Updates on Biomarker-Directed Therapy for Solid Tumors: Focus on NTRK, RET, and NRG-1 - Episode 14
Experts in oncology discuss future directions in biomarker-driven therapy.
Mark Socinski, MD: This has been fantastic. We are at the end of our time. I want to thank all of you for this rich and informative discussion. Before we go, I would like to conclude and get some final thoughts from each of you. I’ll start with Jonathan and pose the question to the 4 panelists. What do you expect to see in the future in terms of biomarker-based oncology? Is there a biomarker out there that you’ve got your eye on that you think is going to change practice? What are your thoughts about the future, in the form of a closing remark?
Jonathan Trent, MD, PhD: I would like to thank the other panelists; this has been a great session. I’ve learned a great deal, and it has helped me and it’s certainly going to impact the way I look at some of these more rare mutations that you might see in thyroid or lung cancer. I have also been surprised at how many targetable, biomarker-detectable mutations and translocations we’re still finding. We’ve been doing NGS [next-generation sequencing] for some time, and we’re still identifying new targets. Academic institutions and pharmaceutical companies are still developing new therapies for rarer and rarer conditions. We just recently identified a mutation in isocitrate dehydrogenase in chondrosarcoma. Seventy percent of patients with chondrosarcoma have this mutation. We have a new targeted therapy that targets the oncometabolite, and it gives me hope that between the biomarkers and the development, we’re going to continue to impact cancer.
Mark Socinski, MD: Thank you. Lori?
Lori Wirth, MD: Mark, thank you so much for being such a great host. It’s really nice to be on this panel with everyone. And thank you to OncLive® for hosting us. Just to build on Jonathan’s comments and then make 1 very specific comment—biomarker-driven treatment is here to stay, and we’re going to be continuing to evolve our treatment and involve our patients in these therapies. Acquired resistance will emerge on the potent, specific inhibitors, and our next-generation inhibitors are in development already. This story does not have an end. Biomarker-driven therapy is here to stay. For advanced thyroid cancer—whatever histology, whether it is anaplastic, medullary, or a differentiated thyroid cancer—patients with advanced thyroid cancer are poster children for gene-specific therapy. There is a very high hit rate across all the various histologies, and we absolutely should be genotyping all those patients who need systemic therapy.
Mark Socinski, MD: Dr Patel?
Jyoti Patel, MD, FASCO: Thanks so much. What a great group. Certainly, I share all the enthusiasm about how we can really transform our patients’ lives with the right drug at the right time. What will also change, and what I look forward to—aside from more targets and an understanding of resistance—is also how we can better personalize therapy for a patient in terms of escalation or de-escalation. Are there opportunities, when treating an early stage patient, to detect minimal residual disease [MRD], as Jonathan had talked about earlier? Can we treat those patients? Are there ways that we can layer on multiple drugs if we do not have the biochemical response that we would like to see? My sense is that, in the next years, we will incorporate prevention of resistance, and also really tailor therapies to patients over a much longer journey.
Mark Socinski, MD: Last but certainly not least, Dr Levy.
Benjamin Levy, MD: It’s tough to go last because everyone stole my thunder. I just want to piggyback on what Jyoti said, because this is a “Go big or go home” comment. Two years from now, I hope we are assembled here again, talking about all the data to leverage these drugs in the early stage of disease for a cure. We’ve sat here for the past 90 minutes talking about the role of these targeted agents, advanced medullary thyroid cancer, lung cancer, and sarcoma. But for these drugs to be truly transformative, we have to leverage them for cure. We have already seen this with ADORA gene and the EGFR story, and this is a call for initiatives, IITs [investigator-initiated studies], cooperative groups, and industry trials looking at these drugs in the neoadjuvant setting—or in the adjuvant setting for better chance for cure. This highlights the importance of testing, not just for patients with advanced-stage diseases but for patients with early stage disease as well. I look forward to that. Jyoti made some really good comments about utilizing CTDNA [circulating tumor DNA], MRD testing, and other technologies to decide who gets these drugs and who does not. That’s important. When we start to consider cost and toxicity, personalization is not about the genotype. It’s about understanding who really needs the drug in the first place. Those are all great points.
Mark Socinski, MD: As the moderator, this has been a complete pleasure. I want to thank the 4 of you—you made my job easy. It was a great discussion. Thank you all, and thank you to our viewing audience. We hope you found this OncLive® Peer Exchange® to be useful, informative, and helpful in your practice.
TRANSCRIPT EDITED FOR CLARITY