Gene therapy has the potential to provide cancer treatments based on novel mechanisms of action with potentially low toxicities. Although multiple genes are involved in carcinogenesis, mutations of the p53 gene are the most frequent abnormality identified in human tumors. Preclinical studies both in vitro and in vivo have shown that restoring p53 function can induce apoptosis in cancer cells. High levels of p53 expression and DNA-damaging agents like cisplatin (Platinol) and ionizing radiation work synergistically to induce apoptosis in cancer cells.
Phase I clinical trials now show that p53 gene replacement therapy using both retroviral and adenoviral vectors is feasible and safe. In addition, p53 gene replacement therapy induces tumor regression in patients with advanced NSCLC and in those with recurrent head and neck cancer. This article describes various gene therapy strategies under investigation, reviews preclinical data that provide a rationale for the gene replacement approach, and discusses the clinical trial data available to date.
Across all types of cancer, the most common genetic mutation doctors have observed involves the p53 tumor-suppressor gene. Many experimental gene-therapy approaches are based on repairing or replacing defective p53 genes. In human DNA, certain genes are responsible for preventing cells from becoming cancerous.
What is p53?
In human DNA, certain genes are responsible for preventing cells from becoming cancerous. The p53 gene is one of the most important of these tumor-suppressor genes.
Healthy cells can become cancerous when carcinogens, such as asbestos, damage their DNA and cause them to start dividing and reproducing uncontrollably.
The p53 gene prevents this by activating proteins that arrest cell division and repair corrupted DNA.
In cases where the DNA damage is irreparable, the p53 gene initiates a process called apoptosis that destroys the cancer cell before it reproduces itself.
The p53 gene can also limit blood flow to tumors, which prevents growth and alerts nearby immune cells to attack cancer cells.
What goes wrong in cancer?
In many cancers the p53 gene itself is corrupted, however, cells lose a natural safeguard against becoming cancerous. Doctors have observed that more than half of human cancer cases involve mutated p53 genes. Improperly functioning p53 genes allow cancer to spread faster and become more resistant to treatment.
If doctors find an effective way to repair or replace mutated p53 genes in cancer cells, it could lead to a radical improvement in the treatment of many types of cancer.
What is our solution?
Our doctors provide patients with a gene therapy treatment that will restore the natural p53 in cells and could be safely combined with traditional cancer treatments such as surgery, chemotherapy or radiation therapy to increase the overall effectiveness of the treatment plan.
Our p53 gene therapy treatment is based on 12 years of commercial use in >30,000 patients, and >30 published clinical studies
Our p53 gene therapy when combined with chemotherapy and radiotherapy has demonstrated significantly higher response rates than for standard therapies alone.
Thirteen published studies that include long-term survival data showed that the p53 gene therapy based combination regimens yield progression-free survival times that are significantly longer than standard therapies alone.
After having been successfully tested in over 30,000 patients no serious adverse events have been reported, except for vector associated transient fever, which occurred in 50-60% of patients and persisted for only a few hours.
Our technology and care, your healthy longevity:
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