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Gene Review

SMYD1  -  SET and MYND domain containing 1

Homo sapiens

Synonyms: BOP, Histone-lysine N-methyltransferase SMYD1, KMT3D, SET and MYND domain-containing protein 1, ZMYND18, ...
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Disease relevance of SMYD1


High impact information on SMYD1

  • Syrian golden hamsters were fed four diets in experiments designed to evaluate the effects of the interaction of dietary fat and protein on carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine [(BOP) CAS: 60599-38-4] [6].
  • At 8 weeks, they were given injections sc of 10 mg BOP/kg body weight and placed on a control diet [9 g corn oil (medium fat) and 18 g casein (medium protein)/385 kcal] [6].
  • The incidence of biliary cystic adenomas was highest in male hamsters that received HF diets, irrespective of BOP treatment, and BOP treatment resulted in increased yields of this lesion in females only in groups given HF-LP diet.(ABSTRACT TRUNCATED AT 400 WORDS)[6]
  • BOP-induced lesions in the lungs, liver, common bile duct, gallbladder, and kidneys are described; results in the pancreas were reported separately [6].
  • Survivors were killed 46 weeks after BOP administration, and the pancreas, common duct, and gallbladder were examined histologically [7].

Chemical compound and disease context of SMYD1


Biological context of SMYD1

  • Pregnant Syrian hamsters (F0 generation) were treated with BOP (10 mg/kg body weight) at the 8th, 10th, 12th, and 14th days of gestation (for a total dose of 40 mg/kg body weight) [13].
  • These data indicate that BOP carcinogenesis is mediated through blood circulation, and that cancer development is not inhibited in the duct-excised lobe for up to 3 days after surgery [14].
  • BOP and BHP were weak mutagens in the Salmonella/S-9 mutagenesis assay using hamster liver S-9 fraction [15].
  • These findings indicated that etodolac reduced both the occurrence of severe cholangitis and the acceleration of biliary epithelial cell kinetics after bilioenterostomy, resulting in the prevention of BOP-induced biliary carcinogenesis in hamsters [16].
  • The results thus suggest that metabolic activation with STase is involved in BOP-induced pancreatic ductal carcinogenesis in hamsters, and support the hypothesis that BOP is metabolized to beta-hydroxyalkylnitrosamines followed by activation to proximate sulfuric acid esters by HSTase [17].

Anatomical context of SMYD1


Associations of SMYD1 with chemical compounds


Analytical, diagnostic and therapeutic context of SMYD1

  • Average tumor weight of animals in all peptide-treated groups, sacrificed 60 days after beginning the peptide treatment, was significantly lower than that of BOP controls [22].
  • Pancreatic tumors were found in 89% of the BOP-treated F0 generation and in 5 (50%) of their male litters, but none was seen in their female progeny or in any hamsters from the F1 control group [13].
  • Animals were treated with a single dose (20 mg/kg body weight) of N-nitrosobis(2-oxopropyl)amine (BOP) either immediately (Group 1) or on Days 1 (Group 2), 3 (Group 3) or 7 (Group 4) after ligation and excision of the duct of the splenic lobe [14].
  • Group 5 received BOP shortly after laparoscopy, and Group 6 consisted of BOP-treated controls [14].
  • Additional groups consisted of animals with PP alone (Group 4), sham operation (laparotomy) followed 30 minutes later by BOP treatment (Group 5), and BOP treatment only (Group 6) [23].


