RASH_HUMAN GTPase HRas ELISA tesk kit
- Known as:
- RASH_HUMAN GTPase HRas Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16656
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- RASH_HUMAN GTPase HRas ELISA tesk kit
Related genes to: RASH_HUMAN GTPase HRas ELISA tesk kit
- Gene:
- HRAS NIH gene
- Name:
- HRas proto-oncogene, GTPase
- Previous symbol:
- HRAS1
- Synonyms:
- -
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: RASH_HUMAN GTPase HRas ELISA tesk kit
Related articles to: RASH_HUMAN GTPase HRas ELISA tesk kit
- Approximately 30% of all human cancers are driven by mutations in genes, , and , resulting in the constitutive activation of RAS proteins and stimulation of MAPK/AKT signaling. Non-mutant, i.e., wild-type (WT) RAS can also become activated through mechanisms such as gene amplification or excessive stimulation by mutated or overexpressed receptor tyrosine kinases (e.g., EGFR), thereby promoting cancer progression. Mutant or activated RAS contributes to multiple hallmarks of cancer, including unchecked cellular proliferation, reprogrammed cellular metabolism, immunosuppression, and metastasis. Hence, RAS is of immense clinical importance, with hundreds of laboratories studying various aspects of RAS biology or developing RAS inhibitors. There is perhaps no greater unmet medical need in oncology than the need for a broadly efficacious but safe inhibitor of mutant and activated RAS. Mutant-specific KRAS G12C inhibitors have shown promising therapeutic efficacy, leading to FDA approval of sotorasib and adagrasib, although their use is limited to patients with the relatively rare G12C KRAS mutation. Mutant-specific KRAS inhibitors are also susceptible to adaptive resistance, in part, due to secondary mutations, and compensatory signaling from WT RAS isozymes. A pan-RAS inhibitor capable of blocking all RAS isozymes, regardless of the underlying mutation, offers the potential for broader efficacy and capacity to avert resistance. While just a few years ago, pan-RAS inhibitors were predicted to be severely toxic or even fatal, the apparent safety profile of RMC-6236 (daraxonrasib), a pan-RAS inhibitor currently in clinical trials, suggests otherwise. Indeed, pan-RAS inhibitors are now considered by many in the RAS field to be the most promising class in development. In this review, we summarize the evolution and current status of pan-RAS and pan-KRAS inhibitors in preclinical and clinical development and highlight emerging human-relevant tumor models that are advancing preclinical evaluation. - Source: PubMed
Publication date: 2026/06/04
Ramesh SindhuWang JunweiHuang Chung-HuiMoore Austin MFadlalla KhaldaBerry Kristy LMaxuitenko Yulia YChen XiKeeton Adam BEl-Rayes BasselBuchsbaum Donald JBudhwani Karim IZhou GangMitra Amit KPiazza Gary A - Risk stratification of thyroid nodules is mainly based on ultrasound examination and fine-needle aspiration (FNA) cytology findings. Molecular testing has increasingly been added to the workup to improve risk of malignancy (ROM) estimation. Here, we evaluated the diagnostic performance of alterations in seven genes, including point mutations in , , , and as well as , , and fusions in 849 FNA samples with cytopathologically indeterminate Bethesda categories (III, IV, and V). In 20.14% of samples, at least one gene alteration was detected, with mutations and the V600E variant occurring most frequently. For 636 of the thyroid nodules, surgical follow-up was available, with a malignancy rate of 22.64%. V600E mutations and fusions were associated with a ROM of 100%, mutations with 13.64%, and fusions with 60.00%. Depending on the Bethesda category, the positive predictive value for malignancy of the seven-gene panel ranged between 18.18% (Bethesda III) and 91.07% (Bethesda V), while the negative predictive value ranged between 93.92% (Bethesda III) and 24.14% (Bethesda V). In conclusion, molecular testing with the seven-gene panel can improve ROM estimation in cytopathologically indeterminate thyroid nodules, but its clinical utility depends on the detected gene alteration. - Source: PubMed
Publication date: 2026/05/30
