National Institutes of Health (NIH)-supported investigators have developed a blood test to find pancreatic ductal adenocarcinoma, one of the deadliest forms of cancer. The new test could improve survival rates from pancreatic cancer, which tends to be diagnosed at late stages when therapy is less likely to be effective. The findings were published in Clinical Cancer Research.

At the 2026 Society of Thoracic Surgeons (STS) Annual Meeting, investigators will present a late-breaking study focused on surgical aortic valve replacement (SAVR) following prior transcatheter aortic valve replacement (TAVR), a clinical scenario increasingly encountered as TAVR use expands. Results demonstrate that operative mortality for isolated SAVR after TAVR has declined substantially over time, while the newly developed risk model showed excellent accuracy for all patients and surgical procedures.

Unrepaired DNA-protein crosslinks (DPCs) – highly toxic tangles of protein and DNA –  cause a process that leads to premature aging and embryonic lethality in mice. The findings reveal a previously unrecognized link between defective DNA repair and immune-driven inflammatory disease. They also suggest that targeting innate immune signaling may offer a therapeutic strategy for human disorders like Ruijs-Aalfs progeria syndrome (RJALS), which are caused by defective DPC repair. DPCs form when proteins become covalently trapped to DNA. These harmful knots block essential cellular processes, including DNA replication and transcription. The protease SPRTN plays a critical role in maintaining genome stability by repairing DPCs during DNA replication. While its role during DNA replication is well established, its functions in other phases of the cell cycle are less understood. Moreover, inherited mutations in SPRTN are known to cause RJALS – a rare disorder marked by premature aging and early-onset liver cancer.

Through cellular analyses, Ines Tomaskovic and colleagues show that SPRTN repairs DPCs not only during DNA replication, but also during mitosis. Loss of SPRTN causes DPC accumulation, leading to chromosome segregation defects and the formation of micronuclei containing persistent DPCs and damaged DNA. DNA released from aberrant nuclei accumulates in the cytoplasm and is detected by the cGAS-STING innate immune pathway, triggering inflammatory signaling. To assess the physiological impact of this response, Tomaskovic et al. generated a mouse model carrying the RJALS-associated SPRTN mutation. The authors found that these animals accumulated unrepaired DPCs and micronuclei, showed a strong innate immune response, and exhibited key features of the human disorder, including reduced body size, craniofacial and eye abnormalities, and premature hair graying, with some defects arising during embryogenesis. Notably, inhibition of cGAS-STING from early development rescued mice from developmental lethality and premature aging caused by DPC accumulation.

An analysis of twin cohort data suggests that human life span is far more heritable than previously believed. The findings of the analysis show that once deaths from external factors, such as accidents or infectious disease, are accounted for, genetics may explain ~50% of how long we live. “[T]he study … has important consequences for aging research,” write Daniela Bakula and Morten Scheibye-Knudsen in a related Perspective. “A substantial genetic contribution strengthens the rationale for large-scale efforts to identify longevity-associated variants, refine polygenic risk scores, and link genetic differences to specific biological pathways that regulate aging.” Understanding the heritability of human life span is a central question in aging research, yet measuring the genetic influence on longevity remains challenging. Although some genes linked to life span have been identified, external environmental forces, such as disease or living conditions, exert a powerful influence on how long someone lives and often obscure or confound potential genetic effects. Moreover, previous studies have produced widely varying estimates of human life-span heritability, fueling skepticism about the role of genetics in aging. These conclusions are striking, given that life span is far more heritable in laboratory mice and that most human physiological traits show much more genetic determination. According to Ben Shenhar and colleagues, this discrepancy may arise from overlooked confounders in previous research, particularly the heavy burden of “extrinsic” mortality – deaths due to external causes – in the historical populations that underpin these studies. These external causes of death likely dilute the measurable impact of genetics, which primarily shapes “intrinsic” mortality driven by aging and internal biological decline.

Shenhar et al. used mathematical models, simulations of human mortality, and multiple large-scale twin cohort datasets to disentangle intrinsic and extrinsic sources of death. According to the findings, extrinsic mortality systematically depresses estimates of life-span heritability. Once deaths from external causes are properly accounted for, the authors show that the genetic contribution to human life span rises dramatically to roughly 55% – more than double previous estimates – suggesting that genetics is a central force in human aging. These revised estimates align human life span with the heritability of most other complex physiological traits and with the life-span heritability observed in other species.