Researchers at Johns Hopkins University and the University of Maryland School of Pharmacy have developed a set of novel, first-in-class drugs that inhibit hypoxia-inducible factors 1 and 2, a pair of transcription factors considered to be “master regulators” of cancer progression. The study, to be published April 2 in the Journal of Experimental Medicine (JEM), shows that these drugs, when combined with immunotherapy, can completely eliminate breast, colorectal, melanoma, and prostate tumors in mice, suggesting that they could eventually be used to treat a broad range of cancers in humans.

A new study led by researchers at the University of Liège highlights the unexpected role of Stard7 in the development of intestinal cancers. Long seen as a transporter of some lipids to mitochondria, Stard7 now appears to be a key player in mitochondrial metabolism and tumour development in the intestine.

The National Comprehensive Cancer Network and NCCN Foundation select five Young Investigator Award recipients from Fred Hutchinson Cancer Center, Memorial Sloan Kettering Cancer Center, O'Neal Comprehensive Cancer Center at UAB, Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine, and The University of Texas MD Anderson Cancer Center.

As survival rates for female-specific cancers continue to rise, therapy-related myeloid neoplasms (t-MN) have become a critical long-term complication threatening survivors’ health. This systematic review by the team from Union Hospital summarizes the multi-factorial pathogenesis of t-MN, analyzes current treatment dilemmas, and puts forward female-focused management strategies. It provides a comprehensive theoretical framework for clinical precision prevention, early monitoring and targeted intervention of t-MN.

Glioma remains one of the deadliest brain cancers, characterized by aggressive growth and limited treatment options. In a new study, researchers from Ningxia Medical University uncovered that choline kinase alpha (CHKA) directly interacts with the epidermal growth factor receptor (EGFR) to activate the MAPK signaling pathway, thereby promoting glioma cell proliferation, migration, and invasion. This discovery sheds light on a previously unrecognized oncogenic axis, the CHKA/EGFR/MAPK pathway, offering fresh opportunities for targeted glioma therapy.

We report the potential target of  Lentinus edodes-derived β-glucan (LNT) in HeLa cancer cells in this study. Our findings demonstrate that LNT could specifically bind to the deleted in malignant brain tumor 1 (DMBT1), a potential target on HeLa cytomembrane. The primary driving force for this binding were mainly hydrogen bonding, hydrophobic interactions, and van der Waals forces. LNT significantly up-regulated the expression of DMBT1 in HeLa cells and reduced HeLa cell viability in a concentration-dependent manner, suggesting that LNT might target DMBT1 to inhibit cancer cell growth. Furthermore, the potential mechanism by which LNT targeted DMBT1 to inhibit HeLa cell viability was investigated using a DMBT1-knockdown HeLa cell model. The results show that LNT-induced proliferation inhibition and apoptosis were significantly lower in DMBT1-knockdown HeLa cells than in non-knockdown HeLa cells, indicating that DMBT1 played a key tumor suppressor role in HeLa cells. Meanwhile, after DMBT1 knockdown, LNT-induced inhibition of PI3K/Akt pathway activation was attenuated in vitro and in vivo, suggesting that LNT induced inhibition of PI3K/Akt pathway activation and HeLa cell viability were closely associated with DMBT1. Therefore, this study proposed a novel strategy for treating cervical cancer by enhancing DMBT1 expression via LNT.