse after the resection of a mediastinal GS.
  • The immunohistological findings showed the features of leukemia, and GS was diagnosed.
  • Despite chemotherapy, the patient died on POD 28 as a result of rapid disease progression.
  • [MeSH-major] Diagnostic Errors. Leukemia, Myeloid, Acute / pathology. Mediastinal Neoplasms / pathology. Sarcoma, Myeloid / pathology. Thymectomy / adverse effects. Thymoma / pathology. Thymus Neoplasms / pathology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Sternum / surgery. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Myeloid sarcoma.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18577899.001).
  • [ISSN] 1341-1098
  • [Journal-full-title] Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia
  • [ISO-abbreviation] Ann Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


53. Konieczna I, Horvath E, Wang H, Lindsey S, Saberwal G, Bei L, Huang W, Platanias L, Eklund EA: Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia. J Clin Invest; 2008 Mar;118(3):853-67
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] Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia.
  • Development of a block in myeloid differentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor prognosis.
  • Interferon consensus sequence binding protein (ICSBP, also known as IRF8) is an interferon-regulatory transcription factor that functions as a leukemia tumor suppressor.
  • Since activity of ICSBP is influenced by tyrosine phosphorylation state, we hypothesized that mutations in molecular pathways that regulate this process might synergize with ICSBP deficiency for progression to AML.
  • Consistent with this, we found that constitutive activation of SHP2 protein tyrosine phosphatase synergized with ICSBP haploinsufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid progression to AML in a murine bone marrow transplantation model.
  • Constitutive SHP2 activation cooperated with ICSBP deficiency to increase the number of progenitors in the bone marrow and myeloid blasts in circulation, indicating a block in differentiation.
  • Since SHP2 activation and ICSBP deficiency may coexist in human myeloid malignancies, our studies have identified a molecular mechanism potentially involved in disease progression in such diseases.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. L-TYROSINE .
  • 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
  • [Cites] Nucleic Acids Res. 2005;33(21):6895-905 [16396836.001]
  • [Cites] Blood. 2005 Sep 15;106(6):1938-47 [15947094.001]
  • [Cites] Mol Cell Biol. 2006 Sep;26(17):6311-32 [16914719.001]
  • [Cites] J Biol Chem. 2007 Jan 26;282(4):2237-49 [17138561.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6629-43 [17200120.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Jun;46(6):517-21 [17330262.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3764-71 [10572090.001]
  • [Cites] J Biol Chem. 2000 Mar 31;275(13):9773-81 [10734131.001]
  • [Cites] J Immunol. 2000 Jul 1;165(1):271-9 [10861061.001]
  • [Cites] Nat Immunol. 2000 Aug;1(2):169-76 [11248811.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3648-50 [11369663.001]
  • [Cites] J Biol Chem. 2001 Oct 12;276(41):37868-78 [11483597.001]
  • [Cites] Cancer Cell. 2002 Jun;1(5):479-92 [12124177.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14925-30 [12417757.001]
  • [Cites] Cytokines Cell Mol Ther. 2002 Dec;7(2):75-82 [12607798.001]
  • [Cites] Nat Genet. 2003 Jun;34(2):148-50 [12717436.001]
  • [Cites] J Immunol. 1980 Jul;125(1):6-12 [7381211.001]
  • [Cites] Nature. 1989 Jun 29;339(6227):718-21 [2662014.001]
  • [Cites] Genes Dev. 1991 May;5(5):868-79 [1851123.001]
  • [Cites] Mol Cell Biol. 1993 Jan;13(1):588-99 [7678054.001]
  • [Cites] J Virol Methods. 1995 Aug;54(2-3):131-43 [8530565.001]
  • [Cites] Cell. 1996 Oct 18;87(2):307-17 [8861914.001]
  • [Cites] J Biol Chem. 1997 Apr 11;272(15):9785-92 [9092512.001]
  • [Cites] Blood. 1998 Jan 1;91(1):22-9 [9414265.001]
  • [Cites] J Biol Chem. 1998 May 29;273(22):13957-65 [9593745.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50874-85 [15371411.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):8816-20 [15604238.001]
  • [Cites] J Biol Chem. 2005 Sep 2;280(35):30984-93 [15987685.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3279-87 [16278304.001]
  • (PMID = 18246201.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095266; United States / NCI NIH HHS / CA / R01-CA095266
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-8; 42HK56048U / Tyrosine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2214847
  •  go-up   go-down


54. Nakamura S, Hirano I, Okinaka K, Takemura T, Yokota D, Ono T, Shigeno K, Shibata K, Fujisawa S, Ohnishi K: The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia. Carcinogenesis; 2010 Nov;31(11):2012-21
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] The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia.
  • However, it is not clearly understood how FOXM1 contributes to acute myeloid leukemia (AML) cell proliferation.
  • In summary, we found that FOXM1B mRNA is predominantly expressed in AML cells and that aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.
  • [MeSH-major] Cell Cycle. Cell Cycle Proteins / metabolism. Cell Proliferation. Forkhead Transcription Factors / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adult. Aged. Aldehyde Dehydrogenase / genetics. Aldehyde Dehydrogenase / metabolism. Apoptosis. Aurora Kinase B. Aurora Kinases. Blotting, Western. Cells, Cultured. Cyclin B1 / genetics. Cyclin B1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Disease Progression. Fluorescent Antibody Technique. Humans. Inhibitor of Apoptosis Proteins. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocytes / metabolism. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Middle Aged. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. S-Phase Kinase-Associated Proteins / genetics. S-Phase Kinase-Associated Proteins / metabolism

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20823107.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / CCNB1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


55. Hentschel N, Krusch M, Kiener PA, Kolb HJ, Salih HR, Schmetzer HM: Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma. Eur J Haematol; 2006 Aug;77(2):91-101
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] Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma.
  • Recently, we demonstrated that low levels of soluble (s) CD137L and high levels of sCD178 correlate significantly with a long progression free survival in patients with myelodysplastic syndrome (MDS).
  • In this study, we correlated sCD137L and sCD178 levels in sera of 42 samples of patients with acute myeloid leukemia (AML) and 46 samples of patients with non-Hodgkin's lymphoma (NHL) with stages, subtypes, and the clinical course of the diseases and determined cut-off values with maximum probability for significant differentiation between cases with higher/lower probability for progress free survival.
  • Furthermore, in AML patients sCD137L levels correlate significantly with the probabilities to achieve complete remission (CR), stay in CR or with progress of the disease.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid / blood. Lymphoma, Non-Hodgkin / blood. Membrane Glycoproteins / blood. Neoplasm Proteins / blood. Tumor Necrosis Factors / blood
  • [MeSH-minor] 4-1BB Ligand. Acute Disease. Adult. Aged. Aged, 80 and over. Blast Crisis / blood. Child, Preschool. Disease Progression. Disease-Free Survival. Fas Ligand Protein. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Lymphoma, B-Cell / blood. Lymphoma, T-Cell / blood. Male. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Prognosis. Retrospective Studies. Solubility. Survival Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16800841.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-1BB Ligand; 0 / Biomarkers, Tumor; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / TNFSF9 protein, human; 0 / Tumor Necrosis Factors
  •  go-up   go-down


56. Loaiza-Bonilla A, Gore SD, Carraway HE: Novel approaches for myelodysplastic syndromes: beyond hypomethylating agents. Curr Opin Hematol; 2010 Mar;17(2):104-9
Hazardous Substances Data Bank. THALIDOMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DNA methyltransferase inhibitors are well tolerated in outpatient settings, with azacitidine prolonging survival and decreasing time to acute myeloid leukemia progression in patients with high-risk myelodysplastic syndromes.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20178141.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / L30 CA111124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoates; 0 / Enzyme Inhibitors; 0 / Hydrazines; 0 / Pyrazoles; 0 / eltrombopag; 4Z8R6ORS6L / Thalidomide; EC 2.1.1.- / Methyltransferases; F0P408N6V4 / lenalidomide
  • [Number-of-references] 48
  •  go-up   go-down


57. Cocco L, Manzoli L, Palka G, Martelli AM: Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia. Adv Enzyme Regul; 2005;45:126-35
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] Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia.
  • PLC beta1 is a well-known example, given that it has been shown that only the enzyme located in the nucleus targets the cyclin D3/cdk4 complex, playing, in turn, a key role in the control of normal progression through the G1 phase of the cell cycle.
  • Moreover, non-specific alterations in chromosome 20 have been found in patients affected by MDS and acute myeloid leukemia AML.
  • The availability of a highly specific probe gave an opportunity to perform in patients affected with MDS/AML, associated with normal karyotype, painting and FISH analysis aimed to check the PLC beta1 gene, given that this signaling molecule is a key player in the control of some checkpoints of the normal progression through the cell cycle.
  • The reported data strengthen the contention of a key role played by PLC beta1 in the nucleus, suggest a possible involvement of PLC beta1 in the progression of MDS to AML and pave the way for a larger investigation aimed at identifying a possible high risk group among MDS patients with a normal karyotype.
  • [MeSH-major] Cell Cycle / physiology. Cell Nucleus / enzymology. Isoenzymes / physiology. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology. Type C Phospholipases / physiology
  • [MeSH-minor] Acute Disease. Gene Deletion. Humans. Phospholipase C beta. Signal Transduction / physiology


58. Vyas P, Sternberg A: Characterization of the hemopoietic defect in early stages of the myelodysplastic syndromes. Adv Enzyme Regul; 2006;46:98-112
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.
  • Myelodysplasia (MDS) is a heterogeneous disorder characterised by bone marrow failure and progression to acute myeloid leukaemia where the molecular and cellular haematopoietic defects are poorly understood.


