Study: Biomarker test may improve risk assessment for HPV-related throat cancer
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Updates every hour. Last Updated: 2-Apr-2026 10:16 ET (2-Apr-2026 14:16 GMT/UTC)
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.
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.
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.
Recent research shows that tumors in different organs host microbial communities capable of influencing cancer biology, immune responses, and the effectiveness of therapies, highlighting the need to standardize methods for studying intratumoral microbes.
In some non-small cell lung cancers (NSCLCs), changes to the RET gene (known as RET fusions) can drive tumor growth. In a phase 1/2 clinical study with a 42-month-long follow-up period, researchers from Mass General Brigham Cancer Institute evaluated the long-term efficacy and safety of the FDA-approved drug pralsetinib, which targets RET. Investigators found that treatment led to durable responses with manageable safety profiles in 281 patients with advanced or metastatic RET fusion-positive NSCLCs. Results are published in Journal of Clinical Oncology.