Le, Dung Dataset for "Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade" Dataset<b> </b>supporting publication: Le, D. T., Durham, J. N., Smith, K. N., Wang, H., Bartlett, B. R., Aulakh, L. K., ... & Wong, F. (2017). Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade. <i>Science</i>, 357(6349), 409-413.<br><br><b>Abstract: </b>The genomes of cancers deficient in mismatch repair contain exceptionally high numbers of somatic mutations. In a proof-of-concept study, we previously showed that colorectal cancers with mismatch repair deficiency were sensitive to immune checkpoint blockade with antibodies to programmed death receptor-1 (PD-1). We have now expanded this study to evaluate the efficacy of PD-1 blockade in patients with advanced mismatch repair-deficient cancers across 12 different tumor types. Objective radiographic responses were observed in 53% of patients, and complete responses were achieved in 21% of patients. Responses were durable, with median progression-free survival and overall survival still not reached. Functional analysis in a responding patient demonstrated rapid in vivo expansion of neoantigen-specific T cell clones that were reactive to mutant neopeptides found in the tumor. These data support the hypothesis that the large proportion of mutant neoantigens in mismatch repair-deficient cancers make them sensitive to immune checkpoint blockade, regardless of the cancers' tissue of origin.<br><br><b>Supplemental Tables included here</b>: Baseline characteristics, response to treatment, and somatic mutations of subjects enrolled in the trial. The data cutoff was 19 December 2016. Mismatch repair deficiency (MMR);microsatellite instability;Anti-programmed cell death-1;Programmed cell death 1;Pembrolizumab monotherapy;immunotherapy;Neoplasms;Colorectal Cancer 2020-05-01
    https://nih.figshare.com/articles/dataset/Dataset_for_Mismatch_repair_deficiency_predicts_response_of_solid_tumors_to_PD-1_blockade_/11991336
10.35092/yhjc.11991336.v1