Ask about this productRelated genes to: CYP2A6 antibody
- Gene:
- CYP2A6 NIH gene
- Name:
- cytochrome P450 family 2 subfamily A member 6
- Previous symbol:
- CYP2A3
- Synonyms:
- CPA6, CYP2A
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-20
- Date modifiied:
- 2015-12-09
Related products to: CYP2A6 antibody
Related articles to: CYP2A6 antibody
- Nasopharyngeal carcinoma (NPC) are geographically restricted malignancies, exhibiting significantly higher incidence in specific regions and among certain ethnic groups, indicating strong genetic and region-specific etiological influences. The pathogenesis of these malignancies illustrates a multifaceted interaction involving host genetic predisposition, viral infections, as well as various environmental and lifestyle factors. This mini review brings together existing evidence regarding the molecular genetic factors influencing both EBV and HR-HPV-associated NPC, focusing on gene polymorphisms, viral biomarkers, and risk modifiers that vary across populations. Recurrent genetic associations involved polymorphisms in GSTM1, CYP1A1, XRCC1, TNF, HLA microsatellites, and xenobiotic metabolism genes, particularly CYP2A6. Markers linked to EBV, including LMP1, EBNA1, and circulating plasma EBV DNA, exhibited a consistent association with NPC susceptibility. Similarly, HR-HPV markers including E6 and E7 oncoproteins, p16INK4a overexpression, and HPV DNA detection serve as critical biomarkers for HPV-driven HNCs, but categorically these associations haven't yet been discovered in regard to NPC. These findings classify NPC as a genetically modified, virus-related cancer and highlight the necessity for population-specific genetic risk assessment, EBVHPV-derived biomarkers, and targeted preventative efforts. - Source: PubMed
Publication date: 2026/04/15
Nath IndrajitRaphael VandanaShunyu Neizekhotuo BrianSiddiqui AyeshaChakraborty SuvamoyDey BiswajitSahoo Om SaswatDhar RubyKarmakar Subhradip - Genotyping of CYP2A6 and CYP2D6 is a cornerstone of personalized medicine; however, current dosing algorithms often assume distinct phenotypic clusters, overlooking the substantial phenotypic overlap among genotypes. This study aimed to quantify genotype-phenotype concordance and identify the mechanistic determinants of prediction discrepancies. Using 90 Chinese human liver specimens, we evaluated CYP2A6 (alleles ∗4, ∗9) and CYP2D6 (100C>T, 1661G>C, ∗2) across enzymatic activity, microsomal kinetics, and predicted in vivo hepatic clearance (CL-) derived via a bias-corrected in vitro-in vivo extrapolation approach. The results revealed significant phenotypic overlap, leading to poor prediction accuracy when relying solely on genotyping. For CYP2A6, the concordance rates were only 50.0%-58.3% for the ∗4 allele and 0% for the ∗9 allele at the microsomal level. Similarly, for CYP2D6, the 100TT genotype exhibited low prediction accuracy (2.4%-14.3%), and the 1661CC genotype showed a 100% discrepancy. Correlation analysis demonstrated that these discrepancies were significantly driven by variations in microsomal enzyme content and cytochrome P450 oxidoreductase activity (for CYP2A6), as well as cytochrome b5 (Cytb5) content (specifically for CYP2D6). In conclusion, genotyping alone is insufficient for precise clearance prediction. Integrating physiological covariates-specifically POR activity and Cytb5 content-into in vitro-in vivo extrapolation models is essential to resolve genotype-phenotype discordance and optimize CYP2A6- and CYP2D6-mediated drug dosing. SIGNIFICANCE STATEMENT: This study addresses a critical limitation in CYP2A6/CYP2D6 genotype-guided therapy: it quantifies their extensive phenotypic overlap (genotyping alone: 0%-58.3% reliable dosing). Its novel multilevel analysis finds cytochrome P450 oxidoreductase/Cytb5 as drivers, aiding precision dosing and genetic-only risks mitigation. - Source: PubMed