59. Gore SD, Hermes-DeSantis ER: Enhancing survival outcomes in the management of patients with higher-risk myelodysplastic syndromes. Cancer Control; 2009 Oct;16 Suppl:2-10
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 myelodysplastic syndromes (MDS) are a collection of clonal myeloid neoplasms characterized by bone marrow failure and cytopenias.
  • The most significant treatment goals in these patients involve prolonging the time to acute myeloid leukemia progression and extending overall survival.


60. Buccisano F, Maurillo L, Tamburini A, Del Poeta G, Del Principe MI, Ammatuna E, Consalvo MI, Campagna S, Ottaviani L, Sarlo C, Renzi D, Faccia S, Fraboni D, Lo Coco F, Amadori S, Venditti A: Evaluation of the prognostic relevance of L-selectin and ICAM1 expression in myelodysplastic syndromes. Eur J Haematol; 2008 Feb;80(2):107-14
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.
  • OBJECTIVES: An aberrant pattern of expression of L-selectin and intercellular adhesion molecule 1 (ICAM1) may characterise CD34+ blast cells in myelodysplastic syndromes (MDS) and secondary acute myeloid leukaemia (sAML).
  • RESULTS: The ratio of L-selectin/ICAM1 expression was identified as a parameter correlated with the percentage of BM blast infiltration and the time to leukaemic progression among MDS patients.
  • Furthermore, MDS patients with a baseline ratio <1 had a higher leukaemic progression rate (41% vs. 19%, P = 0.008); the actuarial risk of disease progression for this subgroup of MDS patients was also higher (64% vs. 11% at 2 yr, P = 0.002).
  • (ii) the ratio of their expression has a prognostic role; and (iii) a ratio <1 significantly predicts progression to overt leukaemia in MDS patients.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Bone Marrow / metabolism. Disease Progression. Female. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / metabolism. Male. Middle Aged. Prognosis. Time Factors

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • 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 = 18028430.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin
  •  go-up   go-down


61. Heilig CE, Löffler H, Mahlknecht U, Janssen JW, Ho AD, Jauch A, Krämer A: Chromosomal instability correlates with poor outcome in patients with myelodysplastic syndromes irrespectively of the cytogenetic risk group. J Cell Mol Med; 2010 Apr;14(4):895-902
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.
  • As for aneuploidy itself, the role of CIN in the evolution and progression of malignancy is a matter still open to debate.
  • Thereby, CIN was measured in 65 patients with myelodysplastic syndromes (MDS), acute myeloid leukaemia (AML) and control subjects.
  • In conclusion, elevated CIN levels may be valuable as an early indicator of poor prognosis in MDS, hence corroborating the concept of CIN as a driving force in tumour progression.
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Risk Factors. Treatment Outcome. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • 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
  • (PMID = 19754665.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3823121
  •  go-up   go-down


62. Wolanskyj AP, Lasho TL, Schwager SM, McClure RF, Wadleigh M, Lee SJ, Gilliland DG, Tefferi A: JAK2 mutation in essential thrombocythaemia: clinical associations and long-term prognostic relevance. Br J Haematol; 2005 Oct;131(2):208-13
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.
  • During this period, thrombotic complications were documented in 62 patients (41.3%) and transformation into acute myeloid leukaemia (AML), polycythaemia vera (PV), or myelofibrosis with myeloid metaplasia (MMM) occurred in 4 (2.7%), 8 (5.3%), and 15 (10%) patients, respectively.
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Hemoglobins / analysis. Humans. Janus Kinase 2. Leukemia, Myeloid, Acute / genetics. Leukocyte Count. Male. Middle Aged. Multivariate Analysis. Polycythemia Vera / genetics. Primary Myelofibrosis / genetics. Risk Factors. Thrombosis / complications

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16197451.001).
  • [ISSN] 0007-1048
  • [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 / Hemoglobins; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


63. Jelínek F, Sobotková E, Vonka V: Characteristics of two mouse bcr-abl-transformed cell lines. II. Pathological lesions induced in mice. Folia Biol (Praha); 2005;51(4):93-102
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.
  • We classified the disease induced by both of the cell lines as acute myeloid undifferentiated leukaemia (AML MO).
  • [MeSH-major] Cell Line, Transformed. Cell Transformation, Neoplastic / genetics. Genes, abl. Leukemia, Myeloid / pathology. Neoplasms, Experimental / pathology
  • [MeSH-minor] Acute Disease. Animals. Disease Progression. Endothelial Cells / pathology. Female. Immunohistochemistry. Leukemic Infiltration. Lung / pathology. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Spine / pathology. Spleen / immunology. Spleen / pathology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16180544.001).
  • [ISSN] 0015-5500
  • [Journal-full-title] Folia biologica
  • [ISO-abbreviation] Folia Biol. (Praha)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  •  go-up   go-down


64. Papadavid E, Panayiotides I, Katoulis A, Pappa V, Dervenoulas I, Stavrianeas N: Stasis dermatitis-like leukaemic infiltration in a patient with myelodysplastic syndrome. Clin Exp Dermatol; 2008 May;33(3):298-300
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report a case of leukaemia cutis presenting as stasis dermatitis-like eruption in a patient with myelodysplastic syndrome progressing to acute myelogenic leukaemia.
  • [MeSH-major] Dermatitis / pathology. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration / pathology. Myelodysplastic Syndromes / pathology. Skin / pathology
  • [MeSH-minor] Aged, 80 and over. Disease Progression. Fatal Outcome. Humans. Hyperpigmentation / etiology. Hyperpigmentation / pathology. Male

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18261141.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


65. Leung EW, Rujkijyanont P, Beyene J, Wei K, Abdelhaleem M, Freedman MH, Dror Y: Shwachman-Diamond syndrome: an inherited model of aplastic anaemia with accelerated angiogenesis. Br J Haematol; 2006 Jun;133(5):558-61
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.
  • Bone marrow angiogenesis is increased in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but has not been studied in inherited or acquired marrow failure syndromes.
  • Future studies should investigate the mechanism for increased angiogenesis in SDS, and whether SDS marrow, with its increased angiogenesis, promotes progression of malignant clones.
  • [MeSH-minor] Acute Disease. Adolescent. Anemia, Aplastic / genetics. Anemia, Aplastic / pathology. Bone Marrow Cells / pathology. Child. Child, Preschool. Female. Gene Expression / genetics. Humans. Infant. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Neovascularization, Pathologic / genetics. Syndrome. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism


66. Sirohi B, Cunningham D, Powles R, Murphy F, Arkenau T, Norman A, Oates J, Wotherspoon A, Horwich A: Long-term outcome of autologous stem-cell transplantation in relapsed or refractory Hodgkin's lymphoma. Ann Oncol; 2008 Jul;19(7):1312-9
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.
  • Median overall survival (OS)/progression-free survival (PFS) from ASCT was 9 years/2.9 years.
  • Twenty (10%) patients developed second cancer (seven secondary acute myeloid leukaemia (AML)/myelodysplastic syndrome (MDS)).

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. Carmustine .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18356139.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q41OR9510P / Melphalan; U68WG3173Y / Carmustine
  •  go-up   go-down


67. Paupert J, Mansat-De Mas V, Demur C, Salles B, Muller C: Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features. Cell Cycle; 2008 Apr 15;7(8):1047-53
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] Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features.
  • The importance of this variant pro-form in tumor progression remains poorly defined.
  • We previously showed that the DNA repair protein Ku interacts at the cell surface of leukaemia cell lines with the 85 Kda pro-form of MMP-9 and these Ku/MMP-9 complexes regulates cell invasion, highlighting their importance in haematological malignancies.
  • We demonstrate here that all samples of acute myeloid leukaemia (AML) blasts purified from bone marrow of 16 affected patients express the 85 Kda form of MMP-9.
  • These results might have important functional significance in the occurrence of extra-medullar infiltrates of leukaemia cells that occurs frequently during the onset of monocyte-related AML sub-types.
  • [MeSH-major] DNA Helicases / metabolism. Leukemia, Myeloid, Acute / metabolism. Matrix Metalloproteinase 9 / metabolism. Membrane Proteins / metabolism. Monocytes / metabolism. Neoplasm Invasiveness / physiopathology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18414048.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / XRCC5 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.4.- / DNA Helicases
  •  go-up   go-down


68. Chehensse C, Braun T, Morin AS, Stirnemann J, Agranat P, Boukari L, Aras N, Kiladjian JJ, Ziol M, Fenaux P, Fain O: [Extramedullary blastic transformation revealed by a prolonged fever during the course of a 5q- syndrome]. Rev Med Interne; 2009 Oct;30(10):886-9
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INTRODUCTION: Fever during a myelodysplastic syndrome can be due to infectious complications, systemic disease or acute transformation with clonal evolution.
  • Neither bone marrow nor blood blasts were detected, but liver biopsy demonstrated significant blast infiltration compatible with the diagnosis of acute myeloid leukaemia (AML).
  • Tissue biopsy may be necessary to confirm the leukaemic progression.

