New imaging technique could transform precision of vocal fold injection procedures
Peer-Reviewed Publication
Updates every hour. Last Updated: 22-Jun-2026 03:16 ET (22-Jun-2026 07:16 GMT/UTC)
An international team of researchers from Trinity College Dublin and the Moffitt Cancer Center in the US has demonstrated a landmark “evolutionary double-bind” strategy to overcome treatment resistance in prostate cancer.
Many patients with metastatic cancers receive therapy that is initially highly effective, often resulting in complete remission. However, cancer cells have a remarkable capacity to evolve resistance to currently available therapies. As a result, resistant cells eventually proliferate causing the tumour to recur, leading to treatment failure and ultimately patient death.
In other words, increasingly the proximate cause of death in cancer patients is evolution, which sees the cancer cells adapt and overcome even highly effective treatments.
The new work found that when cancer cells successfully evolve resistance to DNA damaging treatments, they expose a critical weakness that makes them highly vulnerable to immunotherapy. This represents an “evolutionary double-bind” in which the cancer cell adaptation to one therapy makes them more vulnerable to another therapy and vice-versa.
U.S. counties located closer to operational nuclear power plants (NPPs) have higher rates of cancer mortality than those located farther away, according to a new study led by Harvard T.H. Chan School of Public Health. The study is the first of the 21st century to analyze proximity to NPPs and cancer mortality across all NPPs and every U.S. county. The researchers emphasized that the findings are not enough to establish causality but do highlight the need for further research into nuclear power’s health impacts.
Cancer remains a leading cause of death worldwide, with early and accurate diagnosis being paramount for effective treatment. However, traditional diagnostic methods like biopsies are invasive and carry risks, while non-invasive approaches often struggle to identify reliable biomarkers due to tumor heterogeneity and the complexity of biological data. Integrating information across different molecular layers—genomics, transcriptomics, proteomics, and metabolomics—holds promise but is technically challenging, particularly in capturing the dynamic metabolic state of tumors.
Radiotherapy (RT) is one of the most widely used cancer treatment modalities, applied in over half of all patients with cancer. In clinical oncology, positron emission tomography (PET) with 18F-fluorodeoxyglucose (18F-FDG) is widely used to noninvasively monitor tumor glucose metabolism and evaluate therapeutic responses, including those to RT. However, transient increases in 18F-FDG uptake—referred to as post-RT “metabolic flares”—are frequently observed in responding tumors and have traditionally been attributed to localized inflammatory reactions. Whether these flares reflect underlying immune cell dynamics, particularly tumor-infiltrating T cells, has remained poorly understood.
A new study led by City St George's, University of London provides hope that smarter timing of cancer treatments could improve cure rates.
The standard clinical approach is to wait and see if a tumour regrows before trying a different treatment. By this point, some tumour cells are likely to have gained mutations making them resistant to the second treatment, which then also fails.
Evolutionary theory suggests an alternative strategy. Instead of waiting, it might be better to switch to a second treatment while the tumour is still responding to the first one.
In proof-of-concept study, scientists at Cincinnati Children's discover a method to reduce heart damage risk for people with cancer taking immune checkpoint inhibitors.