The protective effect of parity in hormone receptor-positive, Ki-67 expressing breast cancer

World J Surg. 2014 May;38(5):1065-9. doi: 10.1007/s00268-014-2468-4.

Abstract

Background: Epidemiologic studies showed that the experience of pregnancy is associated with a reduced risk of breast cancer. We hypothesized that parity may differentially be associated with the development of invasive breast cancer by each subtype.

Methods: We reviewed the clinical, radiological, and pathological records of women diagnosed with invasive ductal carcinoma of the breast at Samsung Medical Center between 2005 and 2009. Clinicopathologic results were assessed by χ(2) and Fisher's exact tests with a Bonferroni correction for categorical variables, and by the Kruskal-Wallis test for nonparametric continuous variables. A multinomial logistic regression model was used for multivariate analysis.

Results: Among a total of 3,095 patients, 283 (9.14 %) patients were nulliparous. Older age, higher pN, and expression of HER2 were associated with parity. In the analysis between parity and molecular subtypes, parity also had a variable influence on breast cancer subtypes (p = 0.032). Intergroup analysis with multiple comparison showed that luminal B subtype was related to nulliparity compared with HER2-positive subtypes (p = 0.03).

Conclusions: The effect of parity on the development of breast cancer differed by hormone receptor and HER2 expression. It seems that parity might have a protective effect against hormone receptor-positive breast cancer, especially cancers expressing HR+ and Ki-67. Further basic research to define and understand this result is ongoing.

MeSH terms

  • Adult
  • Breast Neoplasms / epidemiology*
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Female
  • Humans
  • Ki-67 Antigen / biosynthesis*
  • Middle Aged
  • Neoplasm Invasiveness
  • Parity*
  • Protective Factors
  • Receptor, ErbB-2 / biosynthesis*
  • Retrospective Studies

Substances

  • Ki-67 Antigen
  • ERBB2 protein, human
  • Receptor, ErbB-2