A comprehensive multi-cancer study from researchers at The University of Texas MD Anderson Cancer Center has revealed that cancer cells within tumors are genetically diverse, yet all carry the same core genetic changes that can be traced back to a common ancestral cell, providing a single-cell view of how tumors adapt, survive and diversify. Understanding this helps explain why some cancer cells manage to survive treatments, paving the way for more tailored diagnostic and therapeutic strategies.

Bumblebees see the world differently under stress, processing visual information more sharply and making quicker decisions, new research from Newcastle University, UK, reveals.

Female chickadees living in monogamous mating systems will proactively seek out males that have better cognitive skills than their nestmate.

A tropical butterfly has evolved an ingenious anti-ageing strategy by delaying the aging process enabling it to live far longer than its closest relatives, according to a new University of Bristol-led study published in Nature Communications today [16 June].

Young frogs prioritize growing quickly even when infected with a deadly pathogen, shifting energy toward immune defense only when infections become severe.

A new review published in Biogerontology challenges the idea that ageing can be explained by a single biological mechanism. According to Dr. Piotr Chmielewski of Wroclaw Medical University, ageing is more likely to emerge from dynamic interactions among multiple biological processes operating across cells, tissues and organs.

The article examines current theories of ageing, discusses the limitations of popular biomarkers such as epigenetic clocks, and argues that future research may increasingly focus on understanding how organisms maintain resilience, adaptability and functionality despite ongoing biological damage.

Researchers at MUSC Hollings Cancer Center and the University of Arizona have uncovered a previously unknown way that prostate cancer cells can survive treatment, helping explain why some therapies eventually lose effectiveness. The study, led by Noel Warfel, associate professor of Biochemistry and Molecular Biology at MUSC, focused on PIM1, a protein that is active in many prostate cancers and has long been considered a promising drug target.

The team found that while existing PIM1 inhibitors successfully block the protein’s signaling activity, they also cause cancer cells to accumulate larger amounts of the PIM1 protein itself. The excess protein activates a separate survival pathway that helps cancer cells to withstand treatment. Specifically, PIM1 promotes a process called mitophagy, which allows cancer cells to remove damaged mitochondria, reduce oxidative stress and continue surviving despite therapy.

The findings suggest that simply inhibiting PIM1 may not be enough. Instead, researchers showed that completely degrading the protein could be a more effective strategy. Using an experimental drug known as PIMTAC, Warfel’s team removed PIM proteins from cancer cells rather than blocking their activity. In laboratory studies and mouse models, this approach increased oxidative stress in tumor cells and led to greater cancer cell death.

The discovery provides new insight into how prostate cancer develops treatment resistance and highlights a potential path toward more effective therapies. Beyond prostate cancer, the findings could have implications for other cancer types where PIM proteins play a role in tumor survival and drug resistance.