Multiplex imaging analysis of matched primary and metastatic breast tumors provides a phenotypic and spatial map of tumor microenvironments, revealing similar compositions of cancer cells and divergent immunologic features between matched samples.

Cell persistence and senescence are distinct states of proliferative arrest induced by cancer therapy, with persister cells being characterized by the silencing of inflammatory genes through the heterochromatic mark H4K20me3.

STAT3 activity mediated by LSD1 and CoREST2 induces enteroendocrine cell specification in mucinous colorectal cancer, suggesting disrupting interaction among LSD1, CoREST2, and STAT3 as a therapeutic strategy to target neuroendocrine differentiation.

Suppression of angiogenesis by TGFβ1 is mediated by TSP1 upregulation in endothelial cells and abrogated by HIF1α–miR145 activity in the hypoxic tumor microenvironment, providing potential targets to remodel the tumor vasculature.

TCTN1 activates fatty acid oxidation to induce melanoma mesenchymal phenotype switching and invasion by promoting the binding of the subunits of MTP, which can be targeted with fluprostenol to inhibit melanoma metastasis.

The PROTAC SIAIS562055 sustainably degrades SOS1 and inhibits downstream ERK signaling, showing strong antiproliferative activity and synergistic effects with KRAS inhibitors in KRAS-mutant cancers and BCR–ABL inhibitors in chronic myeloid leukemia.

The SOS1 inhibitor BI-3406 both inhibits intrinsic/adaptive resistance and targets drug tolerant persister cells to limit the development of acquired resistance to clinical KRAS^G12C inhibitors in lung adenocarcinoma cells.

Soluble guanylyl cyclase signaling inhibits castration-resistant prostate cancer emergence and can be stimulated with FDA-approved riociguat to resensitize resistant tumors to androgen deprivation, providing a strategy to prevent and treat castration resistance.

EWS–WT1, the unique oncogenic driver of desmoplastic small round cell tumors, confers sensitivity to PARP and ATR inhibitors, supporting the potential of these drugs in treating patients with this aggressive sarcoma subtype.

The development of a reference-free method for deconvolving the identity of cells in spatial transcriptomics datasets enables exploration of tumor architecture to gain deeper insights into the dynamics of the tumor microenvironment.