Ask about this productRelated genes to: KIF5B Blocking Peptide
- Gene:
- KIF5B NIH gene
- Name:
- kinesin family member 5B
- Previous symbol:
- KNS1
- Synonyms:
- KNS
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-24
- Date modifiied:
- 2015-08-28
Related products to: KIF5B Blocking Peptide
Related articles to: KIF5B Blocking Peptide
- fusion is a pathogenic driver factor in lung cancer patients. Currently, the conclusions on the clinical factors of fusion in NSCLC are inconsistent. - Source: PubMed
Publication date: 2026/04/28
Li XiangZhao PeiyanCui HeranZhang TingtingSun WenyuLi Hui - Resistance to third-generation EGFR tyrosine kinase inhibitors (TKIs) such as osimertinib remains a major challenge in the treatment of EGFR-mutated non-small cell lung cancer (NSCLC). While on-target and bypass mechanisms such as MET amplification are well-characterized, oncogenic fusions-particularly RET fusions-are emerging as relevant resistance mechanisms in a subset of patients. The feasibility of dual inhibition strategies and personalized monitoring through liquid biopsy remains underexplored in real-world clinical practice. - Source: PubMed
Publication date: 2026/03/18
Kropf-Sanchen CorneliaFrost NikolajKuon JonasWermke MartinKrüger StefanFuchs FlorianWiesweg MarcelChristopoulos PetrosThomas MichaelGaisa Nadine TJosten MichaelWenzel CarinaButh JanGlanemann FlorianStenzinger AlbrechtFroelich Matthias FJanning MelanieColienne MaikeHaselmann VerenaLoges Sonja - Oncogenic alterations in MET represent therapeutically actionable driver alterations in non-small cell lung cancers (NSCLC). Among these, MET fusions are rare, occurring in approximately 0.1-0.3% of NSCLC. We report the case of a 52-year-old woman with metastatic, TTF1-positive lung adenocarcinoma harboring a KIF5B::MET fusion. After progression on chemotherapy and immunotherapy, she achieved a durable response lasting nearly five years on third-line treatment with the type Ia MET inhibitor crizotinib. At the time of suspected disease progression, two tissue re-biopsies were non-diagnostic due of insufficient tumor cell content. Circulating tumor DNA (ctDNA) analysis identified two newly acquired on-target resistance mutations within the MET kinase domain (L1213V and Y1248C) in addition to the known KIF5B::MET fusion. After re-evaluation by the institutional molecular tumor board, both alterations were considered mediators of resistance to type I MET inhibitors, with available data indicating preserved sensitivity to type II inhibitors. Based on these findings, the patient was switched to cabozantinib, a multikinase type II MET inhibitor, resulting in a radiographic disease stabilization accompanied by a marked decline in tumor marker levels. This case illustrates the clinical utility of liquid biopsy for molecular resistance monitoring, particularly when tissue re-biopsy is not feasible, supports its integration into clinical decision-making, and underscores the therapeutic relevance of MET inhibitor class-switch strategies in MET fusion-positive disease. - Source: PubMed
Publication date: 2026/04/21
Rosnev StanislavKlein KatharinaHeukamp LukasLenk JulianJoosten MariaMöbs MarkusGrob TobiasBenary ManuelaVecchione LoredanaOtt Claus-EricModest Dominik PKnödler MarenKeller UlrichFrost NikolajKeilholz UlrichKiewe PhilippRieke Damian T - To investigate the regulatory role and molecular mechanisms of TSPAN9-mediated mitocytosis in an interleukin-1β (IL-1β)-induced rat chondrocyte senescence model, and to identify novel therapeutic targets for osteoarthritis (OA). - Source: PubMed
Chen QuanDa WaciliLuo NaijiaShen Bin - Juvenile xanthogranuloma (JXG) has historically been defined as a morphologic entity within non-Langerhans cell histiocytosis. Recent studies have demonstrated that a subset of histiocytic lesions with JXG morphology harbor targetable kinase alterations, including ALK and NTRK rearrangements, particularly in systemic or extracutaneous disease. We evaluated an immunohistochemistry (IHC)-based screening strategy for detecting targetable kinase alterations in histiocytic lesions with JXG morphology. IHC screening for ALK and pan-TRK was performed, followed by confirmatory fluorescence in situ hybridization (FISH) and next-generation sequencing (NGS) when feasible.We evaluated an immunohistochemistry (IHC)-based screening strategy for detecting targetable kinase alterations in histiocytic lesions with JXG morphology. IHC screening for ALK and pan-TRK, and BRAF V600E was performed, followed by confirmatory fluorescence in situ hybridization (FISH) and targeted next-generation sequencing (NGS) when feasible. Six of 28 patients (21%) were positive on IHC (ALK, n = 4; pan-TRK, n = 2), all of whom had systemic disease, representing 46% of systemic cases. All IHC-positive cases were confirmed by FISH. Targeted NGS identified fusion genes in analyzable cases, including KIF5B::ALK and TPM3::NTRK1, with RNA-based sequencing being limited by specimen quality in some cases, while DNA-based comprehensive genomic profiling showed higher feasibility in recently processed samples. These findings demonstrate that IHC-based screening followed by confirmatory FISH provides a rapid and cost-effective strategy for identifying cases of non-LCH with JXG morphology harboring actionable kinase alterations. Integration of IHC, FISH, and NGS represents a practical and complementary diagnostic strategy to guide precision therapy in this clinically diverse histiocytic disorder. - Source: PubMed
Publication date: 2026/04/13
Sakamoto KenichiKo KudoYoshioka TakakoMorimoto AkiraShioda YokoNakazawa Atsuko