During therapy, some cancer cells evolve to escape elimination. Newer anticancer drugs that can overcome this resistance are necessary. Now, researchers from Japan demonstrate that aromatic benzaldehyde inhibits the growth of therapy-resistant pancreatic cancer. By preventing various signaling proteins and histone modifiers like Ser²⁸-phosphorylated histone H3 (H3S28ph) from binding to 14-3-3ζ protein, benzaldehyde overcomes therapy resistance and blocks plasticity to prevent the spread of cancer. These findings highlight its potential in cancer treatment.

Scientists have identified a subtype of immune cells that help advanced prostate cancer evade the body’s defenses. In mouse models, blocking a protein produced by those cells made tumors more responsive to immunotherapy, pointing to a potential new treatment approach. The study, with Shenglin Mei of the Fralin Biomedical Research Institute among the corresponding authors, is featured on the July cover of Molecular Cancer Research.

Researchers in the College of Design and Engineering (CDE) at the National University of Singapore and the National Cancer Centre Singapore (NCCS) have developed a hydrogel-based platform that extends the survival of patient-derived tumour tissues in the lab. The platform better replicates the tumour’s natural environment, allowing for more accurate evaluation of cancer drugs - particularly for peritoneal metastases, an advanced stage for abdominal and pelvic cancers. The study, published in Advanced Materials, could pave the way for more personalised and effective treatment strategies.

Amplification-free, highly sensitive, and specific nucleic acid detection is crucial for health monitoring and diagnosis. The type III CRISPR-Cas10 system, which provides viral immunity through CRISPR-associated protein effectors, enables a new amplification-free nucleic acid diagnostic tool. In this study, we develop a CRISPR-graphene field-effect transistors (GFETs) biosensor by combining the type III CRISPR-Cas10 system with GFETs for direct nucleic acid detection. This biosensor exploits the target RNA-activated continuous ssDNA cleavage activity of the dCsm3 CRISPR-Cas10 effector and the high charge density of a hairpin DNA reporter on the GFET channel to achieve label-free, amplification-free, highly sensitive, and specific RNA detection. The CRISPR-GFET biosensor exhibits excellent performance in detecting medium-length RNAs and miRNAs, with detection limits at the aM level and a broad linear range of 10^-15 to 10^-11 M for RNAs and 10^-15 to 10^-9 M for miRNAs. It shows high sensitivity in throat swabs and serum samples, distinguishing between healthy individuals (N = 5) and breast cancer patients (N = 6) without the need for extraction, purification, or amplification. This platform mitigates risks associated with nucleic acid amplification and cross-contamination, making it a versatile and scalable diagnostic tool for molecular diagnostics in human health.

A comprehensive review reveals that blocking natural killer cell checkpoints and employing precision strategies like gene editing and engineered cell therapies could significantly enhance cancer immunotherapy outcomes for solid tumors and blood cancers.

Phosphatases have long been considered undruggable, but recent discoveries are changing that perception. Compared to kinases, phosphatases remain underexplored in cancer therapy, despite their critical roles in tumour progression. Dysregulated phosphatases drive tumour growth, metastasis, angiogenesis, immune evasion, therapy resistance, and intracellular communication—through the modulation of oncogenic signaling pathways.

Phosphatases are governed by a complex regulatory system that must be understood to develop effective targeted therapies. However, phosphatases could be broadly categorized as tumour promoters, tumour suppressors, or having dualistic functions.

This review explores the roles of various phosphatases in cancer cells and immune tumour microenviroment, with a focus on their signaling mechanisms and the current latest therapeutic strategies.

The study investigates the interaction between the human epidermal growth receptor 2 (HER2) and amygdalin, a compound found in peaches, almonds, and apples. To assess the potential of amygdalin, the interaction between HER2 and amygdalin was explored using molecular docking and molecular dynamics simulations. Binding energies were evaluated for both the crystal and equilibrated HER2 structures. The effects of water on binding were also assessed. Molecular dynamics simulations analyzed structural changes in HER2, including interdomain distances, hydrogen bond fluctuations, dihedral angle shifts, and residue-residue distances at the dimerization arm. The free energy landscape was constructed to evaluate stability. Binding energies of −33.472 ​kJ/mol and −36.651 ± 0.867 ​kJ/mol were observed for the crystal and equilibrated HER2 structures, respectively, with water further enhancing binding to −41.212,4 ​± ​1.272,7 and −53.513 ± 1.452,3 ​kJ/mol. Molecular dynamics simulations revealed significant conformational changes in HER2, including a reduction in interdomain distance, fluctuations in hydrogen bond lengths, and a shift in dihedral angles from 60° to −30°. The residue-residue distance at the dimerization arm decreased, indicating conformational changes upon binding. The free energy landscape showed a deeper and more defined minimum in the bound state, reflecting enhanced stability. These findings highlight amygdalin’s potential as a therapeutic agent targeting HER2.