Men who have advanced prostate cancer are prescribed Enzalutamide alone or with hormone therapy to block the effects of testosterone on the cancer cells. The normal dosage is 160mg per day, i.e., 4 Enzalutamide 40 mg tablets. Â
A medical study was conducted to determine the genomic changes that occur upon Enzalutamide treatment. The whole-genome sequencing and RNA sequencing are analyzed to measure the changes. The primary purpose was to determine the character of the molecular mechanism that would be involved with acquiring Enzalutamide resistance.Â
Tumor biopsy samples from 101 men who were diagnosed with metastatic castration-resistant prostate cancer and had not received prior treatment with Enzalutamide or have a condition that is Enzalutamide resistant have been analyzed to derive the results. Among them, 99 tumors had undergone RNA sequencing to identify the gene mutations as well as copy number alterations.Â
ResultsÂ
It had been found out that the increase in Enzalutamide resistant tumors was lesser common compared to the copy number loss. That is why 124 protein-coding genes were identified, which are more likely to get lost within the Enzalutamide resistant samples. The focal deletion of 17q22 locus that includes RNF43 and SRSF1 has been found in 16% of the patients who had metastatic castration-resistant prostate cancer. However, it was not present in patients with the condition of Enzalutamide-resistant metastatic castration-resistant prostate cancer. The loss of 17q22 was associated with lower RNF43 and SRSF1 expression, as well as a feeble overall survival rate from the time of biopsy.Â
Conclusion
At last, it was determined that the loss of 17q22 was linked with the activation of multiple targetable factors that ultimately was successful in demonstrating the potential therapeutic relevance that the loss of 17q22 has in metastatic castration-resistant prostate cancer. Therefore, it is safe to conclude that the copy number loss is more commonly noticed in Enzalutamide-resistant tumors.Â