ISPO

A preliminary study of surgical margins with P53, B72.3 and HER-2/neu to evaluate the molecular basis for tumor field.

G.A.P. Ganepola, M.D., F.A.C.S. ab, A. Gritsman, M.D., PH.D, F.C.A.P.b, A. Yiengpruksawan, M.D., F.A.C.S.b, L. Rizzo b, and R. Vurtser b.

aColumbia University Medical Center, New York, NY, b Cancer Institute, The Valley Hospital, Ridgewood, NJ.

Three surgical resected specimens of breast carcinoma and one esophageal carcinoma specimen were analyzed with immunohistochemistry to study the extent of P53, B72.3 and HER-2/neu molecular markers. This study shows the discrepancy of the hematoxylin-eosin stained histological margins to immunohistochemcial detected molecular margins based on the three markers described above. P53 shows an interesting pattern here. In some cases when its presence is strongly positive, other oncogenic markers like HER-2/neu are absent. As our staining techniques did not differentiate between the mutant and wild-type of P53 nuclear phosphoprotein, it could be postulated that the presence of wild-type P53 may have a suppresive effect on some oncogenes which in fact may be of positive prognostic value. This may become a larger study with a long clinical followup. However, the presence of the P53 mutation in esophageal carcinoma has been reported elsewhere; but this study also confirmed its presence more significantly than even in the breast carcinoma model. The presence of P53 nuclear phosphoproteins away from the primary tumor site signifies that currently acceptable margins may not stand the test of time with further development of molecular genetics and may have to be reconsidered in the surgical management of certain tumors.

KEY WORDS: Wild-Type P53, Molecular Margins, Breast Cancer, Esophageal Cancer.

For more information, contact GANEPOLA@BELLATLANTIC.NET

Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Molecular Pathology.

http://www.cancerprev.org/Journal/Issues/26/101/991/4155