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1. Braig M, Pällmann N, Preukschas M, Steinemann D, Hofmann W, Gompf A, Streichert T, Braunschweig T, Copland M, Rudolph KL, Bokemeyer C, Koschmieder S, Schuppert A, Balabanov S, Brümmendorf TH: A 'telomere-associated secretory phenotype' cooperates with BCR-ABL to drive malignant proliferation of leukemic cells. Leukemia; 2014 Oct;28(10):2028-39
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A 'telomere-associated secretory phenotype' cooperates with BCR-ABL to drive malignant proliferation of leukemic cells.
  • Telomere biology is frequently associated with disease evolution in human cancer and dysfunctional telomeres have been demonstrated to contribute to genetic instability.
  • In BCR-ABL(+) chronic myeloid leukemia (CML), accelerated telomere shortening has been shown to correlate with leukemia progression, risk score and response to treatment.
  • Here, we demonstrate that proliferation of murine CML-like bone marrow cells strongly depends on telomere maintenance.
  • CML-like cells of telomerase knockout mice with critically short telomeres (CML-iG4) are growth retarded and proliferation is terminally stalled by a robust senescent cell cycle arrest.
  • In sharp contrast, CML-like cells with pre-shortened, but not critically short telomere lengths (CML-G2) grew most rapidly and were found to express a specific 'telomere-associated secretory phenotype', comprising secretion of chemokines, interleukins and other growth factors, thereby potentiating oncogene-driven growth.
  • Moreover, conditioned supernatant of CML-G2 cells markedly enhanced proliferation of CML-WT and pre-senescent CML-iG4 cells.
  • Strikingly, a similar inflammatory mRNA expression pattern was found with disease progression from chronic phase to accelerated phase in CML patients.
  • These findings demonstrate that telomere-induced senescence needs to be bypassed by leukemic cells in order to progress to blast crisis and provide a novel mechanism by which telomere shortening may contribute to disease evolution in CML.
  • [MeSH-major] Cell Proliferation. Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Leukemic. Leukemia / pathology. Telomere / ultrastructure
  • [MeSH-minor] Animals. Apoptosis. Bone Marrow Cells / cytology. Cell Aging. Cell Cycle. Cell Line, Tumor. Chemokines / metabolism. Cytokines / metabolism. Disease Progression. Humans. Inflammation / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. Phenotype

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  • (PMID = 24603533.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Chief Scientist Office / / SCD/04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Cytokines; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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2. Jabbour EJ, Hughes TP, Cortés JE, Kantarjian HM, Hochhaus A: Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia. Leuk Lymphoma; 2014 Jul;55(7):1451-62
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  • [Title] Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia.
  • Despite vast improvements in the treatment of Philadelphia chromosome-positive chronic myeloid leukemia (CML) in chronic phase (CP), advanced stages of CML, accelerated phase or blast crisis, remain notoriously difficult to treat.
  • Treatments that are highly effective against CML-CP produce disappointing results against advanced disease.
  • (2) using tyrosine kinase inhibitors that lower risk of disease progression; and (3) more closely observing patients who demonstrate cytogenetic risk factors at diagnosis or during treatment.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Blast Crisis / diagnosis. Blast Crisis / etiology. Blast Crisis / therapy. Disease Management. Disease Progression. Humans. Leukemia, Myeloid, Accelerated Phase / diagnosis. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Accelerated Phase / etiology. Neoplasm Staging. Prognosis. Treatment Outcome


3. Makishima H, Jankowska AM, McDevitt MA, O'Keefe C, Dujardin S, Cazzolli H, Przychodzen B, Prince C, Nicoll J, Siddaiah H, Shaik M, Szpurka H, Hsi E, Advani A, Paquette R, Maciejewski JP: CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia. Blood; 2011 May 26;117(21):e198-206
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  • [Title] CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia.
  • Progression of chronic myelogenous leukemia (CML) to accelerated (AP) and blast phase (BP) is because of secondary molecular events, as well as additional cytogenetic abnormalities.
  • On the basis of the detection of JAK2, CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations in myelodysplastic/myeloproliferative neoplasms, we hypothesized that they may also contribute to progression in CML.
  • We screened these genes for mutations in 54 cases with CML (14 with chronic phase, 14 with AP, 20 with myeloid, and 6 with nonmyeloid BP).
  • We identified 1 CBLB and 2 TET2 mutations in AP, and 1 CBL, 1 CBLB, 4 TET2, 2 ASXL1, and 2 IDH family mutations in myeloid BP.
  • However, none of these mutations were found in chronic phase.
  • Our results indicate that CBL family, TET2, ASXL1, and IDH family mutations and additional cryptic karyotypic abnormalities can occur in advanced phase CML.

