Tumor immune microenvironment of self-identified African American and non-African American triple negative breast cancer

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作者
Michal Marczyk
Tao Qing
Tess O’Meara
Vesal Yagahoobi
Vasiliki Pelekanou
Yalai Bai
Emily Reisenbichler
Kimberly S. Cole
Xiaotong Li
Vignesh Gunasekharan
Eiman Ibrahim
Kristina Fanucci
Wei Wei
David L. Rimm
Lajos Pusztai
Kim R. M. Blenman
机构
[1] Silesian University of Technology,Department of Data Science and Engineering
[2] Yale University,Yale Cancer Center
[3] Yale University,Department of Internal Medicine, Section of Medical Oncology
[4] Yale University,Department of Pathology
[5] Yale University,Department of Computational Biology & Bioinformatics, Biological & Biomedical Sciences
[6] Yale University,Department of Pharmacology
[7] Yale University,Department of Biostatistics
[8] Yale University,Department of Computer Science
[9] Brigham and Women’s Hospital,Department of Internal Medicine
[10] Translational Medicine Early Development,Precision Medicine – Oncology, Translational Medical Oncology
[11] Sanofi,undefined
[12] Sema4 Genomics,undefined
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摘要
Differences in the tumor immune microenvironment may result in differences in prognosis and response to treatment in cancer patients. We hypothesized that differences in the tumor immune microenvironment may exist between African American (AA) and NonAA patients, due to ancestry-related or socioeconomic factors, that may partially explain differences in clinical outcomes. We analyzed clinically matched triple-negative breast cancer (TNBC) tissues from self-identified AA and NonAA patients and found that stromal TILs, PD-L1 IHC-positivity, mRNA expression of immune-related pathways, and immunotherapy response predictive signatures were significantly higher in AA samples (p < 0.05; Fisher’s Exact Test, Mann–Whitney Test, Permutation Test). Cancer biology and metabolism pathways, TAM-M2, and Immune Exclusion were significantly higher in NonAA samples (p < 0.05; Permutation Test, Mann–Whitney Test). There were no differences in somatic tumor mutation burden. Overall, there is greater immune infiltration and inflammation in AA TNBC and these differences may impact response to immune checkpoint inhibitors and other therapeutic agents that modulate the immune microenvironment.
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