Women with unusually enlarged breast tissue may face a higher likelihood of several health problems, including chronic migraine, neck pain and sleep apnea, according to new research. The condition, medically known as macromastia, is often discussed in terms of discomfort or appearance. However, researchers from Wake Forest University School of Medicine say it may be […]

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Plus de 400 000 jeunes Européens, six décennies de mesures, quatre indicateurs suivis. Le déclin de la condition physique n'est uniforme ni dans le temps ni selon les capacités : l'endurance s'est stabilisée depuis 2015, quand la souplesse recule de plus en plus vite depuis 2000.

En quelques années, l’ARN messager est passé du statut de technologie expérimentale à celui d’outil capable de répondre à une pandémie. Rapide à adapter et presque « programmable », il pourrait désormais ouvrir la voie à des vaccins conçus sur mesure contre certains cancers.

A million-person study points to repeated heat injury in the oesophagus.

A federal judge on Tuesday said more than 20 defendants including 3M, DuPont, and Honeywell must face claims by Connecticut firefighters who said their protective gear was contaminated by toxic "forever chemicals" that increased their risk of cancer.

More than 50 years after oil drilling was carried out, Kenya's Kargi community is suing BP, alleging contaminated water contributed to cancers and livestock deaths.

The Diamond Alkali Superfund site covers a sprawling swath of North Jersey, including parts of Newark Bay and the lower Passaic River.

He developed a program that became a model for hospitals around the world, making it easier for poor Black patients to navigate an onerous bureaucratic system.

Opposing teams of attorneys spent hours on Monday battling over a proposed $7.25 billion settlement of the U.S. Roundup cancer litigation that, if approved, would allow Bayer to keep selling its controversial glyphosate weed killers while providing roughly $10,000 to $165,000 for individuals suffering from cancer they blame on Roundup use.

Les radicaux libres ont mauvaise réputation. Ils endommagent l’ADN et sont associés au vieillissement et au cancer. Mais une découverte surprenante vient bousculer cette vision : certaines cellules immunitaires ont besoin de ces molécules pour s’attaquer aux tumeurs, qui ont justement trouvé le...

UCLA scientists engineered ready-made T cells from cord blood stem cells that can hunt solid tumors even when cancer cells hide their main target. T cell receptor therapy, commonly called TCR therapy, is a form of cancer treatment that genetically modifies immune cells known as T cells so they can recognize and attack cancer more [...]

Un médicament cardiaque vieux de 100 ans, dérivé de la digitale, pourrait bouleverser le traitement du cancer. Des chercheurs suisses ont découvert que la digoxine peut dissoudre les amas de cellules cancéreuses en circulation, limitant potentiellement leur propagation dans l'organisme. Cette...

La mort cellulaire programmée joue un rôle essentiel dans le renouvellement et le bon fonctionnement de nos tissus. Mais lorsque ce mécanisme se dérègle, certaines cellules échappent à la mort, se multiplient de façon incontrôlée et peuvent favoriser l’apparition de cancers. Décryptage.

I discuss age-related BPH and prostate cancer screenings, highlighting the unreliability of PSA tests. Having BPH does not increase prostate cancer risk. No advantage is gained from prostate cancer treatment. And there are recent studies linking COVID-19 vaccines to increased cancer risks, particularly prostate cancer.

The myriad horrors of the US healthcare system have spawned generations of medical tourism from the wealthiest country on Earth to the periphery: Cuba, Mexico, Costa Rica, Canada, Turkey, and Thailand, to name just a few.

Now, Shanghai is quickly rising as one of the top destinations for cancer patients, as China’s biotech sector has spun an experimental treatment developed in the US into a standalone industry.

New reporting by the Wall Street Journal took a look at this fast-growth industry, centered around chimeric antigen receptor T-cell therapy, or CAR-T for short.

CAR-T is essentially a personalized form of immunotherapy, in which a patient’s own white blood cells are engineered to identify and attack specific proteins found in cancer cells. Though the process was first developed by US biotech giants, their inability — or unwillingness — to lower the cost and increase supply of the treatment has led to shortages throughout the country.

That’s where China comes in. As director of the CAR-T program at the University of Texas MD Anderson Cancer Center in Houston Sairah Ahmed told the WSJ, this therapy can cost around $150,000 to $230,000 in China — still a life-altering bill, but a sizeable discount compared to an insurmountable $550,000 to $850,000 in the US.

This, Ahmed says, is why she advises some patients to seek out treatment in the People’s Republic.

“China has basically done to CAR-T cell therapy the same thing that it’s done to other industries, which is, they’ve industrialized it,” Ahmed explained.

