E2F1-induced autocrine IL-6 inflammatory loop mediates cancer-immune crosstalk that predicts T cell phenotype switching and therapeutic responsiveness.

Melanoma is a metastatic, drug-refractory cancer with the ability to evade immunosurveillance. Cancer immune evasion involves interaction between tumor intrinsic properties and the microenvironment. The transcription factor E2F1 is a key driver of tumor evolution and metastasis.

A Systems-Based Key Innovation-Driven Approach Infers Co-option of Jaw Developmental Programs During Cancer Progression.

Cancer acquires metastatic potential and evolves via co-opting gene regulatory networks (GRN) of embryonic development and tissue homeostasis. Such GRNs are encoded in the genome and frequently conserved among species. Considering that all metazoa have evolved from a common ancestor via major macroevolutionary events which shaped those GRNs and increased morphogenetic complexity, we sought to examine whether there are any key innovations that may be consistently and deterministically linked with metastatic potential across the metazoa clades.