Every year, 40,000 oncology professionals gather in Chicago for ASCO (American Society of Clinical Oncology), the largest cancer conference in the world. Presenters at this meeting reveal new findings on promising therapies, introduce intriguing theories on anything from cancer biology to clinical practice, and inevitably spark controversial discussions from around the field of oncology research.
Some exciting research showcased at ASCO 2017:
- A drug known as larotrectinib was demonstrated to be markedly effective in its treatment of patients with an NTRK (Neurotrophic Tyrosine Kinase) gene mutation.1 The results of a study presented at ASCO indicated that response to larotrectinib was observed regardless of tumor type or patient age, which may further support a new “pan-cancer” paradigm for modern therapies.
- CAR T cell engineering, the process of genetically modifying T cells to arm them with a chimeric T cell receptor that recognizes a specific neoantigen, demonstrated effectiveness in patients with liquid tumors, and in the near future will be tested in patients whose solid tumors have low TMB (Tumor Mutational Burden). 2,3
- A study indicated that responders and nonresponders to anti-PD-1 therapy have distinct microbiota.4 The results provide additional evidence supporting a growing frontier of immunooncology research, and may lead to patient selection based on their unique makeup of internal microorganisms.
- The results from a study on the clinical utility of a digital symptom monitoring system were presented.5 Compared to patients who did not use the monitoring system, patients who did had a much lower number of emergency room visits and lived an average of five months longer, a difference in overall survival that is greater than that of all but one FDA-approved targeted therapy.
Notably, this year’s conference was prefaced by the FDA approval of Merck’s Keytruda, the first therapy in history approved for a specific genetic feature – the pan-cancer biomarker microsatellite instability (MSI). As such, most of the buzz at ASCO was centered on MSI and tumor mutational burden (TMB), two genomic biomarkers that predict response to checkpoint blockade inhibitors. PGDx currently offers MSI detection in plasma, and is in the validation stage of a TMB assay.
Dr. Luis Diaz, Co-Founder of PGDx, pictured presenting a poster on Pembrolizumab Therapy for Microsatellite Instability High (MSI-H) Colorectal Cancer (CRC) and Non-CRC
As a result of a 2015 study published by PGDx co-founder Dr. Luis Diaz in The New England Journal of Medicine on MSI status and response to checkpoint blockade inhibitors, Dr. Diaz has recently received significant recognition from around the field.6 It’s likely that the results of his study provided much of the core scientific background that propelled Keytruda through the FDA approval process. The two posters he presented at ASCO were both highly anticipated follow-up studies to his 2015 MSI study, and for obvious reasons were visited by crowds of oncologists.7,8 Dr. Diaz was also invited to be the keynote speaker at a special evening event celebrating the partnership between IBM Watson Health and Illumina. It was here that he spoke for nearly an hour about the importance of the recent therapeutic developments and the potential for cancer immunotherapy in the future.
With the approval of Keytruda, and because PGDx is currently the only diagnostics company that offers a plasma assay that detects MSI, we’ve seen an increase in inquiries into our MSI capabilities. This was especially evident at ASCO, which was jam-packed with productive meetings for our Translational Science, Pharma Partnering, Molecular Labs and Clinical teams. Thought-provoking science, uplifting clinical results, and insightful commercial discussions made ASCO 2017 a big success.
1. J Clin Oncol 35, 2017 (suppl; abstr LBA2501)
2. J Clin Oncol 35, 2017 (suppl; abstr TPS7568)
3. J Clin Oncol 35, 2017 (suppl; abstr 7008)
4. J Clin Oncol 35, 2017 (suppl; abstr 3015)
5. J Clin Oncol 35, 2017 (suppl; abstr LBA2)
6. Le et al. NEJM 2015 372:2509-2520
7. J Clin Oncol 35, 2017 (suppl; abstr 3071)
8. J Clin Oncol 35, 2017 (suppl; abstr TPS3618)