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dc.contributor.authorKafshdooz, L
dc.contributor.authorTabrizi, AD
dc.contributor.authorMohaddes, SM
dc.contributor.authorKafshdooz, T
dc.contributor.authorAkbarzadeh, A
dc.contributor.authorGhojazadeh, M
dc.contributor.authorGharesouran, J
dc.date.accessioned2018-08-26T05:48:37Z
dc.date.available2018-08-26T05:48:37Z
dc.date.issued2014
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/41203
dc.description.abstractEndometral carcinoma is the most common malignant tumor of the female genital tract and the fourth most common cancer in women after breast, colorectal and lung cancers Hypoxia-inducible factor -1 (HIF-1) is a key transcription factor that regulates cellular response to hypoxia HIF-1 plays important roles in the development and progression of cancer through activation of various genes that are involved in crucial aspects of cancer biology, including angiogenesis, energy metabolism, vasomotor function, erythropoiesis, and cell survival. In this study, we aimed to investigate the association between HIF-1 1772 C/T polymorphisms and endometrial cancer.75 patients with endometrial carcinoma and 75 patients whose underwent hysterectomy for non tumoral indication selected for evaluation of HIF-1 1772 C/T polymorphisms by PCR-RFLP and sequencing.For the 1772 C/T polymorphism, the analysis showed that the T allele and genotype TT were significantly associated with endometrial cancer risk.Our results suggest that the C1772T polymorphism of the HIF-1a may be associated with endometrial cancers.
dc.language.isoEnglish
dc.relation.ispartofAsian Pacific journal of cancer prevention : APJCP
dc.subjectCarcinoma, Endometrioid
dc.subjectCase-Control Studies
dc.subjectEndometrial Neoplasms
dc.subjectFemale
dc.subjectGenetic Predisposition to Disease
dc.subjectHumans
dc.subjectHypoxia-Inducible Factor 1, alpha Subunit
dc.subjectMiddle Aged
dc.subjectNeoplasms, Cystic, Mucinous, and Serous
dc.subjectPolymorphism, Single Nucleotide
dc.titleThe polymorphism of hypoxia-inducible factor-1a gene in endometrial cancer.
dc.typearticle
dc.citation.volume15
dc.citation.issue23
dc.citation.spage10393
dc.citation.epage6
dc.citation.indexPubmed


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