Comparative study of the immunohistochemical phenotype in breast cancer and its lymph node metastatic location

Cancer Invest. 2004;22(2):219-24. doi: 10.1081/cnv-120030210.

Abstract

At present, an important part of prognostic information, together with particular treatment strategies in breast cancer, take into account the immunohistochemical phenotype of the primary tumor location. However, the changing heterogeneity intrinsic to neoplastic cells in general leads us to consider the possibility that the expression of these proteins is modified during tumoral development and dissemination. With this hypothesis as a starting point, 60 patients with breast cancer were studied with immunohistochemistry, the expression of estrogen and progestagenic receptors, proliferation through the Ki-67 expression, and the overexpression of HER-2 and p53 in both the primary location and the lymph node metastases. If we consider significant change to be loss (from positive to negative) or gain (negative to positive) of expression in some of the studied determinations, we find that this is produced in 60% of the tumors studied. These results demonstrate the modification of immunohistochemical expression of the proteins studied between the primary tumor location and the lymph node metastases.

Publication types

  • Comparative Study

MeSH terms

  • Breast Neoplasms / immunology*
  • Breast Neoplasms / pathology*
  • Female
  • Humans
  • Immunohistochemistry
  • Ki-67 Antigen / analysis
  • Ki-67 Antigen / biosynthesis
  • Lymphatic Metastasis / immunology*
  • Lymphatic Metastasis / pathology*
  • Phenotype
  • Receptor, ErbB-2 / analysis
  • Receptor, ErbB-2 / biosynthesis
  • Receptors, Estrogen / analysis
  • Receptors, Estrogen / biosynthesis*
  • Receptors, Progesterone / analysis
  • Receptors, Progesterone / biosynthesis*
  • Tumor Suppressor Protein p53 / analysis
  • Tumor Suppressor Protein p53 / biosynthesis

Substances

  • Ki-67 Antigen
  • Receptors, Estrogen
  • Receptors, Progesterone
  • Tumor Suppressor Protein p53
  • Receptor, ErbB-2