Abstract
Our recent allelic analysis of head and neck squamous cell carcinomas identified a high incidence of chromosomal loss on 13q. To further define an area of minimal loss, we tested 60 primary head and neck squamous cell carcinomas in 59 patients for loss of heterozygosity (LOH) by using 10 polymorphic microsatellite markers spanning the long arm of chromosome 13. We examined the same primary tumors for inactivation of the retinoblastoma (Rb) gene by immunohistochemical analysis of paraffin-embedded specimens. Thirty-one of 60 (52%) tumors demonstrated LOH in at least one 13q marker. Twenty-nine of 31 (94%) lost a portion of 13q that included D13s133, which lies just telomeric to the Rb gene at 13q14.3. However, immunohistochemical staining revealed absence of Rb protein in only 6 of these 31 tumors (19.4%) with LOH. All but one tumor without LOH on 13q displayed normal Rb protein staining. Although Rb may be inactivated by an unusual mechanism in some head and neck squamous cell carcinomas, our data suggest that another tumor suppressor gene locus at 13q14 is likely to be involved in head and neck tumor progression.
Footnotes
-
↵1 Supported by Lung Cancer Spore Grant CA-58184-01, CA-54672, and a collaborative research agreement with Oncor, Inc. (Gaithersburg, Maryland).
-
↵2 To whom requests for reprints should be addressed, at Department of Otolaryngology—Head and Neck Surgery, Division of Head and Neck Cancer Research, Johns Hopkins University School of Medicine, 818 Ross Research Building, 72 Rutland Avenue, Baltimore, MD 21205-2196.
-
↵3 Under an agreement between Oncor and the Johns Hopkins University, Dr. Sidransky is entitled to a share of sales royalty received by the University from Oncor. Under that agreement, the University and Dr. Sidransky also have received Oncor stock which, per University policy, cannot be traded until products related to this research are sold. The terms of this arrangement have been reviewed and approved by the University in accordance with its conflict of interest policies.
- Received June 28, 1994.
- Accepted July 14, 1994.
- ©1994 American Association for Cancer Research.
Volume 54, Issue 17
