@article {MIYAKE5617, author = {TOMOHIRO MIYAKE and TAKAHIRO NAKAYAMA and NAOFUMI KAGARA and NORIAKI YAMAMOTO and YUKIKO NAKAMURA and YOKO OTANI and KUMIKO UJI and YASUTO NAOI and MASAFUMI SHIMODA and NAOMI MARUYAMA and ATSUSHI SHIMOMURA and KENZO SHIMAZU and SEUNG JIN KIM and SHINZABURO NOGUCHI}, title = {Association of GSTP1 Methylation with Aggressive Phenotype in ER-positive Breast Cancer}, volume = {33}, number = {12}, pages = {5617--5623}, year = {2013}, publisher = {International Institute of Anticancer Research}, abstract = {Aim: We investigated the association of glutathione S-transferase P1 (GSTP1) expression and methylation status with clinicopathological characteristics of estrogen receptor (ER)-positive breast cancers. Materials and Methods: Primary ER-positive breast cancer patients (n=177, stage I-III) were retrospectively analyzed. A quantitative GSTP1 methylation assay was performed using DNA micro-dissected from formalin-fixed and paraffin-embedded (FFPE) breast surgical specimens and GSTP1 expression was examined immunohistochemically. Results: GSTP1 methylation index (MI) was higher for the following patient subsets: Large-size (p=0.029), high-grade (p=0.010), human epidermal growth factor receptor-2 (HER2)-positive (p=0.024) and Ki67-positive (p=0.001) patients. In addition, GSTP1 hyper-methylation was more frequently observed in the luminal-B than the luminal-A subtype (p\<0.001) and there was no significant difference in GSTP1 positivity between the two subtypes (p=0.150). Conclusion: GSTP1 methylation may well be associated with the pathogenesis of the biologically-aggressive phenotype in ER-positive breast cancer.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/33/12/5617}, eprint = {https://ar.iiarjournals.org/content/33/12/5617.full.pdf}, journal = {Anticancer Research} }