Results 61 to 70 of about 427,029 (392)

Chronic Myeloid Leukemia, Version 2.2024, NCCN Clinical Practice Guidelines in Oncology.

The Journal of the National Comprehensive Cancer Network
Chronic myeloid leukemia (CML) is defined by the presence of Philadelphia chromosome resulting from a reciprocal translocation between chromosomes 9 and 22 [t9;22] that gives rise to a BCR::ABL1 fusion gene.
Neil P Shah, Ravi Bhatia, Jessica K Altman, Maria Amaya, K. Begna, Ellin Berman, O. Chan, Joan Clements, Robert H Collins, Peter Curtin, D. DeAngelo, M. Drazer, Lori Maness, L. Metheny, Sanjay R Mohan, Joseph O. Moore, V. Oehler, Keith W Pratz, Iskra Pusic, Michal G. Rose, William Shomali, B. D. Smith, Michael Styler, M. Talpaz, Tiffany N Tanaka, S. Tantravahi, James E. Thompson, Steven Tsai, Jennifer Vaughn, Jeanna Welborn, David T. Yang, Hema M Sundar, K. Gregory   +32 more
semanticscholar   +1 more source

The newfound relationship between extrachromosomal DNAs and excised signal circles

FEBS Letters, EarlyView.
Extrachromosomal DNAs (ecDNAs) contribute to the progression of many human cancers. In addition, circular DNA by‐products of V(D)J recombination, excised signal circles (ESCs), have roles in cancer progression but have largely been overlooked. In this Review, we explore the roles of ecDNAs and ESCs in cancer development, and highlight why these ...
Dylan Casey, Zeqian Gao, Joan Boyes
wiley   +1 more source

Stability and Bifurcation of the Immune Model of Chronic Myeloid Leukemia with Time Delay

Journal of Harbin University of Science and Technology
In order to investigate the effects of the differentiation delay in chronic myeloid leukemia stem cells on the dynamic behaviors among chronic myeloid leukemia stem cells, chronic myeloid leukemia mature cells and effector T cells, a delayed immune ...
WANG Jingnan, SUN Yue
doaj   +1 more source

ABC transporter A3 facilitates lysosomal sequestration of imatinib and modulates susceptibility of chronic myeloid leukemia cell lines to this drug

Haematologica, 2009
Background Inhibition of BCR-ABL tyrosine kinase activity has evolved as a mainstay of therapy for patients with chronic myeloid leukemia. However, a fraction of leukemic cells persists under targeted therapy and can lead to disease progression on ...
Bjoern Chapuy, Melanie Panse, Ulf Radunski, Raphael Koch, Dirk Wenzel, Nobuya Inagaki, Detlef Haase, Lorenz Truemper, Gerald G. Wulf   +8 more
doaj   +1 more source

Detection of BCR-ABL kinase domain mutations in CD34+ cells from newly diagnosed chronic phase CML patients and their association with imatinib resistance [PDF]

, 2011
BCR-ABL kinase domain (KD) mutations, the most common cause of imatinib resistance, are infrequently detected in newly diagnosed chronic-phase chronic myeloid leukemia (CP-CML) patients.
Aamer Aleem, Abdul Qayyum, Abid Jamil, Abid Taj, Ahmad Khalid, Ammara Tahir, Ijaz Shah, Mahwish Khan, Mubashar Naqvi, Mudassar Iqbal, Muhammad Abbad, Muhammad Ferhan, Muhammad Khalid, Najeeb ur-Rehman, Riaz ul-Haq, Shahid Baig, Tanveer Akhtar, Tariq Gill, Weng Qin, Zafar Iqbal   +19 more
core   +1 more source

MTSS1 is a critical epigenetically regulated tumor suppressor in CML [PDF]

, 2015
Chronic myeloid leukemia (CML) is driven by malignant stem cells that can persist despite therapy. We have identified Metastasis suppressor 1 (Mtss1/MIM) to be downregulated in hematopoietic stem and progenitor cells from leukemic transgenic SCLtTA/Bcr ...
Braunschweig, T., Brümmendorf, T. H., Chatain, N., Copland, M., Costa, I. G., Gusmao, E. G., Haenzelmann, S., Hamilton, A., Helgason, G.V., Herrmann, O., Holyoake, T. L., Kintsler, S., Koschmieder, S., Li, S., Merle Reher, M., Müller-Tidow, C., Schemionek, M., Schubert, C., Schwab, A.   +18 more
core   +1 more source

PICALM::MLLT10 translocated leukemia

FEBS Letters, EarlyView.
This comprehensive review of PICALM::MLLT10 translocated acute leukemia provides an in‐depth review of the structure and function of CALM, AF10, and the fusion oncoprotein (1). The multifaceted molecular mechanisms of oncogenesis, including nucleocytoplasmic shuttling (2), epigenetic modifications (3), and disruption of endocytosis (4), are then ...
John M. Cullen, Antonia C. Nakatsugawa, Natalie Barton, Henry Haines, Gary S. Stein, Janet L. Stein, Daniel S. Wechsler, Jessica L. Heath   +7 more
wiley   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

Molecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert, Lauren van den Broecke, Osman Aksoy, Judith Lind, Sonia Vallet, Arne Van der Vreken, Gamze Ates, Ann Massie, Ken Maes, Kim De Veirman, Elke De Bruyne, Karin Vanderkerken, Klaus Podar, Eline Menu   +13 more
wiley   +1 more source

Asciminib in Chronic Myeloid Leukemia after ABL Kinase Inhibitor Failure.

New England Journal of Medicine, 2019
BACKGROUND Asciminib is an allosteric inhibitor that binds a myristoyl site of the BCR-ABL1 protein, locking BCR-ABL1 into an inactive conformation through a mechanism distinct from those for all other ABL kinase inhibitors. Asciminib targets both native
T. Hughes, M. Mauro, J. Cortes, H. Minami, D. Réa, D. DeAngelo, M. Breccia, Y. Goh, M. Talpaz, A. Hochhaus, P. le Coutre, O. Ottmann, M. Heinrich, J. Steegmann, M. Deininger, J. Janssen, F. Mahon, Y. Minami, D. Yeung, D. Ross, M. Tallman, Jae H. Park, B. Druker, David Hynds, Yuyan Duan, C. Meille, F. Hourcade‐Potelleret, K. G. Vanasse, F. Lang, Dong-Wook Kim   +29 more
semanticscholar   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

Molecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 more
wiley   +1 more source