I n this issue of Cancer Cytopathology, Abati et al. 1 , using the cellular material in fine-needle aspiration (FNA) biopsies, demonstrate the feasibility of detecting loss of heterozygosity (LOH) at the p53 locus on chromosome 17, the putative neuroblastoma tumor suppressor locus on chromosome 1, and at the von Hippel-Lindau locus on chromosome 3 in adrenal cortical carcinomas. The most common mechanism of loss of function of a tumor suppressor gene is mutation of one allele and loss of the other (LOH). This makes it possible to use LOH as a marker of loss of tumor suppressor gene function. With the identification of a large number of repeat sequences of 2, 3, or 4 repeating bases (microsatellites) throughout the genome, whose alleles differ only in the number of repeats, it has become possible over the past few years to use the polymerase chain reaction (PCR) to examine LOH at virtually any locus. This approach technically is simpler than sequencing an entire tumor suppressor gene to look for mutations.
Over the past few years, a number of articles have demonstrated the feasibility of determination of LOH at various loci using cellular material obtained by FNA. Tsuda et al. showed LOH on chromosome 16 in FNAs of surgical specimens of 10 of 14 breast carcinomas, with no LOH detected in any of 3 fibroadenomas. Using microdissection of FNA smears, Chuaqui et al. showed LOH at chromosome 11q13 in 10 of 19 breast carcinomas, which demonstrated complete correlation with results obtained from corresponding histologic samples.
Abati et al. 1 apply LOH analysis to cellular material from FNAs of adrenal cortical adenomas and carcinomas. This is of clinical interest because the pathologic distinction of adrenal cortical adenomas from carcinomas is a difficult problem, particularly when based on FNA. Prediction of malignant behavior of primary adrenal cortical neoplasms combines clinical and pathologic characteristics such as weight loss, size, growth pattern, and high mitotic rate of the lesion, broad fibrous bands traversing the tumor, and tumor growth at clinical follow-up. Although FNA is used in the triage of nonfunctional