前列腺癌 z-bo 2020-10-28 434

　　According to a new study published on Oncogene, the compound Temoquinone (TQ) selectively kills prostate cancer cells in late life. The research led by researchers at Kanazawa University reported that prostate cancer cells lacking the SUCLA2 gene can be used as therapeutic targets. Prostate cancer lacking SUCLA2 accounts for the majority of hormone therapy or metastatic resistance, so new treatment options for this disease will bring huge benefits to patients.

　　Hormone therapy is usually chosen to treat metastatic prostate cancer, but nearly half of patients resist it in just two years. B1 is a tumor suppressor gene that controls cell proliferation, one of which is considered to be a particularly powerful driving force for treatment resistance and can be used to predict adverse prognostic reactions in patients. .. Lead author Susumu Kono said: "Mutations in tumor suppressor genes are sufficient to induce the development and malignant progression of prostate cancer, but so far, these have been used to treat prostate cancer. Mutations cannot be directly targeted. And tumor suppressor genes and treatments Initiation related genetic abnormalities."

　　In the genome, SUCLA2 is flanked by RB1, and analysis of prostate cancer cells shows that cells with RB1 deficiency also lack SUCLA2, which matches the RB1 and SUCLA2 deficiency in advanced prostate cancer. Kono et al. analyzed prostate cancer tissue and found that both SUCLA2 and RB1 were lacking in 11% of cases. The researchers screened the compound library to identify drugs that can selectively kill SUCLA2-depleted cells. Among approximately 2,000 compounds, TQ has become a popular candidate compound. TQ is known to have anti-cancer effects and has been proven safe in phase I clinical trials. Kono et al. applied TQ therapy to a mouse model of SUCLA2-deficient prostate cancer to selectively inhibit tumor growth.

　　'S senior writer Chiaki Takahashi said as follows. "These findings suggest that TQ therapy may be an effective treatment for SUCLA2-deficient prostate cancer cells."

　　searched the genetic database of prostate cancer patients. The researchers found the following: At each stage of the disease, the frequency of SUCLA2 deletion is roughly the same as the frequency of RB1. In short, removing SUCLA2 can identify prostate cancer patients who need further treatment.

　　The discovery of the vulnerability of targeting drugs has opened a new door for the treatment of prostate cancer. More work is needed to improve the efficacy of TQ and identify patients who can benefit from such treatments, but this compound is expected to provide new treatment options for advanced prostate cancer.