Multimodal analysis unveils tumor microenvironment heterogeneity linked to immune activity and evasion.

The cellular and molecular heterogeneity of tumors is a major obstacle to cancer immunotherapy. Here, we use a systems biology approach to derive a signature of the main sources of heterogeneity in the tumor microenvironment (TME) from lung cancer transcriptomics. We demonstrate that this signature, which we called , is conserved in different cancers and associated with antitumor immunity.

MAST: a hybrid Multi-Agent Spatio-Temporal model of tumor microenvironment informed using a data-driven approach.

Motivation: Recently, several computational modeling approaches, such as agent-based models, have been applied to study the interaction dynamics between immune and tumor cells in human cancer. However, each tumor is characterized by a specific and unique tumor microenvironment, emphasizing the need for specialized and personalized studies of each cancer scenario.

Results: We present MAST, a hybrid Multi-Agent Spatio-Temporal model which can be informed using a data-driven approach to simulate unique tumor subtypes and tumor-immune dynamics starting from high-throughput sequencing data.

Correction to: Molecular and pharmacological modulators of the tumor immune contexture revealed by deconvolution of RNA-seq data.

It was highlighted that the original article [1] contained a typesetting mistake in the name of Noel Filipe da Cunha Carvalho de Miranda. This was incorrectly captured as Noel Filipe da Cunha Carvahlo de Miranda. It was also highlighted that in Fig.

Molecular and pharmacological modulators of the tumor immune contexture revealed by deconvolution of RNA-seq data.

We introduce quanTIseq, a method to quantify the fractions of ten immune cell types from bulk RNA-sequencing data. quanTIseq was extensively validated in blood and tumor samples using simulated, flow cytometry, and immunohistochemistry data.quanTIseq analysis of 8000 tumor samples revealed that cytotoxic T cell infiltration is more strongly associated with the activation of the CXCR3/CXCL9 axis than with mutational load and that deconvolution-based cell scores have prognostic value in several solid cancers.

Revisiting immune escape in colorectal cancer in the era of immunotherapy.

In colorectal cancer (CRC), T-cell checkpoint blockade is only effective in patients diagnosed with mismatch repair-deficient (MMR-d) cancers. However, defects in Human Leukocyte Antigen (HLA) class I expression were reported to occur in most MMR-d CRCs, which would preclude antigen presentation in these tumours, considered essential for the clinical activity of this immunotherapeutic modality. We revisited this paradox by characterising HLA class I expression in two independent cohorts of CRC.