Loss of expression of transforming growth factor beta type II receptor correlates with high tumour grade in human breast in-situ and invasive carcinomas

H. Gobbi, C. L. Arteaga, R. A. Jensen, J. F. Simpson, W. D. Dupont, S. J. Olson, P. A. Schuyler, W. D. Plummer, D. L. Page

Research output: Contribution to journalArticle

85 Scopus citations


Aims: Loss of transforming growth factor beta type II receptor (TGFβ-RII) expression has been associated with resistance to TGFβ-mediated inhibition of cell proliferation and tumour progression. We investigated whether the expression of TGFβ-RII is related to the progression of human breast cancer and whether there is a correlation between TGFβ-RII expression and phenotypic markers of biological aggressiveness. Methods and results: Immunohistochemical methods were used to detect TGFβ-RII in archival breast samples including benign proliferative lesions, ductal carcinoma in situ (DCIS) and invasive mammary carcinomas (IMC). Neoplastic cells showed reduced expression of TGFβ-RII in comparison to the normal breast tissue and benign lesions. There was a significant inverse correlation between loss of TGFβ-RII expression and tumour grade within both DCIS (P = 0.004) and IMC (P = 0.001) groups. There was an inverse correlation between TGFβ-RII expression and both mitotic count (P = 0.001) and clinical stage (P = 0.004). Oestrogen receptor (P = 0.07) and lymph node status (P = 0.10) were not significantly associated with TGFβ-RII expression. Conclusions: These data indicate that decreased expression of TGFβ-RII may contribute to breast cancer progression and is related to a more aggressive phenotype in both in-situ and invasive carcinomas.

Original languageEnglish (US)
Pages (from-to)168-177
Number of pages10
Issue number2
Publication statusPublished - Jan 1 2000



  • Benign breast disease
  • Ductal carcinoma in situ
  • Immunohistochemistry
  • Invasive mammary carcinoma
  • Transforming growth factor β receptors

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Histology

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