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JNCI Journal of the National Cancer Institute 2001 93(9):666-667; doi:10.1093/jnci/93.9.666
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 9, 666-667, May 2, 2001
© 2001 Oxford University Press

EDITORIAL

p53 in Mammary Ductal Carcinoma In Situ, Mutations in High-Grade Lesions Only?

Jean F. Simpson, David L. Page, Mary E. Edgerton

Affiliations of authors: J. F. Simpson (Division of Anatomic Pathology), D. L. Page (Division of Anatomic Pathology and Department of Preventive Medicine), M. E. Edgerton (Division of Anatomic Pathology and Department of Biomedical Informatics), Vanderbilt University School of Medicine, Nashville, TN.

Correspondence to: Jean F. Simpson, M.D., Division of Anatomic Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232–2561 (e-mail: jean.simpson@mcmail.vanderbilt.edu).

Dissecting the contribution that mutated p53 (also known as TP53) makes to the progression of breast cancer is made difficult by the multiple functions of this tumor suppressor gene and by the study material itself. Most of our data come from the study of well-established, invasive carcinoma; if not already metastatic, these tumors certainly have that capacity.

Although there have been attempts to establish a sequence of epithelial proliferative events that lead to invasive cancer, the only proven precursor to this disease is ductal carcinoma in situ (DCIS) (1). The study of the natural history of DCIS has been difficult . . . [Full Text of this Article]

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