Back

CITEseq analysis of non-small-cell lung cancer lesions reveals an axis of immune cell activation associated with tumor antigen load and TP53 mutations

Leader, A. M.; Grout, J. A.; Chang, C.; Maier, B.; Tabachnikova, A.; Walker, L.; Lansky, A.; LeBerichel, J.; Malissen, N.; Davila, M.; Martin, J.; Magri, G.; Tuballes, K.; Zhoa, Z.; Petralia, F.; Samstein, R.; D'Amore, N. R.; Thurston, G.; Kamphorst, A.; Wolf, A.; Flores, R.; Wang, P.; Beasley, M. B.; Salmon, H.; Rahman, A. H.; Marron, T. U.; Kenigsberg, E.; Merad, M.

2020-07-17 immunology
10.1101/2020.07.16.207605 bioRxiv
Show abstract

Immunotherapy is becoming a mainstay in the treatment of NSCLC. While tumor mutational burden (TMB) has been shown to correlate with response to immunotherapy, little is known about the relation of the baseline immune response with the tumor genotype. Here, we profiled 35 early stage NSCLC lesions using multiscale single cell sequencing. Unsupervised clustering identified in a subset of patients a key cellular module consisting of PDCD1+ CXCL13+ activated T cells, IgG+ plasma cells, and SPP1+ macrophages, referred to as the lung cancer activation module (LCAMhi). Transcriptional data from two NSCLC cohorts confirmed a subset of patients with LCAMhi enrichment, which was independent of overall immune cell content. The LCAMhi module strongly correlated with TMB, expression of cancer testis antigens, and with TP53 mutations in smokers and non-smokers. These data establish LCAM as a key mode of immune cell activation associated with high tumor antigen load and driver mutations.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.