Abstract
Since Bokhman's proposal of dividing endometrial cancer into two broad categories of type I and type II [ [1] Bokhman J.V. Two pathogenetic types of endometrial carcinoma. Gynecol Oncol. 1983; 15: 10-17 Abstract Full Text PDF PubMed Scopus (1759) Google Scholar ] the dogma has been that type I tumors are composed of low-grade endometrioid carcinomas with an excellent prognosis and that type II tumors are represented by serous carcinomas with a poor prognosis. Bokhman divided the groups primarily on clinical, metabolic and endocrine features. Thus, aside from placing “highly differentiated” tumors into the type I group and “poorly differentiated” carcinomas in the type II group, the histologic features of the tumors were not a part of his model. Except for a few case reports, serous carcinoma had been described as a distinctive entity only one year earlier and was not included in Bokhman's model [ [2] Hendrickson M. Ross J. Eifel P. Martinez A. Kempson R. Uterine papillary serous carcinoma: a highly malignant form of endometrial adenocarcinoma. Am J Surg Pathol. 1982; 6: 93-108 Crossref PubMed Scopus (643) Google Scholar ]. Subsequent morphologic, immunohistochemical (IHC) and molecular genetic studies showed that in contrast to low-grade endometrioid carcinomas, which were often associated with atypical hyperplasia, failed to express p53 by IHC and rarely harbored TP53 mutations, serous carcinomas developed in atrophic endometrium from intraepithelial carcinoma [ [3] Ambros R.A. Sherman M.E. Zahn C.M. Bitterman P. Kurman R.J. Endometrial intraepithelial carcinoma: a distinctive lesion specifically associated with tumors displaying serous differentiation. Hum Pathol. 1995; 26: 1260-1267 Abstract Full Text PDF PubMed Scopus (246) Google Scholar ], expressed p53 strongly [ [4] Sherman M.E. Bur M.E. Kurman R.J. p53 in endometrial cancer and its putative precursors: evidence for diverse pathways of tumorigenesis. Hum Pathol. 1995; 26: 1268-1274 Abstract Full Text PDF PubMed Scopus (315) Google Scholar ] and very frequently harbored TP53 mutations [ 5 Tashiro H. et al. p53 mutations are common in uterine serous carcinoma and occur early in their pathogenesis. Am J Pathol. 1997; 150: 177-185 PubMed Google Scholar , 6 Kuhn E. et al. Identification of molecular pathway aberrations in uterine serous carcinoma by genome-wide analyses. J Natl Cancer Inst. 2012; 104: 1503-1513 Crossref PubMed Scopus (183) Google Scholar ]. These reports provide cogent morphologic, IHC and molecular genetic data underpinning the dualistic model as far as low-grade endometrioid and serous carcinomas are concerned but there are only limited data indicating where, for example, clear cell carcinoma and carcinosarcoma should be placed. Moreover, in the intervening years there has been relatively limited information on whether established risk factors for endometrial cancer differ between type I and type II tumors.
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