Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RMI 12,936 (7alpha-methyl-17beta-hydroxy-androst-5-en-one) was tested for androgenic activity in mouse kidney and for antiprogestational activity in guinea-pig uterus. RMI 12,936 stimulated an increase in kidney weight and in the activity of the androgen-responsive renal enzymes, beta-glucuronidase, alcohol dehydrogenase and arginase. RMI 12,936 was bound by the renal androgen receptor with a relative affinity approximately one-third that of testosterone. Although RMI 12,936 did not stimulate glycogen accumulation in guinea-pig endometrium in vivo, it was active in endometrial organ culture. When RMI 12,936 was combined with progesterone, glycogen accumulation in vitro was partly inhibited. RMI 12,936 was bound by the guinea-pig uterine progesterone receptor with a relative affinity of less than 1%. It is concluded that RMI 12,936 is an androgenic steroid with antifertility actions and in-vitro antiglycogenic activity.
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PMID:Androgenic effects of the antiprogestagen RMI 12,936. 63 20

Alcohol consumption has consistently been shown to increase breast cancer (BC) risk. This association may be modified by single nucleotide polymorphisms (SNPs) in alcohol dehydrogenase (ADH) isoenzymes ADH1B and ADH1C. The Netherlands Cohort Study comprises 62 573 women, aged 55-69 years at baseline (1986). Follow-up for postmenopausal BC for 20.3 years was available. Genotyping of six tag SNPs in ADH1B and ADH1C was performed on DNA from toenails. A case-cohort approach was used for analysis (complete data available for nsubcohort = 1301; ncases = 1630). Cox regression models for postmenopausal BC were applied to determine marginal effects of alcohol intake and SNPs using a dominant genetic model, as well as multiplicative interaction of the two. Results were also obtained for subtypes by estrogen receptor (ER) and progesterone receptor (PR) status. Multiple testing was adjusted for by applying the false discovery rate (FDR). Alcohol intake (categorical) increased the risk of postmenopausal BC (Ptrend = 0.031). Trends for ER and PR subgroups followed a similar pattern. Continuous modeling of alcohol resulted in a hazard rate ratio (HR) for overall postmenopausal BC of 1.09 (95% confidence interval: 1.01-1.19) per 10 g/day of alcohol. SNPs were not associated with BC risk. No effect modification of the alcohol-BC association by SNP genotype was seen after FDR correction in overall BC and ER/PR subgroups. In conclusion, alcohol consumption was shown to increase the risk of postmenopausal BC. This association was not significantly modified by common SNPs in ADH1B and ADH1C, neither in overall BC nor in hormone receptor-defined subtypes.
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PMID:Alcohol drinking, ADH1B and ADH1C genotypes and the risk of postmenopausal breast cancer by hormone receptor status: the Netherlands Cohort Study on diet and cancer. 3005 83