Pane budiriro huru muhucheche uropi bundu kuvandudzwa mushonga. Mapundu europi evana chirwere chinouraya chinowanzoitika muvana. Tsvagiridzo ichangoburwa yakawana kuti mushonga mutsva wecocktail unogona kurapa akajairika mamota ehuropi ehudiki.
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 tumamota twakaipa of the cerebellum. This brain tumor grows rapidly and most often occurs in children around the age of 5. Kurapa nzira 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 kenza 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.
Nokubatanidza nemimwe mishonga, makemikari matsva anodzivisa mamota anoongororwa mu vitro uye mu vivo.
Clinical trials 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.
"Kana tikakwanisa kugadzira marapirwo akagadzirwa zvichibva pazvironda zvemota - zano rinowanzonzi kurapwa kwakasarudzika - izvi zvinogona kuunza vhangeri rakakura kuvarwere vane mamwe mapundu."
Kune mhando ina dzakasiyana dzeeuroblastoma, uye varwere veboka rechitatu remamota vane fungidziro yakaipisisa-chete 40% yevarwere vanorarama kwenguva refu. Mukupesana, kurarama kwenguva refu kweimwe neuroblastomas kune tariro, uye vangangoita 80% yevarwere vanogona kurarama kwenguva refu.
Mazhinji eboka rechitatu revarwere vane neuroblastoma vane kutaura kwakanyanya kweMYC oncogene, inova iyo chikonzero chekusagadzikana kwekuparadzanisa maseru uye kuumbwa kwemamota.
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 Medical Centre in Washington, DC
The most effective of these compounds is panobinostat, which has entered clinical trials in other mhando dzekenza, 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 kenza cell kupona.
“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.”
