For nearly half of people diagnosed with lung cancer, immunotherapy can slow the disease but not stop it. Funded through a $4 million joint investment from the Canadian Cancer Society (CCS) and the Weston Family Foundation, a new clinical trial aims to change that. 

Osteosarcoma is an aggressive bone cancer characterized by high rate of recurrence and metastasis. In a new study, researchers show that restoring the RNA-editing enzyme adenosine deaminase acting on RNA 2 (ADAR2) slows tumor growth, reduces invasion, promotes bone-like differentiation, and improves chemotherapy sensitivity in cell and mouse models. The findings identify IGFBP7 RNA editing as a key mechanism underlying these effects, highlighting a potential differentiation-based treatment strategy for pediatric patients with bone cancer.

Researchers have created an innovative paper-based analytical device that can detect microRNA-21—a biomarker associated with multiple cancers—using only a smartphone camera for readout, demonstrating a cost-effective platform with potential for point-of-care cancer diagnostics.

Paligenosis defines a tightly controlled program through which terminally differentiated cells re‑enter the cell cycle and contribute to tissue repair after injury. This review systematically introduces the concept, the three sequential stages of paligenosis—mTORC1 suppression with autophagy initiation, followed by mTORC1 reactivation and stemness gene induction, and finally proliferation with lineage restoration—as well as the underlying molecular networks involving autophagy, metabolic rewiring, and epigenetic remodeling. The article then compares paligenosis with other forms of cellular plasticity such as dedifferentiation, transdifferentiation, epithelial‑mesenchymal transition, and induced pluripotency, highlighting its unique stepwise, reversible and intralineage nature. A major focus is the dual role of paligenosis: while it ensures efficient regeneration in tissues like the stomach and pancreas, its persistent or dysregulated activation under chronic stress or oncogenic signals can drive metaplasia, tumor initiation, metastasis and therapy resistance. The review closes by discussing biomarker prospects for distinguishing adaptive repair from malignant drift, and the therapeutic potential of modulating paligenotic pathways for regenerative medicine and cancer treatment.

N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic mRNA, serves as a pivotal epitranscriptomic mark that dynamically regulates RNA metabolism—including stability, splicing, translation, and localization—thereby shaping cellular identity and function. This modification is installed by writer complexes (e.g., METTL3/METTL14), erased by demethylases (FTO, ALKBH5), and interpreted by reader proteins. Among these readers, YTHDF2 has emerged as a central regulator, primarily known for binding m6A-modified transcripts and promoting their decay, but recent evidence reveals a more complex role extending to m5C reading and even translational enhancement. YTHDF2 functions as a key integrator of intrinsic genetic programs and extrinsic environmental cues, critically governing hematopoietic stem cell (HSC) fate, immune cell development and activation, and tumor-immune interactions. This review synthesizes advances in understanding YTHDF2’s molecular mechanisms—spanning RNA-stability-dependent and -independent pathways—and its multifaceted roles in hematopoiesis, immunity, and cancer, highlighting its potential as a therapeutic target in immune-related diseases and malignancies.

The rapid clinical validation of mRNA technology during the COVID‑19 pandemic has powerfully accelerated its application in oncology, and this comprehensive review provides a state‑of‑the‑art assessment of mRNA cancer vaccines. It systematically covers the molecular design principles of synthetic mRNA, the diverse antigen‑targeting strategies (from conventional tumor‑associated antigens to patient‑specific neoantigens and non‑canonical sources), the major delivery platforms (lipid nanoparticles, lipoplexes, protamine complexes, and cell‑based systems), and the mechanistic pathways by which these vaccines activate both cellular and humoral antitumor immunity. The review then synthesizes preclinical and clinical evidence across solid tumors—melanoma, pancreatic ductal adenocarcinoma, non‑small cell lung cancer, prostate cancer, glioblastoma—and hematologic malignancies, including acute myeloid leukemia, myelodysplastic syndromes, and multiple myeloma. It also critically discusses current challenges, such as the immunosuppressive tumor microenvironment, delivery barriers, and manufacturing complexities, before outlining future directions that involve next‑generation delivery systems, artificial intelligence‑driven vaccine design, and combination strategies with immune checkpoint inhibitors and adoptive T‑cell therapies.

Researchers from The University of Osaka found that only a small subset of tumor-killing T cells undergoes extensive expansion during immunotherapy for multiple myeloma. By tracking individual cells, the team showed that the T-cell clones that later became dominant had already begun expanding shortly after the treatment started. The findings also suggest that highly proliferative immune cells show lower levels of exhaustion-related markers, offering new insights into why some patients respond better to immunotherapy.