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
- Gliomas are the most frequent Central Nervous System (CNS) tumors in children and adolescents. Angiocentric glioma is a rare subtype of pediatric-type diffuse low-- grade gliomas with a relatively favorable prognosis following gross total resection. More recently, the identification of Anaplastic Lymphoma Kinase (ALK) fusions in glioma has led to the development of targeted therapeutics to improve responses and outcomes. - Source: PubMed
Publication date: 2026/05/08
Liu TaoShen GeZhou XiaoyanZhang GairongZou Lei - RET is a transmembrane receptor protein-tyrosine kinase that is required for the (i) survival and maturation of the enteric nervous system, the autonomic nervous system, and sensory neurons, (ii) renal development, and (iii) spermatogenesis. RET activation by its glial-cell derived neurotrophic factor (GDNF) ligands differs from that of all other receptor protein-tyrosine kinases because of the requirement for additional GDNF family receptor-α co-receptors (GFRα1/2/3/4, GFRAL). Activating RET-point mutations occur in multiple endocrine neoplasia syndromes (MEN2A, MEN2B) and in isolated medullary thyroid cancer. RET-fusion proteins, commonly KIF5B-RET, occur in NSCLC. More than three dozen fusion partners of RET have been described in papillary thyroid cancer. Several multikinase blockers targeting RET have been approved by the FDA for the treatment of cancer: (i) vandetanib for medullary thyroid carcinoma and (ii) cabozantinib, lenvatinib, and sorafenib for differentiated thyroid cancer. Pralsetinib is a specific RET blocker that is FDA-approved for the treatment of medullary thyroid cancer, RET-fusion positive thyroid cancer and NSCLC. Selpercatinib is FDA-approved for the management of RET-mutant medullary thyroid cancer, RET-fusion-positive thyroid cancer, and other RET-fusion-positive solid tumors. The RET signaling pathway participates in the pathogenesis of cancer, particularly in thyroid and lung cancer. Currently, the number of new cases of thyroid cancer bearing RET mutations or RET-fusion proteins is about 13,000 per year and the number of cases of RET-driven NSCLC range from about 2000-4000 per year in the United States. Inactivating RET mutations result in Hirschsprung disease, a congenital disorder leading to aganglionosis of the gastrointestinal tract. - Source: PubMed
Publication date: 2026/05/08
Roskoski Robert - 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
Rosnev StanislavKlein KatharinaHeukamp LukasLenk JulianJoosten MariaMöbs MarkusGrob TobiasBenary ManuelaVecchione LoredanaOtt Claus-EricModest Dominik PKnödler MarenKeller UlrichFrost NikolajKeilholz UlrichKiewe PhilippRieke Damian T