title: Association between GSTP1 genotypes and hormone receptor phenotype in invasive ductal carcinomas of breast.
abstract: Eighty six cases of invasive ductal breast carcinomas were utilized to investigate GSTP1 polymorphisms in certain immunohistochemistry (IHC) subtypes of breast cancer with respect to ER, PR and HER2 expression. The frequency of wild allele homozygote, heterozygote and variant allele homozygote genotypes were 46.5%, 52.3% and 1.16% respectively; Whereas 54.3% of the control subjects were GSTP1 wild type allele homozygous, 40.0% were heterozygous and 5.71% mutant allele homozygous. There was dramatic inverted relation between positive IHC ER staining and increasing grade of tumors in general (100%, 88.6%, 40.4%) and especially among tumors with heterozygote genotype of GSTP1 (70%, 35.4%, 22.7). There was increase in positive IHC HER2 staining consistent with higher grades in general (20%, 29.6%, 50.0%), especially among tumors with GSTP1 wild allele homozygote genotype (5.0%, 9.1%, 31.8%). A remarkable reverse relation was also observed between the fraction of IHC hormone receptor phenotype ER+/PR+/ HER2- and increased grade of tumors (60.0%, 45.5%, and 27.3%) especially among tumors with GSTP1 heterozygote genotype, and a similar link was noted regarding ER+/PR-/ HER2- and tumor grade. There was increase in frequency of ER-/PR-/ HER2- (0.0%, 6.8%, and 18.2%) and ER-/PR-/ HER2+ (0.0%, 4.54%, and 40.9%) consistent with the higher grades of tumors in general and especially GSTP1 heterozygote genotype tumors. As a conclusion, there is no correlation between GSTP1 polymorphism and increased risk of breast cancer i.e. the mutant allele is randomly distributed in cancer and control cases. However, there is a link between GSTP1 genotypes and hormone receptor expression status and certain phenotypes of breast cancer, which may have clinical importance.
authors.affiliation: Department of Pathology, Rabigh Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia E-mail : mnkhabaz@kau.edu.sa; nkhabaz@yahoo.co.uk.
authors.forename: Mohamad Nidal
authors.initials: MN
authors.lastname: Khabaz
authors.forename: Mamdooh Abdullah
authors.initials: MA
authors.lastname: Gari
authors.forename: Jaudah Ahmed
authors.initials: JA
authors.lastname: Al-Maghrabi
authors.forename: Taoufik
authors.initials: T
authors.lastname: Nedjadi
authors.forename: Marwan
authors.initials: M
authors.lastname: Bakarman
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001483:Base Sequence; D014408:Biomarkers, Tumor / Q000235:genetics; D001940:Breast / Q000473:pathology; D001943:Breast Neoplasms / Q000235:genetics*; D018270:Carcinoma, Ductal, Breast / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D051549:Glutathione S-Transferase pi / Q000235:genetics*; D006801:Humans; D008875:Middle Aged; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*; D017422:Sequence Analysis, DNA; D055815:Young Adult
chemical_list: D014408:Biomarkers, Tumor; D051549:Glutathione S-Transferase pi; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C496556:GSTP1 protein, human; C508053:ERBB2 protein, human