  • Genetic Alliance. consumer health - 5q- Syndrome.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Fever.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19748163.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


69. Bai J, Xue Y, Ye L, Yao J, Zhou C, Shao Z, Qian L, Yang R, Li H, Zhang H, Zheng Y: Risk factors of long-term incidences of thrombosis, myelofibrosis and evolution into malignance in polycythemia vera: a single center experience from China. Int J Hematol; 2008 Dec;88(5):530-5
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.
  • To find out risk factors of incidences of long-term complications of thrombosis, myelofibrosis with myeloid metaplasia (MMM) and evolution into malignance in Chinese PV patients, we evaluated 320 PV patients referred to our center from April 1984 to June 2005 by Kaplan-Meier estimation and Cox proportional hazards models.
  • A total of 43 patients progressed into MMM at a median time of 84 (7-240) months, higher white blood cell (WBC) count, splenomegaly, receiving alkylating agent and hydroxycarbamide were associated with the progression into MMM.
  • During the follow-up time, 11 and 2 patients died of fatal complications of thrombosis and acute myeloid leukaemia (AML), respectively.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Polycythemia Vera / mortality. Primary Myelofibrosis / mortality. Thromboembolism / mortality


70. Stefanowicz J, Grabiec-Wiśniewska A, Stachowicz-Stencel T, Adamkiewicz-Drozyńska E, Bień E, Kaczorowska-Hać B, Połczyńska K, Szołkiewicz A, Sierota D, Maciejka-Kapuścińska L, Płoszyńska A, Izycka-Swieszewska E, Szutowicz E, Czauderna P, Reiter M, Hennig M, Balcerska A: [Second neoplasms in children with solid tumours in the years 1992-2007. Experiences of Gdańsk medical academy]. Med Wieku Rozwoj; 2008 Oct-Dec;12(4 Pt 2):1141-7
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.
  • The second neoplasms were: acute non lymphoblastic leukaemia - 2, soft tissue sarcoma - 2, osteosarcoma - 2, chondrosarcoma - 1, renal cell carcinoma - 1 and glioblastoma multiforme - 1 case.
  • Treatment failed in 5 out of 9 children treated for osteosarcoma (2/2), chondrosarcoma (1/1), soft tissue sarcoma (1/2) and acute non lymphoblastic leukaemia (1/2).
  • These patients died of progression of neoplastic disease during 2 to 20 months after the diagnosis of the second tumour.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Neoplasms, Neuroepithelial / epidemiology. Neoplasms, Second Primary / epidemiology. Sarcoma / epidemiology. Wilms Tumor / epidemiology
  • [MeSH-minor] Adolescent. Adult. Child. Disease Progression. Female. Humans. Incidence. Male. Poland / epidemiology. Prognosis. Young Adult


71. Capello D, Deambrogi C, Rossi D, Lischetti T, Piranda D, Cerri M, Spina V, Rasi S, Gaidano G, Lunghi M: Epigenetic inactivation of suppressors of cytokine signalling in Philadelphia-negative chronic myeloproliferative disorders. Br J Haematol; 2008 May;141(4):504-11
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 investigated epigenetic and genetic inactivation of SOCS3, SOCS1 and PTPN6 in 112 CMPD and 20 acute myeloid leukaemia (AML) post-CMPD.
  • [MeSH-minor] Chronic Disease. DNA Methylation. Disease Progression. Humans. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Philadelphia Chromosome. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / genetics. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Signal Transduction

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18318760.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / SOCS1 protein, human; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
  •  go-up   go-down


72. Ponassi R, Biasotti B, Tomati V, Bruno S, Poggi A, Malacarne D, Cimoli G, Salis A, Pozzi S, Miglino M, Damonte G, Cozzini P, Spyrakis F, Campanini B, Bagnasco L, Castagnino N, Tortolina L, Mumot A, Frassoni F, Daga A, Cilli M, Piccardi F, Monfardini I, Perugini M, Zoppoli G, D'Arrigo C, Pesenti R, Parodi S: A novel Bim-BH3-derived Bcl-XL inhibitor: biochemical characterization, in vitro, in vivo and ex-vivo anti-leukemic activity. Cell Cycle; 2008 Oct;7(20):3211-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The antiapoptotic molecule Bcl-X(L), involved in cancer development/progression and tumour resistance to cytotoxic drugs, is a target for Bim.
  • Multiparameter flow cytometry demonstrated that the 072RB dose-dependent growth inhibition of leukaemia cell lines was due to apoptotic cell death.
  • Ex-vivo derived leukemic cells from acute myeloid leukaemia (AML) patients underwent cell death when cultured in vitro in the presence of 072RB.
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis / physiology. Cells, Cultured. Female. Humans. Leukemia, Myeloid, Acute / metabolism. Lymphocytes / cytology. Lymphocytes / physiology. Mice. Mice, Inbred NOD. Mice, SCID. Molecular Sequence Data. Neoplasm Transplantation. Protein Structure, Tertiary. Transplantation, Heterologous. Tumor Cells, Cultured. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Cell Cycle. 2008 Oct;7(20):3111 [18843203.001]
  • [ErratumIn] Cell Cycle. 2012 Oct 1;11(19):3703. Spyraki, Francesca [corrected to Spyrakis, Francesca]
  • (PMID = 18843207.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 072RB peptide; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / Peptides; 0 / Proto-Oncogene Proteins; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein
  •  go-up   go-down


73. Jabbour EJ, Giles FJ: New agents in myelodysplastic syndromes. Curr Hematol Rep; 2005 May;4(3):191-9
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.
  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic disorders characterized by ineffective hematopoiesis resulting in peripheral cytopenia and by increased progression to acute myeloid leukemia (AML).

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15865871.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Arsenicals; 0 / Benzamides; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Growth Substances; 0 / Immunosuppressive Agents; 0 / Oligonucleotides, Antisense; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; M801H13NRU / Azacitidine
  • [Number-of-references] 89
  •  go-up   go-down


74. Parker TM, Klaassen RJ, Johnston DL: Spontaneous remission of myelodysplastic syndrome with monosomy 7 in a young boy. Cancer Genet Cytogenet; 2008 Apr 15;182(2):122-5
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.
  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder that often results in progression to acute myeloid leukemia (AML), particularly when additional genetic abnormalities are present, such as monosomy 7.


75. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 8. Clone Cells. Disease Progression. Humans. Male. Mutation. Neoplasms, Second Primary. Trisomy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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
  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  •  go-up   go-down


