{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T21:20:52Z","timestamp":1760908852818},"reference-count":40,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2013,9,23]],"date-time":"2013-09-23T00:00:00Z","timestamp":1379894400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2013,10]]},"abstract":"Abstract<\/jats:title>Background and Aim<\/jats:title>Angiogenesis plays a key role in growth, progression, and metastasis of various cancers. Vascular endothelial growth factor (VEGF<\/jats:styled-content>) polymorphism has been associated with several cancers. Role of VEGF<\/jats:styled-content> has not been reported in gallbladder cancer (GBC<\/jats:styled-content>). Present study was designed to investigate the role of VEGF<\/jats:styled-content> polymorphism in GBC<\/jats:styled-content> and in other (benign) gallbladder diseases, that is chronic cholecystitis (CC<\/jats:styled-content>) and xanthogranulomatous cholecystitis (XGC<\/jats:styled-content>).<\/jats:p><\/jats:sec>Methods<\/jats:title>Blood samples were collected from 195 GBC<\/jats:styled-content>, 140 CC<\/jats:styled-content>, and 47 XGC<\/jats:styled-content> patients and 300 normal healthy controls. VEGF<\/jats:styled-content> polymorphisms were investigated using amplification refractory mutation system polymerase chain reaction for g.43737830A<\/jats:styled-content>>G<\/jats:styled-content> and g.3437A<\/jats:styled-content>>C<\/jats:styled-content>, polymerase chain reaction\u2010restriction fragment length polymorphism for c.*237C<\/jats:styled-content>>T<\/jats:styled-content>, and g.43736418delT<\/jats:styled-content>insG<\/jats:styled-content> amplified by polymerase chain reaction.<\/jats:p><\/jats:sec>Results<\/jats:title>At g.43737830A<\/jats:styled-content>>G<\/jats:styled-content>, GA<\/jats:styled-content> genotype showed susceptibility (odds ratio [OR<\/jats:styled-content>]\u2009=\u20091.65 and OR<\/jats:styled-content>\u2009=\u20091.68) and GG<\/jats:styled-content> genotype showed protective association (OR<\/jats:styled-content>\u2009=\u20090.58 and OR<\/jats:styled-content>\u2009=\u20090.50) with GBC<\/jats:styled-content> and CC<\/jats:styled-content>. Allele A<\/jats:styled-content> of VEGF<\/jats:styled-content> g.43737830A<\/jats:styled-content>>G<\/jats:styled-content> was risk associated with GBC<\/jats:styled-content> and CC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20091.48 and OR<\/jats:styled-content>\u2009=\u20091.70), while G<\/jats:styled-content> allele was risk protective for GBC<\/jats:styled-content> and CC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20090.67 and OR<\/jats:styled-content>\u2009=\u20090.58). At g.3437A<\/jats:styled-content>>C<\/jats:styled-content>, genotype CA<\/jats:styled-content> was risk protective for GBC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20090.61). TT<\/jats:styled-content> genotype of c.*237C<\/jats:styled-content>>T<\/jats:styled-content> was susceptible for GBC<\/jats:styled-content> and CC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20092.59 and OR<\/jats:styled-content>\u2009=\u20093.48), while CC<\/jats:styled-content> genotype was risk protective for GBC<\/jats:styled-content> and CC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20090.61 and OR<\/jats:styled-content>\u2009=\u20090.34). T<\/jats:styled-content> allele of c.*237C<\/jats:styled-content>>T<\/jats:styled-content> polymorphism was risk associated with GBC<\/jats:styled-content> and CC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20091.63 and OR<\/jats:styled-content>\u2009=\u20092.90), while C<\/jats:styled-content> allele was risk protective for GBC<\/jats:styled-content> and CC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20090.38 and OR<\/jats:styled-content>\u2009=\u20090.28). Haplotype I<\/jats:styled-content>\u2010C<\/jats:styled-content>\u2010A<\/jats:styled-content>\u2010C<\/jats:styled-content> was risk protective for GBC<\/jats:styled-content> (OR<\/jats:styled-content>\u2009=\u20090.27).<\/jats:p><\/jats:sec>Conclusion<\/jats:title>The present study suggests that c.*237C<\/jats:styled-content>>T<\/jats:styled-content> and g.43737830A<\/jats:styled-content>>G<\/jats:styled-content> polymorphisms are useful markers of susceptibility to GBC<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.12343","type":"journal-article","created":{"date-parts":[[2013,8,21]],"date-time":"2013-08-21T09:58:36Z","timestamp":1377079116000},"page":"1678-1685","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Vascular endothelial growth factor single\u2010nucleotide polymorphism in gall bladder cancer"],"prefix":"10.1111","volume":"28","author":[{"given":"Kumudesh","family":"Mishra","sequence":"first","affiliation":[{"name":"Department of Surgical Gastroenterology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anu","family":"Behari","sequence":"additional","affiliation":[{"name":"Department of Surgical Gastroenterology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vinay Kumar","family":"Kapoor","sequence":"additional","affiliation":[{"name":"Department of Surgical Gastroenterology Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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