Results 111 to 120 of about 19,649 (222)

MYC in chronic myeloid leukemia: Induction of aberrant DNA synthesis and association with poor response to imatinib [PDF]

, 2012
El pdf es la versión post-print.-- et al.Untreated chronic myeloid leukemia (CML) progresses from chronic phase to blastic crisis (BC). Increased genomic instability, deregulated proliferation, and loss of differentiation appear associated to BC, but the
Acosta, Juan C., Albajar, Marta, Delgado, M. Dolores, Gómez-Casares, M. Teresa, León, Javier, Mauleon, Itaso, Vaqué, José P.   +6 more
core   +2 more sources

Progression significance for low‐level aberrant B‐lymphoblasts in chronic myeloid leukaemia patients

Clinical and Translational Medicine, Volume 15, Issue 11, November 2025.
Haoren Wang, Huijun Wang, Yuanyuan Li, Bin Zheng, Qiuyun Fang, Yan Li, Yuntao Liu, Runxia Gu, Ying Wang, Yingchang Mi, Bingcheng Liu, Hui Wei, Jianxiang Wang   +12 more
wiley   +1 more source

BCR-ABL mutational studies for predicting the response of patients with chronic myeloid leukaemia to second-generation tyrosine kinase inhibitors after imatinib fail [PDF]

, 2009
Imatinib is the standard treatment for chronic myeloid leukaemia. BCR-ABL kinase domain mutation is the commonest mechanism implicated in imatinib resistance. In in-vitro studies, kinase domain mutations are variably resistant to second-line agents.
Chan, YY, Kwan, TK, Lie, AKW, Liu, HSY, Ma, ESK, Sim, JPY, Wan, TSK, Yeung, YM, Yip, SF   +8 more
core  

ABCB1 Overexpression Is a key initiator of resistance to tyrosine kinase inhibitors in CML cell lines [PDF]

, 2016
The tyrosine kinase inhibitor (TKI) imatinib has resulted in excellent responses in the majority of Chronic Myeloid Leukaemia (CML) patients; however, resistance is observed in 20-30% of patients.
Eadie, L., Hughes, T., White, D.
core   +4 more sources

Cooperation of imipramine blue and tyrosine kinase blockade demonstrates activity against chronic myeloid leukemia [PDF]

, 2016
The use of tyrosine kinase inhibitors (TKI), including nilotinib, has revolutionized the treatment of chronic myeloid leukemia (CML). However current unmet clinical needs include combating activation of additional survival signaling pathways in ...
Arbiser, Arbiser, Bellamkonda, Bellamkonda, Bhatia, Bruner-Klisovic, Cao, Cao, Cao, Cao, Cao, Cao, Cao, Chandra, Chen, Dikalov, Gallo, Goris, Holyoake, Holyoake, Holyoake, Holyoake, Holyoake, Jordan, Kantarjian, Kogan, Larsson, Lehn, Li, Lozzio, Marcucci, Miyoshi, Neviani, Omay, Passegue, Passegue, Passegue, Perrotti, Rousselot, Rowntree, Shah, Skorski, Stoklosa, Suda, Tonks, White, Yang, Zhang   +47 more
core   +3 more sources

Insertion (22;9)(q11;q34q21) in a patient with chronic myeloid leukemia characterized by fluorescence in situ hybridization [PDF]

, 2001
An unusual cytogenetic rearrangement, described as ins(22;9)(q11;q34q21), was detected in a 49-year-old male patient diagnosed with chronic myeloid leukemia (CML). Reverse transcriptase polymerase chain reaction (RT-PCR) revealed a b3a2 fusion transcript.
Calasanz-Abinzano, M.J. (Maria Jose), Ferreira, C. (C.), García-Delgado, M. (Marina), Giraldo, P. (P.), Gomez, E. (Emilio), Lahortiga, I. (Idoya), Larrayoz, M.J. (María J.), Martin-Subero, J.I. (Jose Ignacio), Novo-Villaverde, F. J. (Francisco Javier), Odero, M.D. (Maria Dolores)   +9 more
core   +1 more source

TREATMENT WITH IMATINIB MESILAT IN CHRONIC MYELOGENOUS LEUKEMIA – OUR EXPERIENCE

Zdravniški Vestnik, 2004
Background. Chronic myelogenous leukemia (CML) is a malignant clonal disorder of hematopoietic stem cell. In majority of patients we find reciprocal chromosomal translocation t (9.22) which result in fusion oncoprotein with tyrosine kinase activity.
Mateja Grat, Joško Vučkovič
doaj  

BCR-ABL1 mutation development during first-line treatment with dasatinib or imatinib for chronic myeloid leukemia in chronic phase [PDF]

, 2015
BCR-ABL1 mutations are a common, well-characterized mechanism of resistance to imatinib as first-line treatment of chronic myeloid leukemia in chronic phase (CML-CP). Less is known about mutation development during first-line treatment with dasatinib and
A Hochhaus, A Hochhaus, E Jabbour, E Jabbour, E Jabbour, E Jabbour, FE Nicolini, FX Gruber, H de Lavallade, H Kantarjian, HA Bradeen, HM Kantarjian, HM Kantarjian, IJ Griswold, J Cortes, JE Cortes, JE Cortes, JE Cortes, JF Apperley, JS Ahn, JS Khorashad, M Baccarani, M Baccarani, M Deininger, M Talpaz, MC Müller, MC Müller, NP Shah, NP Shah, RA Larson, S Branford, S Branford, S Branford, S Redaelli, S Soverini, S Soverini, S Soverini, S Soverini, S Soverini, SG Willis, T Ernst, T Hughes, T Hughes, T Lange, T O'Hare, T O’Hare, WS Kim, WT Parker, WT Parker, X Jiang, Z Iqbal   +50 more
core   +2 more sources

An in vitro model for cytogenetic conversion in CML. Interferon-alpha preferentially inhibits the outgrowth of malignant stem cells preserved in long-term culture [PDF]

, 1998
IFN-alpha has been shown to prolong survival in chronic myeloid leukemia patients, but its mechanism of action is still not understood.
Borsboom, A. (Astrid), Cornelissen, J.J. (Jan), Hagemeijer, A. (Anne), Kluin-Nelemans, J.C. (Hanneke), Löwenberg, B. (Bob), Ploemacher, R.E. (Robert), Wognum, B.W.   +6 more
core   +1 more source

Hydroxychloroquine for chronic myeloid leukemia: complete cure on the horizon? [PDF]

, 2011
No abstract ...
Amaravadi, Arunima Mukhopadhyay, Bellodi, Belloni, Boya, Druker, Furst, Gordon, Gozuacik, Gudmundur V Helgason, Jiang, Kalia, Kim, Maria Karvela, Munster, Naka, Ozvegy-Laczka, Savarino, Sharma, Tessa L Holyoake, Zaidi   +20 more
core   +1 more source