Cell Death Dis: Drug CBL0137 Effectively Inhibits MYC Amplified Type 3 Myeloma (MYCamp-G3-MB)

Myeloma (MB) as the most common malignant childhood brain tumor, it can be divided into WNT, SHH, Group3, Group4 four major molecular subgroups.
type 3 MB (MYCamp-G3-MB) with MYC amplification has been shown to be extremely invasive and has the worst prognosm.
, there is an urgent need for new and effective treatments for the subsope.
recent studies have shown that a number of oscic genetically targeted treatment strategies can effectively treat preclinical models of MYCamp-G3-MB, including the inhibition of BET, hdAC and SETD8, which also provides a promising direction for further research into the disease.
in this study, the researchers performed a systematic bio-informational analysis of the published MB data set and the main MYCamp-G3-MB functional genomic screening dataset to look for other potential therapeutic targets associated with ostogenesic genetic regulation.
Comprehensive Screening identified SSRP1 as a preferred drug candidate and prognostic marker researchers identified SSRP1 (hismoprotein-molecular partner FACT complex sub-base) as the preferred drug target, which is highly dependent on cancer in genome-wide CRISPR-Cas9 screening across multiple MYCamp-G3-MB systems.
the expression level of the gene in MYCamp-G3-MB increased significantly compared to the normal cer cerebrocephaly and most of the remaining subsypes of MB;
researchers have further discovered that it has a target drug that penetrates the blood-brain barrier and has conducted relevant early clinical trials.
researchers used RNA interference to verify the cancer dependence of SSRP1 in multiple MYCamp-G3-MB cell line and further confirmed the efficacy of the target ACT drug curaxin CBL0137 for the treatment of MYCamp-G3-MB preclinical models.
in the intracranial intestoma model, CBL0137 was able to effectively inhibit the growth transcription group analysis of MYCamp-G3-MB, showing that CBL0137 was able to suppress the biological processes associated with cell cycles and DNA repair as a priority.
addition, it can selectively destroy transcription of two key carcinogenic transcription factors, MYC and NEUROD1, in MYCamp-G3-MB by consuming factual compounds from the promoter region.
all, the results show that the drug CBL0137 for FACT is effective in treating MYCamp-G3-MB and provides another potential treatment strategy for the most destructive MB.
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