Dataset for "Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade"

Dataset 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. Science, 357(6349), 409-413.

Abstract: 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.

Supplemental Tables included here: Baseline characteristics,
response to treatment, and somatic mutations of subjects enrolled in the
trial. The data cutoff was 19 December 2016.