within the field. These results are compelling enough to justify moving towards carefully designed human studies for further validation, safety studies, and, if regulatory approvals and funding align, early-phase human clinical trials.

The study demonstrates a potential treatment in experimental models, not in people- yet. However, independent cancer researchers not involved in the study have noted that durable responses without relapse are exceptionally rare in pancreatic cancer models, making the results particularly significant

patients and grown in the laboratory. The important finding of the study was that, unlike traditional chemotherapy, which often causes severe side effects, the triple-drug combination showed low toxicity in animals. The mice tolerated the treatment well, a crucial factor if the therapy is ever to

move into human trials. Researchers did note that this is the FIRST time a complete, durable response with low toxicity has been achieved in these experimental models.

The results show that in mouse models designed to closely mimic human pancreatic cancer, tumours completely disappeared. Even more striking, they did not return for more than 200 days after treatment stopped. The same effect was seen in genetically engineered mice AND in tumours taken from HUMAN

In simpler terms, this combination therapy cut the engine, sealed the exits, and disabled the emergency backup, all at the SAME TIME.

So, why is this different?

KRAS has long been considered “untouchable.” This approach shut it down completely- at least in experimental models.

•The first drug, daraxonrasib, blocks the main KRAS growth signal.

•The second, afatinib, shuts down EGFR and HER2 pathways, which cancers often use as escape routes.

•The third, SD36, disables STAT3, an stress-response system that helps tumour cells survive treatment.

a drug already approved for lung cancer, with a protein degrader, resulting in tumours disappearing WITHOUT significant side effects in THREE DIFFERENT experimental models. Essentially, instead of hitting one target, researchers attacked the cancer from three directions at once:

In pancreatic cancer, this ability to “rewire” itself is a major reason single-drug treatments fail. The key to THIS breakthrough lies in avoiding the resistance that appears when the KRAS oncogene molecular pathway is blocked at a single point. The CNIO team combined an experimental KRAS inhibitor,

struggled to block it. Relatively new KRAS-blocking drugs, including one called daraxonrasib, have shown promise and can extend survival. But cancer finds ways to grow. When one pathway is blocked, tumours often activate alternative routes- molecular detours that let them survive and return.

cancer has remained one of oncology’s toughest challenges. At the core of most pancreatic cancers lies a faulty gene called KRAS, which constantly sends signals telling cancer cells to grow and divide. KRAS mutations are found in over 90% of pancreatic cancers. For decades, researchers have

long-lasting tumour regression. In Spain, more than 10,300 cases of this type of cancer are diagnosed each year, with a five-year survival rate of less than 10%. Standard chemotherapy often slows the disease only briefly, because tumors rapidly adapt and find new ways to grow. This is why pancreatic

tumors in experimental models and prevent them from recurring using triple combination therapy. The results, published in the journal Proceedings of the National Academy of Sciences (PNAS), show that simultaneously targeting three key points of the KRAS oncogene molecular pathway achieves

Pancreatic cancer is one of the most aggressive tumors with the worst prognosis, partly because of the rapid emergence of resistance to treatment. But a new study from the Spanish National Cancer Research Centre (CNIO), led by Dr. Mariano Barbacid, reveals that it is possible to eliminate pancreatic

Researchers managed to overcome tumors using a triple combination therapy, which also avoids the common problem of treatment resistance. Currently, drugs for pancreatic cancer lose effectiveness within months because the tumour becomes resistant.
• www.timesnownews.com/world/who-is...

The study has been published in PNAS (Proceedings of the National Academy of Sciences). YES, it is PEER-REVIEWED.
• www.pnas.org/doi/10.1073/...

NOTE: THIS IS PRECLINICAL. Results were also shown in tumors taken from HUMAN patients and grown in the laboratory.

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