O uso cada vez mais freqüente de métodos diagnósticos simples e efetivos tem contribuído significativamente para um aumento no diagnóstico de câncer da tiróide nos últimos anos. Entretanto, existem importantes evidências de que muitos dos microcarcinomas papilíferos têm um comportamento indolente e podem nunca evoluir para cânceres clínicos. Existe, portanto, uma necessidade urgente de desenvolver novas ferramentas capazes de predizer quais os tumores tiroidianos que permanecerão silenciosos e quais desenvolverão comportamento agressivo. Há uma série de marcadores clínicos de evolução bem estabelecidos e alguns estudos recentes sugerem que dados laboratoriais e métodos de imagem podem ser úteis. Marcadores moleculares também vêm sendo ativamente investigados e alguns, como BRAF, os genes GST e polimorfismos de p53, parecem promissores. Além disso, marcadores imunocitoquímicos e a medida da natureza fractal da cromatina podem aumentar a especificidade do diagnóstico anatomopatológico e ajudar a predizer o prognóstico. Existe uma necessidade imperiosa de elaborarmos diretrizes destinadas a selecionar os nódulos que merecem prosseguimento em sua avaliação, assim como novos métodos capazes de identificar lesões mais agressivas entre os geralmente indolentes tumores tiroidianos.

The large use of simple and effective diagnostic tools has significantly contributed to the increase in diagnosis of thyroid cancer over the past years. However, there is compelling evidence that most micropapillary carcinomas have an indolent behavior and may never evolve into clinical cancers. Therefore, there is an urgent need for new tools able to predict which thyroid cancers will remain silent, and which thyroid cancers will present an aggressive behavior. There are a number of well-established clinical predictors of malignancy and recent studies have suggested that some of the patient’s laboratory data and image methods may be useful. Molecular markers have also been increasingly tested and some of them appear to be very promising, such as BRAF, a few GST genes and p53 polymorphisms. In addition, modern tools, such as immunocytochemical markers, and the measure of the fractal nature of chromatin organization may increase the specificity of the pathological diagnosis of malignancy and help ascertain the prognosis. Guidelines designed to select nodules for further evaluation, as well as new methods aimed at distinguishing carcinomas of higher aggressiveness among the usually indolent thyroid tumors are an utmost necessity.

Background: p53 is a nuclear protein that exerts an important role in the negative control of cellular proliferation, as well as in masterminding signaling cascades important in DNA repair and/or apoptosis. Mutations of p53 have been reported with high frequency in many cancer types and are highly prevalent in poorly differentiated and undifferentiated thyroid carcinomas, but they are not found in benign tumors and are infrequent in well-differentiated cancer. Most mutations are located in exons 5-8 of the gene. Recently, a germline mutation in the seldom investigated exon 10, on codon 337 of p53 was described in Brazilian children who had adrenocortical tumors. Aim: To study codon 337 of exon 10 of p53 mutation in thyroid tumors. Material and methods: Seventy four thyroid tumors were studied (5 follicular carcinomas including 3 widely invasive, 22 papillary carcinomas including 6 tall cell variants, 11 follicular adenomas, 1 medullary carcinoma and 35 benign goiters). DNA was extracted from a central part of all tumors and contralateral normal thyroid tissue samples or blood from 38 of these patients. The products of PCR for exon 10 of p53 were examined by single strand conformation polymorphism (SSCP) analysis. We sequenced 2 samples suspected of presenting aberrant migrating bands and 3 additional PCR products from tumor samples with normal SSCP patterns but all were wild type. Results: In all samples studied, a wild type sequence was found. Conclusions: Exon 10 of p53 gene does not present mutations in thyroid tumors, suggesting that this mutation is specific of adrenocortical cancers. (Rev Méd Chile 2004; 132: 1513-6)