Researchers at Baylor College of Medicine have uncovered a strategy that triple negative breast cancer (TNBC) cells use to boost their ability to metastasize, or spread to other organs. Metastasis is the leading cause of cancer-related deaths and scientists are investigating ways to prevent it. These findings highlight new possibilities for developing clinical interventions to treat metastatic TNBC patients for whom there are no specific therapies.

A study coordinated by the Institut de Neurociències of the Universitat Autònoma de Barcelona proposes a new treatment for glioblastoma, the most aggressive brain tumor. The approach involves patches tested in cell cultures and in excised pig brains that induce a high level of cellular oxidation in a local and controlled manner, thereby minimizing potential systemic side effects.

Cancer research is undergoing a profound transformation. Advances in molecular and cellular biology, genomics, immunology, engineering, and computational science have reshaped our understanding of cancer as a complex, multiscale disease. Yet the gap between biological discovery and durable clinical benefit remains a central challenge. Addressing this gap increasingly requires integration across disciplines, technologies, and conceptual frameworks. Advanced Cancer Research is an international, peer-reviewed, open-access journal publishing original cancer research spanning basic, translational, and clinical investigation. The journal prioritizes studies that provide mechanistic depth, introduce conceptual or technological innovation, or offer system-level insight into cancer biology and therapy, with particular emphasis on work that bridges disciplinary boundaries and advances translational relevance.

Recently, the research team led by Professor Jun Pang from the Department of Urology at The Seventh Affiliated Hospital of Sun Yat-sen University discovered that cyclin-dependent kinase 12 (CDK12) can directly phosphorylate the pioneer transcription factor FOXA1, thereby activating a critical new pathway that drives prostate cancer progression. This study is the first to identify a novel phosphorylation site (S234) on the FOXA1 protein and elucidates the complete mechanism by which phosphorylation at this site upregulates the expression of the oncogene MDM2, leading to the degradation of the tumor suppressor protein p53, ultimately promoting tumor cell survival and proliferation. Targeted inhibition of CDK12 can effectively block this pathway, restore p53 function, and induce cancer cell apoptosis, providing a highly promising new strategy for the treatment of advanced prostate cancer. The related findings have been published in Research under the title "CDK12-Mediated Phosphorylation of FOXA1 Promotes Prostate Cancer Progression via the MDM2–p53 Axis."

Overcoming tumor resistance to chemotherapy drugs has long been a challenge for oncology clinicians and researchers. Now, a new study suggests that blocking a key protein, p300, may force damaged cancer cells into a state of uncontrolled transcriptional activity, thereby creating a novel form of cellular stress that can make even chemo-resistant tumors sensitive again to treatment.

The new method developed by Rutgers researchers distinguishes between existing microbes and contamination in tissue samples.