76. Issa JP: Epigenetic changes in the myelodysplastic syndrome. Hematol Oncol Clin North Am; 2010 Apr;24(2):317-30
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.
  • Myelodysplastic syndrome (MDS) is characterized by frequent epigenetic abnormalities, including the hypermethylation of genes that control proliferation, adhesion, and other characteristic features of this leukemia.
  • Aberrant DNA hypermethylation is associated with a poor prognosis in MDS that can be accounted for by more rapid progression to acute myeloid leukemia.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • [Cites] Cell. 2004 Jan 23;116(2):259-72 [14744436.001]
  • [Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147.001]
  • [Cites] Nature. 2004 May 27;429(6990):457-63 [15164071.001]
  • [Cites] Mol Cell Biol. 2004 Jun;24(12):5475-84 [15169908.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1266-9 [15155466.001]
  • [Cites] EMBO J. 2004 Oct 13;23(20):4061-71 [15385962.001]
  • [Cites] Cell. 1980 May;20(1):85-93 [6156004.001]
  • [Cites] Nature. 1983 Jan 6;301(5895):89-92 [6185846.001]
  • [Cites] Cell. 1985 Mar;40(3):485-6 [2578884.001]
  • [Cites] J Biol Chem. 1985 Jul 25;260(15):8653-6 [4019444.001]
  • [Cites] J Biol Chem. 1986 Feb 5;261(4):1594-8 [2418016.001]
  • [Cites] Cell. 1988 Apr 8;53(1):3-4 [3280142.001]
  • [Cites] Am J Hum Genet. 1991 May;48(5):880-8 [1673287.001]
  • [Cites] Leukemia. 1993 Feb;7(2):263-7 [8426480.001]
  • [Cites] J Natl Cancer Inst. 1993 Aug 4;85(15):1235-40 [8331684.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):8891-5 [8415627.001]
  • [Cites] Nature. 1993 Nov 25;366(6453):362-5 [8247133.001]
  • [Cites] Environ Health Perspect. 1993 Dec;101 Suppl 5:169-72 [8013405.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):9700-4 [7937876.001]
  • [Cites] J Biol Chem. 1995 Jan 27;270(4):1595-601 [7829490.001]
  • [Cites] Science. 1995 Dec 8;270(5242):1610-3 [7502071.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10366-70 [8816806.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):808-11 [9041175.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1403-9 [9269757.001]
  • [Cites] Mutat Res. 1997 Sep 5;379(1):33-41 [9330620.001]
  • [Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]
  • [Cites] Annu Rev Genet. 1997;31:571-610 [9442908.001]
  • [Cites] Cancer Res. 1998 Feb 15;58(4):591-3 [9485004.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2985-90 [9531610.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6870-5 [9618505.001]
  • [Cites] Nature. 1998 Sep 3;395(6697):89-93 [9738504.001]
  • [Cites] Leuk Res. 2008 Oct;32(10):1541-5 [18367246.001]
  • [Cites] Cancer. 2008 Sep 15;113(6):1351-61 [18618511.001]
  • [Cites] Nat Cell Biol. 2008 Nov;10(11):1291-300 [18931660.001]
  • [Cites] Nat Rev Genet. 2009 Jan;10(1):32-42 [19065135.001]
  • [Cites] Blood. 2009 Feb 5;113(6):1315-25 [18832655.001]
  • [Cites] Cancer Lett. 2009 Aug 8;280(2):192-200 [19345475.001]
  • [Cites] Gastroenterology. 2009 Jun;136(7):2149-58 [19375421.001]
  • [Cites] Clin Cancer Res. 2009 Jun 15;15(12):3938-46 [19509174.001]
  • [Cites] Br J Haematol. 2009 Jun;145(6):788-800 [19388938.001]
  • [Cites] Blood. 2009 Oct 15;114(16):3448-58 [19652201.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):605-13 [20038729.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2865-8 [11675364.001]
  • [Cites] Nature. 2001 Nov 15;414(6861):277-83 [11713521.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8094-9 [11719434.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Nature. 2002 Apr 4;416(6880):552-6 [11932749.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Curr Opin Cell Biol. 2002 Jun;14(3):286-98 [12067650.001]
  • [Cites] Genes Dev. 2002 Jul 15;16(14):1739-42 [12130533.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5400-13 [12154403.001]
  • [Cites] Nature. 2002 Sep 26;419(6905):407-11 [12353038.001]
  • [Cites] Adv Cancer Res. 2002;86:41-65 [12374280.001]
  • [Cites] Nature. 2002 Oct 10;419(6907):624-9 [12374981.001]
  • [Cites] Leukemia. 2002 Nov;16(11):2177-84 [12399959.001]
  • [Cites] Int J Hematol. 2002 Aug;76 Suppl 2:228-38 [12430930.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6456-61 [12438235.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):206-15 [12482974.001]
  • [Cites] Haematologica. 2002 Dec;87(12):1324-41 [12495905.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7213-8 [12499261.001]
  • [Cites] Leuk Res. 2003 Feb;27(2):95-120 [12526916.001]
  • [Cites] Cancer Cell. 2003 Jan;3(1):89-95 [12559178.001]
  • [Cites] Blood Rev. 2003 Jun;17(2):71-97 [12642121.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):1062-5 [12648079.001]
  • [Cites] Genomics. 1998 Nov 1;53(3):260-8 [9799591.001]
  • [Cites] Science. 1999 Jan 15;283(5400):387-90 [9888853.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Nat Genet. 1999 Feb;21(2):163-7 [9988266.001]
  • [Cites] Nucleic Acids Res. 1999 Jun 1;27(11):2291-8 [10325416.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2302-6 [10344733.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8681-6 [10411935.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):673-8 [15637150.001]
  • [Cites] Br J Haematol. 2005 Apr;129(1):60-5 [15801956.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1367-75 [15902282.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):23-32 [16343268.001]
  • [Cites] Nat Med. 2007 Jan;13(1):78-83 [17159988.001]
  • [Cites] Mol Cell. 2007 Feb 9;25(3):473-81 [17289593.001]
  • [Cites] Exp Hematol. 2007 Mar;35(3):394-406 [17309820.001]
  • [Cites] Cell. 2007 Feb 23;128(4):669-81 [17320505.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1997-2005 [17332327.001]
  • [Cites] Genes Dev. 2007 May 1;21(9):1050-63 [17437993.001]
  • [Cites] Clin Cancer Res. 2007 Jul 15;13(14):4225-32 [17634552.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):7107-12 [18056190.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1060-6 [17962510.001]
  • [Cites] Nat Genet. 2008 Jun;40(6):741-50 [18488029.001]
  • [Cites] Semin Cancer Biol. 1999 Oct;9(5):339-47 [10547342.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):88-91 [10615135.001]
  • [Cites] Leukemia. 2000 Apr;14(4):586-93 [10764143.001]
  • [Cites] Nat Genet. 2000 Jul;25(3):269-77 [10888872.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):148-54 [11167795.001]
  • [Cites] Ann Intern Med. 2001 Apr 3;134(7):573-86 [11281740.001]
  • [Cites] Curr Opin Cell Biol. 2001 Jun;13(3):263-73 [11343896.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] Br J Haematol. 2001 Aug;114(2):349-57 [11529854.001]
  • [Cites] J Biol Chem. 2001 Sep 28;276(39):36734-41 [11473107.001]
  • [Cites] Jpn J Clin Oncol. 2003 Apr;33(4):153-60 [12810828.001]
  • [Cites] Cancer. 2003 Aug 1;98(3):522-8 [12879469.001]
  • [Cites] Curr Opin Pharmacol. 2003 Aug;3(4):344-51 [12901942.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1813-9 [12970781.001]
  • [Cites] Semin Hematol. 2003 Oct;40(4):268-73 [14582077.001]
  • [Cites] Science. 2003 Nov 14;302(5648):1153; author reply 1153 [14615517.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Mol Cell. 2003 Dec;12(6):1577-89 [14690609.001]
  • [Cites] Mol Cell. 2003 Dec;12(6):1591-8 [14690610.001]
  • [Cites] Blood. 2004 Jan 15;103(2):698-700 [14504087.001]
  • (PMID = 20359628.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631-050003; United States / NCI NIH HHS / CA / P50 CA100632-06S1; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / R01 CA121104-03; United States / NCI NIH HHS / CA / CA100632-060001; United States / NCI NIH HHS / CA / R01 CA121104; United States / NCI NIH HHS / CA / CA100632-06S1; United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / P50 CA100632-060001; United States / NCI NIH HHS / CA / CA108631-050003; United States / NCI NIH HHS / CA / R01 CA098006; United States / NCI NIH HHS / CA / CA121104-03; United States / NCI NIH HHS / CA / CA098006; United States / NCI NIH HHS / CA / P50 CA100632-010001; United States / NCI NIH HHS / CA / CA121104; United States / NCI NIH HHS / CA / CA100632-010001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Histones; 776B62CQ27 / decitabine; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Number-of-references] 107
  • [Other-IDs] NLM/ NIHMS177428; NLM/ PMC2848959
  •  go-up   go-down


77. Poppe B, Yigit N, De Moerloose B, De Paepe A, Benoit Y, Speleman F: HOXA gene cluster rearrangement in a t(7;9)(p15;q34) in a child with MDS. Cancer Genet Cytogenet; 2005 Oct 1;162(1):82-4
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.
  • We describe the molecular characterization of a t(7;9)(p15;q34) found in a 15-month-old female patient, diagnosed with refractory anemia with excess blasts in transformation (RAEBt), in progression to acute myeloid leukemia (AML) M7.

