All articles tagged with #metastasis
Research published in Nature reveals that circulating tumor cells shed migrasomes during metastasis, which deliver tumor antigens to immune cells and trigger anti-tumor responses. This process, mediated by Tspan4, paradoxically enhances tumor immunogenicity and constrains metastatic growth.
A multi-omics analysis of lethal metastatic bladder cancer from a rapid-autopsy program shows metastasis-to-metastasis seeding as the dominant spread pattern and polyclonal migration linked to worse survival. Histology-driven differences include early founder alterations in plasmacytoid and neuroendocrine variants, with cisplatin resistance in plasmacytoid tumors associated with Fanconi anaemia pathway activity. Single-nucleus RNA sequencing reveals substantial transcriptional and microenvironmental heterogeneity across subtypes, while post-mortem cfDNA captures the majority of driver alterations, offering a noninvasive readout of tumor identity and aggressiveness to guide therapy.
Lucy Davis, the UK The Office star, revealed on Instagram that a stage-four breast cancer diagnosis from a year and a half ago has metastasized to her spine, right hip, and ribs, making the disease incurable and ending chemotherapy. She says she's at peace and intends to live life to the fullest while continuing acting and animal-rights activism, despite pain and wheelchair use, and she urges others to seek medical checks for unusual symptoms.
A Nature Aging study shows fructose secreted by chemotherapy‑induced senescent ovarian cancer cells acts as a signaling molecule that reduces cell adhesion and promotes detachment and metastasis in cell cultures and mice; altering fructose metabolism blocked movement, and high-fructose intake worsened spread in animals, suggesting dietary fructose restriction and senolytic therapies could improve treatment outcomes—though findings are preclinical and not yet applicable to humans.
Sildenafil (Viagra) appears to disrupt cholesterol trafficking in cancer cells, limiting their ability to spread in mouse models of breast, lung, and colon cancer, while a retrospective analysis of health records from over 40,000 male cancer patients linked combined sildenafil and statin use to about a 31% lower five-year mortality versus neither drug. The results are observational and require clinical trials to confirm causality.
A Weizmann Institute study suggests sildenafil (Viagra’s active ingredient) may slow cancer metastasis by disrupting how cancer cells use cholesterol, potentially reducing the spread to distant tumors. The work combines human data, cell and mouse experiments, and suggests that pairing PDE5 inhibitors with statins could help limit tumor spread, but the human evidence is observational and does not prove causation; more research is needed before clinical application.
Researchers at The Wistar Institute found that fructose released by treatment-surviving ovarian cancer cells acts as a signal that weakens cell–cell adhesion and promotes detachment and spread. The effect can occur even without chemotherapy, and higher dietary fructose may influence tumor behavior, with cholesterol-lowering statins also weakening cancer cell adhesion. The study, published in Nature Aging, raises the possibility that this mechanism could occur in other torso-spreading cancers, though clinical studies are needed.
A study identifies the RNA-binding protein ZFP36L2 as a stress-responsive switch that binds AU-rich 3′ UTRs in stress-related mRNAs, drives condensate formation and targeted degradation to terminate the stress response, and enables dedifferentiation into LGR5+ intestinal stem cells necessary for regeneration and canonical metastasis. In ZFP36L2-deficient colorectal cancer, canonical metastasis seeding is impaired but non-canonical, heterogeneous cell states emerge, linking ZFP36L2 to cancer plasticity and patient outcomes.
New research suggests sildenafil (Viagra) may slow cancer metastasis by disrupting cholesterol transport inside cancer cells, effectively starving tumors of a key resource. The findings—spanning mouse models, patient-derived cancer cells, and large health records—also point to better survival when sildenafil is used with statins, highlighting the influence of a patient’s metabolic state on cancer progression.
Researchers at The Wistar Institute report that fructose released by chemotherapy-surviving ovarian cancer cells acts as a signal to neighboring tumor cells, promoting detachment and metastatic spread. In preclinical tests, high dietary fructose could enhance cancer spread by lowering cholesterol production in nearby cells, weakening cell adhesion; the finding also suggests interactions with cholesterol-lowering drugs (statins). While intriguing, these effects have not been tested in patients, and researchers caution against changing medications yet. More studies are planned to see if this pathway affects other cancers and whether diet or statin use could influence outcomes.
A new study suggests fructose, a common sugar in fizzy drinks, can act as a signal for surviving cancer cells after chemotherapy, helping them spread by suppressing cholesterol in neighboring cells and reducing adhesion; higher fructose intake may promote cancer spread even without chemo.
A study led by the Weizmann Institute of Science suggests sildenafil (Viagra) may prevent cancer cells from spreading by causing cholesterol to accumulate in recycling compartments, depriving tumors of cholesterol needed for invasion; while promising, clinical trials are needed to confirm it can reduce metastasis in patients.
Researchers at Umeå University and collaborators developed a fully human antibody that stopped growth and metastatic spread of an aggressive prostate cancer in preclinical tests, via a newly identified mechanism that may carry a lower risk of side effects. While promising, the therapy requires further safety studies and regulatory approval before clinical use, and researchers plan to explore its potential against other solid tumors.
Researchers at Florida A&M University tested polyisoprenylated cysteinyl amide inhibitors (PCAIs) against pancreatic cancer cells to disrupt mutant KRAS signaling. The leading compound NSL-YHJ-2-27 blocked more than 90% of cell migration at low concentrations, altered gene and protein markers related to movement, disrupted actin filaments, and dismantled 3D mini-tumor models; however, these findings are limited to lab studies and require animal testing and safety assessment before any human trials.
Real-world TriNetX data presented at ASCO 2026 show GLP-1 receptor agonists used after cancer diagnosis linked to reduced metastatic progression across several obesity-related cancers, notably NSCLC, breast, colorectal, and hepatocellular carcinoma; in NSCLC, progression to stage IV was 10.0% with GLP-1 RAs vs 22.3% with DPP-4 inhibitors (HR 0.50). GLP-1 receptor expression also correlated with better overall survival, suggesting a potential class effect and the need for further study.