Akwai babban nasara a ci gaban ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar yara. Ciwan ƙwaƙwalwar yara ya zama cuta mafi haɗari ga yara. Binciken da aka yi kwanan nan ya gano cewa sabon magani na hadaddiyar giyar na iya magance cututtukan ƙwaƙwalwar yara na yau da kullun.
Cancer Cell” magazine recently announced that in the UK, about 400 children develop brain ciwan kansa 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 m ciwace -ciwacen daji of the cerebellum. This ƙwaƙwalwar ƙwayar cuta grows rapidly and most often occurs in children around the age of 5. Jiyya zažužžukan 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 ciwon daji 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.
Ta hanyar haɗawa tare da wasu magunguna, ana yin sabbin mahadi waɗanda ke hana ciwace ciwace a cikin injin da ingin.
Gwajin gwaji 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.
"Idan za mu iya inganta ci gaba da keɓaɓɓun jiyya dangane da ƙwayoyin cuta na ƙwayoyin cuta - dabarun da aka fi sani da magani na mutum - wannan na iya kawo babbar bishara ga marasa lafiya da wasu ciwace-ciwacen."
Akwai nau'ikan nau'ikan neuroblastoma guda huɗu, kuma marasa lafiya tare da rukuni na uku na ciwace-ciwacen daji suna da mummunan hangen nesa-kashi 40% ne kawai na marasa lafiya ke rayuwa na dogon lokaci. Sabanin haka, rayuwar sauran neuroblastomas na da kyakkyawan fata, kuma kusan kashi 80% na marasa lafiya na iya rayuwa na dogon lokaci.
Yawancin rukuni na uku na marasa lafiya tare da neuroblastoma suna da babban bayyanar MYC oncogene, wanda shine sanadin rabewar kwayar halitta da ba za'a iya shawo kanta ba da samuwar kumburi.
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 Cibiyar Kiwon lafiya a Washington, DC
The most effective of these compounds is panobinostat, which has entered clinical trials in other nau'ikan cutar kansa, 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 ciwon daji tsira.
“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.”