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • 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 = 16157206.001).
  • [ISSN] 0165-4608
  • [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 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  •  go-up   go-down


78. Jabbour E, Giles FJ: New agents in myelodysplastic syndromes. Curr Hematol Malig Rep; 2006 Mar;1(1):25-33
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.
  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic disorders characterized by ineffective hematopoiesis resulting in peripheral cytopenia and by increased progression to acute myeloid leukemia (AML).
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Blood Transfusion. Clinical Trials as Topic. Combined Modality Therapy. Disease Progression. Drug Design. Enzyme Inhibitors / therapeutic use. Erythropoietin / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Multicenter Studies as Topic. Prognosis. Risk. Tretinoin / therapeutic use

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 1996 Jan;10(1):40-2 [8558935.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1499-507 [12886236.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):251-6 [12542482.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):481-7 [12181402.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1201-7 [12149198.001]
  • [Cites] Cell. 1980 May;20(1):85-93 [6156004.001]
  • [Cites] Blood. 2002 Dec 1;100(12):3897-902 [12393738.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1570-4 [12176872.001]
  • [Cites] Br J Haematol. 1998 Oct;103(1):176-88 [9792306.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1635-40 [14604977.001]
  • [Cites] Clin Immunol. 2003 Oct;109(1):89-102 [14585280.001]
  • [Cites] Blood. 2002 Aug 1;100(3):1088-91 [12130532.001]
  • [Cites] Nature. 1995 Jul 6;376(6535):62-6 [7596435.001]
  • [Cites] Blood. 2003 Oct 15;102(8):3025-7 [12829603.001]
  • [Cites] J Clin Oncol. 2001 Nov 1;19(21):4165-72 [11689585.001]
  • [Cites] Leuk Res. 2002 Oct;26(10):899-902 [12163050.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):1071-9 [10071302.001]
  • [Cites] Ann Intern Med. 2002 Aug 6;137(3):156-63 [12160363.001]
  • [Cites] Blood. 2001 Aug 15;98(4):958-65 [11493439.001]
  • [Cites] Leukemia. 2004 Jan;18(1):113-9 [14586479.001]
  • [Cites] Blood. 2003 Aug 1;102(3):795-801 [12649163.001]
  • [Cites] Blood. 1993 Jul 15;82(2):677-81 [8329721.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1578-84 [11861271.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:297-317 [15561689.001]
  • [Cites] Science. 1999 Sep 3;285(5433):1553-8 [10477517.001]
  • [Cites] Leuk Res. 2003 Feb;27(2):95-120 [12526916.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2985-90 [9531610.001]
  • [Cites] Br J Haematol. 1990 Feb;74(2):151-5 [2180469.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4527-34 [12947010.001]
  • [Cites] Curr Opin Oncol. 1991 Feb;3(1):44-53 [1710505.001]
  • [Cites] N Engl J Med. 1999 May 27;340(21):1649-60 [10341278.001]
  • [Cites] Chem Biol Interact. 1998 Apr 24;111-112:225-38 [9679557.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1805-11 [7475266.001]
  • [Cites] Cancer. 2004 Jul 15;101(2):226-41 [15241818.001]
  • [Cites] Blood. 1995 Jul 1;86(1):268-76 [7795232.001]
  • [Cites] Blood. 1996 Jul 1;88(1):358-65 [8704196.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4370-8 [12036864.001]
  • [Cites] Haematologica. 2003 May;88(5):ECR18 [12745287.001]
  • [Cites] Br J Haematol. 2000 Jun;109(4):842-6 [10929039.001]
  • [Cites] Leuk Lymphoma. 1995 Aug;18(5-6):457-63 [8528053.001]
  • [Cites] Blood. 2002 Aug 1;100(3):791-8 [12130488.001]
  • [Cites] Curr Opin Hematol. 2002 May;9(3):228-33 [11953669.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1388-92 [10942382.001]
  • [Cites] Br J Haematol. 2003 Feb;120(4):679-84 [12588356.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6489-96 [14528273.001]
  • [Cites] Ann Intern Med. 2001 Apr 3;134(7):573-86 [11281740.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Semin Hematol. 1995 Apr;32(2):132-51 [7652581.001]
  • [Cites] Nature. 1997 Feb 20;385(6618):729-33 [9034190.001]
  • [Cites] J Exp Med. 1995 Dec 1;182(6):1777-83 [7500022.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):1037-46 [12648074.001]
  • [Cites] Br J Haematol. 1982 Jun;51(2):189-99 [6952920.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1427-34 [11222390.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2760-6 [12767088.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1287-92 [15051776.001]
  • [Cites] Science. 1989 Dec 8;246(4935):1306-9 [2479986.001]
  • [Cites] Semin Hematol. 2000 Jan;37(1):15-29 [10676908.001]
  • [Cites] Blood. 1990 Jul 1;76(1):36-43 [1694702.001]
  • [Cites] Bone Marrow Transplant. 1992 Nov;10(5):445-50 [1464008.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Cancer Treat Res. 2001;108:93-100 [11702608.001]
  • [Cites] J Clin Oncol. 1999 Sep;17(9):2819-30 [10561358.001]
  • [Cites] Br J Haematol. 2002 Feb;116(2):334-7 [11841434.001]
  • [Cites] J Clin Oncol. 1990 Oct;8(10):1707-14 [2213106.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3553-60 [12411319.001]
  • [Cites] Oncologist. 1997;2(1):28-39 [10388027.001]
  • [Cites] Br J Cancer. 1999 Dec;81(8):1398-401 [10604739.001]
  • [Cites] Leukemia. 2000 Jan;14(1):2-8 [10637470.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):620-30 [10997974.001]
  • (PMID = 20425328.001).
  • [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 / Angiogenesis Inhibitors; 0 / Drugs, Investigational; 0 / Enzyme Inhibitors; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5688UTC01R / Tretinoin
  • [Number-of-references] 89
  •  go-up   go-down


79. Bernasconi P, Boni M, Cavigliano PM, Calatroni S, Giardini I, Rocca B, Zappatore R, Dambruoso I, Caresana M: Clinical relevance of cytogenetics in myelodysplastic syndromes. Ann N Y Acad Sci; 2006 Nov;1089:395-410
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.
  • In addition, chromosome abnormalities are independent prognostic factors predicting overall survival and the likelihood of progression in acute myeloid leukemia.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • 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
  • (PMID = 17261783.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 18
  •  go-up   go-down


80. de Melo Campos P, Traina F, da Silva Santos Duarte A, Lorand-Metze I, Costa FF, Saad ST: Reduced expression of FLIP SHORT in bone marrow of low risk myelodysplastic syndrome. Leuk Res; 2007 Jun;31(6):853-7
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.
  • Apoptosis is dysregulated in patients with myelodysplastic syndrome (MDS) and acute myelogenous leukaemia (AML).
  • Furthermore, FLIP(SHORT) mRNA expression was significantly lower in low risk MDS, compared to MDS-AML/AML de novo (P=0.0006), according to FAB classification.
  • Increased levels of FLIP(SHORT) in RAEB and AML may be related to apoptosis resistance in these diseases and to MDS progression.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. CASP8 and FADD-Like Apoptosis Regulating Protein / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism


81. Follo MY, Mongiorgi S, Finelli C, Clissa C, Ramazzotti G, Fiume R, Faenza I, Manzoli L, Martelli AM, Cocco L: Nuclear inositide signaling in myelodysplastic syndromes. J Cell Biochem; 2010 Apr 15;109(6):1065-71
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.
  • Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML).
  • Inositides are key cellular second messengers with well-established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide-specific phospholipase C (PI-PLC) beta1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions.
  • [MeSH-minor] Animals. Humans. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Phosphatidylinositols / metabolism. Phospholipase C beta / metabolism. Proto-Oncogene Proteins c-akt / metabolism


82. Hara T, Schwieger M, Kazama R, Okamoto S, Minehata K, Ziegler M, Löhler J, Stocking C: Acceleration of chronic myeloproliferation by enforced expression of Meis1 or Meis3 in Icsbp-deficient bone marrow cells. Oncogene; 2008 Jun 19;27(27):3865-9
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.
  • Interferon consensus sequence-binding protein (ICSBP) is a tumor suppressor, whose downregulation cooperates with BCR-ABL and NUP98-TOP1 gene products to accelerate leukemia induction in mouse models.
  • Similarly, Meis1 synergizes with HoxA9 or NUP98-HOX (but not NUP98-TOP1) fusion genes to promote the early onset of leukemia.
  • Secondary mutations, such as activation of Mn1, led to the progression to acute myeloid leukemia in a few mice.
  • These results reveal a novel collaboration between Icsbp deficiency and Meis1/Meis3 in the acceleration of chronic myeloid leukemia-like disease.
  • [MeSH-minor] Animals. Cell Division. Gene Expression Regulation. Kinetics. Leukemia, Myeloid, Acute / genetics. Mice. Mice, Knockout. Mutation

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18223676.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Interferon Regulatory Factors; 0 / Meis3 protein, mouse; 0 / Neoplasm Proteins; 0 / Transcription Factors; 0 / interferon regulatory factor-8; 0 / myeloid ecotropic viral integration site 1 protein
  •  go-up   go-down