Jochum Ann-KristinRenström FridaBischofberger-Baumann BarbaraDemmer IzadoraSchönegg RenéBrändle MichaelBilz StefanJochum Wolfram - Aristolochic acid (AA), a naturally occurring compound found in Aristolochia plants, is a well-established nephrotoxin and Group 1 carcinogen. Emerging evidence suggests a potential link between AA exposure and hepatocellular carcinoma (HCC), one of the leading causes of cancer-related mortality worldwide. This review critically evaluates current knowledge on AA's hepatic metabolism, its formation of persistent DNA adducts, and the induction of inflammatory responses in the liver. Based on preclinical and indirect human evidence, we propose a working hypothesis that AA may contribute to hepatocarcinogenesis through a dual mechanism: genotoxic (primarily via H-ras and p53 mutations resulting from AA-DNA adducts) and non-genotoxic (via chronic inflammation involving IL-6, TNF-α, and NF-κB activation, as well as epithelial-mesenchymal transition). We note, however, that these mechanisms remain to be validated in human cohorts and do not yet establish causality. Recent studies have identified novel mechanisms, including PDK4-mediated mitochondrial dysfunction, ferroptosis inhibition via p53 hijacking, and ARID1A deficiency as a susceptibility factor. A recent meta-analysis quantified a significantly increased risk of liver cancer following AA exposure in epidemiological studies. While direct causal evidence in humans remains limited, the high mutational burden observed in AA-exposed liver tissues warrants caution. Nevertheless, the primary public health priority pertains to the prevention of AA exposure. Further epidemiological and mechanistic studies are urgently needed. - Source: PubMed
Publication date: 2026/05/25
Wang YupengZhang YikunRen TianqiYuan LiyongGeng Xingchao - The identification of the cancer cell of origin is a fundamental question in cancer biology. We used fluorescent lineage tracing of independent mouse skin stem cell populations, single cell transcriptomics, and Duplex sequencing, to identify the origin of chemically induced skin tumors. Tumors arose predominantly from and / or stem cells of the upper hair follicle, but only very rarely from the + and + hair follicle bulge. + stem cells initiated by dimethylbenzanthracene responded to tumor promoter treatment resulting in clonal expansion of initiated cells carrying the canonical Q61L mutation. Spontaneous mutations in also clonally expanded, but did not generate tumors unless the gene was deleted, thus revealing a competitive interaction between and pathways that influences clonal selection. - Source: PubMed
Publication date: 2026/06/11
Kandyba EveJabouille ArnaudCalvet FerriolLi Yun RoseCurtabbi AndreaCristea DianaShin JoyceDelrosario ReynoAnzules JonathanWu DiQuigley DavidTaylor MarkZanette CamilaLo Fang YinHiggins JacobSalk JesseLopez-Bigas NuriaBalmain Allan - RASopathies are a group of developmental disorders caused by variations in genes of the RAS/mitogen activated protein kinase (MAPK) pathway and affect 1 in 1000 individuals worldwide. Due to overlapping clinical features, accurate diagnosis is challenging and therefore we used next-generation sequencing (NGS) panels as an effective molecular diagnostic tool. Targeted sequencing was performed on 130 samples using a multigene panel comprising of 21 RASopathy genes. Molecular analysis revealed variations in 74 individuals (57%). Pathogenic or likely pathogenic variations were observed in 60/74 (81%) of the cases, 13 (17.5%) had variant(s) of uncertain significance (VUS), and one novel variant was identified in RASA2 whose pathogenicity has not yet been established. In individuals with Noonan Syndrome, pathogenic variants were identified in eight different genes mainly and . Nine clinically diagnosed Cardio-facio-cutaneous syndrome cases harboured variations in and The c.34G>A variant in was seen in all nine individuals diagnosed with Costello syndrome. This study provides a comprehensive molecular and clinical profile of the largest Indian RASopathy cohort. The use of targeted gene panel has increased the variation detection rate in affected individuals. - Source: PubMed
Srikanth AmbikaKumar Tejashwini VittalAthota Jeevana PraharshaMorris MonishaBhat MeenakshiNarayanachar Sanjeeva GhantiNampoothiri SheelaYeshodharan DhanyaGowrishankar KalpanaArunachal GauthamShetty Swathi