Það er mikil bylting í þróun heilaæxlislyfja í æsku. Heilaæxli barna eru algengari illkynja sjúkdómur hjá börnum. Nýlegar rannsóknir hafa leitt í ljós að nýtt kokteillyf getur meðhöndlað algeng heilaæxli í æsku.
Cancer Cell” magazine recently announced that in the UK, about 400 children develop brain æxli á hverju ári, þar af er algengi drengja aðeins hærra en stúlkna.
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 illkynja æxli of the cerebellum. This heilaæxli grows rapidly and most often occurs in children around the age of 5. Meðferðarmöguleikar 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 lifa af, samanborið við önnur æxli af minna alvarlegri gerð - með lifunarhlutfall sem er meira en 80%.
Vísindamenn í Bandaríkjunum hafa uppgötvað nýja samsetta meðferð til að meðhöndla mjög árásargjarn taugaæxli. In laboratory tests, the drug killed krabbamein 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.
Með því að sameina önnur lyf eru ný efnasambönd sem hindra æxli skimuð in vitro og in vivo.
Klínískar rannsóknir 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.
„Ef við getum þróað sérsniðnar meðferðir byggðar á æxlisgenum - stefnu sem almennt er kölluð einstaklingsbundin meðferð - þá gæti þetta fært mikið fagnaðarerindi fyrir sjúklinga með ákveðin æxli.“
Það eru fjórar mismunandi gerðir af taugaæxli og sjúklingar með þriðja hóp æxla eru með verstu horfurnar - aðeins 40% sjúklinga lifa langtíma. Aftur á móti er langtíma lifun annarra taugaæxla tiltölulega bjartsýnn og um 80% sjúklinga geta lifað til lengri tíma.
Flestir í þriðja hópi sjúklinga með taugaæxli hafa mikla tjáningu á MYC krabbameini, sem er orsök óviðráðanlegra frumuskiptinga og myndun æxla.
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 Center í Washington, DC
The most effective of these compounds is panobinostat, which has entered clinical trials in other tegundir krabbameins, 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 Krabbamein Cell lifun.
“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.”
