Terobosan di ubar tumor otak budak leutik

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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Aya narabas badag dina ngembangkeun ubar tumor otak budak leutik. Tumor otak murangkalih mangrupikeun panyakit ganas anu langkung umum di barudak. Panaliti anyar mendakan yén ubar cocktail énggal tiasa ngubaran tumor otak budak leutik anu umum.

Cancer Cell” magazine recently announced that in the UK, about 400 children develop brain tumor 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 tumor ganas of the cerebellum. This tumor uteuk grows rapidly and most often occurs in children around the age of 5. pilihan perlakuan 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 medulloblastoma 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 neuroblastoma. In laboratory tests, the drug killed kangker 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.

Ku ngagabungkeun sareng ubar sanésna, sanyawa anyar anu ngahambat tumor diayak dina vitro sareng vivo.

percobaan klinis 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.

"Upami urang tiasa ngembangkeun pangobatan anu didasarkeun dumasar kana tumor gen-strategi anu biasa disebut perlakuan individual-ieu tiasa nyayogikeun Injil anu ageung pikeun penderita tumor anu tangtu."

Aya opat jinis neuroblastoma anu bénten-bénten, sareng pasién sareng gugus tumor katilu ngagaduhan ramalan parah-ngan 40% pasién anu salamet jangka panjang. Kontras, salamet jangka panjang neuroblastomas sanés kawilang optimis, sareng sakitar 80% pasién tiasa salamet jangka panjang.

Kaseueuran kelompok katilu pasién sareng neuroblastoma gaduh éksprési tinggi oncogene MYC, anu mangrupikeun panyabab pembagian sél teu kabendung sareng pembentukan tumor.

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 médis Center di Washington, DC

The most effective of these compounds is panobinostat, which has entered clinical trials in other jinis kanker, 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 sél kanker kasalametan.

“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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