On 05 – 06 November 2026, the Josep Carreras Leukaemia Research Institute will host its 2026 Scientific Symposium: "Immunity in Haematological Malignancies: From Molecular Mechanisms to Transformative Therapies". Held at the headquarters of the Institute in Badalona, Barcelona, the Symposium will foster scientific exchange and collaboration to accelerate the translation of discoveries into new treatments for patients with blood cancers.

Developing radiosensitizing agents to amplify tumor-eradicating effects on primary, regional recurrence, and distant metastases plays a transformative role in modern cancer care. Here, we report the de novo design of biocatalytic artificial metalloenzymes with an IrMn-cluster-based redox center (IMM) to achieve radiosensitized systemic antitumor responses for preventing malignant tumor metastasis and recurrence. Notably, our findings indicate that Mn-organic ligands substantially enrich the electron density of Ir clusters, thereby optimizing their interaction with oxygen species and markedly enhancing the production of both reactive oxygen species and molecular oxygen. When combined with radiotherapy, the IMM effectively amplifies DNA damage and induces pronounced apoptosis by alleviating intratumoral hypoxia. This shift reprograms the tumor microenvironment, enhancing radiosensitivity and facilitating the infiltration and activation of intratumoral CD8⁺ T cells and dendritic cells. Moreover, when integrated with anti-PD-1 therapy, this coordinated therapeutic regimen elicits potent systemic immune responses and durable antitumor memory, effectively suppressing tumor recurrence and metastasis while markedly improving therapeutic efficacy and long-term survival. We anticipate that this conceptual design could offer a promising and translationally relevant nanomedicine platform for radiotherapies.

Pushing the accelerator and the brake at the same time is rarely a good idea. But researchers at the University of Gothenburg are using this approach to treat leukemia. A new drug forces cancer cells to keep working hard even though they have run out of energy. The first study in mice shows very promising results.

- A joint research team of KAIST, Seoul St. Mary's Hospital, and Konyang University College of Medicine identifies how an active vitamin A metabolite suppresses "terminal exhaustion" in cancer-attacking CD8⁺ T cells

- Activates T cells' "function-preserving switch" to sustain anti-cancer function even during prolonged combat with cancer.

- In mouse glioma models, combination with anti-PD-1 immunotherapy — which releases the 'brake' cancer cells impose on immune cells — enhances treatment efficacy and points to the potential to suppress recurrent brain tumors

Researchers from Cambridge and Basel have developed small molecules that could make cancer immunotherapies more effective. They work in two ways: They prompt macrophages to engulf cancer cells and alter the surrounding tissue, reducing its ability to suppress immune attacks on the tumor.