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Category: biotech/medical – Page 124

Metastatic Recurrence in Adolescent and Young Adult Cancer—Key Drivers of Early Mortality

Editorial: Metastatic recurrence nearly triples mortality risk in Breast Cancer among young adults and increases death risk in sarcoma and colorectal cancer—highlighting the need for earlier detection and novel treatments.

Survivors of adolescent and young adult cancer (aged 15 to 39 years at diagnosis) are a large and growing population at risk for early mortality, with death due to primary cancer recurrence/progression a large contributor to increased mortality among survivors.1-3 In JAMA Oncol ogy, using linked data between the California Cancer Registry, Kaiser Permanente Northern California, and the Department of Health Care Access and Information, Brunson and colleagues4 report on patterns of metastatic recurrence among adolescents and young adults with cancer and compare the risk of death between those with metastatic recurrence and those with metastatic disease at diagnosis. These data provide valuable insights into the burden of metastatic disease among adolescents and young adults with cancer and identify cancer types for which adolescents and young adults face high risk for metastatic recurrence and associated mortality. Findings largely parallel trends in metastatic recurrent disease incidence and mortality among populations with broader age ranges, with some notable exceptions.

In this analysis, Brunson and colleagues4 found that 9.2% of adolescents and young adults had metastatic disease at diagnosis and 9.5% had metastatic recurrence, with the incidence of metastatic recurrence differing by cancer type. These findings have important implications for prognosis, treatment planning, disease surveillance, and survivorship care. Despite a 5-year overall survival of 86% for cancer in adolescents and young adults, a critical unmet need remains for those who do not reach long-term survival.5 Future efforts should prioritize understanding biologic mechanisms driving metastasis, identifying novel therapeutic targets, improving monitoring of minimal residual disease, and addressing disparities in treatment access and adherence, particularly for cancers that present with metastatic disease or have a high risk for metastatic recurrence.

Notably, the 5-year cumulative incidence of metastatic recurrence was highest for adolescents and young adults with sarcoma and colorectal cancer, at 24.5% and 21.8%, respectively. Additionally, compared to having metastatic disease at diagnosis, metastatic recurrence was associated with approximately 1.5-fold increased risk for mortality among adolescents and young adults with sarcoma and colorectal cancer. Compared to other common cancer types for this age range that have seen improvements in 5-year survival across recent decades, improvements in sarcoma survival have been muted, particularly among older adolescents and young adults.5, 6 Findings from the current study demonstrate that, in addition to poor prognosis compared to other cancer types, adolescents and young adults with sarcoma face a high burden of metastatic disease at diagnosis and high incidence of metastatic recurrence associated with increased risk of mortality.

Elon Musk Holds Surprise Talk At The World Economic Forum In Davos

The musk blueprint: navigating the supersonic tsunami to hyperabundance when exponential curves multiply: understanding the triple acceleration.

On January 22, 2026, Elon Musk sat down with BlackRock CEO Larry Fink at the World Economic Forum in Davos and delivered what may be the most important articulation of humanity’s near-term trajectory since the invention of the internet.

Not because Musk said anything fundamentally new—his companies have been demonstrating this reality for years—but because he connected the dots in a way that makes the path to hyperabundance undeniable.

[Watch Elon Musk’s full WEF interview]

This is not visionary speculation.

This is engineering analysis from someone building the physical infrastructure of abundance in real-time.

Continue reading “Elon Musk Holds Surprise Talk At The World Economic Forum In Davos” | >

Neutrophil extracellular trapping network-associated biomarkers in liver fibrosis: machine learning and experimental validation

The diagnostic and therapeutic potential of neutrophil extracellular traps (NETs) in liver fibrosis (LF) has not been fully explored. We aim to screen and verify NETs-related liver fibrosis biomarkers through machine learning.

In order to obtain NETs-related differentially expressed genes (NETs-DEGs), differential analysis and WGCNA analysis were performed on the GEO dataset (GSE84044, GSE49541) and the NETs dataset. Enrichment analysis and protein interaction analysis were used to reveal the candidate genes and potential mechanisms of NETs-related liver fibrosis. Biomarkers were screened using SVM-RFE and Boruta machine learning algorithms, followed by immune infiltration analysis. A multi-stage model of fibrosis in mice was constructed, and neutrophil infiltration, NETs accumulation and NETs-related biomarkers were characterized by immunohistochemistry, immunofluorescence, flow cytometry and qPCR. Finally, the molecular regulatory network and potential drugs of biomarkers were predicted.