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  • (PMID = 21346257.001).
  • [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 / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [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 / ASXL1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / TET2 protein, human; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl; EC 6.3.2.19 / CBLB protein, human
  • [Other-IDs] NLM/ PMC3110035
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4. Ito T, Kwon HY, Zimdahl B, Congdon KL, Blum J, Lento WE, Zhao C, Lagoo A, Gerrard G, Foroni L, Goldman J, Goh H, Kim SH, Kim DW, Chuah C, Oehler VG, Radich JP, Jordan CT, Reya T: Regulation of myeloid leukaemia by the cell-fate determinant Musashi. Nature; 2010 Aug 5;466(7307):765-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of myeloid leukaemia by the cell-fate determinant Musashi.
  • Chronic myelogenous leukaemia (CML) can progress from a slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this transition remains poorly understood.
  • Here we have used mouse models of CML to show that disease progression is regulated by the Musashi-Numb signalling axis.
  • Specifically, we find that the chronic phase is marked by high levels of Numb expression whereas the blast crisis phase has low levels of Numb expression, and that ectopic expression of Numb promotes differentiation and impairs advanced-phase disease in vivo.
  • As a possible explanation for the decreased levels of Numb in the blast crisis phase, we show that NUP98-HOXA9, an oncogene associated with blast crisis CML, can trigger expression of the RNA-binding protein Musashi2 (Msi2), which in turn represses Numb.
  • Notably, loss of Msi2 restores Numb expression and significantly impairs the development and propagation of blast crisis CML in vitro and in vivo.
  • Finally we show that Msi2 expression is not only highly upregulated during human CML progression but is also an early indicator of poorer prognosis.
  • These data show that the Musashi-Numb pathway can control the differentiation of CML cells, and raise the possibility that targeting this pathway may provide a new strategy for the therapy of aggressive leukaemias.

