Staging is an essential part of cancer treatment. It is crucial to both cancer care practice and the reporting of cancer data and statistics. The staging system serves multiple fundamental purposes across cancers. First, the staging system allows for the assignment of appropriate treatment. In particular, in the case of clinical trials, the stage of disease is always part of the inclusion criteria, thus allowing the appropriate assignment of patients to experimental therapy that is addressing specific treatment question(s). Second, the staging system allows health care providers to offer prognostic information regarding the cancer to their patient. This information should factor into both treatment planning and establishment of goals of life care. Third, the staging system allows a standard categorization of cancer and a recognized and accepted terminology that then facilitates data collection and reporting. Finally, the ideal staging system is based on the current scientific understanding of how the particular cancer grows and metastasizes.The recently revised International Federation of Gynecology and Obstetrics (FIGO) staging system for epithelial ovarian cancer and the accompanying introductory text re-reported in this issue of Cancer 1 together make an attempt to incorporate the most up-to-date scientific understanding of ovarian cancer within the staging system. The first point is the incorporation of new data identifying the etiology of ovarian cancer by recognizing that most (if not all) high-grade serous Mullerian cancers (most likely) arise in the fallopian tube epithelium. This science is paradigm-shifting as serous tubal intraepithelial carcinoma (STIC) is the first accepted precursor lesion for epithelial ovarian cancer. Transition zones from STIC to invasive malignancy have been identified to demonstrate the continuity of the pathology (Figs. 1-3). That FIGO has recognized this discovery in the current publication 1 formally acknowledges its importance. However, the problem with this acknowledgment lies in the potential assumption that the STIC lesion is relevant for all epithelial ovarian cancers. In fact, it is likely that STIC is a precursor lesion only for high-grade serous tumors.2 As the authors themselves note, other epithelial ovarian cancer types have different biologic origins.1 For example, low-grade serous tumors do not arise from STIC but rather progress from serous low malignant potential, or borderline, tumors.
3Clear cell ovarian cancers are biologically, genetically, and prognostically different from serous tumors, with the current belief that most if not all clear cell cancers arise in endometriosis. 4 Clear cell cancers have mutations in ARID1a, a member of the SWI/SNF complex; these mutations also have been identified in the endometriosis precursors. Furthermore, transition zones have been observed between endometriosis and clear cell cancers.5 Germ cell and stromal ovarian tumors do not arise from STICs and are not epithelial cancers. Thus, the updated staging system with the i...