| Literature DB >> 24891321 |
Mohini Rajasagi1, Sachet A Shukla2, Edward F Fritsch2, Derin B Keskin1, David DeLuca2, Ellese Carmona3, Wandi Zhang1, Carrie Sougnez4, Kristian Cibulskis4, John Sidney5, Kristen Stevenson6, Jerome Ritz7, Donna Neuberg6, Vladimir Brusic8, Stacey Gabriel4, Eric S Lander4, Gad Getz9, Nir Hacohen10, Catherine J Wu7.
Abstract
Genome sequencing has revealed a large number of shared and personal somatic mutations across human cancers. In principle, any genetic alteration affecting a protein-coding region has the potential to generate mutated peptides that are presented by surface HLA class I proteins that might be recognized by cytotoxic T cells. To test this possibility, we implemented a streamlined approach for the prediction and validation of such neoantigens derived from individual tumors and presented by patient-specific HLA alleles. We applied our computational pipeline to 91 chronic lymphocytic leukemias (CLLs) that underwent whole-exome sequencing (WES). We predicted ∼22 mutated HLA-binding peptides per leukemia (derived from ∼16 missense mutations) and experimentally confirmed HLA binding for ∼55% of such peptides. Two CLL patients that achieved long-term remission following allogeneic hematopoietic stem cell transplantation were monitored for CD8(+) T-cell responses against predicted or confirmed HLA-binding peptides. Long-lived cytotoxic T-cell responses were detected against peptides generated from personal tumor mutations in ALMS1, C6ORF89, and FNDC3B presented on tumor cells. Finally, we applied our computational pipeline to WES data (N = 2488 samples) across 13 different cancer types and estimated dozens to thousands of predicted neoantigens per individual tumor, suggesting that neoantigens are frequent in most tumors.Entities:
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Year: 2014 PMID: 24891321 PMCID: PMC4102716 DOI: 10.1182/blood-2014-04-567933
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113