50P - Distinct immune microenvironments stratify triple-negative breast cancer and predict outcome

Date 04 May 2017
Event IMPAKT 2017
Session Welcome reception and Poster Walk
Topics Breast Cancer
Pathology/Molecular Biology
Basic Scientific Principles
Presenter Tina Gruosso
Authors T. Gruosso1, M. Gigoux1, N. Bertos1, V.S.K. Manem2, M. Guiot3, L. Buisseret4, R. Salgado5, G. Van den Eyden5, B. Haibe-Kains2, M. Park1
  • 1Goodman Cancer Research Center, McGill University, H3A 1A3 - Montreal/CA
  • 2Princess Margaret Bioinformatics And Computational Genomics Laboratory, University of Toronto, M5G 2M9 - Toronto/CA
  • 3Pathology, McGill University Health Centre, H4A 3J1 - Montreal/CA
  • 4Breast Cancer Translational Research Laboratory, Institut Jules Bordet, Université Libre de Bruxelles, 1000 - Bruxelles/BE
  • 5Oncology, Jules Bordet Institute, B-1000 - Brussels/BE



Triple negative breast cancer (TNBC) are especially difficult to treat effectively. While only 20-30% of TNBC patients respond to chemotherapy in the neoadjuvant setting, overall outcome remains poor for non-responding patients. Engaging the immune system promises optimal personalized cancer therapy as mounting evidence suggests that immune-checkpoint inhibitor immunotherapies may become a therapeutic option for TNBC patients. The presence of CD8+ T cells, a crucial component of the cytotoxic arm of the adaptive immune response, is associated with good clinical outcome in TNBC patients. Specifically, it is the efficient CD8+ T cell invasion and infiltration in the tumor that is associated with good outcome. On the other hand, some tumors accumulate CD8+ T cells in the tumor-associated stroma with poor infiltration in the tumor epithelium. These patients show poor outcome.

As CD8+ T cell infiltration in the tumor is a crucial step to mount an efficient anti-tumor response, we thus wondered how the tumor microenvironment affects CD8+ T cell invasion into the tumor epithelial compartment of the TNBC tumors.

To identify potential stroma-dependent mechanisms that potentiate or inhibit CD8+ T cells invasion into the tumor epithelium, we performed gene expression profiling of laser-capture microdissected tumor-associated stroma (as well as matched epithelium and bulk tumor) from 38 TNBC chemotherapy-naive primary cases. Here we identify several pathways and phenotypes that may explain heterogeneity of the CD8+ T cell distribution.

These newly identified distinct immune microenvironments of TNBC have implications for patient stratification for immunotherapies.

Clinical trial identification