83. Ryningen A, Stapnes C, Paulsen K, Lassalle P, Gjertsen BT, Bruserud O: In vivo biological effects of ATRA in the treatment of AML. Expert Opin Investig Drugs; 2008 Nov;17(11):1623-33
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.
  • BACKGROUND: All-trans retinoic acid (ATRA) is mandatory in the treatment of acute promyelocytic leukaemia (APL).
  • Experimental studies suggest that ATRA can induce differentiation and apoptosis in leukaemia cells also for other acute myelogenous leukaemia (AML) subtypes, but the clinical observations are conflicting.
  • Serum/plasma samples were collected before and after 2 days of ATRA, peripheral blood AML cells were collected from all 12 patients with circulating leukaemia cells (ClinicalTrials.gov NCT00175812; EudraCT no. 2004-001663-22).
  • Circulating leukaemia cells derived during therapy had increased intracellular levels of P21 (mean increase in mean fluorescence intensity (MFI) being 18.2%, p = 0.017), and decreased levels of Gata-2 (mean decrease in MFI 19%, p = 0.026), NF-kappaB p65 (mean decrease in MFI 15.4%, p = 0.033) and Bcl-2 (mean decrease in MFI 7.2%, p = 0.005).
  • CONCLUSIONS: In vivo ATRA treatment in AML affects leukaemic cell morphology, regulation of cell cycle progression and apoptosis, and possibly also microvascular endothelial cell functions.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Tretinoin / therapeutic use

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18922099.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00175812
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


84. Post SM, Quintás-Cardama A: Closing in on the pathogenesis of the 5q- syndrome. Expert Rev Anticancer Ther; 2010 May;10(5):655-8
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.
  • Patients with 5q- syndrome are characterized by macrocytic anemia, normal to elevated platelet counts, and a propensity to develop acute myeloid leukemia.
  • Two recently published studies using genetic approaches have unraveled a small array of genes whose alteration recapitulates critical features of the 5q- syndrome including dysplasia, clonal dominance, and progression to acute myeloid leukemia.
  • [MeSH-major] Anemia, Macrocytic / etiology. Anemia, Macrocytic / genetics. Chromosomes, Human, Pair 5 / genetics. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics

  • Genetic Alliance. consumer health - 5q- Syndrome.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20469997.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 18
  •  go-up   go-down


85. Götze K, Platzbecker U, Giagounidis A, Haase D, Lübbert M, Aul C, Ganser A, Germing U, Hofmann WK: Azacitidine for treatment of patients with myelodysplastic syndromes (MDS): practical recommendations of the German MDS Study Group. Ann Hematol; 2010 Sep;89(9):841-50
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.
  • Myelodysplastic syndromes (MDS) are a group of common bone marrow disorders characterized by ineffective hematopoiesis, peripheral cytopenias, and a substantial risk of progression to acute myeloid leukemia (AML).

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20567826.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] M801H13NRU / Azacitidine
  • [Number-of-references] 50
  •  go-up   go-down


86. Musolino C, Sant'antonio E, Penna G, Alonci A, Russo S, Granata A, Allegra A: Epigenetic therapy in myelodysplastic syndromes. Eur J Haematol; 2010 Jun;84(6):463-73
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 wide spectrum of clonal hematopoietic disorders that fall under the broad diagnostic category of myelodysplastic syndromes (MDS) consist of a family of bone marrow malignancies - with ineffective, inadequate, and dysplastic hematopoiesis, and with an increased risk of life-threatening infections, bleeding, and progression to acute myeloid leukemia (AML) - that are characterized by a deep heterogeneity on the clinical, biologic and prognostic level.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20192987.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
  • [Number-of-references] 76
  •  go-up   go-down


87. Pons A, Nomdedeu B, Navarro A, Gaya A, Gel B, Diaz T, Valera S, Rozman M, Belkaid M, Montserrat E, Monzo M: Hematopoiesis-related microRNA expression in myelodysplastic syndromes. Leuk Lymphoma; 2009 Nov;50(11):1854-9
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.
  • The present study sought to link hematopoiesis-relevant miRNAs with myelodysplastic syndromes (MDS) and MDS progression to acute myeloid leukemia (AML).
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Bone Marrow / metabolism. Bone Marrow / pathology. Disease Progression. Female. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • 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
  • [CommentIn] Leuk Lymphoma. 2009 Nov;50(11):1735-6 [19883302.001]
  • (PMID = 19883312.001).
  • [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
  • [Chemical-registry-number] 0 / MIRN15 microRNA, human; 0 / MIRN16 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
  •  go-up   go-down


88. Epling-Burnette PK, Bai F, Painter JS, Rollison DE, Salih HR, Krusch M, Zou J, Ku E, Zhong B, Boulware D, Moscinski L, Wei S, Djeu JY, List AF: Reduced natural killer (NK) function associated with high-risk myelodysplastic syndrome (MDS) and reduced expression of activating NK receptors. Blood; 2007 Jun 1;109(11):4816-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis with potential for progression to acute myeloid leukemia (AML).
  • Collectively, these findings suggest that impairment of NK cytolytic function derives in part from reduced activating NK receptors such as NKG2D in association with disease progression.
  • Evasion of NK immunosurveillance may have importance for MDS disease progression.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 2002 May 17;296(5571):1323-6 [11950999.001]
  • [Cites] Int J Cancer. 2006 Feb 1;118(3):684-7 [16094621.001]
  • [Cites] J Immunol. 2002 Oct 15;169(8):4098-102 [12370336.001]
  • [Cites] Leukemia. 2002 Nov;16(11):2253-8 [12399970.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6178-86 [12414645.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2002;:136-61 [12446422.001]
  • [Cites] Leuk Res. 2003 Feb;27(2):95-120 [12526916.001]
  • [Cites] Eur J Immunol. 2003 May;33(5):1235-41 [12731048.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1389-96 [12714493.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1797-805 [12750175.001]
  • [Cites] Leuk Lymphoma. 2003 Oct;44(10):1683-9 [14692519.001]
  • [Cites] Blood. 2004 May 1;103(9):3431-9 [14726391.001]
  • [Cites] Trends Immunol. 2004 Jun;25(6):328-33 [15145323.001]
  • [Cites] Lancet. 1982 Feb 20;1(8269):449 [6121114.001]
  • [Cites] Blut. 1982 Oct;45(4):243-8 [6982087.001]
  • [Cites] Leuk Res. 1983;7(3):389-95 [6310273.001]
  • [Cites] Leuk Res. 1984;8(2):239-47 [6717064.001]
  • [Cites] Br J Haematol. 1984 Sep;58(1):71-81 [6466573.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):9996-10000 [1438250.001]
  • [Cites] J Virol. 1995 Feb;69(2):1328-33 [7815516.001]
  • [Cites] Virology. 1996 Dec 15;226(2):167-75 [8955035.001]
  • [Cites] J Exp Med. 1998 May 18;187(10):1681-7 [9584146.001]
  • [Cites] Blood. 1998 Oct 15;92(8):2886-92 [9763574.001]
  • [Cites] Eur J Immunol. 1999 May;29(5):1656-66 [10359120.001]
  • [Cites] J Exp Med. 1999 Nov 15;190(10):1505-16 [10562324.001]
  • [Cites] Hum Immunol. 2000 Jan;61(1):18-27 [10658974.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2012-21 [10979941.001]
  • [Cites] Br J Haematol. 2000 Sep;110(4):876-9 [11054073.001]
  • [Cites] Immunity. 2001 Feb;14(2):123-33 [11239445.001]
  • [Cites] Annu Rev Immunol. 2001;19:197-223 [11244035.001]
  • [Cites] Nat Immunol. 2001 Jan;2(1):23-7 [11135574.001]
  • [Cites] Immunol Rev. 2001 Jun;181:185-92 [11513139.001]
  • [Cites] Science. 2001 Oct 19;294(5542):605-9 [11567106.001]
  • [Cites] J Immunol. 2002 Jan 15;168(2):671-9 [11777960.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):636-40 [11895890.001]
  • [Cites] J Immunol. 2002 Apr 1;168(7):3155-64 [11907067.001]
  • [Cites] Blood. 2002 May 15;99(10):3661-7 [11986221.001]
  • [Cites] Leukemia. 2002 May;16(5):855-60 [11986947.001]
  • [Cites] Science. 1999 Jul 30;285(5428):727-9 [10426993.001]
  • [Cites] Science. 1999 Jul 30;285(5428):730-2 [10426994.001]
  • [Cites] Ann Oncol. 1999 Jul;10(7):825-9 [10470430.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:297-317 [15561689.001]
  • [Cites] Oncogene. 2004 Dec 9;23(57):9220-9 [15516985.001]
  • [Cites] Nat Immunol. 2005 Sep;6(9):928-37 [16116470.001]
  • [Cites] Immunol Lett. 2005 Aug 15;100(1):7-13 [16109445.001]
  • [Cites] Ann Intern Med. 2002 Aug 6;137(3):156-63 [12160363.001]
  • (PMID = 17341666.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 112112-01; United States / NCI NIH HHS / CA / R01 CA112112; United States / NIAID NIH HHS / AI / AI 056213; United States / NCI NIH HHS / CA / CA 098080; United States / NCI NIH HHS / CA / R01 CA098080; United States / NIAID NIH HHS / AI / R01 AI056213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Other-IDs] NLM/ PMC1885518
  •  go-up   go-down


