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ePoster Display

709P - Serial circulating tumor (ct)-DNA alterations using amplicon-based next-generation sequencing (NGS) to identify resistance mechanisms to immune checkpoint inhibitors (ICIs) for metastatic urothelial carcinoma (mUC)

Date

16 Sep 2021

Session

ePoster Display

Topics

Targeted Therapy;  Immunotherapy;  Translational Research

Tumour Site

Urothelial Cancer

Presenters

Praful Ravi

Citation

Annals of Oncology (2021) 32 (suppl_5): S678-S724. 10.1016/annonc/annonc675

Authors

P. Ravi1, A. Ravi1, I. Bin Riaz1, D. Freeman1, C. Curran1, C. Mantia1, B.A. McGregor1, K. Kilbridge1, C. Pan1, M. Pek2, Y. Choudhury2, N. Corsaro1, M. Tan2, G.P. Sonpavde1

Author affiliations

  • 1 Department Of Medical Oncology, Dana Farber Cancer Institute, 02215 - Boston/US
  • 2 Research, Lucence Diagnostics, 94303 - Palo Alto/US

Resources

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Abstract 709P

Background

Most mUC patients (pts) develop resistance to ICI therapy. Study of serial ctDNA alterations during therapy may provide a non-invasive method of exploring mechanisms of resistance to ICI.

Methods

Pts with mUC at DFCI who had ≥2 ml plasma available pre- and post-ICI or cisplatin-based chemotherapy (chemo) were eligible. Paired pre and post samples underwent ctDNA evaluation with 7 to 30 ng of DNA using an 80-gene panel which employs an amplicon-based NGS assay, including fusions (Lucence LiquidHallmark). The primary objective was to evaluate ctDNA alterations pre- and post-ICI, and to correlate with objective response.

Results

39 pts with pre and post-ICI and 6 with pre and post-chemo samples were included. Median age was 68 years, 79% of pts were male, and 97% had urothelial histology. The majority (82%) received single-agent ICI (PD1/L1 inhibitor). Median duration between pre and post samples was 6.2 months. The most common variants pre- and post-ICI were in TP53 (54% and 49%), TERT (49% and 49%) and BRCA1/2 (36% and 33%). 9 pts were responding to ICI at time of post-ICI blood collection, with 7 (78%) showing clearance of ≥1 ctDNA variants, most commonly in TP53 (n=4), PI3KCA (n=2) and BRCA1/2 (n=2). 18 of 20 pts (90%) who were progressing at time of post-ICI collection had emergence of a new alteration, most commonly in BRCA1/2 (n=6), PI3KCA (n=4), CCND2/RB (n=4) and TP53 (n=3). BRCA1 and PIK3CA mutations emerged in only 1 and 0 chemo pts. Pts who cleared TP53 alterations during ICI had a higher likelihood of response compared to those who did not (50% vs. 17%, p=0.04). No responses were seen in pts who had emergence of a BRCA1/2 (n=9) or PIK3CA variants (n=4) on therapy, while none of 3 patients with a driver FGFR2/3 alteration responded to ICI.

Conclusions

ctDNA alterations were detected in 96% of pre/post-ICI samples overall. Clearance of TP53 alterations during ICI therapy was associated with response, while emergence of BRCA1/2 or PI3KCA variants appeared to be associated with resistance. Exploration of therapeutic combinations of ICI with PARP and PI3K/Akt inhibition in mUC may be warranted.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Lucence.

Disclosure

B.A. McGregor: Financial Interests, Personal, Advisory Board: Bayer; Financial Interests, Personal, Advisory Board: Astellas; Financial Interests, Personal, Advisory Board: AstraZeneca; Financial Interests, Personal, Advisory Board: Seattle Genetics; Financial Interests, Personal, Advisory Board: Exelixis; Financial Interests, Personal, Advisory Board: Nektar; Financial Interests, Personal, Advisory Board: Pfizer; Financial Interests, Personal, Advisory Board: Janssen; Financial Interests, Personal, Advisory Board: Genentech; Financial Interests, Personal, Advisory Board: Eisai; Financial Interests, Personal, Advisory Board: EMD Serono; Financial Interests, Institutional, Research Grant: BMS; Financial Interests, Institutional, Research Grant: Calithera; Financial Interests, Institutional, Research Grant: Exelixis; Financial Interests, Institutional, Research Grant: Seattle Genetics. M. Pek: Financial Interests, Personal, Other, Employee: Lucence. Y. Choudhury: Financial Interests, Personal, Other, Employee: Lucence. M. Tan: Financial Interests, Personal, Other, Employee: Lucence. G.P. Sonpavde: Financial Interests, Personal, Advisory Board: Pfizer; Financial Interests, Personal, Advisory Board: BMS; Financial Interests, Personal, Advisory Board: Genentech; Financial Interests, Personal, Advisory Board: EMD Serono; Financial Interests, Personal, Advisory Board: Novartis; Financial Interests, Personal, Advisory Board: Merck; Financial Interests, Personal, Advisory Board: Sanofi; Financial Interests, Personal, Advisory Board: Seattle Genetics; Financial Interests, Personal, Advisory Board: Astellas; Financial Interests, Personal, Advisory Board: AstraZeneca; Financial Interests, Personal, Advisory Board: Exelixis; Financial Interests, Personal, Advisory Board: Janssen; Financial Interests, Personal, Advisory Board: Amgen; Financial Interests, Personal, Advisory Board: Eisai; Financial Interests, Personal, Advisory Board: Bicycle Therapeutics; Financial Interests, Institutional, Research Grant: Boehringer Ingelheim; Financial Interests, Institutional, Research Grant: Bayer; Financial Interests, Institutional, Research Grant: Pfizer; Financial Interests, Institutional, Research Grant: Merck; Financial Interests, Institutional, Research Grant: Sanofi; Financial Interests, Institutional, Research Grant: AstraZeneca. All other authors have declared no conflicts of interest.

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