Tokyo, Japan – Researchers from Tokyo Metropolitan University have discovered a new pathway by which cells counteract the action of alovudine, an important antiviral and anticancer drug. The protein flap endonuclease-1 (Fen1) was found to improve cell tolerance by counteracting the toxic accumulation of another protein, 53BP1. A renewed spotlight on the underappreciated role of Fen1 promises not only new cancer treatments, but a way to gauge the efficacy of existing treatments.

New research from Memorial Sloan Kettering Cancer Center (MSK) develops a powerful new resource for studying gene regulation across eukaryotes; uncovers how “jumping genes” can drive cancer growth; describes how an unexpected oxygen sensor regulates ferroptosis; establishes a technique to map chromatin architecture in 3D; creates new models for studying schizophrenia-associated defects; and finds transcription factor 19 is critical for the responses of natural killer cells to viral infection.

The growing healthcare burden posed by hepatocellular carcinoma, the most common subtype of liver cancer, has prompted the establishment of a Commission comprising a wide range of medical and public health experts. Now, they present their findings in a recent report, which defines concrete goals for the reduction of hepatocellular carcinoma cases, and presents a set of evidence-based recommendations to help stakeholders work together to achieve these goals.

Professor Xun Lan from the School of Basic Medical Sciences at Tsinghua University and Director Hongxing Liu from Hebei Yanda Lu Daopei Hospital have published a research article entitled “Integrative scATAC-seq and mtDNA mutation analysis reveals disease-driven regulatory aberrations in AML” in Science Bulletin. This study leverages single-cell multi-omics technologies to investigate the regulatory aberrations caused by mutations in the transcription factor WT1 and in cis-regulatory elements that drive acute myeloid leukemia (AML). The research also uncovers tumor clones and relapse-associated markers linked to AML relapse, offering new insights into the mechanisms of disease progression and potential avenues for therapeutic intervention.

This review introduces a novel paradigm in cancer biology, focusing on the nuclear phosphoinositide (PIPn)-p53 signalosome and its crucial role in regulating cell motility. Traditionally associated with cytoplasmic and membrane-bound signaling, PIPns are now recognized for orchestrating nuclear events including the stabilization of p53 and activation of nuclear AKT. The review emphasizes the interplay between wild-type or mutant p53 and nuclear PIPn metabolism, opening new directions for therapeutic strategies targeting metastasis.

This study reveals that dynamin 1 (DNM1) promotes N-cadherin recycling through caveolae-mediated endocytosis, maintaining epithelial-to-mesenchymal transition (EMT) plasticity and driving ovarian cancer metastasis. DNM1 deficiency disrupts N-cadherin/Rab11 co-localization, while β-1,3-galactosyltransferase 1 (B3GALT1) inhibits this process. Clinically, elevated DNM1 expression correlates with poor prognosis in high-grade serous ovarian cancer and enhances nanoparticle uptake, providing a novel therapeutic target.

This review discusses the evolution, challenges, and innovations of antibody-drug conjugates (ADCs) in cancer treatment. It focuses on the importance of precise target selection and engineering to improve efficacy while minimizing off-target toxicities. Recent advances such as pH-dependent antibodies, dual-epitope targeting, and AI-guided profiling are highlighted as promising strategies to enhance safety and therapeutic impact.

Neuroblastoma, a cancer mainly affecting children, is often difficult to treat. A team led by Jan Dörr and Anton Henssen at the Experimental and Clinical Research Center report in “Cancer Discovery,” a potential reason treatment sometimes fails and a new strategy to combat particularly resistant tumors.