TP53 is a tumor suppressor gene which participates in regulation of cell cycle check points, DNA repair, and apoptosis. Somatic mutations of TP53 are more frequent in advanced stage or in cancer subtypes with aggressive behavior (such as triple negative or HER2-amplified breast cancers). The aim of this study was to compare TP53 germline gene polymorphisms (c.[215G > C]) wild – type homozygotes GG with heterozygotes GC according to clinicopathological factors.
We reviewed the medical records of 65 (29% TP53 gene homozygotes and 71% heterozygotes) breast cancer patients who were diagnosed and treated in COI in Gliwice. Mutation profile was assessed by RFLP-PCR technique. We evaluated the presence of polymorphism TP53 (c.[215G > C]). Statistical analysis was carried out using STATISTICA 7 software.
The median age of patients was 51 years (range from 32 to 77). There was no difference according to median age between TP53 gene homozygotes and heterozygotes (51 vs. 52 years, p = 0.903). Lobular invasive carcinoma was observed insignificantly more frequently in TP53 gene homozygotes in comparison to heterozygotes (21% vs. 9%, p = 0.218). Tumor size (T3-T4) was detected in 15% of pts. Pts being TP53 gene heterozygotes had larger tumor size (T > 2) than homozygotes (20% vs. 5%, p = 0.258). Ki67 > 20% was detected in 56% of tumors and was more often reported in TP53 gene homozygotes (75% vs. 46%, p = 0.157). There was observed tendency to the presence of lymph node metastases (53% vs. 35%, p = 0.266) and triple negative breast cancer (16% vs. 7%, p = 0.347) in patients with TP53 gene homozygotes in comparison to heterozygotes (53% vs. 35%, p = 0.266). There were no associations between type of TP53 gene polymorphisms (homozygotes vs. heterozygotes) and steroid receptor status (68% vs. 74%, p = 0.762), higher histological grade (G > 2) (38% vs. 35%, p = 1.00) or HER2 overexpression (26% vs. 21%, p = 0.761).
TP53 gene homozygotes were characterized by lymph node metastases, lobular histological type, triple negative breast cancer and higher Ki67 (>20%). In contrary, larger tumor size (T > 2) was mostly presented in TP53 gene heterozygotes.
Clinical trial identification
Legal entity responsible for the study
Clinical and Experimental Oncology Department MSC Memorial Cancer Center and Institute of Oncology, Gliwice Branch
Center for Translational Research and Molecular Biology of Cancer Clinical and Experimental Oncology Department MSC Memorial Cancer Center and Institute of Oncology, Gliwice Branch
All authors have declared no conflicts of interest.