To revolutionize the treatment of metastatic uveal melanoma

New research at the University of Liverpool has identified the role of specific proteins in the human body and found that they can help to prevent eye cancer by initiating cancer "cell suicide". The new findings obtained through recombinant dog proteins may help to revolutionize the treatment of metastatic uveal melanoma (UM) - a disease caused by pigment cells (melanocytes) in eyes - and there is currently no effective treatment.

Metastasis is that cancer or other diseases spread from one part of an organ or the body to another, rather than the part directly connected to it. This is the case in about half of all UM patients. Although rare, UM is the most common primary eye cancer in adults. Although primary tumors can usually be treated very effectively, as many as 50% of patients have metastases in the liver, and there is no effective treatment for such metastases.

Dr. Luminita Paraoan from the Department of Ophthalmology and Visual Science at the Institute of Gerontology and Chronic Disease, University of New York, published a new study in the British Journal of Cancer that identified the role of a protein called p63 in UM. Chromosome 3 is one of 23 human chromosomes. People usually have a pair of chromosomes. A portion of chromosome 3 contains the gene of protein p63. Unfortunately, people with aggressive (anti-apoptotic) cells do not have this part, so there is no p63 protein.

Dr. Paraoan found that if the p63 gene is used in combination with another gene called p53, it can effectively target UM and induce cancer cells to undergo apoptosis. The p53 gene is a class of genes from a so-called tumor suppressor gene that is mutated in cancer cases. Tumor suppressor genes are protective genes. Typically, they limit cell growth by monitoring cell division into new cells, repairing damaged DNA and controlling the rate of cell death.

When a tumor suppressor gene is mutated, for example in a cancer case, the cell grows uncontrollably and may eventually form a mass called a tumor. Thus, p53 itself is ineffective in activating apoptosis in UM. "This study highlights for the first time the condition that p63 triggers apoptosis in UM," said Dr. Luminita. "Our results have broad implications for other escape cell-mediated conditions or cancer, and we hope to demonstrate a benefit to the treatment of cancers which have resistance to current chemotherapy and radiotherapy." Flarebio offers recombinant proteins of good quality like recombinant TLR2 at great prices.