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• W2003205710 abstract "Molecular genetic techniques have permitted an unprecedented exploration of cancer progression, perhaps the most broadcasted being the unlocking of the genetic and epigenetic events leading to colon tumor formation (7). These discoveries could not have been achieved without the coexistence of the following two important factors: 1) the organizational infrastructure to collect critical human tissues and 2) the advent of the polymerase chain reaction (PCR), which permitted the investigation of genetic mutations in minuscule amounts of archival tissues. These efforts in molecular sleuthing often lead to surprising observations that cause us to re-evaluate our basic assumptions with regard to disease progression. The presence of HER-2 amplification in almost 50% of ductal carcinomas in situ compared with 20% of lymph node-positive breast cancers suggested that HER-2 is not a progression factor as originally thought, but may indeed mark a more virulent etiologic subtype (2). Similarly, the early reports of frequent p53 mutations in colon cancer raised suspicions that p53 may play a major role in the induction of colon tumors. The absence of p53 aberrations in premalignant lesions and the observation that Li-Fraumeni patients harboring germline p53 mutations do not have high rates of colon cancer, however, indicated that p53 may not be involved in the initiation of colorectal carcinomas. These and other results have led to the hypothesis that the APC gene, and not p53, functions as the gatekeeper maintaining normal, nonmalignant colonic epithelial growth. The article by Zheng et al. (5) appearing in this issue of the Journal again raises some intriguing questions about cancer progression, specifically ovarian cancer progression. Zheng et al. have found that p53 mutations can be detected in 52% of 46 ovarian carcinomas compared with none of 21 ovarian tumors of low malignant potential and none of 16 solitary cystadenomas. They found that all six cystadenocarcinomas with p53 mutations and adjacent, morphologically benign cysts harbored the same p53 mutation in both tissues. In fact, all benign cysts were also concordant with their contiguous carcinomas when examined for loss of heterozygosity (LOH) at the p53 locus (17p). In one tumor, they observed that the cyst and the adenocarcinoma not only carried the same p53 mutation and LOH at 17p but also carried LOH at l ip. Thus, benign and adjacent malignant ovarian tissues are related in multiple genetic loci. The simple explanation for their findings is that a small proportion of benign ovarian cysts or tumors of low malignant potential (fewer than one in 37) harbor p53 mutations. These mutations then mark the affected tissues as predestined to become ovarian carcinomas through several possible pathways (progression models I and II; Fig. 1). Such a progression model of p53 action can be clinically applied, since a patient carrying a cyst with malignant potential (i.e., carrying a p53 mutation) may need to, at least, undergo more vigorous postoperative surveillance. To prove this point, however, many more benign ovarian cysts will need to be screened for aberrations of the p53 gene so that the prevalence of p53 mutations may be estimated. In other disease systems in which p53 or ras mutations are common in the malignant cells, genetic mutations at these loci have been readily detected in the premalignant counterparts. In breast cancer, p53 mutations are present in approximately 25%-50% of invasive cancers (4,5), in 20%-30% of in situ carcinomas (<5), and in 5% of biopsy specimens of tissues taken from patients with benign breast disease (7). The ras mutations are found in 50% of colon carcinomas (8) and in 10%-of polyps (8) and are detectable in the earliest precancerous lesions, the aberrant crypt foci (9,10). In ovarian cancers, however, there has not been the same level of molecular scrutiny to ascertain the frequency of genetic alterations in purely benign ovarian tissues. Thus, if the true prevalence of p53 mutations in ovarian cysts is small (e.g., one in 200), then proving the clinical utility of a p53 assay in this situation would require large trials and long follow-up. Moreover, at this frequency, the molecular screening of benign ovarian masses for p53 alterations would not be cost-effective." @default.
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• W2003205710 title "Molecular Sleuthing: Tracking Ovarian Cancer Progression" @default.
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• W2003205710 doi "https://doi.org/10.1093/jnci/87.15.1099" @default.
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