Closing out their program on HR+/HER2- metastatic breast cancer, panelists look toward future evolutions in the treatment landscape.
Transcript:
Joyce A. O’Shaughnessy, MD: I’d like to thank you for being here today.… And I think…we want to front-load our endocrine therapy as much as we possibly can. We are going to get more and more tools to both understand mechanisms of resistance that are coming both at the tissue level and in the blood ctDNA [circulating tumor DNA] level and understand, I hope, with the help of you all there at Memorial [Sloan Kettering] and your tumor board, to understand the role of co-mutations and serial evolution of different clones coming up. And it’s going to be a lot of very important work over a lot of years to understand how to best help patients get the most durable benefit in endocrine therapy. Right now, we’re fortunate to be able to find PIK3CA mutations. Hopefully, soon, AKT mutations, PTEN loss. Or maybe we won’t even have to find those. We’ll be able to give capivasertib to everybody who’s progressing on CDK [inhibitors].… And then ESR1 mutations. It’s both good news but frustrating. Good news is it’s still an ER [estrogen receptor]-dependent breast cancer. Bad news is our traditional agents really don’t work well. But thankfully, we have a new agent that really can give the patient the opportunity to get a very durable response. About 25% of the patients going out about a year, 23%, I think, to be exact.… So we’ve got to find those ESR1 mutations. So thank you so much for your really thoughtful, comprehensive discussions and analysis. And I really want to thank our viewing audience as well and thank Targeted Oncology™ for putting together this tumor board so we can get together. I hope this is a valuable use of your time and, most importantly, that this will [provide] some practical application to your practice. Thank you all very much.
Transcript is AI-generated and edited for clarity and readability.
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