Latest Research
All publications from the Cancer3.AI database, newest first.
RYK silencing-modified bone marrow-derived mesenchymal stem cells suppress gastric cancer progression.
Fu Y, et al
Researchers investigated whether bone marrow-derived mesenchymal stem cells (BMSCs) engineered to silence a gene called RYK (receptor-like tyrosine kinase) could suppress the growth and spread of gastric cancer cells. The study used laboratory co-culture experiments pairing these modified BMSCs with the human gastric cancer cell line NCI-N87, examining effects on cell proliferation, invasion, colony formation, and programmed cell death. Results showed that unmodified BMSCs actually promoted cancer cell growth and reduced apoptosis, while RYK-silenced BMSCs reversed this effect, inhibiting proliferation, colony formation, and invasion while triggering cancer cell death and cell cycle arrest at the G2/M phase. Molecular analysis confirmed activation of key apoptotic proteins including cleaved caspases and PARP1, alongside suppression of survival proteins Bcl-2 and Bcl-xL. These findings suggest that genetically engineering BMSCs to silence RYK may offer a promising cell-based therapeutic strategy for gastric cancer, which remains one of the leading causes of cancer-related mortality worldwide.
In vitro cellular & developmental biology. Animal
Source →Engineering a vascularized-osteogenic microenvironment to enhance bone regeneration via a 3D-printed composite scaffold with progressive-release bio-factors.
Shao T, et al
Researchers developed a 3D-printed composite scaffold designed to simultaneously promote blood vessel formation and bone tissue growth, addressing a major challenge in bone regeneration medicine. The scaffold was engineered to progressively release biological factors over time, creating a coordinated microenvironment that supports both vascularization and osteogenesis at the repair site. By combining additive manufacturing precision with controlled bio-factor delivery, the system aims to overcome the limitations of conventional bone grafts, which often fail due to poor vascularization and inadequate healing signals. Published in the Journal of Translational Medicine, this work represents a significant step toward clinically viable engineered bone substitutes that could benefit patients with large bone defects from trauma, cancer resection, or degenerative disease.
Journal of translational medicine
Source →The Atypical and Suspicious for Malignancy Categories of the WHO Reporting System for Lymph Node, Spleen, and Thymus Cytopathology: Review of their Diagnostic Utility, Limitations, and Clinical Impact.
Cozzolino I, et al
Researchers reviewed the diagnostic value and limitations of two intermediate categories — 'Atypical' and 'Suspicious for Malignancy' — within the World Health Organization Reporting System for Lymph Node, Spleen, and Thymus Cytopathology, which is used to classify results from fine-needle aspiration biopsies of lymph nodes. The study found that cases labeled 'Atypical' carry a widely variable risk of malignancy ranging from 28.6% to 76.9%, while 'Suspicious for Malignancy' cases show a consistently high risk of 82% to 100%, yet both categories suffer from very poor agreement between pathologists. Common diagnostic pitfalls include mistaking benign tissue changes for aggressive lymphoma or missing diagnoses of Hodgkin lymphoma and certain T-cell cancers, and even ancillary molecular tests can mislead clinicians by detecting abnormal cell populations in non-cancerous conditions. The authors conclude that while these diagnostic categories are essential tools for guiding clinical decisions, their reliability is hampered by subjective interpretation and inconsistent application across institutions. To improve patient outcomes, the authors call for standardized diagnostic criteria, institutional consistency, and the integrated use of cell morphology, immune marker, and molecular data when evaluating lymph node biopsies.
Diagnostic cytopathology
Source →Pseudo-senescence induced by palbociclib does not sensitise pleural mesothelioma cells to combinations with senolytics.
Sreeram I, et al
Researchers investigated whether the CDK4/6 inhibitor palbociclib could sensitize pleural mesothelioma cells — an aggressive and difficult-to-treat lung cancer — to so-called senolytic drugs, which are designed to kill cells that have entered a state of permanent growth arrest known as senescence. Although palbociclib caused mesothelioma cells to display classic hallmarks of senescence, including increased cell size, elevated inflammatory secretions, and reduced proliferation, the cells resumed growth once the drug was removed, indicating the senescence was not permanent. Combinations of palbociclib with several senolytic agents, including BH3 mimetics such as navitoclax, venetoclax, and S63845, as well as inhibitors of the Src, STAT3, and mTORC1 signalling pathways, failed to enhance cancer cell death. In contrast, the established chemotherapy drug cisplatin induced a stronger and more consistent permanent cell cycle arrest and genuine senescence across multiple mesothelioma cell lines, as confirmed by sorting cells based on size and enzyme activity. These findings highlight that not all therapy-induced senescence is equivalent and that the type of senescence a tumour enters determines whether senolytic strategies will succeed, which has direct implications for how future combination therapies are designed for mesothelioma patients.
Cell death & disease
Source →NEK2 promotes oral squamous cell carcinoma progression and serves as a diagnostic and therapeutic target.
Wu H, et al
Researchers investigated the role of NEK2 (NIMA-related kinase 2) in oral squamous cell carcinoma (OSCC), a common and often deadly form of mouth cancer, to determine whether it could serve as a diagnostic marker or treatment target. Using patient tissue samples and laboratory cancer cell lines, the team found that NEK2 protein levels were significantly higher in OSCC tumors compared to healthy oral tissue, and that patients with elevated NEK2 expression had worse overall survival and progression-free survival. Experiments in cell cultures showed that NEK2 promotes the spread of cancer cells by triggering epithelial-mesenchymal transition (EMT), a process that makes cancer cells more mobile and invasive, while studies in mice confirmed that NEK2 drives tumor growth and lung metastasis in living organisms. The researchers also demonstrated that INH1, a chemical inhibitor of NEK2, effectively suppressed tumor growth and metastasis in animal models, suggesting therapeutic potential. Pathway analysis indicated that NEK2 likely exerts its cancer-promoting effects by activating the PI3K-Akt and IL-17 signaling pathways, which are well-known drivers of cancer progression. These findings position NEK2 as a promising biomarker for OSCC diagnosis and a viable molecular target for future therapies aimed at improving outcomes for patients with this disease.
Scientific reports
Source →