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.

Next-generation deconvolution of transcriptomic data to investigate the tumor microenvironment.

Methods for in silico deconvolution of bulk transcriptomics can characterize the cellular composition of the tumor microenvironment, quantifying the abundance of cell types associated with patients' prognosis and response to therapy. While first-generation deconvolution methods rely on precomputed, transcriptional signatures of a handful of cell types, second-generation methods can be trained with single-cell data to disentangle more fine-grained cell phenotypes and states. These novel approaches can also be applied to spatial transcriptomic data to reveal the spatial organization of tumors.

The circadian transcription factor ARNTL2 is regulated by weight-loss interventions in human white adipose tissue and inhibits adipogenesis.

Misalignment of physiological circadian rhythms promotes obesity which is characterized by white adipose tissue (WAT) expansion. Differentiation of Adipose stem/progenitor cells (ASCs) contributes to WAT increase but the importance of the cellular clock in this process is incompletely understood. In the present study, we reveal the role of the circadian transcription factor Aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) in human ASCs, isolated from subcutaneous (s)WAT samples of patients undergoing routine elective plastic abdominal surgery.