China’s CAR-T services aren’t just cheaper, either. They’re also faster, and come with a host of complimentary after-care treatments, the WSJ notes. As MD Anderson Cancer Center’s explainer on CAR-T therapy advises, the process of extracting and bio-engineering a patient’s cells to fight cancer can take over three weeks in the US. Compare that to China, where the WSJ reports labs near Shanghai can “crank out” the therapy in just a matter of days.

An important caveat here is that CAR-T cell therapy isn’t a catch-all for every type of cancer, and it’s typically only administered after other treatments have failed. It’s not exactly a walk in the park, either, requiring months of recovery and check-ups from a range of physical, neurological, and psychological health specialists. Still, if you had to go through with it, your first step should clearly be pricing out some flights to China.

More on healthcare: Bougie Health Startups Offering Full-Body Diagnostic Scans for Rich People While the Rest of Us Suffer a Crumbling Healthcare System

The post America’s Health Care System Is So Screwed That Patients Are Flying to China for Cancer Treatment appeared first on Futurism.

A new study presents alarming findings linking mRNA COVID-19 vaccines to aggressive heart tumors, as plasmid DNA fragments from the vaccine were found in a 35-year-old patient’s cardiac tumor developed shortly after vaccination. This evidence prompts calls for the immediate removal of mRNA technology from global markets, challenging prior dismissals of "turbo cancer."

A mammogram does more than search for suspicious lumps. It can also show whether a woman’s breasts contain a large amount of dense tissue, a feature that has long been associated with a higher chance of developing breast cancer. For many years, breast density was especially important because it could hide small tumors on mammograms. […]

The post Dense Breasts May Create a Hidden Cancer-Friendly Environment appeared first on Knowridge Science Report.

North Carolina has secured $455 million in payments from Chemours, DuPont and Corteva over PFAS pollution, along with a separate $135 million reserve intended to protect future drinking water and cleanup work.

For more than four decades, pathologists have glimpsed something unsettling under the microscope in the earliest stages of certain cancers: cells with nuclei far larger than they should be, swollen and distorted, lurking in tissue that otherwise appears on the verge of catastrophe. These so-called giant-nucleus cells, or karyomegalic cells, were first spotted in the 1980s in animal experiments involving iron-induced oxidative stress, yet their biological identity and their role in the genesis of cancer remained stubbornly obscure. Now, a team of researchers in Japan has provided the most detailed portrait of these cells to date, and their findings suggest that the enormous nuclei may be far more than a curiosity—they could be the founding population of early cancer, visible before any tumor exists, and potentially useful as a predictor of patient outcomes.

The study, led by Shinya Toyokuni, professor emeritus at Nagoya University Graduate School of Medicine, together with assistant professor Yingyi Kong and colleagues, was published in Redox Biology. The work addresses a deceptively simple question: when iron overload kills most cells in a tissue through oxidative damage, who survives, and what do the survivors become? Iron is an essential micronutrient, but in excess it is a potent carcinogen. Its chemistry is both the reason we need it and the reason it can harm us. Iron catalyzes the formation of hydroxyl radicals from hydrogen peroxide through the Fenton reaction, and these radicals shred DNA, oxidize lipids, and damage proteins. When the damage is severe enough, a form of programmed cell death called ferroptosis is triggered—an iron-dependent demise characterized by lipid peroxidation cascades that rupture the cell membrane. Ferroptosis has become one of the hottest topics in cancer biology precisely because it links iron metabolism, oxidative stress, and cell fate in a single mechanism.

Toyokuni’s team reasoned that if ferroptosis sweeps through iron-damaged tissue, the cells that escape it must be exceptional in some way, and those exceptions might be the seed of malignancy. To find out, they turned to a well-established animal model in which ferric nitrilotriacetate, a carcinogenic iron compound, is injected into rats, delivering a bolus of iron to the kidneys. The compound accumulates in the proximal tubules, where it catalyzes oxidative damage and, over months, produces renal cell carcinoma. In the experiments, the researchers collected kidney tissue before the injection and again one and three weeks afterward. Crucially, they also included a second experimental group: rats carrying a single mutated copy of the BRCA1 gene, the same gene that, when mutated in humans, dramatically raises the risk of breast and ovarian cancers and is associated with renal carcinoma in certain contexts.

The methodological heart of the study lies in its marriage of two technologies. The first is spatial transcriptomics, a technique that maps gene activity across individual cells within a tissue section while preserving the tissue’s original architecture—so researchers can see not only which genes are active but where in the tissue those transcriptional programs are operating. The second is computational nuclear morphometry, which quantifies the size, shape, and density of cell nuclei in the same samples. By overlaying the two datasets, the team could link the physical appearance of each cell—above all, the size of its nucleus—to its underlying transcriptional state. This integration is important because morphological atypia has long been the currency of diagnostic pathology, but connecting that atypia to molecular signatures at single-cell resolution is a recent capability.

