Ask about this productRelated genes to: UGT1A1 Blocking Peptide
- Gene:
- UGT1A1 NIH gene
- Name:
- UDP glucuronosyltransferase family 1 member A1
- Previous symbol:
- UGT1, GNT1
- Synonyms:
- UGT1A
- Chromosome:
- 2q37.1
- Locus Type:
- complex locus constituent
- Date approved:
- 1989-02-13
- Date modifiied:
- 2019-04-23
Related products to: UGT1A1 Blocking Peptide
Related articles to: UGT1A1 Blocking Peptide
- Pharmacogenomic-related adverse drug reactions and treatment failure contribute to global morbidity. Evidence for PGx-guided therapy in sub-Saharan Africa remains limited with few implementation studies. This study evaluated the potential clinical utility and projected population-level impact of pharmacogenomic testing in Zimbabwe. - Source: PubMed
Publication date: 2026/07/31
Mazhindu Tinashe AdrianChikwambi ZediasGrimes Kevin VBorok Margaret ZNdlovu NtokozoMasimirembwa Collen - Pharmacogenetics plays an increasingly important role in oncology by supporting individualized therapeutic strategies based on patient genetic profiles. ClinicalTrials.gov provides a valuable platform for evaluating global trends in pharmacogenetic anticancer clinical trials. This systematic review aimed to evaluate pharmacogenetic-focused anticancer clinical trials registered on ClinicalTrials.gov and summarize trends in study design, cancer types, targeted biomarkers, therapeutic interventions, and geographic distribution. - Source: PubMed
Ashour Ahmed MAlhayyan AliahAlhayyan Rawan - Hepatic sexual dimorphism is critical for maintaining sex-specific metabolic pathways and xenobiotic clearance. We have demonstrated that in fibroblast growth factor 15 (Fgf15) transgenic (Tg) mice, FGF15 overexpression significantly reduced bile acid (BA) levels and induced hepatic feminization in males, marked by a male-to-female shift in expression of the drug metabolizing enzymes. This feminization is linked to the disruption of pulsatile growth hormone (GH) secretion pattern and signaling. However, it remained unclear whether FGF15 overexpression broadly disrupts hepatic sexual dimorphism or specifically drives a directional feminization program independent of biological sex. In this study, we profiled the hepatic transcriptome of female Fgf15 Tg mice and replenished male Fgf15 Tg mice with exogenous, pulsatile GH to test to what degree changes in the GH axis maintain liver dimorphism under low BA conditions. Beyond suppressing BA synthesis and altering steroid metabolism, female Tg mice altered expression of genes in xenobiotic metabolism and detoxification pathways, suggesting that the FGF15/BA axis regulates xenobiotic processing in females as well. Notably, FGF15 overexpression further amplified the baseline female expression profile of drug-metabolizing enzymes, characterized by the upregulation of female-predominant genes (Cyp2b9, Cyp3a41, Sult1e1, and Ugt1a1) and the suppression of male-predominant genes (Cyp7b1, Cyp2d9, Hsd3b5, and Igf1). Furthermore, pulsatile GH replenishment in male Tg mice partially restored male-predominant gene expression patterns. Taken together, these findings demonstrate that overexpression of intestine-derived FGF15 drives the feminization of sexually dimorphic hepatic gene expression independent of biological sex, a process that is at least partially mediated by impaired GH signaling. SIGNIFICANCE STATEMENT: Fibroblast growth factor 15 (Fgf15) overexpression intensified hepatic feminization of drug-metabolizing enzyme expression in female Fgf15 transgenic mice, similar to male Fgf15 transgenic mice. Restoring growth hormone signaling partially rescued the male-predominant gene expression pattern in male Fgf15 transgenic mice. This indicates that disruptions to growth hormone pulsatility, alongside sustained hepatic signal transducer and activator of transcription 5 activation, contribute to FGF15-induced hepatic gene feminization. - Source: PubMed
Publication date: 2026/07/15
Dai ManyunShi HongBasaly VeroniaMeadows VikKong BoGuo Grace L - Interpatient variability in chemotherapy response and toxicity remains a major challenge in oncology. Pharmacogenomics (PGx) is an approach to address this challenge by combining somatic alterations that affect tumour sensitivity with germline variants that affect drug metabolism, transport and toxicity. This review provides a critical evaluation of clinically validated PGx biomarkers for chemotherapeutics and targeted therapy with a focus on translational relevance and strength of evidence. High-impact germline markers such as DPYD, TPMT, NUDT15 and UGT1A1 are highlighted as key determinants of genotype-guided dosing for improving safety without compromising efficacy. Somatic biomarkers such as EGFR, RAS, BRAF, and HER2 remain central to treatment selection, while resistance underscores the need for ongoing molecular assessment. A tiered implementation framework, barriers to progress, and future directions involving polygenic models, multi-omics, and artificial intelligence (AI) are discussed to advance safe, effective, and personalized chemotherapy. - Source: PubMed
Publication date: 2026/08/06
Vishwash Satyam KumarSoni Ram BabuKosey SourabhSood Ratima - There is an unmet need for optimal third- or later-line treatment options for refractory or metastatic colorectal cancer (mCRC) patients. This phase II study investigated whether high-dose irinotecan rechallenge based on genotype improves the 12-week disease control rate (12w DCR), objective response rate (ORR), progression-free survival (PFS), overall survival (OS), and safety in refractory mCRC patients. - Source: PubMed
Publication date: 2026/07/22
Kim HanaHong JoohyunKong Sun-YoungChoi Moon Ki