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Critical questions for this Forum

  1. The biology and anatomy of HGSC work against early detection and the best efforts have failed to date. Therefore...
  2. Management of genetic risk associated with HGSC has saved countless lives and to further progress disease prevention we should…
  3. We don’t know why BRCA mutations manifest in a subset of cells/tissues, particularly considering their function should plausibly be widespread. Understanding the tropism of BRCA mutations to fallopian tube secretory cells may provide new clues to prevention.
  4. To find another PARPi/synthetic lethal for HGSC we’d have to…
  5. In most cancer types small molecule monotherapy almost always results in resistance in weeks to months in most patients, and therefore…
  6. There are still no biomarkers of likely response to bevacizumab or systematic analysis of resistance.
  7. The benefit of HIPEC is unresolved and there is global variation in PDS versus NACT.
  8. Umbrella and platform trials would allow a more efficient and patient friendly approach to molecular stratification and testing of new agents, but such studies are rare in HGSC.
  9. HGSC has a moderate mutation burden, but immune control appears to be present in some patients. To move beyond checkpoint inhibitors, we need to…..
  10. The TME may both contain the disease as well as support tumor growth, hinder immune control or therapy and therefore…
  11. There are a lot of non-productive cell cell interactions in the TME and to understand any logic we’d need to…
  12. The complex multi-omic and spatial studies have not yet led to new therapeutic approaches – will 3D approaches be more useful?
  13. The T cell response to HGSC is somewhat of a red herring. Other immune cell types are essential for tumour control – we need to figure out how they work, and how to activate them via immunotherapy.
  14. A tumour’s first exposure to chemotherapy is like a “big bang” event in its evolution. Everything changes virtually overnight: cell composition, architecture, genome, epigenome, immune response, stroma, vasculature. “One and done” patients are cured during this process. Which changes are critical for complete, durable regression, and how do we promote them?