Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043346 (xeroderma pigmentosum)
2,924 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a study to investigate the role of excision repair cross-complimentary group 1 gene (ERCC1)-xeroderma pigmentosum complementation group F (XPF) gene polymorphisms in response to chemotherapy and clinical outcome of gastric patients. Three SNPs in ERCC1 (rs11615, rs3212986, and rs2298881) and two SNPs in XPF (rs2276465 and rs6498486) were extracted using Tiangen DNA kit (Tiangen Biotech, Beijing, China) according to the manufacturer's instructions. The median follow-up time was 36.4 months, and ranged from 2-60 months. During the follow-up period, 112 patients died from gastric cancer. Individuals carrying ERCC1 rs11615 AA and XPF rs6498486 CC genotypes were associated with poorer response to chemotherapy when compared with wild-type genotype, with the ORs (95 % CI) of 0.48 (0.25-0.94) and 0.38 (0.14-1.00). In the Cox proportional hazards model, individuals carrying ERCC1 rs11615 GA and AA genotype had 1.91 and 2.66 risk of death when compared with those carrying GG genotype. Patients carrying the XPF rs6498486 AC and CC genotype were associate with 2.17 and 4.91-fold risk of death when compared with wild-type genotype. In conclusion, we found that ERCC1 rs11615 and XPF rs2276465 may substantially contribute to the future design of individualized cancer treatment in gastric cancer patients.
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PMID:Association of DNA repair gene polymorphisms with response to chemotherapy and prognosis of gastric cancer in a Chinese population. 2479 15

Folic acid is a necessary micronutrient for normal human growth and development. Benzo(a)pyrene (BaP) is a ubiquitously distributed environmental pollutant and its metabolite, benzo(a)pyrene-diol-epoxide, is known to exert a strong teratogenic and carcinogenic effect on the body's tissues and cells. The aim of this study was to investigate the mechanism by which folic acid can inhibit the toxic effects of BaP both in vivo and in vitro. We measured changes in 16HBE cell activity affected by the intervention of folic acid on BaP using the cell counting kit-8 assay and that of cell cycle distribution by flow cytometry. At the same time, we assessed the xeroderma pigmentosum group A, xeroderma pigmentosum group C, excision repair cross complementation group 1, cyclinD1, and CKD4 mRNAs, and their related protein expression both in mouse lung tissue and in 16HBE cells. In conclusion, the mechanisms by which this effect is mediated were not entirely elucidated by our study, possibly because folic acid antagonizes the toxic effects of BaP by upregulating the levels of excision repair cross complementation group 1, xeroderma pigmentosum group A, and xeroderma pigmentosum group C gene expression to improve the rate of DNA repair, in turn accelerating the speed of repair for DNA damage caused by BaP. Meanwhile, folic acid could restrain BaP-induced cyclinD1 protein expression, which could help cells return to their normal cell cycle.
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PMID:The intervention mechanism of folic acid for benzo(a)pyrene toxic effects in vitro and in vivo. 3002 Jan 14