oncolytic viral gene editing
Strategies for oncolytic viral gene editing
To further enhance the therapeutic efficacy and minimize potential adverse impacts, the functional optimization and attenuation of immunogenicity or toxicity of oncolytic viruses have emerged as pivotal research foci. A proven strategy entails the genetic engineering of oncolytic viruses targeting specific genes.
TP53: TP53 gene mutations or deletions are prevalent in diverse genitourinary tumors, including renal cell carcinoma and bladder cancer. Gene therapy that fixes or adds the normal TP53 gene can bring back its role in stopping tumors. This approach can trigger the programmed death of tumor cells and also prevent tumor cells from growing and multiplying.
RB: Mutations or deletions in the RB gene disrupt cell-cycle regulation, predisposing to abnormal tumor cell proliferation. In genitourinary tumors like prostate cancer, RB gene abnormalities are prevalent. Editing the RB gene or promoting its overexpression can restore normal cell-cycle control and impede tumor cell growth.
PSA: The prostate-specific antigen (PSA) gene is specifically expressed in prostate cancer cells. Engineering a PSA/hTERT-driven oncolytic virus can downregulate the expression of CD24, CD44, and PSCA in cancer cells and tissues, decrease cancer tissue weight, inhibit angiogenesis within cancer tissues, and modulate the immune response in tumor tissues.
HER2: Human epidermal growth factor receptor-2 (HER-2) is overexpressed in certain urogenital tumors, like bladder cancer. The HER2 gene is a good target for gene therapy. Stopping the HER2 gene from working or blocking the way it sends signals can slow down the growth and stop the spread of tumor cells. It also can help the immune system better identify and kill tumor cells.
IL12: IL-12 promotes the proliferation and activation of T cells, NK cells, and other immune cells. Engineering an oncolytic virus to express the IL12 can enhance the body's anti-tumor immune response. By infecting tumor cells, it improves the ability of immune cells to kill tumor cells.
Estimated Timeframe:
Pre-requirement communication: 1-2 weeks
Design and construction of oncolytic viruses: 3-4 weeks
Mass production of oncolytic viruses: 2-3 weeks
Function and properties of oncolytic viruses in vivo and in vitro: 3-4 weeks
Results analysis and test report: 1-2 weeks
Product delivery and shipping: 2-3 weeks
Case Study
The employment of genetically-altered oncolytic viruses in commonly utilized in vivo murine models and in vitro cell-culture models of genitourinary malignancies has yielded a significant improvement in tumor-elimination effectiveness. Findings retrieved from an array of research reports offer crucial outlooks on its promising potential for the treatment of genitourinary malignancies.