Transposable elements in cancer therapy.

Transposable elements (TEs) are a major source of immunogenic nucleic acids that can be therapeutically reactivated in cancer cells to induce a state of viral mimicry.

TE expression can trigger innate immune sensing pathways, including type I interferon responses, and promote immunogenic cell death via sensors such as RIGI, MDA5, cGAS, and Z-DNA binding protein 1.

Although initially described in the context of epigenetic therapies, viral mimicry is now recognized as a shared response to diverse cancer treatment modalities, including chemotherapies and targeted therapies.

Despite their distinct primary mechanisms, these treatments converge on TE reactivation through disruption of DNA/histone methylation, p53 activation, and perturbation of mRNA splicing.

Therapeutic resistance to chemotherapy, radiation, and targeted agents is associated with TE silencing, identifying TE repression as a targetable axis of resistance.

Combination strategies to induce immunogenic TE expression can further enhance viral mimicry and boost antitumor immunity. https://sciencemission.com/Viral-mimicry-in-cancer-therapy

A new study reveals that bacteria can survive antibiotic treatment through two fundamentally different “shutdown modes,” not just the classic idea of dormancy. The paper is published in the journal Science Advances.

The researchers show that some cells enter a regulated, protective growth arrest, a controlled dormant state that shields them from antibiotics, while others survive in a disrupted, dysregulated growth arrest, a malfunctioning state marked by vulnerabilities, especially impaired cell membrane stability. This distinction is important because antibiotic persistence is a major cause of treatment failure and relapsing infections even when bacteria are not genetically resistant, and it has remained scientifically confusing for years, with studies reporting conflicting results.

By demonstrating that persistence can come from two distinct biological states, the work helps explain those contradictions and provides a practical path forward: different persister types may require different treatment strategies, making it possible to design more effective therapies that prevent infections from coming back.

In laboratory models, researchers at The University of Texas MD Anderson Cancer Center discovered that a mother’s circadian rhythms, or internal body clock, can influence the immune system states of her offspring, which can accurately predict the risk of bacterial infection.

These findings offer novel insights into non-genetic factors shaping immune defenses and provide a framework to study circadian rhythms as a possible reason why some patients might be more vulnerable to getting infections during disease treatment. The study, published in Science Advances, was led by Alejandro Aballay, Ph.D., professor of Genetics and dean of the UTHealth Houston Graduate School of Biomedical Sciences.

“These findings reveal a circadian mechanism that can create significant differences in infection outcomes even when genetics and environment are similar,” Aballay said. “This circadian control may help explain why patients with comparable risk profiles often experience very different responses to infection.”