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Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

4703 - PD-L1 expression is strongly associated with TIGIT, FOXP3 and LAG3 across advanced cancers, but not OX40, TIM3 and IDO

Date

20 Oct 2018

Session

Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

Topics

Translational Research

Tumour Site

Presenters

Sumanta Pal

Citation

Annals of Oncology (2018) 29 (suppl_8): viii400-viii441. 10.1093/annonc/mdy288

Authors

S.K. Pal1, A.M. Vanderwalde2, C. Szeto3, S. Reddy3, O. Hamid4

Author affiliations

  • 1 Medical Oncology And Therapeutics Research, City of Hope, 91010 - Duarte/US
  • 2 Hematology/oncology, University of Tennessee, 38104 - Memphis/US
  • 3 Bioinformatics, NantOmics, Culver City/US
  • 4 Research/immuno-oncology, The Angeles Clinic and Research Institute, Los Angeles/US

Resources

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Abstract 4703

Background

Multiple trials are ongoing to evaluate combinations of immune checkpoint inhibitors (ICIs) across a variety of tumor types. Most of these studies utilize programmed death-1(PD-1) or programmed death-ligand 1 (PD-L1) inhibitors as a backbone. We interrogate the relationship of PD-L1 with other immune checkpoints to inform rational combination strategies.

Methods

We performed whole transcriptomic sequencing (RNA-Seq; ∼200x106 reads/tumor) across 1,467 unselected clinical cases (NantHealth; Culver City, CA). Cases reflected 38 distinct histologies; the most common histologies were breast (17.8%), colon (9.5%) and lung (7.9%). High and low PD-L1 was delineated as the top and bottom 15th percentile of expression values. Co-expression of checkpoint markers (TIGIT, FOXP3, LAG3, OX40, TIM3 and IDO) was analyzed within PD-L1-defined categories, along with putative markers of ICI resistance (e.g, VEGF-A/B/C). Tumor mutational burden (TMB; defined as exonic nonsynonymous mutations) was characterized across checkpoints.

Results

High PD-L1 expression was strongly associated with high expression of TIGIT, FOXP3 and LAG3 (P < 0.001 for each). In contrast, there was no significant difference in expression of OX40, TIM3 and IDO in groups subdivided by high and low PD-L1 expression. High expression of PD-L1 was associated with elevated levels of VEGF-C, but there was no relationship with VEGF-A or VEGF-B expression. Very limited concordance was seen between elevated TMB (> 200 nonsynonymous mutations) and checkpoint expression.

Conclusions

Recent results of combination trials assessing IDO and PD-1 inhibitors may be attributable to a lack of concomitant expression of these markers, thereby limiting synergy. Combinations of PD-1/-L1-directed therapies with TIGIT and LAG3 inhibitors may therefore be of greater interest. Enrichment strategies using TMB for these combinations may be challenging, given the lack of association with checkpoint expression.

Clinical trial identification

Legal entity responsible for the study

Sumanta Pal.

Funding

Has not received any funding.

Editorial Acknowledgement

Disclosure

S.K. Pal: Consultant: Pfizer, Inc., Novartis, Aveo Pharmaceuticals, Inc., Myriad Genetics, Genentech, Inc., Exelixis, Bristol-Myers Squibb Company, Astellas Pharma, Inc.; Research/grant support: Medivation, Inc,; Honorarium: Novartis, Medivation, Inc., and Astellas Pharma, Inc. C. Szeto, S. Reddy: Employee and stockholder: NantOmics LLC. O. Hamid: Consultant: Amgen, Novartis, Roche, BMS, Merck; Speaker: BMS, Genentech, Novartis, Amgen; Contracted research (for institution): AstraZeneca, BMS, Celldex, Genentech, Immunocore, Incyte, Merck, Merck-Serono, MedImmune, Novartis, Pfizer, Rinat, Roche. All other authors have declared no conflicts of interest.

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