89. Zhang WW, Habeebu S, Sheehan AM, Naeem R, Hernandez VS, Dreyer ZE, López-Terrada D: Molecular monitoring of 8p11 myeloproliferative syndrome in an infant. J Pediatr Hematol Oncol; 2009 Nov;31(11):879-83
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.
  • Typical pathologic findings include myeloid hyperplasia, lymphadenopathy, precursor T-lymphoblastic lymphoma, and eosinophilia.
  • The disease is usually associated with an aggressive course and progression to acute myeloid leukemia is frequent.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19829149.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / ZMYM2 protein, human; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
  •  go-up   go-down


90. van Luijn MM, van den Ancker W, Chamuleau ME, Ossenkoppele GJ, van Ham SM, van de Loosdrecht AA: Impaired antigen presentation in neoplasia: basic mechanisms and implications for acute myeloid leukemia. Immunotherapy; 2010 Jan;2(1):85-97
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] Impaired antigen presentation in neoplasia: basic mechanisms and implications for acute myeloid leukemia.
  • During onset, treatment and progression of acute myeloid leukemia (AML), inadequate immune responses against certain myeloid leukemic blasts might be associated with the occurrence of minimal residual disease and subsequent relapse.
  • In tumor cells that can express HLA class II molecules, such as myeloid leukemic blasts, abnormalities in the processing pathways of endogenous antigens could also result in impaired HLA class II-restricted tumor-associated antigen presentation to CD4(+) T helper cells.
  • More insight into impaired tumor-associated antigen presentation by myeloid leukemic blasts could explain their escape from immune recognition and might be crucial for selecting appropriate strategies to improve whole-cell or dendritic cell-based tumor vaccine efficacy in the treatment of AML patients.
  • [MeSH-major] Antigen Presentation / immunology. Leukemia, Myeloid / immunology. Neoplasm, Residual / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Acute Disease. Cancer Vaccines / immunology. Dendritic Cells / immunology. Humans. Immunotherapy / methods. Neoplasms / immunology. Neoplasms / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20635891.001).
  • [ISSN] 1750-7448
  • [Journal-full-title] Immunotherapy
  • [ISO-abbreviation] Immunotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
  •  go-up   go-down


91. Carlsten M, Baumann BC, Simonsson M, Jädersten M, Forsblom AM, Hammarstedt C, Bryceson YT, Ljunggren HG, Hellström-Lindberg E, Malmberg KJ: Reduced DNAM-1 expression on bone marrow NK cells associated with impaired killing of CD34+ blasts in myelodysplastic syndrome. Leukemia; 2010 Sep;24(9):1607-16
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.
  • Myelodysplastic syndromes (MDS) comprise a heterogeneous group of clonal stem-cell disorders characterized by ineffective hematopoiesis and risk of progression to acute myeloid leukemia.
  • Thus, given the emerging evidence for NK cell-mediated immune surveillance of neoplastic cells, we speculate that reduced expression of DNAM-1 on bone marrow NK cells may facilitate disease progression in patients with MDS.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Flow Cytometry. Humans. Male. Middle Aged


92. Jiang Y, Dunbar A, Gondek LP, Mohan S, Rataul M, O'Keefe C, Sekeres M, Saunthararajah Y, Maciejewski JP: Aberrant DNA methylation is a dominant mechanism in MDS progression to AML. Blood; 2009 Feb 5;113(6):1315-25
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] Aberrant DNA methylation is a dominant mechanism in MDS progression to AML.
  • Myelodysplastic syndromes (MDSs) are clonal hematologic disorders that frequently represent an intermediate disease stage before progression to acute myeloid leukemia (AML).
  • In 184 patients with MDS and AML, DNA methylation microarray and high-density single nucleotide polymorphism array (SNP-A) karyotyping were used to assess the relative contributions of aberrant DNA methylation and chromosomal deletions to tumor-suppressor gene (TSG) silencing during disease progression.
  • However, the ubiquity, extent, and correlation with disease progression suggest that aberrant DNA methylation is the dominant mechanism for TSG silencing and clonal variation in MDS evolution to AML.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • Guide to Pharmacology. gene/protein/disease-specific - FZD9 - data and references .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2007 Oct 15;26(47):6697-714 [17934479.001]
  • [Cites] Histol Histopathol. 2007 Dec;22(12):1413-24 [17701921.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):7107-12 [18056190.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):132-8 [10655057.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6481-6 [10823896.001]
  • [Cites] Blood. 2001 May 1;97(9):2823-9 [11313277.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2957-64 [12351408.001]
  • [Cites] J Biol Chem. 2002 Oct 4;277(40):37479-86 [12138115.001]
  • [Cites] Hematol Oncol. 2002 Dec;20(4):167-76 [12469326.001]
  • [Cites] Haematologica. 2002 Dec;87(12):1324-41 [12495905.001]
  • [Cites] Leuk Res. 2004 Feb;28(2):171-7 [14654082.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] Int J Hematol. 2004 Aug;80(2):128-35 [15481440.001]
  • [Cites] Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3 [5279523.001]
  • [Cites] J Clin Oncol. 1985 Jan;3(1):3-11 [3965632.001]
  • [Cites] Blood. 1986 Jun;67(6):1721-30 [3708158.001]
  • [Cites] Eur J Haematol. 1988 Oct;41(4):341-6 [3197821.001]
  • [Cites] Cancer Res. 1996 Mar 1;56(5):973-77 [8640788.001]
  • [Cites] Cancer Res. 1997 May 1;57(9):1678-81 [9135007.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2985-90 [9531610.001]
  • [Cites] Blood. 1998 Oct 15;92(8):2981-3 [9763591.001]
  • [Cites] Nature. 1998 Dec 17;396(6712):643-9 [9872311.001]
  • [Cites] Forum (Genova). 1999 Jan-Mar;9(1):17-31 [10101208.001]
  • [Cites] Cancer Res. 1999 Jul 1;59(13):3215-21 [10397268.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Aug;25(4):384-92 [10398433.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3730-40 [10446989.001]
  • [Cites] Semin Cancer Biol. 1999 Aug;9(4):245-54 [10448112.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Carcinogenesis. 2005 Dec;26(12):2031-45 [16150895.001]
  • [Cites] Ann Hematol. 2005 Dec;84 Suppl 1:39-46 [16231140.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S4-11 [16341240.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):23-32 [16343268.001]
  • [Cites] Cancer Lett. 2006 Jan 28;232(1):90-8 [16242838.001]
  • [Cites] Blood Rev. 2006 Jan;20(1):1-13 [16426940.001]
  • [Cites] Genome Res. 2006 Mar;16(3):383-93 [16449502.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6118-28 [16778185.001]
  • [Cites] Genome Res. 2006 Sep;16(9):1075-83 [16899657.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] PLoS Med. 2006 Dec;3(12):e486 [17194187.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1370-7 [17283175.001]
  • [Cites] Haematologica. 2007 May;92(5):605-11 [17488683.001]
  • [Cites] Br J Haematol. 2007 Jul;138(1):3-11 [17489980.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Science. 2007 Nov 16;318(5853):1108-13 [17932254.001]
  • (PMID = 18832655.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [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 / FZD3 protein, human; 0 / Frizzled Receptors; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2637194
  •  go-up   go-down


93. Komrokji RS, Bennett JM: Evolving classifications of the myelodysplastic syndromes. Curr Opin Hematol; 2007 Mar;14(2):98-105
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The International Prognostic Scoring System is very important to define patient risk of progression to acute myeloid leukemia and predict overall survival.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17255786.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
  •  go-up   go-down


94. Nowicki M, Ostalska-Nowicka D, Konwerska A, Miskowiak B: The predicting role of substance P in the neoplastic transformation of the hypoplastic bone marrow. J Clin Pathol; 2006 Sep;59(9):935-41
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: The expression of substance P (as evidenced by both immunocytochemical and hybridisation techniques) was confirmed in the cytoplasm of B lymphocytes in 8 of 11 children who developed acute leukaemia in 45 (SD 12) days.
  • The risk of development of leukaemia secondary to bone marrow hypoplasia was found to be significant (p<0.001) in those children who expressed substance P in normal-looking lymphocytes at the initial bone marrow evaluation.
  • A marked correlation between substance P-positive bone marrow pattern and the expansion of tumour cells may prove the potential value of this oligopeptide in the pathogenesis of leukaemia.
  • [MeSH-major] Bone Marrow Diseases / metabolism. Cell Transformation, Neoplastic / metabolism. Leukemia / metabolism. Substance P / physiology
  • [MeSH-minor] Adolescent. B-Lymphocytes / metabolism. Bone Marrow Examination / methods. Child. Child, Preschool. Disease Progression. Humans. Immunoenzyme Techniques. Immunophenotyping. In Situ Hybridization. Ki-67 Antigen / metabolism. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Prognosis

