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Loss of Heterozygosity for Genes on 11p and the Clinical Course of Patients with Lung Carcinoma¹

Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710 [M. A. S., G. H., J. D. I.]; Department of Pathology, Durham Veterans Administration Medical Center, Durham, North Carolina 27710 [R. V.]; and Division of Cardiothoracic Surgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104 [P. A.]

Forty-five primary human lung carcinomas were evaluated for the loss of heterozygosity for genes on the short end of chromosome 11. Of 40 evaluable heterozygous cases, loss of the 11p genes c-H-ras and insulin was documented in nine cases (22%). The clinical parameters investigated for each patient included the disease stage at presentation, the presence of metastatic disease in either bronchial or mediastinal lymph nodes, and the presence of positive parietal pleural margins in the surgically resected specimen. There were no differences found with respect to these indicators when patients exhibiting the loss of heterozygosity were compared with those who did not have such genetic loss. In addition, when the clinical courses of the two patient groups were compared, there was no difference in survival. We conclude that the loss of heterozygosity for c-H-ras and insulin on 11p is a common finding in primary non-small cell human lung carcinomas but does not confer a more aggressive phenotype on these tumors. Although this genetic lesion may be important in the initial transformation of the cells to carcinoma, the available data for lung carcinoma are insufficient to prove causality.

¹ This investigation was supported by USPHS Grant CA-40640 awarded to J. D. I. by the National Cancer Institute.

² To whom requests for reprints should be addressed, at Department of Surgery, Box 3873, Duke University Medical Center, Durham, NC 27710.

Received 10/10/89. Revised 12/27/89.

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