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Synthetic biology experiments show that MYC is a general transcription amplifier acting at two or more sites in the transcription-cycle and that MYC-turnover contributes to its activity.

The presented primary epithelial acinus-based platform for studying interactions between normal and malignant cells will enable in depth analysis of the tumor initiation process on a molecular level.

The HOXB13 binding partner MEIS1 suppresses prostate cancer proliferation, invasion, and metastasis by promoting expression of the anti-oncogenic extracellular proteoglycan Decorin.

3D culture of breast cancer in biologically relevant ECM potentiates the growth-inhibitory effects of unacylated ghrelin and AZP-531, and clinical response may be predictable based on a MAPK gene signature.

Cancer systems immunology is a highly interdisciplinary field that is advancing our ability to understand and predict the complex behavior that orchestrates the interplay between tumors and the immune system.

CHK2 directly binds the AR to mediate transient suppression of AR activity and thus loss of CHK2 function in prostate cancer increases AR activity, DNA damage response and radiation resistance.

DNA-PK and PTEN protect breast cancer cells from lethal replication stress induced by the WEE1 inhibitor AZD1775 and constitute new potential biomarkers for AZD1775 sensitivity.

A novel toxicophore, a 1H-1,2,3-triazole, has been identified in a wide-number of therapeutically-relevant compounds, including two anti-cancer chemotherapeutics, which inhibits mitochondria function and is mechanistically linked to adverse cardiac-cell events.

A structural motif that is found in two cancer drugs may be responsible for their ability to tackle cancers and for the side-effects caused by the drugs.

In lung adenocarcinoma, deleting one glucose transporter, whether it is Glut1 or Glut3 is insufficient, whereas their dual deletion reduces tumor growth.