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  • (PMID = 20639863.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK063031-02; United States / NCI NIH HHS / CA / R01 CA122206; United States / NIDDK NIH HHS / DK / DK072234; United States / NCI NIH HHS / CA / CA140371; United States / NCI NIH HHS / CA / CA18029; United States / NIAID NIH HHS / AI / U19 AI067798-020006; United States / NCI NIH HHS / CA / R01 CA140371; United States / NIDDK NIH HHS / DK / R01 DK063031-06; United States / NIDDK NIH HHS / DK / DK063031-07S1; United States / NIGMS NIH HHS / GM / T32 GM007184; United States / NIDDK NIH HHS / DK / DK072234-02; United States / NIDDK NIH HHS / DK / R01 DK072234-02; United States / NCI NIH HHS / CA / P01 CA018029; United States / NIDDK NIH HHS / DK / R01 DK072234-01A1; United States / NHLBI NIH HHS / HL / HL097767; United States / NIDDK NIH HHS / DK / R01 DK072234-03; United States / NIDDK NIH HHS / DK / DK063031-06; United States / NIDDK NIH HHS / DK / DK063031-01; United States / NIDDK NIH HHS / DK / R01 DK072234; United States / NIH HHS / OD / DP1 OD006430; United States / NIDDK NIH HHS / DK / DK063031-07; United States / NIH HHS / OD / OD006430-02; United States / NIH HHS / OD / DP1 OD006430-01; United States / NIAID NIH HHS / AI / AI067798; United States / NIH HHS / OD / DP1OD006430; United States / NIDDK NIH HHS / DK / R01 DK063031-03; United States / NIAID NIH HHS / AI / U19 AI067798-050006; United States / NIAID NIH HHS / AI / AI067798-040006; United States / NIDDK NIH HHS / DK / DK072234-04; United States / NIDDK NIH HHS / DK / R01 DK063031-01S1; United States / NIDDK NIH HHS / DK / R01 DK063031-07; United States / NIAID NIH HHS / AI / AI067798-050006; United States / NIAID NIH HHS / AI / U19 AI067798-030006; United States / NIAID NIH HHS / AI / AI067798-020006; United States / NIDDK NIH HHS / DK / R01 DK063031-01; United States / NIDDK NIH HHS / DK / R01 DK063031-04; United States / NCI NIH HHS / CA / DP1 CA174422; United States / NIDDK NIH HHS / DK / DK063031-03; United States / NIAID NIH HHS / AI / AI067798-030006; United States / NIH HHS / OD / OD006430-01; United States / NIDDK NIH HHS / DK / DK63031; United States / NHLBI NIH HHS / HL / R01 HL097767; United States / NIDDK NIH HHS / DK / DK063031-04; United States / NIDDK NIH HHS / DK / DK072234-01A1; United States / NCI NIH HHS / CA / CA122206; United States / NIDDK NIH HHS / DK / DK063031-01S1; United States / NIAID NIH HHS / AI / U19 AI067798-010006; United States / NIDDK NIH HHS / DK / DK072234-03; United States / NIAID NIH HHS / AI / U19 AI067798; United States / NIDDK NIH HHS / DK / R01 DK063031-02; United States / NIAID NIH HHS / AI / U19 AI067798-040006; United States / NHLBI NIH HHS / HL / R01 HL097767-01; United States / NHLBI NIH HHS / HL / HL097767-01; United States / NIH HHS / OD / DP1 OD006430-02; United States / NIAID NIH HHS / AI / AI067798-010006; United States / NIDDK NIH HHS / DK / R01 DK063031; United States / NIDDK NIH HHS / DK / R01 DK063031-08; United States / NIDDK NIH HHS / DK / R01 DK072234-04; United States / NHLBI NIH HHS / HL / R01 HL097767-02; United States / NIGMS NIH HHS / GM / T32 GM007184-33; United States / NIDDK NIH HHS / DK / DK063031-08; United States / NIDDK NIH HHS / DK / R01 DK063031-07S1; United States / NIDDK NIH HHS / DK / R01 DK063031-05; United States / NIDDK NIH HHS / DK / DK063031-05; United States / NHLBI NIH HHS / HL / HL097767-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MSI2 protein, human; 0 / Membrane Proteins; 0 / Msi2h protein, mouse; 0 / Nerve Tissue Proteins; 0 / Notch1 protein, mouse; 0 / Nuclear Pore Complex Proteins; 0 / Numb protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Proteins; 0 / Receptor, Notch1; 0 / Tumor Suppressor Protein p53; 0 / homeobox protein HOXA9; 0 / nuclear pore complex protein 98; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS206659; NLM/ PMC2918284
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5. Helbig G, Bober G, Seweryn M, Wichary R, Tukiendorf A, Sedlak L, Oleksy T, Kyrcz-Krzemień S: Occurrence of secondary malignancies in chronic myeloid leukemia during therapy with imatinib mesylate-single institution experience. Mediterr J Hematol Infect Dis; 2015;7(1):e2015003
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  • [Title] Occurrence of secondary malignancies in chronic myeloid leukemia during therapy with imatinib mesylate-single institution experience.
  • INTRODUCTION: Imatinib mesylate (IM) remains the treatment of choice for chronic myeloid leukemia (CML) showing a remarkable efficacy and offers a perspective for long disease-free survival.
  • OBJECTIVE: To investigate the incidence and clinical outcome of secondary malignancies during IM therapy for CML.
  • MATERIAL AND METHODS: The records of 221 CML patients treated with IM between 2003-2013 in a single institution were reviewed.
  • The Poisson regression model was used to estimate the relative risks for SM and death in CML patients.
  • Two patients were diagnosed with their CML at accelerated phase whereas 6 had chronic phase.
  • One patient did not receive treatment due to disseminated disease.
  • All CML patients were in hematologic and complete cytogenetic response (CCR) at the time of SM development.
  • All of them also met the criteria for major molecular response (BCR-ABL(IS) ≤0.1%).
  • The risks for SM development as well as death due to SM in CML patients were not statistically increased if compared to age-adjusted population.
  • CONCLUSIONS: The association between IM therapy for CML and SM development has not been found.

