Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

ePoster Display

369P - Characterization of the inflammatory tumor microenvironment composition in brain metastases after failure of immune checkpoint inhibitor therapy

Date

16 Sep 2021

Session

ePoster Display

Topics

Tumour Immunology;  Immunotherapy;  Translational Research

Tumour Site

Central Nervous System Malignancies

Presenters

Angelika M. Starzer

Citation

Annals of Oncology (2021) 32 (suppl_5): S516-S529. 10.1016/annonc/annonc674

Authors

A.M. Starzer1, M. Kleinberger1, K. Feldmann1, J. Kreminger2, S. Traint2, A. Steindl1, G. Widhalm3, B. Gatterbauer3, K. Dieckmann4, M. Preusser1, A.S. Berghoff1

Author affiliations

  • 1 Division Of Oncology, Department Of Medicine I, Medical University of Vienna, 1090 - Vienna/AT
  • 2 Division Of Oncology, Department Of Medicine I, Medical University of Vienna, Vienna/AT
  • 3 Department Of Neurosurgery, Medical University of Vienna, 1090 - Vienna/AT
  • 4 Department Of Radiotherapy, Medical University of Vienna, 1090 - Vienna/AT

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 369P

Background

Immunotherapy (IO) is an important pillar in the treatment of various advanced solid cancers, but resistance is frequent. We aimed to characterize the inflammatory tumor microenvironment of patients with brain metastasis (BM) progression after IO to gain insight on potential inflammatory resistance mechanisms.

Methods

Patients with BM resection after failure of IO were identified (IO cohort). Tumor-infiltrating lymphocytes (TILs; CD3, CD8, FOXP3) as well as immune checkpoint molecules (PD-L1) were investigated. A control group of BM patients without prior IO was included for comparison (no immunotherapy cohort, NIO).

Results

Twenty-three IO patients (9/23 (39.1%) females, 14/23 (60.9%) males; 11/23 (47.8%) lung cancer patients; 1/23 (4.3%) breast cancer patient; 5/23 (21.7%) melanoma patients; 6/23 (26.1%) patients with other cancer entities) and 79 NIO patients were included in the analyses. Thirteen/23 (56.5%) IO patients showed tumor PD-L1 expression (TPS range 0-100) in BM. FOXP3+ TIL density was statistically significantly higher in IO compared to NIO patients (Mann-Whitney U test; p=0.001, 83.5 cells/mm2 vs. 28.1 cells/mm2). Median CD8+ TIL density was numerically higher in IO (327.0 cells/mm2) compared to NIO (129.8 cells/mm2, p=0.05) whereas median CD3+ TIL density was lower in IO (226.4 cells/mm2) vs. NIO (459.0 cells/mm2, p=0.08) patients, respectively. There was no correlation of time from last IO application to BM resection with TIL density (Spearman correlation coefficient <±0.3).

Conclusions

Higher infiltration with regulatory immunosuppressive FOXP3+ T cells could be an immunological escape mechanism in BM from solid cancers. New immunological targets are warranted to increase the likelihood of response to IO in BM patients.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Financial support by the Austrian Federal Ministry for Digital and Economic Affairs, the National Foundation for Research, Technology and Development and the Christian Doppler Research Association.

Disclosure

A.M. Starzer: Financial Interests, Personal, Other, Travel support: PharmaMar. M. Preusser: Financial Interests, Personal, Advisory Board: Roche; Financial Interests, Personal, Advisory Board: BMS; Financial Interests, Personal, Advisory Board: Merck Sharp & Dome; Financial Interests, Personal, Advisory Board: Daiichi Sankyo; Financial Interests, Personal, Advisory Board: Bayer; Financial Interests, Personal, Advisory Board: Novartis; Financial Interests, Personal, Advisory Board: Gerson Lehrman Group; Financial Interests, Personal, Advisory Board: CMC Contrast; Financial Interests, Personal, Advisory Board: GlaxoSmithKline; Financial Interests, Personal, Advisory Board: Mundipharma; Financial Interests, Personal, Advisory Board: BMJ Journals; Financial Interests, Personal, Advisory Board: MedMedia; Financial Interests, Personal, Advisory Board: AstraZeneca; Financial Interests, Personal, Advisory Board: AbbVie; Financial Interests, Personal, Advisory Board: Lilly; Financial Interests, Personal, Advisory Board: Medahead; Financial Interests, Personal, Advisory Board: Sanofi; Financial Interests, Personal, Advisory Board: Tocagen; Financial Interests, Institutional, Sponsor/Funding: Boehringer-Ingelheim; Financial Interests, Institutional, Sponsor/Funding: BMS; Financial Interests, Institutional, Sponsor/Funding: Roche; Financial Interests, Institutional, Sponsor/Funding: Daiichi Sankyo; Financial Interests, Institutional, Sponsor/Funding: Merck Sharp & Dome; Financial Interests, Institutional, Sponsor/Funding: Novocure; Financial Interests, Institutional, Sponsor/Funding: GlaxoSmithKline; Financial Interests, Institutional, Sponsor/Funding: AbbVie. A.S. Berghoff: Financial Interests, Institutional, Research Grant: Roche; Financial Interests, Institutional, Sponsor/Funding: Daiichi Sankyo; Financial Interests, Personal, Advisory Board: Roche; Financial Interests, Personal, Advisory Board: BMS; Financial Interests, Personal, Advisory Board: Merck; Financial Interests, Personal, Advisory Board: Daiichi Sankyo; Financial Interests, Personal, Other, Travel support: Roche; Financial Interests, Personal, Other, Travel support: Amgen; Financial Interests, Personal, Other, Travel support: Daiichi Sankyo; Financial Interests, Personal, Other, Travel support: AbbVie. All other authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.