N_ras binding protein EMSA Probe Set
- Known as:
- N_ras binding protein EMSA Probe Set
- Catalog number:
- AY1368P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- N_ras binding protein EMSA Probe Set
Related genes to: N_ras binding protein EMSA Probe Set
- Gene:
- NRAS NIH gene
- Name:
- NRAS proto-oncogene, GTPase
- Previous symbol:
- -
- Synonyms:
- N-ras
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: N_ras binding protein EMSA Probe Set
Related articles to: N_ras binding protein EMSA Probe Set
- Juvenile myelomonocytic leukemia (JMML) is a rare and very aggressive pediatric myelodysplastic/myeloproliferative neoplasm with molecular heterogeneity and constitutive activation of the RAS signaling pathway. The aim of this study was to identify the mutational landscape, driver genes, mutational signatures, functional pathways, and therapeutic targets of mutations that affect receptor tyrosine kinases (RTKs) and RAS pathways in JMML. - Source: PubMed
Publication date: 2026/09/18
Goel HarshMajhi Ravi KumarMeena Jagdish PrasadChopra AnitaBakhshi SameerSingh LataSeth RachnaKar BibekanandaTanwar PranayGupta Aditya Kumar - : Right-sided metastatic colon cancer represents a clinically distinct subgroup with inferior outcomes and uncertain optimal biologic treatment selection, even among patients with RAS wild-type disease. Real-world data focusing specifically on right-sided RAS wild-type metastatic colon cancer remain limited. This study aimed to describe clinicopathologic characteristics, metastatic patterns, treatment approaches, and survival outcomes in this population using a national multicenter registry. : This retrospective multicenter cohort study was conducted using data from the ONKO-KOLON Türkiye registry. Patients with pathologically confirmed KRAS/NRAS wild-type metastatic colorectal cancer and available primary tumor localization were evaluated. The main analytic cohort included patients with right-sided metastatic colon cancer, defined as right colon or transverse colon tumors. Left-sided colon cancer patients were used as a contextual comparator, while rectal cancer patients were excluded from sidedness-based colon comparisons. Survival outcomes were estimated using the Kaplan-Meier method, and prognostic factors were evaluated using Cox regression analyses. : Among 1079 patients in the source cohort, primary tumor localization was available in 1065 patients. Of these, 213 had right-sided colon cancer, 464 had left-sided colon cancer, and 388 had rectal cancer. In the right-sided cohort, median age was 61.5 years, 64.3% were male, and 66.7% had synchronous/de novo metastatic disease. Liver metastasis was the most common metastatic site (63.4%), followed by lymph node (31.0%), lung (21.1%), and peritoneal metastases (15.5%). First-line anti-VEGF-based treatment was used in 46.0% of patients, while anti-EGFR-based treatment was used in 40.8%. Among evaluable patients, the objective response rate was 46.8% and the disease control rate was 79.2%. Median progression-free survival was 10.0 months, and median overall survival was 24.0 months. In unadjusted exploratory analysis, median OS was 27.0 months with anti-EGFR-based treatment and 17.0 months with anti-VEGF-based treatment (log-rank = 0.022), whereas median PFS was 10.0 months in both groups. In an extended covariate-adjusted multiple-imputation sensitivity model, the anti-EGFR OS estimate did not meet statistical significance (adjusted HR 0.66, 95% CI 0.43-1.00; = 0.051). In a secondary contextual comparison, median overall survival was shorter in the right-sided than in the left-sided colon cancer group (24.0 vs. 28.0 months; HR 1.47, 95% CI 1.19-1.82; < 0.001), whereas progression-free survival did not differ significantly. : This study provides a descriptive account of metastatic patterns, treatment approaches, and outcomes in a dedicated right-sided RAS wild-type metastatic colon cancer cohort. The unadjusted OS difference between biological treatment groups was not confirmed after measured covariate adjustment and should not be interpreted as evidence of comparative treatment effectiveness. Because molecular profiling was incomplete, this study cannot identify biomarker-defined treatment subgroups. Prospective studies with complete, predefined molecular characterization are needed before molecularly informed treatment selection hypotheses can be evaluated in this population. - Source: PubMed
Publication date: 2026/08/24
Yildiz Nur DenizArslan ÇağatayOkten İlker NihatKefeli UmutYildirim Mahmut EmreKaradurmus NuriBaydas TubaKarabulut BülentCicin IrfanBilir CemilOzcelik MelikeCil TimucinCelik SinemisBozkurt OktayHarputluoglu HakanOven Bala BaşakArtaç MehmetTürk Hacı MehmetAlacacıoğlu AhmetGumus MahmutYalcin Şuayib - Lacrimal gland (LG) choristomas are ectopically located lacrimal gland tissue that present as mass lesions, and their diagnosis is confirmed by histopathology. The current study reviews cases of lacrimal gland choristoma published between 2016 and 2025 and reports a rare case of bilateral epibulbar lacrimal gland choristoma associated with a limbal dermoid and ocular colobomatous anomalies in a young female. LG choristomas have been reported in the conjunctiva, eyelid, orbit, lacrimal drainage system, and intraocular structures. They can be simple or have associated syndromic presentations such as Goldenhar syndrome, linear nevus sebaceous syndrome, epidermal nevus syndrome, and craniofacial microsomia. Molecular studies in syndromic cases demonstrated postzygotic somatic mutations in HRAS, KRAS, and NRAS, affecting the RAS-MAPK signaling pathway. Histopathology demonstrated mature lacrimal gland acini and ductal structures within fibrofatty stroma. Whole-exome sequencing did not identify pathogenic mutations associated with choristoma syndromes, ectodermal dysgenesis, or neuroectodermal developmental disorders. - Source: PubMed
Publication date: 2026/09/24
Maniktala YaminiGavara SuneethaSankar LekshmySucharita SoumyaSingh Swati - - Source: PubMed
Publication date: 2026/09/24
- In myelodysplastic neoplasms, autoinflammatory syndromes result from dysregulated innate immunity and cause severe, organ-dominant inflammation. Interleukin-1 signaling through the NLRP3 inflammasome is implicated in the pathogenesis of myelodysplastic disease and related inflammatory complications, especially in the context of RAS-pathway activation. Reports describing therapy-related myelodysplastic syndrome with pulmonary autoinflammatory syndromes are rare, and the efficacy of interleukin-1 blockade in this setting has not been previously documented. A man in his 60s with therapy-related myelodysplastic syndrome (del 5q) following rectal chemoradiation developed a recurrent, lung-predominant autoinflammatory syndrome refractory to corticosteroids and Janus kinase inhibition. Next-generation sequencing identified gain-of-function mutations in NRAS, PTPN11, SF3B1, and ASXL1. On two separate occasions, anakinra produced rapid clinical improvement with normalization of inflammatory biomarkers and radiographic resolution; on both occasions, discontinuation of anakinra led to prompt relapse within days, with ferritin rising to above 5500 ng/mL and C-reactive protein exceeding 300 mg/L. This case demonstrates that interleukin-1-mediated inflammation can drive pulmonary complications in therapy-related myelodysplastic syndrome. Targeted cytokine blockade with anakinra produced reproducible and measurable clinical improvement when conventional therapies were insufficient. The recurrence of symptoms following anakinra withdrawal, and rapid improvement upon re-administration, underscores the functional link between interleukin-1-driven inflammation and clinical outcomes. The RAS/MAPK mutational context and the observed on-off response to anakinra further support an interleukin-1-driven mechanism that merits further investigation. - Source: PubMed
Publication date: 2026/09/20
Smith QuinnArar-Cauley Anna