TRKC, Active Human Recombinant Protein
- Known as:
- TRKC, Active Human Recombinant Protein
- Catalog number:
- 40282
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biotech support group
- Gene target:
- TRKC Active Human Recombinant Protein
Related genes to: TRKC, Active Human Recombinant Protein
- Gene:
- NTRK3 NIH gene
- Name:
- neurotrophic receptor tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- TRKC
- Chromosome:
- 15q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-18
- Date modifiied:
- 2016-10-05
Related products to: TRKC, Active Human Recombinant Protein
Related articles to: TRKC, Active Human Recombinant Protein
- , , and gene fusions are rare oncogenic driver alterations found in diverse tumor types of adults and children. They are clinically important biomarkers as tumors harboring these genomic alterations have high response rates to targeted therapy. Routine testing for fusions and treatment with TRK inhibitors has been recommended in multiple tumor types; however, differences between testing technologies used for detecting fusions can result in variable likelihoods of identification. - Source: PubMed
Publication date: 2025/05/02
Wallen Zachary DTierno MarniSchnettler EricaRoos AlisonGreen MichelleAmoah KobinaPrevis Rebecca AHastings StephaniePabla SarabjotJensen Taylor JCaveney BrianEisenberg MarciaSathyan PratheeshRamkissoon Shakti HSeverson Eric A - The NTRK fusion gene is detected in most salivary gland secretory carcinomas. While tropomyosin receptor kinase (TRK) inhibitors are used for various solid tumors with the fusion gene, there are no reports regarding TRK inhibitor use for unresectable parotid gland carcinomas that subsequently shrink and become resectable. Here, we report a case of salivary gland secretory carcinoma in which conversion surgery was performed after TRK inhibitor use. - Source: PubMed
Publication date: 2025/05/19
Nagano ArisaMatoba TakumaKawakita DaisukeMinohara KiyoshiIwaki ShoTsuge HiroshiTsukamoto KojiKikuchi SekaiNakano SatsukiMurase TakayukiTada YuichiroIwasaki Shinichi - On the basis of exploring the efficacy of XSF, the material basis and mechanism of XSF for the prevention of exercise-induced fatigue were clarified by network pharmacology using blood-absorbed components as the research object. - Source: PubMed
Publication date: 2025/05/13
Xuan QiwenRuan YiYin ZifeiGu WeiLing Changquan - Thyroid cancer is the primary endocrine malignancy, exhibiting distinct genomic drivers. The frequency of genetic alterations varies between adult and pediatric groups and across geographic regions and ethnicities. Molecular markers may serve as prognostic tools and/or specific treatment-selection tools in papillary thyroid carcinoma (PTC) in children. We sought to characterize molecular alterations in pediatric PTC from Argentina and test a future laboratory algorithm for molecular diagnosis and stratification. Immunohistochemistry, fluorescence in situ hybridization, and Sanger sequencing were performed on 57 pediatric PTC samples. This study assesses multiple genetic alterations, including fusions in RET, ALK, MET, BRAF, and NTRK genes, as well as the BRAF V600E single nucleotide variant. Fusions in known oncogenes were observed in 29.8% of cases (6 in RET, 5 in ALK, 4 in NTRK3, 1 in BRAF, and 1 in MET). The BRAF V600E SNV was detected in 12.3% of cases. Larger tumor size and higher initial risk were associated with genetic alterations (P = 0.027 and P = 0. 036, respectively). Designing a laboratory algorithm following an increasing order of complexity provided a reliable molecular testing platform that reduces the requirement for NGS screening. These results also broaden the data on PTC alterations in children from Argentina. - Source: PubMed
Publication date: 2025/05/08
Colli Sandra LorenaBoycho Marisa EstherPapendieck PatriciaMangone Franco MauricioChiesa AnaGarcía Lombardi MercedesMedín MartínDe Matteo Elena NoemíLorenzetti Mario AlejandroPreciado María Victoria - gene is responsible for encoding , which consists of three family members: , , and . These family members encode different proteins known as , , and , respectively. fusion genes are the clearest driving factor for carcinogenesis. gene fusion detection and inhibitors are effective measures for the treatment of malignant tumors. The development of anti-tumor drugs targeting proteins has been favored by various scientific research institutions and pharmaceutical companies. The first-generation inhibitors, larotrectinib and entrectinib, have been approved for the treatment of pediatric and adult patients with metastatic or locally advanced solid tumors harboring fusion proteins, demonstrating remarkable anticancer efficacy in clinical settings. However, the issue of acquired resistance to inhibitors has emerged. Currently, efforts are underway to develop next-generation inhibitors based on sequence, structural, and kinetic methodologies, as well as to explore the intracellular signaling pathways of and the mechanisms underlying resistance. The main focus of this review was to discuss the fusion of genes and the application of inhibitor treatment. - Source: PubMed
Li JielinLiang Yuan