Results 101 to 110 of about 81,803 (228)

DNA Replication Stress‐Induced Transcriptome of Human Burkitt's Lymphoma Identifies Reciprocal Regulation Between MBD1 and BCL6 During Germinal Center‐Derived B‐Lymphomagenesis

Hematological Oncology, Volume 44, Issue 5, September 2026.
ABSTRACT BCL6 is a master transcriptional regulator of germinal center (GC) B cells. BCL6 is frequently translocated at the major translocation cluster (MTC) within intron 1 of the BCL6 locus, a hotspot commonly rearranged in diffuse large B cell lymphomas (DLBCLs).
Santosh Kumar Gothwal, Kyoko Oichai, Hongtae Kim, Kyungjae Myung, Jacqueline H. Barlow   +4 more
wiley   +1 more source

Oncogenic KRAS Rewires Stress Granule Dynamics: Mechanisms and Therapeutic Opportunities

The Kaohsiung Journal of Medical Sciences, Volume 42, Issue 9, September 2026.
ABSTRACT Stress granules (SGs) are dynamic, membrane‐less structures that form in response to various cellular stresses, including metabolic, oxidative, and therapeutic challenges. They function as adaptive hubs and reorganize protein synthesis and signaling networks to help cells survive under stress. In cancer, these condensates are often hijacked to
Msimisi Ndzinisa, Birhanetensay Masresha Altaye, Yuh‐Pyng Sher   +2 more
wiley   +1 more source

Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia [PDF]

, 2001
Chronic myeloid leukemia (CML) is characterized by formation of the BCR-ABL fusion gene, usually as a consequence of the Philadelphia (Ph) translocation between chromosomes 9 and 22.
Reid, AG, Campbell, LJ, Telford, N, Grace, C, Nacheva, EP, Shepherd, P, Szer, J, Green, AR, Bench, AJ, Prince, HM, Huntly, BJP, Turner, P   +11 more
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Cross-talk between Bcr-abl and the Thioredoxin System in Chronic Myeloid Leukaemia: Implications for CML Treatment

, 2020
Chronic myeloid leukaemia (CML) is currently treated with inhibitors of the CML specific oncoprotein, bcr-abl. While this strategy is initially successful, drug resistance can become a problem.
Sicong Wang, Wang, Sicong, Di Trapani, Giovanna, Prahlad V. Raninga, Clapper, Erin, Tonissen, Kathryn F, Erin Clapper, Raninga, Prahlad V, Kathryn F. Tonissen, Giovanna Di Trapani   +9 more
core   +1 more source

Cyclins and Cyclin‐Dependent Kinases: Structure, Biological Functions, and Innovative Targeting Strategies in Cancer

MedComm, Volume 7, Issue 9, September 2026.
This work synthesizes recent insights into the pathological roles of cyclins and cyclin‐dependent kinases (CDKs) across human cancers, highlights state‐of‐the‐art innovative approaches (especially targeted degradation and redistribution of CDK/cyclin proteins) for cancer therapy, and outlines future directions for CDK/cyclin‐related biomedical research.
Suya Zheng, Zhipeng Shen, Yuanfang Wu, Xingze Huang, Zhongyuan Zhang, Jiangyu Liu, Qichun Wei, Wenhao Chen, Ye Chen, Liang Xu   +9 more
wiley   +1 more source

Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide through glutathione-depletion in imatinib-resistant cells

Haematologica, 2007
The development of resistance to imatinib mesylate may partly depend on high Bcr-Abl-expression levels. Arsenic trioxide (ATO) has Bcr-Abl suppressing activity in vitro.
Heiko Konig, Nicolai Härtel, Beate Schultheis, Michael Schatz, Christian Lorentz, Junia V. Melo, Rüdiger Hehlmann, Andreas Hochhaus, Paul La Rosée   +8 more
doaj   +1 more source

Heat Shock Proteins in Cancer: Mechanisms and Therapeutic Targeting

MedComm, Volume 7, Issue 9, September 2026.
This review illustrates heat shock proteins (HSPs) as central regulators of cancer metabolic reprogramming. By stabilizing key metabolic enzymes and coordinating glycolysis, oxidative phosphorylation, redox homeostasis, and stress adaptation, HSPs support tumor growth, metastasis, and therapeutic resistance. Targeting HSP networks may therefore provide
Sheng Ma, Chen‐Qian Liu, Si‐Yang Ma, Shao‐Gang Wang, Qi‐Dong Xia, Meng‐Yao Xu   +5 more
wiley   +1 more source

Targeting USP10–FAK pathway sensitizes BCR-ABL+ leukemia cells to tyrosine kinase inhibitors

Cell Investigation
BCR-ABL+ leukemia is driven by constitutive tyrosine kinase activity, and tyrosine kinase inhibitors (TKIs) are the standard therapy. However, resistance to TKIs remains a significant clinical challenge.
Kangjie Qiu, Xianfeng Wang, Zhen Liu, Xueting Peng, Shuxin Zhong, Zhangshuai Dai, Xianfeng Zha, Peipei Wang, Chengwu Zeng   +8 more
doaj   +1 more source

Update on Non‐Biological and RNA‐Based Therapeutics in Chronic Inflammatory Diseases: Precision Medicine Through Small Molecules: An EAACI Position Paper

Allergy, Volume 81, Issue 9, Page 3039-3070, September 2026.
ABSTRACT In the last decades, critical advancements in research technology and knowledge on disease mechanisms steered therapeutic approaches for chronic inflammatory diseases towards unprecedented target specificity. For allergic and chronic lung diseases, biologic drugs pioneered this goal, acquiring on the way—through the clinical use of monoclonal ...
Franziska Roth‐Walter, Ian M. Adcock, Cristina Benito‐Villalvilla, Rodolfo Bianchini, Leif Bjermer, Gaetano Caramori, Luigi Cari, Kian Fan Chung, Zuzana Diamant, Ibon Eguiluz‐Gracia, Edward F. Knol, Milos Jesenak, Francesca Levi‐Schaffer, Giuseppe Nocentini, Liam O'Mahony, Oscar Palomares, Frank Redegeld, Milena Sokolowska, Betty Van Esch, Marco Zurlo, Cristiana Stellato   +20 more
wiley   +1 more source

Importância da investigação da mutação JAK2V617F em pacientes com neoplasia mieloproliferativa crônica BCR/ABL negativa e sua associação com a expressão da proteína antiapoptótica survivina como marcador diagnóstico [PDF]

, 2012
Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Programa de Pós-Graduação em Farmácia, Florianópolis, 2011As neoplasias mieloproliferativas crônicas (NMPC) são neoplasias originadas por uma proliferação ...
Barcelos, Michelle Maccarini
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