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. 2019 Mar 4;3:PO.18.00321. doi: 10.1200/PO.18.00321

FIG 1.

FIG 1.

Spectrum of B2M mutations and expression. (A) Fifty-nine patients with colorectal cancer (CRC) harbored B2M mutations. Although several scattered missense (green) mutations were seen, truncating (gray) mutations were more frequent at several hotspots. These included microsatellite loci: 21 mutations at p. L15Ffs*41, 16 at p. V69Wfs*34, 11 at p.T93Hfs*2/Lfs*10, and 10 at the splice site p.X23. (B) Oncoprint summarizing the immunopathologic data with genomic information. Each dot above the sample indicates the patient was treated with a checkpoint inhibitor. (C) Loss of B2M expression and retained major histocompatibility complex (MHC) class I expression in a microsatellite instability-high B2M double-mutant (p. V69Wfs*34, p. S16Afs*27) CRC with high tumor-infiltrating lymphocyte level. A medullary carcinoma of the colon shows immune-cell expression of programmed death-1 ligand at the tumor-stroma interface, loss of B2M expression in tumor cells, retention of strong diffuse MHC class I expression in tumor cells, > 150 CD3+ lymphocytes per high-powered field (HPF), and average of 69 CD8+ cells per HPF.