Hidden threat lurks post-cure: T-MN risks in female cancer survivors
Peer-Reviewed Publication
Updates every hour. Last Updated: 22-Jun-2026 08:16 ET (22-Jun-2026 12:16 GMT/UTC)
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.
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.
Tumour suppressor BAP1 protein is implicated in several aggressive cancers, but the mechanisms behind it are not well understood.
Scientists from the National Cancer Centre Singapore (NCCS) and Duke-NUS Medical School (Duke-NUS) have uncovered new ways that BAP1 repairs DNA and regulates cell function, leading to promising new therapeutic targets for BAP1-deficient cancers.
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.