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p16(INK4a) expression and breast cancer risk in women with atypical hyperplasia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Radisky, Derek C. Santisteban, Marta Berman, Hal K. Gauthier, Mona L. Frost, Marlene H. Reynolds, Carol A. Vierkant, Robert A. Pankratz, V. Shane Visscher, Daniel W. Tlsty, Thea D. Hartmann, Lynn C.
Description	Country affiliation: United States Author Affiliation: Radisky DC ( Division of Biochemistry/Molecular Biology, Mayo Clinic in Jacksonville, Jacksonville, Florida 32224, USA. radisky.derek@mayo.edu)
Abstract	p16, a nuclear protein encoded by the p16(INK4a) gene, is a regulator of cell-cycle regulation. Previous studies have shown that expression of p16 in tissue biopsies of patients with ductal carcinoma in situ (DCIS) is associated with increased risk of breast cancer, particularly when considered in combination with other markers such as Ki-67 and COX-2. Here, we evaluated how expression of p16 in breast tissue biopsies of women with atypical hyperplasia (AH), a putative precursor lesion to DCIS, is associated with subsequent development of cancer. p16 expression was assessed by immunohistochemistry in archival sections from 233 women with AH diagnosed at the Mayo Clinic. p16 expression in the atypical lesions was scored by percentage of positive cells and intensity of staining. We also studied coexpression of p16, with Ki-67 and COX-2, biomarkers of progression in AH. Risk factor and follow-up data were obtained via study questionnaire and medical records. Forty-seven patients (20%) developed breast cancer with a median follow-up of 14.5 years. Staining of p16 was increased in older patients relative to younger patients (P = 0.0025). Although risk of developing breast cancer was not associated with increased p16 expression, joint overexpression of Ki-67 and COX-2 was found to convey stronger risk of breast cancer in the first 10 years after diagnosis as compared with one negative marker (P < 0.01). However, the addition of p16 levels did not strengthen this association. p16 overexpression, either alone or in combination with COX-2 and Ki-67, does not significantly stratify breast cancer risk in women with AH.
File Format	HTM / HTML
ISSN	19406207
e-ISSN	19406215
DOI	10.1158/1940-6207.CAPR-11-0282
Journal	Cancer Prevention Research
Issue Number	12
Volume Number	4
Language	English
Publisher	American Association for Cancer Research
Publisher Date	2011-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Oncology Tumor Markers, Biological Metabolism Breast Neoplasms Cyclin-dependent Kinase Inhibitor P16 Hyperplasia Precancerous Conditions Pathology Cyclooxygenase 2 Immunoenzyme Techniques Ki-67 Antigen Risk Factors Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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