Results 71 to 80 of about 52,225 (202)

Unveiling Candidate Markers for Drug Resistance or Synthetic Lethality in Cervical Cancer: Integrative Analysis of Genetic and Pharmacoprofiling

open access: yesCancer Reports, Volume 9, Issue 6, June 2026.
ABSTRACT Introduction Systemic cervical cancer management continues to be challenging. Numerous chemotherapies have been approved, but predicting response is difficult due to the lack of biomarkers. Here, we analyze the genetic and protein profiles of 20 cervical cancer cell lines (CCCLs) and explore their correlation with drug response patterns to ...
Suzy Scholl   +10 more
wiley   +1 more source

Quinacrine Depletes BCR-ABL and Suppresses Ph-Positive Leukemia Cells

open access: yesCancer Investigation, 2019
Drug resistance to TKIs and the existance of CML leukemia stem cells is an urgent problem. In this study, we demonstrate that quinacrine (QC) induces apoptosis in BCR-ABL positive CML and acute lymphoblastic leukemia (ALL) cells. Interestingly, QC inhibits the colony formation of primary CD34+ progenitor/stem leukemia cells from CML patients.
Hu Lei   +8 more
openaire   +2 more sources

Dynamics of mutant BCR-ABL-positive clones after cessation of tyrosine kinase inhibitor therapy

open access: yesHaematologica, 2011
Background Point mutations of the BCR-ABL tyrosine kinase domain are considered the predominant cause of imatinib resistance in chronic myeloid leukemia.
Benjamin Hanfstein   +9 more
doaj   +1 more source

Multifaceted actions of 8-amino-adenosine kill BCR–ABL positive cells [PDF]

open access: yesLeukemia & Lymphoma, 2012
Survival of chronic myelogenous leukemia (CML) cells is dependent on BCR-ABL kinase, the activity of which is contingent on the level of BCR-ABL protein and the availability of adenosine triphosphate (ATP). We hypothesized that 8-amino-adenosine (8-amino-Ado)-mediated reduction in cellular ATP level and inhibition of mRNA synthesis leading to a ...
Rathi N, Pillai   +7 more
openaire   +2 more sources

RAPSYN-mediated neddylation of BCR-ABL alternatively determines the fate of Philadelphia chromosome-positive leukemia

open access: yeseLife
Philadelphia chromosome-positive (Ph+) leukemia is a fatal hematological malignancy. Although standard treatments with tyrosine kinase inhibitors (TKIs) have achieved remarkable success in prolonging patient survival, intolerance, relapse, and TKI ...
Mengya Zhao   +10 more
doaj   +1 more source

Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism

open access: yesBMC Cancer, 2012
Background Philadelphia positive leukemias are characterized by the presence of Bcr-Abl fusion protein which exhibits an abnormal kinase activity. Selective Abl kinase inhibitors have been successfully established for the treatment of Ph (+) leukemias ...
Khateb Mamduh   +7 more
doaj   +1 more source

Evidence-based guidelines for the use of tyrosine kinase inhibitors in adults with Philadelphia chromosome-positive or BCR-ABL-positive acute lymphoblastic leukemia: a Canadian consensus.

open access: yesCurrent Oncology, 2014
Adult Philadelphia chromosome-positive (Ph+) or BCR-ABL-positive (BCR-ABL+) acute lymphoblastic leukemia (all) is an acute leukemia previously associated with a high relapse rate, short disease-free survival, and poor overall survival.
S. Couban   +9 more
semanticscholar   +1 more source

BCR‐ABL enhances the prolyl isomerase activity of Pin 1 by interacting with DAPK1 in ph+ ALL

open access: yesCancer Medicine, 2018
Philadelphia chromosome (Ph)/BCR‐ABL‐positive (ph+) ALL is the most common genetic abnormality associated with ALL and has been shown to confer the worst prognosis to both children and adults.
Wen‐bin Cao   +12 more
doaj   +1 more source

Oxidative Stress in the Tumor Immune Microenvironment: Mechanisms and Therapeutic Perspectives

open access: yesMedComm – Oncology, Volume 5, Issue 2, June 2026.
Oxidative stress is involved in several key processes in cancer, including redox regulation, DNA damage, post‐translational modifications, transcriptional regulation, epigenetic modifications, metabolic reprogramming, cell death, and immune modulation. These mechanisms collectively influence tumor progression, immune evasion, and therapeutic responses,
Zhen Wang   +14 more
wiley   +1 more source

PF-114, a Novel Inhibitor of Bcr-Abl Chimeric Tyrosine Kinase, Attenuates Intracellular CrkL Phosphorylation and Kills Chronic Myeloid Leukemia Cells

open access: yesКлиническая онкогематология, 2016
Background & Aims. The chimeric tyrosine kinase Bcr-Abl triggers malignant transformation of myeloid cells via phosphorylation of a number of substrates including the CrkL adaptor protein.
E. S. Kolotova   +9 more
doaj   +1 more source

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