What emerged within a week of iron administration was striking. Giant-nucleus cells appeared in the damaged kidneys, and these cells were not simply wounded cells awaiting death. They showed elevated expression of potent oncogenes, including Myc and Met, and they had acquired resistance to ferroptosis—the very cell death pathway that was eliminating their neighbors. In other words, the extreme oxidative environment had functioned as a brutal selective pressure, and the cells best adapted to survive it had activated a program that resembles, in miniature, the hallmark machinery of cancer. The enrichment of Myc, a transcription factor that drives cell growth and proliferation, and Met, a receptor tyrosine kinase involved in invasive growth, paints a picture of cells that are not merely enduring damage but reorganizing themselves around it.

The BRCA1 connection proved equally consequential. BRCA1 is best known as a guardian of the genome, a scaffold for the homologous recombination machinery that repairs double-strand DNA breaks. In the BRCA1-mutant rats, giant-nucleus cells emerged with distinctly different biological profiles from those in wild-type animals. The interpretation the researchers offer is that BRCA1 deficiency cripples DNA repair, so more of the damaged cells that would otherwise die or be repaired instead survive in their injured, genome-compromised state—becoming precancerous giant-nucleus cells. Electron microscopy and cellular respiration measurements reinforced this idea at the subcellular level: cells from BRCA1-mutant rats showed mitochondrial remodeling, with impaired iron handling and compromised respiratory function. Mitochondria, long appreciated as power plants, are also central regulators of ferroptosis and iron metabolism, and their disarray in the mutant animals may be both a consequence of BRCA1 loss and a driver of the abnormal iron biology that feeds karyomegaly.

Using their combined gene-expression and nuclear-shape data, the researchers went further and classified the giant-nucleus cells into six distinct types. One type possessed extremely large nuclei and gene signatures of stress-induced growth arrest—cells that appear to have locked themselves into a senescent-like state, consistent with profiles reported in earlier studies. Another type, found more frequently in BRCA1-mutant kidneys, showed heightened activity of cancer-related genes alongside elongated nuclei, a combination the authors interpret as a potential precancerous state. The taxonomy matters because it reframes giant-nucleus cells from a single enigmatic category into a spectrum, some members of which may be harmless or even protective while others carry genuine malignant potential.

One of the most provocative findings concerns the cells surrounding the giants. Even morphologically normal cells near giant-nucleus cells exhibited gene expression changes that appear to promote survival, suggesting that the karyomegalic cells remodel their local microenvironment in ways that extend beyond their own borders. In BRCA1-mutant kidneys, the team also documented a substantial increase in stromal cells—non-cancerous supportive cells including immune and connective tissue elements—around the damaged regions. The local tissue environment, the tumor niche in the language of modern oncology, was being reshaped long before any tumor could be called a tumor. This raises the possibility that a single conspicuous cell, easily identified by its nucleus under a conventional microscope, could serve as a sentinel for a whole neighborhood of incipient malignancy.

The leap from rat kidneys to human medicine came through two complementary analyses. First, the researchers mined TCGA-KIRC, a large public database of kidney cancer patients, asking whether tumors carrying gene-expression patterns resembling the cancer-prone giant-nucleus cells were associated with different clinical trajectories. They were: patients whose tumors shared the gene patterns of the cancer-prone giant-nucleus cells had shorter survival times, while those with patterns resembling the healthier giant-nucleus cell types had better outcomes. Not all giant-nucleus cells, in other words, are created equal, and the transcriptional fingerprints defined in the rat model appear to carry prognostic weight in human disease. Second, in a small pilot study, the team examined breast tissue from seven individuals with inherited BRCA1 mutations and fifteen without, observing abnormal nuclear features similar to those in the animal model in the mutation carriers. While the sample size is modest, the parallel hints that karyomegaly may be a cross-tissue marker of BRCA1-linked precancerous change.

The broader implications run in two directions. Clinically, the promise is that giant-nucleus cells, being easy to spot under the microscope, could function as early indicators of cancer—visible warnings in tissue that would otherwise be classified as merely damaged or inflamed. The TCGA survival data suggest that their gene-expression signatures might even stratify patients by risk once a tumor has formed. Scientifically, the study offers a concrete mechanism connecting an environmental exposome factor—iron-catalyzed oxidative stress—to a defined, transcriptionally characterized precancerous population, with ferroptosis resistance as the pivot. It also implies testable therapeutic hypotheses: if blocking mitochondrial remodeling or reversing ferroptosis resistance could prevent the persistence of the precancerous cells, early intervention might stop cancer before it starts. Toyokuni and his colleagues are careful to note that long-term studies will be needed to determine how giant-nucleus cells actually progress into tumor cells, whether such interventions can work, and whether nuclear shape combined with gene patterns can be validated as a diagnostic in larger patient cohorts. But the central message is already legible: some of the earliest chapters of cancer may be written in cells that have grown too large to be ignored.