Dissecting structural, cellular and molecular differences between transplanted and spontaneous mouse tumor models, highlighting their relevance for predicting the efficacy of anti-cancer treatments in patients.
ST recruitment of STRIPAK facilitates PP2A-mediated dephosphorylation of MAP4K4 and induces cell transformation highlighting that STRIPAK complex plays a key role in defining PP2A specificity and activity.
The gluconeogenic enzyme PCK1 and pyrimidine nucleotide biosynthetic enzyme DHODH drive hypoxic pyrimidine nucleotide biosynthesis and liver metastatic colonization in colorectal cancer, which is therapeutically exploitable by DHODH pharmacologic inhibition.
Cancer cell expression of the T-cell co-stimulatory molecule CD80, or treatment with agonistic antibodies targeting the T-cell co-stimulatory receptors OX-40 or 4-1BB, enhances the anti-tumor activity of FAK inhibition.
A mechanistic link between TLE3 loss and glucocorticoid receptor-mediated androgen receptor inhibitor resistance supports the rationale to target GR during anti-hormonal treatment in castrate-resistant prostate cancer.
The oncogenic role ligand-dependent BMP signaling plays in suppressing differentiation in melanoma is a reiteration of its physiological roles during melanocyte development.
MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.
In small cell lung cancer, the transition from a neuroendocrine state to a more neuronal state endows these cancer cells with increased migration and metastatic potential.
When pioneer metastatic cells enter a sentinel lymph node through afferent lymphatics subcapsular sinus, macrophages provide them soil to proliferate and colonize lymph node.
