TKI treatment promotes mitochondrial fission and metabolic reprogramming toward oxidative phosphorylation in residual EGFR‐mutant lung cancer cells. Targeting this metabolic vulnerability restores TKI sensitivity and provides a promising strategy to overcome acquired resistance.
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Comprehensive transcriptomic characterization of two melanoma cell lines with acquired dual resistance to BRAF and MEK inhibitors. [PDF]
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Nobiletin in cancer therapy: Emerging insights into multi-target mechanisms, overcoming drug resistance and therapeutic translation (Review). [PDF]
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Phenotypic alterations and PI3K-AKT pathway regulation in senescence of human tonsil mesenchymal stem cells. [PDF]
Qiu X, Lin Z, Sun Y, Zhao A, Chen X.
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Avapritinib for targeting KIT D816V-mutated acute myeloid leukemia relapsed after allogeneic hematopoietic stem cell transplant with extramedullary and central nervous system involvement. [PDF]
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Copy Number Amplification and c-Myc Transcriptional Activation-Mediated RNA-Binding Protein MEX3A Promotes EGFR-TKI Resistance in Non-Small-Cell Lung Cancer. [PDF]
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Genomic Subtype Influences BH3 Mimetic Drug Sensitivity and Synergy with Cytotoxic Chemotherapeutics in T-cell Acute Lymphoblastic Leukemia. [PDF]
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Expression and Function of the c-kit Proto-Oncogene Protein in Mouse Sperm
The Journal of Urology, 1998The presence and role of the c-kit protein were examined in mature sperm of the mouse. Monoclonal antibodies (mAbs) against the c-kit protein were used to perform immunohistochemical staining, electron microscopy studies, and Western blot analysis. The acrosomal region of both fixed and unfixed noncapacitated sperm stained with the antibodies.
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Proto-oncogene c-kit expression in malignant melanoma: protein loss with tumor progression.
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 1997The c-kit gene encodes a transmembrane receptor that has tyrosine kinase activity. c-kit plays a role in hematopoiesis, gametogenesis, and melanogenesis. c-kit is found in melanocytes, and there is evidence that expression is lost in melanoma. We studied 85 melanocytic lesions for c-kit by immunohistochemical techniques using a monoclonal antibody. The
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