Cell Suicide Protein Is Key to Eye Cancer Treatment
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Recent research from investigators of the University of Liverpool has shown that a specific protein in the human body is able to prevent the growth and spread of eye cancer by starting a series of events that will eventually lead to cell suicide. These new findings may help change the course of eye cancer treatment in cases of metastatic uveal melanoma (UM), a type of eye cancer that is from the pigment cells of the eye called melanocytes. This type of eye cancer has no known effective treatment.
The spread of cancer cells in other organs or parts of the body either adjacent or remote to the place of origin is known as metastasis. This spread often occurs in almost half of patients with metastatic uveal melanoma. Though the condition is rare, metastatic uveal melanoma is said to be the most common primary eye cancer among adults. While the primary tumor can be treated effectively with conventional treatments, almost half of the patients may develop metastasis most commonly in the liver. When it reaches this stage, there may be no effective treatment available.
Programmed cell death or apoptosis is a natural process wherein there is a fast and irreversible death and elimination of damaged cells in the body. One characteristic of cancer cells is that it is able to evade the process of apoptosis, especially if the cancer cells are malignant cells.
Dr Luminita Paraoan of the University’s Department of Eye and Vision Science in the Institute of Ageing and Chronic Disease has previously published new findings about the requirement of p63, a protein that generates apoptosis in UM. These findings are published in the British Journal of Cancer.
To note, Chromosome 3 is one of the 23 chromosome pairs in humans. Normally, humans have two copies of each chromosome. Chromosome 3 contains a part that has the gene for protein p63. However, people with aggressive UM don't have this part and so they don't have the p63 protein.
The present study was able to find out that of the p63 gene is used along with another gene called p53, Um can be effectively targeted and apoptosis would occur in cancer cells. The p53 gene belongs to a class of genes called tumor suppressor genes which are abnormal in cancer. They are supposedly protective genes that limit the growth and development of cells. When these tumor suppressor genes are mutated, the cells can grow without control and can form a tumor.
The researchers noted that this study is able to highlight for the first time for p63 can initiate apoptosis in cells in UM. This can have broad implications in the treatment of other cancers in which there is impaired apoptosis. Hopefully, the findings of this study can help design new therapeutic approaches that can treat cancers which are resistant to chemotherapy and radiation treatment.