A total of 166 NETs-DEGs were identified. Through enrichment analysis, these genes were mainly enriched in chemokine signaling pathway and cytokine-cytokine receptor interaction pathway. Machine learning screened CCL2 as a NETs-related liver fibrosis biomarker, involved in ribosome-related processes, cell cycle regulation and allograft rejection pathways. Immune infiltration analysis showed that there were significant differences in 22 immune cell subtypes between fibrotic samples and healthy samples, including neutrophils mainly related to NETs production. The results of in vivo experiments showed that neutrophil infiltration, NETs accumulation and CCL2 level were up-regulated during fibrosis. A total of 5 miRNAs, 2 lncRNAs, 20 function-related genes and 6 potential drugs were identified based on CCL2.

Peripheral cancer attenuates amyloid pathology in Alzheimer’s disease via cystatin-c activation of TREM2

Now online! Peripheral cancer inhibits amyloid pathology and rescues cognition of Alzheimer’s disease through secretion of cystatin-c (Cyst-C), which binds amyloid oligomers and activates TREM2 in microglia and enables microglia to degrade pre-existing plaques.

Can Aging Be Measured—and Eventually Reversed?

A former professor at the University of California, Los Angeles, Horvath is now principal investigator of the U.K. research arm of Altos Labs, a longevity biotech company that says it is developing therapies that could reverse age-related diseases and disabilities.

Having precise and meaningful ways to measure aging could make it possible for drug developers like Altos Labs to test longevity treatments in people, Horvath says: “It’s a quintessential tool to find interventions for rejuvenation.”

As part of TIME’s series interviewing longevity leaders and influencers, we spoke to Horvath about his pioneering invention and what he thinks might be possible for human life extension.

Scientists May Have Discovered a Way to Rejuvenate The Immune System

As we age, the immune system gradually declines in function, leaving the body more vulnerable to disease. Scientists have discovered a new way to rejuvenate a key component of immune function, potentially boosting health in later years.

A team from the Broad Institute of MIT and Harvard focused on the thymus, a small organ in front of the heart that’s crucial for the development of T cells. These immune cells act as guards, identifying and fighting threats such as cancer and infections.

From early adulthood, the thymus shrinks and slows, limiting T cell production. In mouse models, the researchers were able to repurpose part of the liver as a thymus substitute, sending the molecular signals that stimulate T-cell production.

Using lab-grown lung tumors as test subjects for tailored cancer therapies

Lung cancer varies widely from patient to patient, and that diversity makes it hard to find effective treatments. Researchers at the Berlin Institute of Health at Charité (BIH) have developed a method to evaluate multiple therapeutic approaches on patient-derived “tumoroids”—miniature tumors grown from tissue removed during surgery at Charité

By testing drug responses across these tumoroids, the team showed that therapeutic success depends on a complex interplay of tumor characteristics rather than a single factor. Their results suggest that tumoroid-based testing could help physicians tailor treatments to individual patients and improve clinical decision-making.

The BIH researchers have published their findings in Nature Biomedical Engineering.

A novel mechanism for cancer-associated weight loss

Combined metabolomics and transcriptomics analysis in eight different organs of tumor-bearing mice with and without cachexia allowed researchers to create metabolic signatures typical of cancer-associated weight loss. High-throughput analyses identified a cachexia-specific metabolic and genetic signature that provides insight into the progression of these metabolic changes.

The researchers found that all organs showed increased activation of the so-called “one carbon cycle”, a biochemical process essential for the synthesis of nucleotides, amino acids, and cell regeneration. Products of this cycle, such as sarcosine or dimethylglycine, could potentially serve as biomarkers for cachexia in the future.

The study also revealed that hyperactivation of the one carbon cycle in muscle is associated with increased glucose metabolism (glucose hypermetabolism) and muscle atrophy. Early experiments suggest that inhibiting this process could prevent muscle loss. Comparative analyses across eight different mouse tumor models (lung, colon, and pancreatic cancer) confirmed that the one carbon signature represents a universal cachexia signature, independent of cancer type.

Currently, there is no approved drug for cancer cachexia in Germany. New approaches are being explored to address cancer-related appetite loss. This study provides the first evidence of how metabolism itself could potentially be normalized. Early experiments in cell cultures show that interventions targeting the one carbon cycle can have positive effects. sciencenewshighlights ScienceMission.

Cachexia is a metabolic disorder that causes uncontrolled weight loss and muscle wasting in chronic diseases and cancer. A new study shows that cachexia affects more than just muscles. Numerous organs respond in a coordinated manner, ultimately contributing to muscle loss. Analysis of metabolome and transcriptome data, along with glucose tracing in tumor-bearing mouse models, identified a novel mechanism that plays a key role in cancer-associated weight loss.

A loss of 10% of body weight within six months – what may sound desirable in some contexts – often causes uncertainty and frustration in cancer patients with cachexia, as they are unable to maintain or gain body weight despite wanting to. Cachexia (from the Greek kakós, “bad,” and héxis, “condition”) affects 50–80% of all cancer patients, reduces quality of life, diminishes the effectiveness of cancer therapies, and increases mortality.

Continue reading “A novel mechanism for cancer-associated weight loss” | >

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