© 1998 by Oxford University Press
Journal of the National Cancer Institute, Vol. 90, No. 20, 1545-1551,
October 21, 1998
©Copyright 1998 Oxford University Press
ARTICLES |
Phenotype and Genotype of Advanced Premalignant Head and Neck Lesions After Chemopreventive Therapy
Affiliations of authors: L. Mao, V. Papadimitrakopoulou, D. M. Shin, Y. Fan, X. Zhou, J. S. Lee, W. K. Hong (Department of Thoracic/Head and Neck Medical Oncology), A. K. El-Naggar, H. C. Shin (Department of Pathology), G. Clayman (Department of Head and Neck Surgery), J. J. Lee (Department of Biomathematics), W. N. Hittelman (Department of Clinical Investigation), S. M. Lippman (Department of Clinical Cancer Prevention), The University of Texas M. D. Anderson Cancer Center, Houston.
Correspondence to: Li Mao, M.D., Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030.
Background: The goal of chemoprevention is to reduce the
risk of cancer development
by reversing or blocking the tumorigenic process through the use
of pharmacologic or natural
agents. To determine the potential role of genetic alterations in
assessing cancer risk and in
evaluating the efficacy of chemopreventive agents, we studied 22
patients with advanced
premalignant lesions of the head and neck who were part of a
prospective cancer prevention trial
that is investigating a regimen of 13-cis-retinoic acid,
interferon alfa, and
-tocopherol administered for 12 months or until disease
progression. Methods: We
used polymerase chain reaction analysis of microsatellite DNA
sequences in cells from
precancerous lesions to determine the frequencies of genetic
alterations—namely, loss of
heterozygosity (LOH) and microsatellite instability—at
chromosomal loci that are
commonly deleted in head and neck cancer. Results: Prior
to treatment, 17 (81%)
of 21, eight (44%) of 18, and eight (42%) of 19
patients who were informative (i.e.,
heterozygous) at chromosomes 9p21, 3p14, and 17p13, respectively,
exhibited LOH in at least
one of their lesion biopsy specimens. Among nine patients who
exhibited LOH at chromosome
9p21 in pretreatment biopsy specimens and who had completed at
least 5 months of therapy, the
genetic loss persisted in eight—including three of the four
patients who exhibited
complete histologic responses (i.e., no evidence of dysplasia in
their biopsy specimens). Implication: Our data suggest
that clinical and histologic assessments of the response to
chemopreventive agents may be insufficient to determine their
efficacy and that critical genetic
alterations could be used as independent biomarkers to augment
the ability to evaluate the
efficacy of such agents. [J Natl Cancer Inst
1998;90:1545-51]
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