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  • (PMID = 25574362.001).
  • [ISSN] 2035-3006
  • [Journal-full-title] Mediterranean journal of hematology and infectious diseases
  • [ISO-abbreviation] Mediterr J Hematol Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC4283924
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6. Salimizand H, Amini S, Abdi M, Ghaderi B, Azadi NA: Concurrent effects of ABCB1 C3435T, ABCG2 C421A, and XRCC1 Arg194Trp genetic polymorphisms with risk of cancer, clinical output, and response to treatment with imatinib mesylate in patients with chronic myeloid leukemia. Tumour Biol; 2016 Jan;37(1):791-8
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  • [Title] Concurrent effects of ABCB1 C3435T, ABCG2 C421A, and XRCC1 Arg194Trp genetic polymorphisms with risk of cancer, clinical output, and response to treatment with imatinib mesylate in patients with chronic myeloid leukemia.
  • There are a paucity and contradicted data about the impact of concurrent heredity of polymorphic genes and risk of chronic myeloid leukemia (CML).
  • In the present study, the concurrent effects of three polymorphisms affecting the integrity of DNA consist of ABCB1 C3435T, ABCG2 C421A, and XRCC1 Arg194Trp on development of chronic myeloid leukemia were studied.
  • In this case-control study, 70 CML patients and 140 healthy individuals were enrolled in the study.
  • The clinical features of patients such as phase of disease and response to treatment and laboratory data before and after treatment with imatinib mesylate were collected.
  • TT genotype of ABCB1 and TT genotype of XRCC1 were associated with higher risk of chronic myeloid leukemia development.
  • CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 were also correlated with a higher risk of CML.
  • Patients with C allele of ABCB1 had poor cytogenetic response, and correlation of CC421 ABCG2/TT3435 ABCB1 diplotype with accelerated phase of CML was significant.
  • Patients with CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 diplotypes might be at higher risk to rapid and severe development of CML and have weaker response to treatments with imatinib.
  • [MeSH-major] Imatinib Mesylate / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Neoplasms / drug therapy. Neoplasms / genetics

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  • (PMID = 26250462.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / DNA-Binding Proteins; 0 / P-Glycoproteins; 0 / X-ray repair cross complementing protein 1; 8A1O1M485B / Imatinib Mesylate
  • [Keywords] NOTNLM ; ABCB1 / ABCG2 / Chronic myeloid leukemia / Imatinib mesylate / Polymorphism / XRCC1
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7. Kantarjian H, le Coutre P, Cortes J, Pinilla-Ibarz J, Nagler A, Hochhaus A, Kimura S, Ottmann O: Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance. Cancer; 2010 Jun 1;116(11):2665-72
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  • [Title] Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance.
  • BACKGROUND: : INNO-406, a dual v-abl Abelson murine leukemia viral oncogene homolog (Abl)/v-yes-1 Yamaguchi sarcoma viral-related oncogene homolog (Lyn) tyrosine kinase inhibitor (TKI), has demonstrated specific Lyn kinase inhibitory activity with no or limited activity against other sarcoma (Src) family member kinases.
  • Several breakpoint cluster region (Bcr)-Abl kinase domain mutations are sensitive to INNO-406 in vitro, including mutations that involve a phenylalanine-to-leucine or phenylalanine-to-valine substitution at codon 317 (F317L and F317V, respectively).
  • In the current study, the authors evaluated the use of INNO-406 in patients with Philadelphia (Ph) chromosome-positive chronic myelogenous leukemia (CML) or acute lymphocytic leukemia (ALL) after imatinib resistance or intolerance.
  • Of 31 patients with CML in chronic phase who received INNO-406, the major cytogenetic response rate was 19%.
  • No responses were observed in patients who had CML in accelerated phase, CML in blastic phase, or Ph-positive ALL.
  • CONCLUSIONS: : INNO-406 had anti-CML efficacy in a heavily pretreated study population.
  • On the basis of the classic determinations of both DLT and MTD, the recommended phase 2 dose of oral INNO-406 was 240 mg twice daily.

