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Coexistence of a novel , double-fusion in a lung poorly differentiated adenocarcinoma patient and response to alectinib: a case report and literature review.
Front Oncol
December 2024
Department of Pathology, China-Janpan Friendship Hospital, Beijing, China.
Background: Anaplastic lymphoma kinase () rearrangement, the most common oncogenic rearrangement in lung adenocarcinoma, occurs in approximately 5% of non-small cell lung cancer (NSCLC) patients. gene is the most common partner of rearrangement, and distinct EML4-ALK fusions differ in their responsiveness to ALK tyrosine kinase inhibitors. However, the concurrence of two rearrangements in one patient and whose response to ALK-TKIs have rarely been reported so far.
View Article and Find Full Text PDFFusion circRNA F-circEA1 facilitates EML4-ALK1 positive lung adenocarcinoma progression through the miR-4673/SMAD4/ADAR1 axis.
Cell Signal
December 2024
Department of Respiratory Medicine, Jinling Hospital, Nanjing Medical University, Jiangsu Province, China. Electronic address:
Circular RNA (circRNA) can sponge miRNA participate in the tumorigenesis and progression of various cancers. We substantiate for the first time that the fusion circular RNA (F-circRNA) F-circEA1 is involved in driving the echinoderm microtubule associated-protein like 4-anaplastic lymphoma kinase variant 1-positive (EML4-ALK1) lung adenocarcinoma (LUAD) progression and the expression of the parental gene EML4-ALK1, molecular mechanisms of F-circEA1 in the EML4-ALK1 LUAD remain unknown. Bioinformatics analysis showed that only miR-4673 can bind to F-circEA1 and bind to EML4-ALK1 3'-UTR to regulate the expression of EML4-ALK1.
View Article and Find Full Text PDFMicrotubule Association of EML4-ALK V3 Is Key for the Elongated Cell Morphology and Enhanced Migration Observed in V3 Cells.
Cells
November 2024
Department of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 7RH, UK.
The EML4-ALK oncogene drives tumour progression in approximately 5% of cases of non-small-cell lung cancers. At least 15 EML4-ALK variants have been identified, which elicit differential responses to conventional ALK inhibitors. Unfortunately, most, if not all, patients eventually acquire resistance to these inhibitors and succumb to the disease, which warrants the need for alternative targets to be identified.
View Article and Find Full Text PDFDesign and evaluation of anaplastic lymphoma kinase degraders using a covalent fumarate handle.
Bioorg Med Chem Lett
March 2025
Therapeutics and Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon 34114, Republic of Korea; Medicinal Chemistry and Pharmacology, Korea University of Science and Technology, Daejeon 34113, Republic of Korea. Electronic address:
Targeted protein degradation has emerged as a novel therapeutic paradigm in drug discovery. Despite the FDA approval of anaplastic lymphoma kinase (ALK) inhibitors, the pursuit of compounds with enhanced potency and prolonged efficacy remains crucial to mitigate inevitable adverse effects. In this context, we endeavored to develop ALK degraders utilizing FDA-approved ALK inhibitors-crizotinib, ceritinib, brigatinib, and alectinib-as ALK binders, along with 4-methoxyphenylfumarate as a covalent handle to bind to RNF126 E3 ligase.
View Article and Find Full Text PDFA novel double fusion of EML4-ALK and PLEKHA7-ALK contribute to rapid progression of lung adenocarcinoma: a case report and literature review.
Discov Oncol
November 2024
Department of Respiratory and Critical Care Medicine, Changzheng Hospital, Naval Medical University, Shanghai, 200003, China.
A 40-year-old male with EML4-ALK (E6:A20) fusion variant 3 and previously unreported PLEKHA7-ALK (P3:A20) fusion in lung adenocarcinoma exhibited resistance to alectinib and chemotherapy. Subsequent next-generation sequencing (NGS) from the plasma specimen revealed the co-existing mutation in the KEAP1 gene, which may represent an intrinsic resistance to ALK-TKI. Furthermore, the presence of double fusion PLEKHA7-ALK (P3:A20) may also have played a critical role in the resistance to alectinib.
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