  1. Modification of pancreatic carcinogenesis in the hamster model. XI. Inhibitory effect of pilocarpine hydrochloride. Pour, P.M., Lawson, T., Donnelly, T., Stepan, K. J. Natl. Cancer Inst. (1984) [Pubmed]
  2. Modifying factors in pancreatic carcinogenesis in the hamster model. IV. Effects of dietary protein. Pour, P.M., Birt, D.F. J. Natl. Cancer Inst. (1983) [Pubmed]
  3. Enhancement of experimental pancreatic cancer in Syrian golden hamsters by dietary fat. Birt, D.F., Salmasi, S., Pour, P.M. J. Natl. Cancer Inst. (1981) [Pubmed]
  4. Modification of pancreatic carcinogenesis in the hamster model. X. Effect of streptozotocin. Pour, P.M., Patil, K. J. Natl. Cancer Inst. (1983) [Pubmed]
  5. Interaction of dietary fat and protein on pancreatic carcinogenesis in Syrian golden hamsters. Birt, D.F., Stepan, K.R., Pour, P.M. J. Natl. Cancer Inst. (1983) [Pubmed]
  6. Effects of the interaction of dietary fat and protein on N-nitrosobis(2-oxopropyl)amine-induced carcinogenesis and spontaneous lesions in Syrian golden hamsters. Birt, D.F., Pour, P.M. J. Natl. Cancer Inst. (1985) [Pubmed]
  7. Modification of pancreatic carcinogenesis in the hamster model. VIII. Inhibitory effect of exogenous insulin. Pour, P.M., Stepan, K. J. Natl. Cancer Inst. (1984) [Pubmed]
  8. A potent pancreatic carcinogen in Syrian hamsters: N-nitrosobis(2-oxopropyl)amine. Pour, P., Althoff, J., Krüger, F.W., Mohr, U. J. Natl. Cancer Inst. (1977) [Pubmed]
  9. Carcinogenic effect of N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine, a postulated proximate pancreatic carcinogen in Syrian hamsters. Pour, P., Wallcave, L., Gingell, R., Nagel, D., Lawson, T., Salmasi, S., Tines, S. Cancer Res. (1979) [Pubmed]
  10. Modification of pancreatic carcinogenesis in the hamster model. 3. Inhibitory effect of alloxan. Pour, P.M., Donnelly, K., Stepan, K. Am. J. Pathol. (1983) [Pubmed]
  11. Inhibitory effect of butylated hydroxyanisole administration on pancreatic carcinogenesis in Syrian hamsters initiated with N-nitrosobis(2-oxopropyl)amine. Mizumoto, K., Ito, S., Kitazawa, S., Tsutsumi, M., Denda, A., Konishi, Y. Carcinogenesis (1989) [Pubmed]
  12. Hematologic malignancies developing in Syrian golden hamsters during induction of pancreatic carcinoma. Cualing, H.D., Povoski, S.P., Yassin, R.S., Fenoglio-Preiser, C.M., Bell, R.H. Carcinogenesis (1996) [Pubmed]
  13. Induction of exocrine pancreatic, bile duct, and thyroid gland tumors in offspring of Syrian hamsters treated with N-nitrosobis(2-oxopropyl)amine during pregnancy. Pour, P.M. Cancer Res. (1986) [Pubmed]
  14. Modification of pancreatic carcinogenesis in the hamster model. 6. The effect of ductal ligation and excision. Pour, P.M., Donnelly, T., Stepan, K. Am. J. Pathol. (1983) [Pubmed]
  15. High mutagenic activity of N-nitrosobis(2-oxopropyl)amine and N-nitrosobis(2-hydroxypropyl)amine in the host-mediated assay in hamsters: evidence for premutagenic methyl and hydroxylpropyl adducts. Guttenplan, J.B., Kokkinakis, D. Carcinogenesis (1993) [Pubmed]
  16. Chemopreventative effect of a cyclooxygenase-2-specific inhibitor (etodolac) on chemically induced biliary carcinogenesis in hamsters. Tsuneoka, N., Tajima, Y., Kitazato, A., Fukuda, K., Kitajima, T., Kuroki, T., Onizuka, S., Kanematsu, T. Carcinogenesis (2005) [Pubmed]
  17. Inhibitory effects of sulfation inhibitors on initiation of pancreatic ductal carcinogenesis by N-nitrosobis(2-oxopropyl)amine in hamsters. Tsutsumi, M., Noguchi, O., Okita, S., Horiguchi, K., Kobayashi, E., Tamura, K., Tsujiuchi, T., Denda, A., Konishi, Y., Iimura, K. Carcinogenesis (1995) [Pubmed]
  18. Experimental induction of pancreatic carcinomas in the hamster with N delta-(N-methyl-N-nitrosocarbamoyl)-L-ornithine. Longnecker, D.S., Curphey, T.J., Kuhlmann, E.T., Schaeffer, B.K. J. Natl. Cancer Inst. (1983) [Pubmed]
  19. Modification of pancreatic carcinogenesis in the hamster model. XII. Dose-related effect of ethanol. Pour, P.M., Reber, H.A., Stepan, K. J. Natl. Cancer Inst. (1983) [Pubmed]
  20. Metabolism of pancreatic carcinogens N-nitroso-2,6-dimethylmorpholine and N-nitrosobis(2-oxopropyl)amine by microsomes and cytosol of hamster pancreas and liver. Kokkinakis, D.M., Scarpelli, D.G., Rao, M.S., Hollenberg, P.F. Cancer Res. (1983) [Pubmed]
  21. Alterations in pancreatic islet function produced by carcinogenic nitrosamines in the Syrian hamster. Zucker, P.F., Archer, M.C. Am. J. Pathol. (1988) [Pubmed]
  22. Programmed cell death (apoptosis) in pancreatic cancers of hamsters after treatment with analogs of both luteinizing hormone-releasing hormone and somatostatin. Szende, B., Zalatnai, A., Schally, A.V. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  23. Modification of pancreatic carcinogenesis in the hamster model. 2. The effect of partial pancreatectomy. Pour, P.M., Donnelly, T., Stepan, K., Muffly, K. Am. J. Pathol. (1983) [Pubmed]
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