I Agree

"The most common gene mutations that cause prostate cancer are: AR, 62.7%; ETS family, 56.7%; TP53, 53.3%; and PTEN, 40.7%." Shen Qi drafted a preliminary gene therapy plan for Han Meng.

According to the results of his genetic testing, Han Meng was most likely to die of prostate cancer.

So they would start by treating the genes associated with prostate cancer.

The first step in the plan was to lay out the disease mechanisms of prostate cancer at the genetic level.

"Additionally, BRCA2 mutations have been found in 13% of patients with advanced prostate cancer." Cui Hualin assisted Shen Qi with this work.

"Among mutations unrelated to the androgen receptor, the PI3K signaling pathway accounts for 49%, the DNA repair system for 19%, cyclin-dependent kinases, or CDKs, for 7%, BRAF for 3%, and the WNT signaling pathway for 5%." Like everyone else, Du Yuan took an evidence-based approach, grounding every experimental design in data that had been confirmed or could be predicted.

"I'm pretty familiar with the next part we're analyzing. Heterozygous loss of the PTEN gene lowers PTEN protein expression, destabilizes the genome, and induces high-grade prostatic intraepithelial neoplasia. Yes, that's right." Tang Yaxing continued.

Wu Junqiang added, "When the genome is unstable, chromosomes are prone to rearrangements and recombination. For example, the TMPRSS2-ERG gene fusion promotes the development of prostate cancer. When the PTEN gene is homozygously deleted, the downstream molecule AKT becomes continuously activated, inducing the invasion and metastasis of prostate cancer... Hey, guys, this was the subject of my master's thesis. Back then, I asked my advisor: Since we've figured out the genetic mechanisms behind thousands of diseases, including cancer, why don't we widely apply gene therapy in clinical practice? There are risks in modifying genes, sure, but someone who undergoes treatment might live another twenty