Blog – Page 15

Two modeling studies suggest that making more people eligible for lung cancer screening would prevent tens of thousands of deaths in the US each year — but at what cost?

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Two new modeling studies suggest that expanding lung cancer screening — to include more smokers or even lifelong nonsmokers — would save thousands more lives in the US every year. But not everyone is convinced the projected benefits would outweigh the harms.

In one study, published in JAMA, researchers at the American Cancer Society (ACS) found that only about 19% of currently eligible Americans underwent lung cancer screening in 2024.

That, the study projected, could translate to roughly 15,000 lung cancer deaths averted over 5 years. But 100% screening uptake would save three times as many lives.

Cao et al. show that Trichoderma harzianum detoxifies fusaric acid into the non-toxic metabolite 10OH-FSA, thereby suppressing disease and fostering beneficial microbial networks. This work reveals toxin neutralization as an ecological strategy for sustainable control of soil-borne plant diseases.

Like a phoenix rising from the ashes, our skin tissue—and in fact many types of epithelial tissue that lines and covers the body’s organs—can respond to death and destruction with a burst of regeneration. This phenomenon, known as compensatory proliferation, was first described in the 1970s in fly larvae, which regrew fully functional wings after their epithelial tissue had been severely damaged by high-dose radiation. Since then, this surprising ability has been documented in many species, including humans, yet its molecular basis has remained unclear.

A new study from the Weizmann Institute of Science, published in Nature Communications, reveals that the very enzymes responsible for cellular destruction—caspases—may also render certain cells resistant to death, enabling damaged tissue not only to regenerate but even to become more resilient.

Unfortunately, this same mechanism may be hijacked by many types of cancer and may help explain why some tumors recur in a more aggressive and treatment-resistant form. The new findings could thus open avenues for therapies that speed up wound repair and help prevent cancer relapse.

A new study published in Science Translational Medicine by researchers at The University of Texas MD Anderson Cancer Center details a therapeutic vulnerability in patients with an aggressive subtype of triple-negative breast cancer.

Led by Khandan Keyomarsi, Ph.D., professor of Experimental Radiation Oncology, the study shows that simultaneous inhibition of ATR and PKMYT1 triggers a type of cell death in Rb1-deficient breast cancer models.

Using genomic profiling, proteomics and patient-derived xenografts, the researchers found that loss of Rb1—a gene important for normal cell division—disrupts DNA repair processes and forces tumor cells to rely on ATR and PKMYT1 dependent pathways for survival, creating a vulnerability that can be selectively targeted.