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Editors' Summary: This Replication Study did not reproduce those experiments in the original paper that it attempted to reproduce.

Cancer is a consequence of the release of basal cellular functions inherited from our unicellular ancestors from the control of regulatory networks that evolved during the emergence of multicellularity.

Endothelial cells express a soluble isoform of the L1CAM cell adhesion molecule that is generated by the splicing factor NOVA2 and induces angiogenesis, with relevant implications for ovarian cancer vascularization.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

Inhibition of FGF2-FGFR1 signaling in bone marrow stroma attenuates secretion of FGF2-laden exosomes and subsequent protection of leukemia cells.

The MondoA transcription factor localizes to the outer mitochondrial membrane where it coordinates an adaptive transcriptional response to elevated cellular energy represented by high cytoplasmic glucose and high mitochondrial ATP.

In addition to increasing glycolysis, some proliferating cells exhibiting the Warburg effect also increase oxidative phosphorylation through mitochondrial fusion.

Prostate cancer cells maintain heterogeneous androgen receptor transcriptional activity through upregulation of AR-regulated coactivator GREB1, and cells with high activity rapidly develop resistance to antiandrogen therapy in a GREB1-dependent manner.

Bazedoxifene's SERD activities enable it to resist the impact of activating ESR1 mutations in breast cancer.

A drug used in hormone replacement therapy can target estrogen receptors that have become resistant to breast cancer treatments.