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Background: The role of ABL1 in hepatocellular carcinoma (HCC) is still unclear. Therefore, this study aims to explore the potential role of ABL1 in the progression of HCC using bioinformatics methods.
Methods: We analyzed the expression, prognostic potential, and immune cell effect of ABL1 in HCC by using a variety of datasets.
Results: ABL1 is highly expressed in HCC and associated with unfavorable overall survival (OS) and disease-free survival (DFS). Functional network analysis revealed that ABL1 plays an important role in mitochondrial activity, ATP metabolism, protein translation and metabolism, various neurological diseases, nonalcoholic fatty liver disease, and notch signaling pathway. In addition, we found that ABL1 expression was closely correlated with B cells, CD8 + T cells, CD4 + T cells, macrophages, neutrophils, and dendritic cells. Furthermore, ABL1 expression was positively associated with the expression levels of immune checkpoint genes, such as PD-1L, TIM3, TIGIT, and CTLA4.
Conclusion: ABL1 is associated with immune infiltration and prognosis of HCC.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8413061 | PMC |
http://dx.doi.org/10.1155/2021/1379706 | DOI Listing |
Br J Haematol
September 2025
Department of Pediatrics, Stanford University, Stanford, California, USA.
Chronic myeloid leukaemia (CML) accounts for 2% of leukaemias in children and 9% in adolescents. While the BCR::ABL1 fusion gene remains a hallmark across all age groups, emerging evidence suggests that paediatric CML exhibits unique biological and clinical characteristics compared to its adult counterpart. Children often present with more aggressive clinical features and show distinct treatment response patterns.
View Article and Find Full Text PDFNAR Cancer
September 2025
Department of Molecular Genetics and Microbiology, Duke University School of Medicine, 213 Research Drive, Durham, NC 27710, United States.
Treatment of patients with platinum-resistant ovarian cancer is a major clinical challenge. We found that high expression of a meiotic protein, Synaptonemal Complex Protein 2 (SYCP2), is associated with platinum resistance and tyrosine kinase ABL1 inhibitor sensitivity in ovarian cancer. We demonstrate that tyrosine kinase ABL1 inhibitors inhibit cancer cell proliferation more efficiently in ovarian cancer cell lines with SYCP2 overexpression.
View Article and Find Full Text PDFLeuk Res Rep
August 2025
Department of Hematology, The Second Hospital & Clinical Medical School, Lanzhou University, No. 82, Cuyingmen, Lanzhou, Gansu Province 730030, China.
The use of TKIs has significantly improved the prognosis of CML. However, a small subset of patients still experience poor outcomes. We present a rare case of Ph-AML following a diagnosis of CML.
View Article and Find Full Text PDFFuture 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 PDFUnlabelled: Tyrosine kinases (TKs) are frequently mutated or overexpressed in cancer, and TK inhibitors (TKIs) are an important therapeutic modality against TK-driven cancers, but many patients show an underwhelming response to TKIs prescribed on the basis of tumor genotype. To find cell-intrinsic TK signaling patterns which might be predictive of poor response to TKI exposure, we used high-sensitivity multiplexed mass spectrometry to quantify endogenous levels of 1,222 phosphotyrosine (pY) sites across the proteomes of TK-driven human cancer cell lines with variable response to genotype-matched TKIs. In direct comparisons between TKI-tolerant and TKI-sensitive lines with a common driver TK, we found that TKI treatment was equally effective at blocking driver TK signaling, and higher basal activity of the driver TK did not always predict higher sensitivity to TKI.
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