Proboj u lijekovima za tumore mozga u djetinjstvu

Breakthrough In Childhood Brain Tumor Drugs
Recent breakthroughs in childhood brain tumor drugs promise improved outcomes. Innovative therapies target specific genetic mutations, minimizing side effects and enhancing efficacy. Clinical trials show promising results, offering hope for children facing these challenging diagnoses. These advancements mark a significant step forward in pediatric oncology, driving optimism for better treatment options.

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Došlo je do velikog pomaka u razvoju lijekova za dječji tumor mozga. Dječji tumori mozga češća su maligna bolest u djece. Nedavno istraživanje pokazalo je da novi koktel lijek može liječiti uobičajene tumore mozga u djetinjstvu.

Cancer Cell” magazine recently announced that in the UK, about 400 children develop brain tumori each year, of which the prevalence of boys is slightly higher than that of girls.

Are we able to take advantage of the results of tumor gene testing and tailor-made treatments, a strategy often referred to as personalized medicine? This treatment strategy can produce very good results for patients with brain tumors.

Neural myeloblastoma (medulloblastoma) is one of the most common maligni tumori of the cerebellum. This tumor na mozgu grows rapidly and most often occurs in children around the age of 5. Mogućnosti liječenja include surgery, radiation, and chemotherapy. Although great progress has been made in treatment methods and techniques, the success rate of treating myeloblastoma still lags far behind other children’s malignancies. In particular, myeloblastoma is a highly aggressive malignancy. Only 40% of patients with meduloblastoma survive, compared with other tumors of a less severe type-with a survival rate of more than 80%.

Researchers in the United States have discovered a new combination therapy for the treatment of highly aggressive neuroblastom. In laboratory tests, the drug killed Raka cells without any toxicity to normal cells, and researchers hope to conduct clinical trials of the drug. Robert Wechsler-Reya, an adjunct professor at the Sanford Burnham Prebys Medical Institute, said: “Our goal is to confirm that the drug has low toxicity properties. Because doctors and patients in this case urgently require new clinical treatment options, we will soon apply the drug from the laboratory to clinical treatment.

Kombinacijom s drugim lijekovima, novi spojevi koji inhibiraju tumore pregledavaju se in vitro i in vivo.

Klinička ispitivanja for neuroblastoma are often very challenging because of the limited number of patients. In addition, coupled with the variability of the disease, most treatments are only effective for one subtype of patient. Understanding which patients will respond to this treatment is one of the main goals of the trial.

"Ako uspijemo razviti terapije po mjeri na temelju tumorskih gena - strategiju koja se obično naziva individualiziranim tretmanom - to bi moglo donijeti ogromno evanđelje pacijentima s određenim tumorima."

Postoje četiri različite vrste neuroblastoma, a bolesnici s trećom skupinom tumora imaju najgoru prognozu - samo 40% pacijenata preživi dugoročno. Suprotno tome, dugoročno preživljavanje ostalih neuroblastoma relativno je optimistično i oko 80% pacijenata može dugoročno preživjeti.

Većina treće skupine bolesnika s neuroblastomom ima visoku ekspresiju MYC onkogena, što je uzrok nekontrolirane diobe stanica i stvaranja tumora.

There was a study on mice with a third type of neural tube cell tumors that showed histone deacetylase inhibitors (HDACIs) and phosphatidylinositol 3-kinase inhibitors (PI3KIs) might stop mice and people from making neurotubular glioblastomas without doing too much damage to normal cells.

We found several histone deacetylase inhibitors that can kill MYC oncogene-activated neural tube cell tumors without harming normal cell agents (HDACIs),” said Pei Yanxin, an assistant professor at the National Children’s Medicinski centar u Washingtonu, DC

The most effective of these compounds is panobinostat, which has entered clinical trials in other vrste raka, but has not yet been tested on neuroblastoma.” Dr. Kun-Wei, a postdoctoral researcher at Stanford University, added: “Several other studies have revealed that the mechanism of action of panobinostat is to promote the activation of the FOXO1 gene that can interfere with the oncogenes of MYC.

Phosphatidylinositol 3-kinase inhibitors (PI3KIs) are also thought to have the effect of activating the FOXO1 gene. We hypothesized that panobinostat and phosphatidylinositol 3-kinase inhibitors (PI3KIs) could work together to block stanica raka opstanak.

“It is true that the combined treatment of these two drugs can significantly increase the survival of patients with tumors carrying the MYC gene compared to using a single drug alone.”

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