Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Cofilin (CFL1) is one critical member of the actin deploy family (ADF). Overexpression of CFL1 is associated with aggressive features and poor prognosis in malignancies. We evaluated the expression of CFL1 in patients with chronic myeloid leukemia in the chronic phase (CML-CP), acute myelocytic leukemia (AML) and healthy controls. The role of CFL1 in imatinib therapy was also investigated using cell line. We found that the expression of CFL1 was lower in CML patients than that in healthy controls, and was significantly upregulated after imatinib therapy (p<0.05). CML patients with lower CFL1 achieved higher Major molecular response (MMR) rate after 6 months of imatinib therapy (p<0.05). Cofilin, P-cofilin and F-actin, especially branched F-actin were all upregulated after imatinib therapy. The lower CFL1 expression before treatment may predicts a better response to imatinib. Imatinib affects F-actin remodeling in CML patients by regulating CFL1 expression and activity.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10937266 | PMC |
| http://dx.doi.org/10.7150/jca.92202 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Targeting yes-associated protein to overcome imatinib resistance in gastrointestinal stromal tumor drug-tolerant persister cells.
Gastric Cancer
September 2025
Department of Gastroenterological Surgery, The University of Osaka Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Background: The tyrosine kinase inhibitor (TKI) imatinib targets KIT and PDGFRA, offering significant therapeutic benefits in advanced gastrointestinal stromal tumors (GISTs). However, the high rate of recurrence following treatment discontinuation suggests that drug-tolerant persister cells (DTPs) may contribute to therapy resistance. Elucidating the mechanisms underlying DTP survival is critical for the development of curative strategies.
View Article and Find Full Text PDFHistopathologic and Clinical Characteristics of Cutaneous Toxicities of Tyrosine Kinase Inhibitors: Insights Into Pathologic Mechanisms From a Retrospective Cohort.
Am J Dermatopathol
September 2025
Dermatology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY.
Background: Dermatologic adverse events (dAEs) are prevalent with BCR-ABL tyrosine kinase inhibitors (TKIs), affecting quality of life and treatment adherence. Despite their prevalence, underlying mechanisms of toxicity remain unclear. We sought to characterize dAEs across TKI generations to elucidate mechanisms driving toxicities.
View Article and Find Full Text PDFLeveraging artificial intelligence and machine learning in kinase inhibitor development: advances, challenges, and future prospects.
RSC Med Chem
August 2025
Pharmaceutical Organic Chemistry Department, Faculty of Pharmacy, Suez Canal University 4.5 Km the Ring Road Ismailia 41522 Egypt.
Protein kinases are central regulators of cell signaling and play pivotal roles in a wide array of diseases, most notably cancer and autoimmune disorders. The clinical success of kinase inhibitors-such as imatinib and osimertinib-has firmly established kinases as valuable drug targets. However, the development of selective, potent inhibitors remains challenging due to the conserved nature of the ATP-binding site, off-target effects, resistance mutations, and patient-specific variability.
View Article and Find Full Text PDFHow I treat Ph+ acute lymphoblastic leukemia.
Future Oncol
September 2025
Division of Leukemia, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is characterized by the fusion gene which produces a constitutively active tyrosine kinase which drives disease pathogenesis and is associated with resistance to conventional chemotherapy. Intensive cytotoxic chemotherapy followed by allogeneic hematopoietic stem cell transplantation (HSCT), the historical treatment paradigm for Ph+ ALL, was associated with poor outcomes. The introduction of inhibitors of ABL1 revolutionized the treatment of Ph+ ALL.
View Article and Find Full Text PDFGrowth factors involved in vascular remodeling in pulmonary arterial hypertension.
J Smooth Muscle Res
September 2025
Department of Physiology, Aichi Medical University, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan.
Pulmonary arterial hypertension (PAH) is a rare and fatal cardiovascular disease characterized by pulmonary vascular remodeling, leading to a progressive increase in pulmonary vascular resistance and pulmonary arterial pressure (PAP). Elevated PAP induces right ventricular hypertrophy and eventually progresses to right heart failure. Pulmonary vascular remodeling is primarily caused by the excessive proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs) in the medial layer.
View Article and Find Full Text PDF