- We can identify patients who will and will not benefit from neoadjuvant chemotherapy (basal versus other)
- We can identify patients who will (GU) or will not (luminal papillary/uroA) benefit from immunotherapy
- We can identify variant histologies (ie. micropapillary, neuroendocrine, etc)
- We can identify high risk pT1 and/or pT2 tumors, specifically with regards to the basal subtype
McConkey makes several important points as to why we need to wait on molecular subtyping before it is ready for ‘prime time’. First, the basal subtype neoadjuvant chemotherapy benefit has not been confirmed in prospective trials. Second, a similar argument can be made for the relationship between molecular subtypes and response to ICB. Finally, we do not know whether molecular subtyping is an ‘intrinsic’ property of a given tumor.
McConkey concluded this rebuttal talk by noting that clinical correlations must be tested prospectively and this is where we are ultimately lacking for molecular subtyping. More work needs to be done to characterize the stability of subtype membership and immunohistochemistry is even further behind in this matter. For now, McConkey states that DNA-based biomarkers, such as DDR mutations and tumor mutational burden, appear to be the most robust entities.
Presented by: David J. McConkey, Johns Hopkins University, Baltimore, MD
Written by: Zachary Klaassen, MD, Urologic Oncology Fellow, University of Toronto, Princess Margaret Cancer Centre at the 2018 AUA Annual Meeting - May 18 - 21, 2018 – San Francisco, CA USA
Read the Opposing Presentation: Molecular Profiling Influences My Treatment Selection