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  • [Copyright] (c) 2010 American Cancer Society.
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  • (PMID = 20310049.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632-070007; United States / NCI NIH HHS / CA / CA100632-070007; United States / NCI NIH HHS / CA / P01CA049639; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P01 CA049639
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 859212-16-1 / bafetinib; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS189694; NLM/ PMC2876208
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8. DeFilipp Z, Khoury HJ: Management of advanced-phase chronic myeloid leukemia. Curr Hematol Malig Rep; 2015 Jun;10(2):173-81
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  • [Title] Management of advanced-phase chronic myeloid leukemia.
  • The management of chronic myeloid leukemia (CML) in accelerated or blast phase (advanced phase) remains a significant challenge despite the introduction of very effective tyrosine kinase inhibitors (TKIs).
  • The biology of advanced-phase CML is complex and engages several pathways that are not optimally targeted by TKIs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Chronic-Phase / therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Blast Crisis / therapy. Consolidation Chemotherapy / methods. Disease Management. Humans. Molecular Targeted Therapy / methods

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  • (PMID = 25929768.001).
  • [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 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors
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9. Foran J, Ravandi F, Wierda W, Garcia-Manero G, Verstovsek S, Kadia T, Burger J, Yule M, Langford G, Lyons J, Ayrton J, Lock V, Borthakur G, Cortes J, Kantarjian H: A phase I and pharmacodynamic study of AT9283, a small-molecule inhibitor of aurora kinases in patients with relapsed/refractory leukemia or myelofibrosis. Clin Lymphoma Myeloma Leuk; 2014 Jun;14(3):223-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I and pharmacodynamic study of AT9283, a small-molecule inhibitor of aurora kinases in patients with relapsed/refractory leukemia or myelofibrosis.
  • Two patients with accelerated-phase chronic myeloid leukemia showed evidence of benefit, manifested as a cytogenetic response in 1 case; 1 patient completed 6 cycles of treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Leukemia / drug therapy. Leukemia / pathology. Primary Myelofibrosis / drug therapy. Primary Myelofibrosis / pathology. Protein Kinase Inhibitors / therapeutic use. Urea / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Drug Administration Schedule. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Recurrence. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2014 Elsevier Inc. All rights reserved.
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  • (PMID = 24355079.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCATS NIH HHS / TR / UL1 TR000371
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Protein Kinase Inhibitors; 8W8T17847W / Urea
  • [Other-IDs] NLM/ NIHMS593260; NLM/ PMC4096861
  • [Keywords] NOTNLM ; Blood cancer / Clinical / Dose escalation / Response / Tolerability
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10. Al-Achkar W, Moassass F, Ikhtiar A, Liehr T, Othman MA, Wafa A: Hyperdiploidy associated with T315I mutation in BCR-ABL kinase domain in an accelerated phase-chronic myeloid leukemia case. Mol Cytogenet; 2014;7(1):89
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  • [Title] Hyperdiploidy associated with T315I mutation in BCR-ABL kinase domain in an accelerated phase-chronic myeloid leukemia case.
  • BACKGROUND: Chronic myeloid leukemia (CML) is genetically characterized by the occurrence of a reciprocal translocation t(9;22)(q34;q11), resulting in a BCR/ABL gene fusion on the derivative chromosome 22, i.e. the Philadelphia (Ph) chromosome.
  • During CML progression 60-80% of the cases acquire additional genetic changes.
  • Even though hyperdiploidy is not a rare finding in advanced phase-CML, hyperdiploidy together with a T315I kinase domain (KD) mutation in the BCR-ABL gene has not yet been reported.
  • RESULTS: A complete cytogenetic and molecular cytogenetic analysis; molecular biology methods such as quantitative reverse transcription polymerase chain reaction (RQ-PCR) and allele-specific oligonucleotide (ASO)-PCR; and immunophenotypically confirmed CML in acceleration phase (AP).
  • Our case revealed the presence of hyperdiploidy including multiple copies of the Ph chromosome, presence of b3a2 fusion transcript,T315I mutation in BCR-ABL KD in pre imatinib mesylate (IM) treatment.
  • The ratio of BCR-ABL/ABL expression in post nilotinib treatment was 0.07% on international scale.

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  • (PMID = 25621010.001).
  • [ISSN] 1755-8166
  • [Journal-full-title] Molecular cytogenetics
  • [ISO-abbreviation] Mol Cytogenet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4305221
  • [Keywords] NOTNLM ; Chronic myeloid leukemia / Hyperdiploidy / Philadelphia chromosome / Prognostic factors / T315I mutation
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