Fig. 5: HLA loss as a mechanism of immune escape.

a, Left, distribution over cells of chromosome arm 6p BAF in scRNA-seq data with ranking by median 6p BAF per cell type. Right, allelic imbalance in 6p BAF across cancer cell clusters. White vertical lines indicate the median. Chr., chromosome. b, Left, percentage of cancer cells with 6p LOH per patient. Right, site- and clone-specific percentage of cancer cells with 6p LOH. Het., heterozygous. c, Percentage of cancer cells with 6p LOH per sample as a function of mutational signature. Pie charts show the fraction of samples with heterozygous, subclonal LOH and clonal LOH 6p status. d, Percentage of patients with LOH of any HLA class I gene in the MSK-IMPACT HGSOC cohort (n = 1,298 patients) for BRCA1-, BRCA2- and CDK12-mutant and CCNE1-amplified tumours, mapping to HRD-Dup, HRD-Del, TD and FBI signatures, respectively. Error bars, 95% binomial confidence intervals. e, Percentage of cancer cells with 6p LOH per sample as a function of anatomical site. Pie charts show the fraction of samples by 6p status. f, UMAP plots of cancer cells from representative HRD-Dup and FBI cases. Density plots show site-specific 6p BAF. g, Fraction of naive and dysfunctional T cells in CD45⁺ samples as a function of the 6p LOH clonality of cancer cells in matched CD45⁻ samples. *P < 0.05; brackets indicate two-sided Wilcoxon pairwise comparisons. In b, c, e and g, 6p LOH status is defined as follows: heterozygous, percentage 6p LOH ≤ 20%; subclonal LOH, 20% < percentage 6p LOH ≤ 80%; clonal LOH, percentage 6p LOH > 80%. In c, e and g, box plots and violin plots show the median, top and bottom quartiles; whiskers correspond to 1.5× IQR. In a–e, only BAF estimates from cells with ≥10 reads aligning to 6p were considered and allelic imbalance states were assigned on the basis of the mean 6p BAF per cell as follows: balanced, BAF ≥ 0.35; imbalanced, 0.15 ≤ BAF < 0.35; LOH, BAF < 0.15 (Methods).