Bradley Monk, MD, FACOG, FACS: This has been extremely informative. Before we end this discussion, I’d like final thoughts from each of our panelists. Dr Birrer, can you summarize our discussion here talking across multiple gynecologic cancers: ovarian, cervix, and endometrial cancer? What’s the unifying theme?

Michael J. Birrer, MD, PhD: Tom doesn’t know what TWiST is.

Thomas Herzog, MD: Maybe you can explain it.

Michael J. Birrer, MD, PhD: I’m the oldest person here, so I may have a slightly different perspective. But 15 years ago we were arguing about IP [intraperitoneal] versus IV [intravenous], or Taxol versus Taxotere. We’ve seen a revolution here, and now it’s in all 3 tumors. It’s been in the ovaries a little bit over the last 5 to 10 years, but now it’s in the endometrium and it’s in the cervix. It involves accurate stratification of patients, active drugs that we didn’t have. And potentially, we’re beginning to see some payoff and cures.

Bradley Monk, MD, FACOG, FACS: Krish, give me your summary.

Krishnansu S. Tewari, MD: Yeah, I think the bottom line is we’re finally catching up with where we need to be and we’re sequencing our tumors.

Bradley Monk, MD, FACOG, FACS: So biomarkers.

Krishnansu S. Tewari, MD: Yes, biomarkers. We’re not sitting there thinking: “Should we keep the chemotherapy up? Should we pour it in the belly? Should we use an analog? Should we change the dose?” You know we’re moving forward, finally.

Bradley Monk, MD, FACOG, FACS: So BRCA HRD [homologous recombination deficiency] in ovary.

Krishnansu S. Tewari, MD: Yup.

Bradley Monk, MD, FACOG, FACS: PD-L1 [programmed death-ligand 1] and HER2.

Krishnansu S. Tewari, MD: To a lesser extent.

Bradley Monk, MD, FACOG, FACS: In cervical cancer.

Krishnansu S. Tewari, MD: Yeah.

Bradley Monk, MD, FACOG, FACS: And MSI [microsatellite instability] and HER2 in endometrial.

Krishnansu S. Tewari, MD: Yeah.

Jubilee Brown, MD: Great. This is a time of incredible progress, and I think that’s the word that is underlined in all these discussions. You know we have incredible technology and a lot of different compounds, and now I think over the next few years we’re going to see how we need to tweak it. How we should use these compounds to best benefit our patients.

Bradley Monk, MD, FACOG, FACS: Sequencing, right?

Jubilee Brown, MD: Absolutely, that’s part of it.

Bradley Monk, MD, FACOG, FACS: Tom?

Thomas Herzog, MD: I think the themes that emerge from looking at where we are today and where we’re heading in the immediate future are really combinations. It’s about the science, and it remains about clinical trials, and that’s really been the driver for all the content that we’ve been able to hopefully convey today that has changed practice for our patients. And I think we need to continue to do that. And the other note I would say is that I think it’s increasingly harder to keep up because of all these complex studies and these combinations and so forth. So if you’re going to treat ovarian cancer, if you’re going to treat cervical cancer, if you’re going to treat endometrial cancer, it’s changed. And it’s going to be a challenge for physicians and providers to keep up with.

Bradley Monk, MD, FACOG, FACS: If I was to choose 1 unifying theme, it would be antiangiogenesis. Krish, with your passion, you got bevacizumab FDA approved in cervical cancer. We have 3 approvals in ovarian cancer. And now, Michael, you told me that lenvatinib may improve the efficacy of pembrolizumab in mismatch repair proficient tumors. That is a unifying theme across all 3 tumor types. But each of your points, whether they’re clinical trials or following the science, I really appreciate them.

On behalf of our panelists, I’d like to thank you so much for being with us. I hope you’ve enjoyed this OncLive® Peer Exchange® discussion and found it to be useful and informative. Thank you, and so long for now.

Transcript Edited for Clarity