  • MedlinePlus Health Information. consumer health - Bone Marrow Diseases.
  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Folia Histochem Cytobiol. 2003;41(1):33-6 [12705477.001]
  • [Cites] Pathol Int. 1999 Jul;49(7):626-32 [10504523.001]
  • [Cites] Semin Hematol. 1973 Jul;10(3):195-223 [4577645.001]
  • [Cites] Clin Haematol. 1978 Oct;7(3):431-65 [363321.001]
  • [Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]
  • [Cites] Pharmacol Rev. 1983 Jun;35(2):85-141 [6196797.001]
  • [Cites] J Clin Invest. 1984 Oct;74(4):1532-9 [6207205.001]
  • [Cites] Exp Hematol. 1985 Mar;13(3):194-9 [3884357.001]
  • [Cites] J Immunol. 1985 Aug;135(2 Suppl):755s-765s [2861231.001]
  • [Cites] Semin Oncol. 1985 Jun;12(2):105-21 [3892693.001]
  • [Cites] Anal Biochem. 1985 Aug 15;149(1):1-28 [2416238.001]
  • [Cites] Annu Rev Neurosci. 1988;11:13-28 [3284438.001]
  • [Cites] J Immunol. 1988 Aug 1;141(3):961-6 [2456338.001]
  • [Cites] Ann Intern Med. 1988 Nov 1;109(9):695-704 [2847613.001]
  • [Cites] J Immunol. 1989 May 1;142(9):3256-61 [2496164.001]
  • [Cites] Am J Clin Pathol. 1989 Dec;92(6):836-43 [2480062.001]
  • [Cites] Peptides. 1989 Sep-Oct;10(5):957-62 [2481848.001]
  • [Cites] Circ Res. 1990 May;66(5):1178-83 [1692268.001]
  • [Cites] Br J Pharmacol. 1990 May;100(1):11-4 [1695530.001]
  • [Cites] Immunology. 1990 Sep;71(1):52-6 [1698717.001]
  • [Cites] Acta Oncol. 1991;30(4):509-17 [1713037.001]
  • [Cites] Int J Tissue React. 1992;14(3):101-11 [1332929.001]
  • [Cites] Blood. 1993 Jan 15;81(2):391-8 [7678516.001]
  • [Cites] Regul Pept. 1993 Jan 22;43(1-2):21-35 [8381237.001]
  • [Cites] Hum Pathol. 1993 Apr;24(4):359-63 [8098317.001]
  • [Cites] Life Sci. 1994;54(26):2035-47 [8208061.001]
  • [Cites] Blood. 1995 Jul 15;86(2):482-90 [7541664.001]
  • [Cites] Immunol Today. 1995 Jul;16(7):318-22 [7576063.001]
  • [Cites] Blood. 1996 Jul 1;88(1):98-106 [8704207.001]
  • [Cites] Am J Clin Pathol. 1997 Mar;107(3):268-74 [9052376.001]
  • [Cites] J Histochem Cytochem. 1997 Mar;45(3):327-43 [9071315.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1096-9 [12764374.001]
  • (PMID = 16935970.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 33507-63-0 / Substance P
  • [Other-IDs] NLM/ PMC1860490
  •  go-up   go-down


95. Saracco P, Quarello P, Iori AP, Zecca M, Longoni D, Svahn J, Varotto S, Del Vecchio GC, Dufour C, Ramenghi U, Bacigalupo A, Locasciulli A, Bone Marrow Failure Study Group of the AIEOP (Italian Association of Paediatric Haematology Oncology): Cyclosporin A response and dependence in children with acquired aplastic anaemia: a multicentre retrospective study with long-term observation follow-up. Br J Haematol; 2008 Jan;140(2):197-205
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.
  • This study, of 42 consecutive children with AAA treated with IST, assessed the incidence of CyA-dependence, CyA and granulocyte colony-stimulating factor (G-CSF) tapering schedules and the impact of drug accumulation on progression to myelodysplasia/acute myeloid leukaemia (MDS/AML).
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease Progression. Drug Administration Schedule. Drug Evaluation. Drug Therapy, Combination. Epidemiologic Methods. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Infant. Male. Recurrence. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Aplastic Anemia.
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18173756.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83HN0GTJ6D / Cyclosporine
  •  go-up   go-down


96. List AF: Iron overload in myelodysplastic syndromes: diagnosis and management. Cancer Control; 2010 Jan;17 Suppl:2-8
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.
  • Transfusion dependence is associated with shorter survival and an increased risk for progression to acute myeloid leukemia (AML) in transfusion-dependent patients.


97. Xiao W, Jiang F, Wang Z: ELL binding regulates U19/Eaf2 intracellular localization, stability, and transactivation. Prostate; 2006 Jan 1;66(1):1-12
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Eleven-nineteen Lysine-rich Leukemia (ELL) is an RNA polymerase II transcription elongation factor, initially identified as a fusion partner gene of MLL in the t(11;.
  • 19) (q23; p13.1) chromosomal translocation in acute myeloid leukemia.
  • These findings suggest that ELL-U19/Eaf2 interaction is potentially important in prostate cancer progression and/or acute myeloid leukemia.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16114057.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA90386; United States / NIDDK NIH HHS / DK / R01 DK51193
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EAF1 protein, human; 0 / EAF2 protein, human; 0 / Oligodeoxyribonucleotides; 0 / Transcription Factors; EC 1.13.12.- / Luciferases
  •  go-up   go-down


98. Xiao L, Qiong L, Yan Z, Zheng Z, Luxi S, Li X, Ying T, Yizhi L, Quan P: Experimental and clinical characteristics in myelodysplastic syndrome patients with or without HLA-DR15 allele. Hematol Oncol; 2010 Jun;28(2):98-103
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 noted the following observations with regard to disease progression: None of the 46 HLA-DR15 positive patients with international prognostic scoring system (IPSS) scores <or=1 developed acute myeloid leukaemia (AML) during the follow-up period, while six of the 63 DR15-negative patients with the same IPSS score developed AML within a shorter follow-up period (p = 0.039).
  • We concluded that the presence of the HLA-DR15 allele is indicative of a genetic susceptibility to MDS and, the presence of the HLA-DR15 allele showed less association with disease progression and greater association with BM failure.
  • [MeSH-minor] Alleles. Asian Continental Ancestry Group / genetics. Bone Marrow / chemistry. Bone Marrow / pathology. CD4 Lymphocyte Count. CD4-CD8 Ratio. Disease Progression. Gene Frequency. Genetic Predisposition to Disease. HLA-DR Serological Subtypes. Humans. Interferon-gamma / analysis. Tumor Necrosis Factor-alpha / analysis

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • 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
  • [Copyright] (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19593744.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DR Antigens; 0 / HLA-DR Serological Subtypes; 0 / HLA-DR15 antigen; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


99. Park S, Grabar S, Kelaidi C, Beyne-Rauzy O, Picard F, Bardet V, Coiteux V, Leroux G, Lepelley P, Daniel MT, Cheze S, Mahé B, Ferrant A, Ravoet C, Escoffre-Barbe M, Adès L, Vey N, Aljassem L, Stamatoullas A, Mannone L, Dombret H, Bourgeois K, Greenberg P, Fenaux P, Dreyfus F, GFM group (Groupe Francophone des Myélodysplasies): Predictive factors of response and survival in myelodysplastic syndrome treated with erythropoietin and G-CSF: the GFM experience. Blood; 2008 Jan 15;111(2):574-82
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.
  • Multivariate adjusted comparisons of survival between our cohort and the untreated MDS cohort used to design IPSS showed similar rate of progression to acute myeloid leukemia in both cohorts, but significantly better overall survival in our cohort, suggesting that epoetin or DAR treatment may have a favorable survival impact in MDS.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • 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
  • (PMID = 17940203.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


100. Drexler HG, Dirks WG, Macleod RA: Many are called MDS cell lines: one is chosen. Leuk Res; 2009 Aug;33(8):1011-6
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.
  • Myelodysplastic syndromes (MDS) comprise a heterogenous group of clonal disorders of hematopoietic progenitors, showing genetic instability and in many cases progression to acute myeloid leukemia (AML).
  • When MDS progress towards AML (AML/MDS), additional genetic lesions cause a block in differentiation and an accumulation of blast cells.
  • Leukemia cell lines are key resources for modelling hematological malignancies.
  • However, a significant minority of these has proved false after DNA profiling which revealed their cross-contamination with older established leukemia cell lines.
  • Most remaining ("authentic") MDS cell lines were established during the leukemic phase of the disease progression rather than during the MDS phase.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Genomic Instability. Humans. Leukemia, Myeloid, Acute. Models, Biological






Advertisement