1. Loss of expression of transforming growth factor beta type II receptor correlates with high tumour grade in human breast in-situ and invasive carcinomas
- Author
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Walton D. Plummer, Carlos L. Arteaga, Helenice Gobbi, Jean F. Simpson, Sandy Olson, Peggy A. Schuyler, Roy A. Jensen, David L. Page, and William D. Dupont
- Subjects
Pathology ,medicine.medical_specialty ,Histology ,Carcinoma in situ ,Mammary gland ,Cancer ,hemic and immune systems ,chemical and pharmacologic phenomena ,General Medicine ,Hyperplasia ,Biology ,Ductal carcinoma ,medicine.disease ,Pathology and Forensic Medicine ,medicine.anatomical_structure ,Breast cancer ,Growth factor receptor ,Tumor progression ,medicine - Abstract
Aims Loss of transforming growth factor beta type II receptor (TGFbeta-RII) expression has been associated with resistance to TGFbeta-mediated inhibition of cell proliferation and tumour progression. We investigated whether the expression of TGFbeta-RII is related to the progression of human breast cancer and whether there is a correlation between TGFbeta-RII expression and phenotypic markers of biological aggressiveness. Methods and results Immunohistochemical methods were used to detect TGFbeta-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 TGFbeta-RII in comparison to the normal breast tissue and benign lesions. There was a significant inverse correlation between loss of TGFbeta-RII expression and tumour grade within both DCIS (P = 0.004) and IMC (P = 0.001) groups. There was an inverse correlation between TGFbeta-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 TGFbeta-RII expression. Conclusions These data indicate that decreased expression of TGFbeta-RII may contribute to breast cancer progression and is related to a more aggressive phenotype in both in-situ and invasive carcinomas.
- Published
- 2000
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