Ovarian cancer – where are we today?

The keynote lecture given by Robert Kurman was one of several highlights of the first joint IAP/ESP Congress in Cologne. With the development of a dualistic model of ovarian cancer a paradigm shift has occurred. What does this mean for the pathologist, the clinician and – most important – the patient?

Paradigm shift in ovarian carcinomas origins research

The keynote lecture given by Robert Kurman was one of several highlights of the first joint IAP/ESP Congress in Cologne. With the development of a dualistic model of ovarian cancer a paradigm shift has occurred. What does this mean for the pathologist, the clinician and – most important – the patient?

Does the vast majority of ovarian carcinomas originate from the ovarian epithelium as understandably has been believed for a long time? No, says Professor Robert Kurman (Johns Hopkins Medicine, USA), one of the world’s leading pathologists. In a very comprehensive and lively presentation he made clear why he thinks the time has come for a true paradigm shift. Recently evidence has amounted suggesting that fallopian tube epithelium – be it benign or malignant – that implants on the ovary acts as the source of low-grade and high-grade serous carcinoma (LGSC and HGSC, respectively).

Also endometrioid and clear cell carcinomas can be regarded as involving the ovary secondarily. It is widely accepted that endometriosis develops from retrograde menstruation and serves as precursor for these malignancies. Maybe even the mucinous and transitional cell (Brenner) tumors might possibly be not derived from the ovary initially, but from transitional epithelial nests located in paraovarian locations at the tubo-peritoneal junction.

Major characteristics of type I and type II tumors

Clinicopathologic and molecular features of type I and type II ovarian carcinomas are:

Type I:

Type II:

"It now appears that type I and type II ovarian tumors develop independently along different molecular pathways and outside the ovary", Kurman stated. In conclusion the only true primary ovarian neoplasms would be gonadal stromal and germ cell tumors similar to testicular tumors. According to Kurman a large number of molecular and histopathologic studies back the adapted dualistic model that initially has been proposed more than a decade ago. Looking at it in more detail it describes entirely different groups of diseases.

What are the clinical implications of the new paradigm?

Shifting the early events of ovarian carcinogenesis to the fallopian tube and endometrium instead of the ovary has important clinical implications. For example, preventive salpingectomy with ovarian conservation may improve patient care by reducing the burden of ovarian cancer while preserving hormonal function and fertility. Kurman presented several further examples, some of which we briefly summarize here:

Robert Kurman ended up his philosophically underlaid presentation with an inspiring picture of the particular value pathology has to contribute to health care: "Pathologists are biology watchers: We are in a unique position to take advantage of the data generated by the most powerful techniques in the laboratory, combine it with our knowledge of clinical behaviour, integrate it with what we see under the microscope and elucidate mechanisms of disease."

Source:
1. Kurman RJ, Shih I-M. The Dualistic Model of Ovarian Carcinogenesis: Revisited, Revised, and Expanded.Am J Pathol. 2016;186(4):733-47.
2. Kurman R. Keynote lecture: The dualistic model of ovarian cancer. Implications for early detection, prevention and treatment (ESP Symeonidis Lecture). IAP/ESP Congress. Cologne, 28 September 2016.