TTN/OBSCN 'Double-Hit' predicts favourable prognosis, 'immune-hot' subtype and potentially better immunotherapeutic efficacy in colorectal cancer

J Cell Mol Med. 2021 Apr;25(7):3239-3251. doi: 10.1111/jcmm.16393. Epub 2021 Feb 23.

Abstract

Colorectal cancer (CRC) remains a leading cause of cancer-related deaths worldwide. Although treatment strategies for solid tumours have been revolutionized by immunotherapy, only a small subset of CRC patients benefit. Using two-independent cohorts, we found the common frequently mutated genes TTN and OBSCN had the significant correlation with higher tumour mutation burden (TMB) and favourable overall survival. TTN and OBSCN also displayed significant commutation phenomenon. Therefore, based on the status of TTN and OBSCN, we stratified patients into 'Double-WT' phenotype, 'Single-Hit' phenotype and 'Double-Hit' phenotype. Importantly, the 'Double-Hit' phenotype had favourable prognosis, low malignant events propensity, and highest TMB, immune cells infiltration abundance, POLE mutation rate, microsatellite instability ratio, as well as immune checkpoints expression compared with the other two phenotypes. These results indicated that the 'Double-Hit' phenotype suggested 'immune-hot' tumours and potentially better immunotherapeutic efficacy. Bioinformatic algorithm assessment of immunotherapy responses also confirmed this conclusion, and the 'Double-Hit' phenotype was found to be a better predictor of immunotherapy than PD-L1, PD-1, CTLA-4, TMB and microsatellite status. This study revealed CRC patients with TTN/OBSCN 'Double-Hit' was significantly associated favourable prognosis, 'immune-hot' subtype and potentially better immunotherapeutic efficacy.

Keywords: OBSCN; TTN; colorectal cancer; immunotherapy; mutation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / genetics
  • Colorectal Neoplasms / drug therapy
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / immunology
  • Colorectal Neoplasms / pathology
  • Computational Biology
  • Connectin / genetics*
  • DNA Polymerase II / genetics
  • Humans
  • Immune Checkpoint Inhibitors / therapeutic use
  • Mutation
  • Poly-ADP-Ribose Binding Proteins / genetics
  • Protein Serine-Threonine Kinases / genetics*
  • Rho Guanine Nucleotide Exchange Factors / genetics*

Substances

  • Biomarkers, Tumor
  • Connectin
  • Immune Checkpoint Inhibitors
  • Poly-ADP-Ribose Binding Proteins
  • Rho Guanine Nucleotide Exchange Factors
  • TTN protein, human
  • OBSCN protein, human
  • Protein Serine-Threonine Kinases
  • DNA Polymerase II
  • POLE protein, human