Tumors escape killing by the immune system through generating transient spatial cell-in-cell structures that are impenetrable to cytotoxic compounds including lytic granules and chemotherapy.

Prostate cancer resistance to androgen receptor antagonist therapy occurs by way of tumors impeding local glucocorticoid metabolism and inactivation and thereby permitting sustained glucocorticoids to stimulate up-regulated glucocorticoid receptor.

Analyses of genetically engineered mouse models reveal the androgen receptor-independent properties of a luminal stem/progenitor cell in the prostate epithelium, and its ability to serve as a cell of origin for castration-resistant prostate cancer.

Pre-clinical and patient data show that inhibition of autophagy with an approved, inexpensive, well-tolerated drug can overcome resistance to BRAF^V600E inhibition in multiple brain tumor subtypes with different resistance mechanisms.

Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.

SOX2 causes resistance to anti-EGFR therapies in EGFR-mutant lung cancer.

Oncoprotein BCL6 confers tumor adaptive resistance to genotoxic stress through the IFN-BCL6-PTEN axis in solid tumors and presents a promising combinational target for chemo-sensitization.

A microfluidic device induces doxorubicin-resistant polyaneuploid cancer cells from triple negative breast cancer cells, revealing NUPR1/HDAC11 axis dysfunction drives chemoresistance, increasing tumor heterogeneity and impacting clinical outcomes.

A genetic discovery screen for epigenetic factors accelerating melanoma development in vivo identifies SATB2 as a driver of tumor invasion and resistance to FDA-approved BRAF-targeted inhibitor Vemurafenib.

A novel first-in-class small molecule (ERX-11) that interacts with and disrupts the interactome of the estrogen receptor (ER), blocks the growth of ER-positive breast cancers, including those that are resistant to currently approved hormonal agents.