Publication date: 2026/03/04
Fang YanWang JiyaoLiu DemengLi JunleTian XinGao NaZhang HaifengWen QiangQiao Hailing - The cytochrome P450 (CYP) system plays a central role in drug metabolism and pharmacokinetic variability, influencing drug-drug interaction risk. The newly synthesized 4-propoxy-2-arylquinoline derivatives (MW1-3) are dual inhibitors of epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK) with potent anticancer activity. This study aimed to assess their potential inhibitory effects on major human CYP enzymes to predict metabolic liabilities and interaction risks. - Source: PubMed
Publication date: 2026/04/08
Elbarbry FawzyEspiritu MichaelHecker BethanyElbadawi Mostafa MEldehna Wagdy M - We investigated whether markers, genes or terms of the associated with genetic or rare diseases (GARDs) that affect airway or lung function are associated with lung cancer. - Source: PubMed
Publication date: 2026/04/01
Rosenberger AlbertBickeböller HeikeChristiani David CCaporaso Neil ELiu GeoffreyBojesen Stig ELe Marchand LoicAlbanes DemetriosAldrich Melinda CTardon AdoninaFernández-Tardón GuillermoRennert GadField John KDavies Michael P AKiemeney Lambertus ALazarus PhilipZienolddiny ShanbehLam StephenSchabath Matthew BAndrew Angeline SArnold Susanne MGoodman Gary EDoherty Jennifer ATaylor FionaCox AngelaWoll Penella JRisch AngelaJohansson MikaelBrennan PaulLandi Maria TeresaShete Sanjay SHung Rayjean JAmos Christopher I - Tobacco use remains the leading cause of preventable death worldwide. The major metabolic pathway for nicotine, the addictive component in tobacco, is via cytochrome P450 (CYP) 2A6-mediated metabolism to cotinine. Cannabidiol has been shown to reduce cigarette consumption in vivo and inhibit CYP2A6-mediated nicotine metabolism in vitro. In the present study, Δ-8-tetrahydrocannabinol (Δ8-THC), an isomer of Δ-9-tetrahydrocannabinol, was examined as a potential inhibitor of CYP2A6-mediated nicotine metabolism. While Δ-9-tetrahydrocannabinol showed no significant inhibition of nicotine metabolism to cotinine, Δ8-THC demonstrated unbound IC values of 0.57 ± 0.04 μM in microsomes from recombinant wild-type CYP2A6 overexpressing human embryonic kidney 293 cells and 0.70 ± 0.16 μM in human liver microsomes (HLMs). A similar unbound IC value was observed for recombinant CYP2A6∗5 microsomes (0.52 ± 0.17 μM) and was modestly elevated in recombinant CYP2A6∗2 microsomes (1.00 ± 0.12 μM). IC shift experiments were consistent across pooled HLM (5.3-fold) and microsomes from liver specimens exhibiting the CYP2A6 (∗2/∗2) and (∗9/∗9) genotypes (6.1- and 4.0-fold, respectively) but were reduced in CYP2A6 (∗35/∗35) microsomes (1.0-fold). Irreversible inhibition kinetics in pooled HLMs by Δ8-THC yielded a k value of 0.022 ± 0.001 min and an unbound K value of 0.232 ± 0.062 μM. Static modeling predicted that oral dosing with 10 mg Δ8-THC increased the nicotine plasma area under the curve by 189%, with further increases observed at 20 mg and 40 mg; interactions were also observed with inhalation doses ≥70 mg. These findings suggest that, based on CYP2A6 genotype, Δ8-THC could be a candidate for smoking cessation therapy. SIGNIFICANCE STATEMENT: This study is the first, to the best of our knowledge, to identify Δ-8-tetrahydrocannabinol as a potent and irreversible inhibitor of nicotine metabolism to cotinine. The extent of inhibition is modulated by genetic variation in cytochrome P450 2A6. These findings suggest that further investigations focusing on Δ-8-tetrahydrocannabinol and its potential as a candidate for smoking cessation therapy are warranted. - Source: PubMed
Publication date: 2026/01/13
Zhao MengqiLuo ShamanLazarus Philip