Early UVA light exposure ‘doesn’t cause melanoma’

Washington, May 5 (ANI): Scientists from The University of Texas MD Anderson Cancer Center have found that early life exposure to ultraviolet A light does not cause melanoma.

The researchers, therefore, concluded that UVA exposure is unlikely to have contributed to the rise in the incidence of melanoma over the past 30 years

UVA is a carcinogen responsible for squamous cell carcinomas that also causes premature aging of the skin and suppresses the immune system. It”s also possible, the authors note, that long-term chronic exposure to UVA can hasten the progression to malignancy of melanocytes in the skin that are already on the path to becoming melanoma.

Study’s lead author David Mitchell, professor in M. D. Anderson”s Department of Carcinogenesis located at its Science Park – Research Division in Smithville, Texas, and colleagues tested the effects of UVA and ultraviolet B (UVB) light exposure in melanoma-prone fish hybrids that develop the disease spontaneously 15-20 percent of the time without exposure to UV light.

The scientists exposed a hybrid form of the genus Xiphophorus, more commonly known as platyfishes and swordtails, to either UVA or UVB daily between their fifth and 10th day of life. The fish were then scored for melanoma 14 months after exposure.

“We found that UVB exposure induced melanoma in 43 percent of the 194 treated fish, a much higher rate than the 18.5 percent incidence in the control group that received no UV exposure,” Mitchell said.

This was expected because UVB exposure at an early age is a well-established cause of melanoma.

Only 12.4 percent of 282 fish exposed to UVA developed the disease, which is not statistically different from the control group.

The study has been reported in the online early edition of the Proceedings of the National Academy of Sciences. (ANI)

Novel genetic regulator involved in head, throat cancers discovered

Washington, Apr 29 (ANI): In a major scientific advancement, pharmacy researchers at Oregon State University have discovered a genetic regulator, called CTIP2, which is expressed at higher levels in the most aggressive types of head and neck cancers.

The study might help in the identification of these cancers earlier or even offer a new therapy at some point in the future.

In a recent research, the “transcriptional regulator” CTIP2 was demonstrated to be a master regulator that has important roles in many biological functions, ranging from the proper development of enamel on teeth to skin formation and the possible treatment of eczema or psoriasis.

But, in the latest study, scientists found for the first time that levels of CTIP2 were more than five times higher in the “poorly differentiated” tumour cells that caused the most deadly types of squamous cell carcinomas in the larynx, throat, tongue and other parts of the head.

The researchers even found a high correlation between greater CTIP2 expression and the aggressive nature of the cancer.

They said that head and neck squamous cell cancers are the sixth most common cancers in the world, and a significant cause of mortality. They have been linked to such things as tobacco use and alcohol consumption.

“Serious head and throat cancer is pretty common, and mortality rates from it haven’t improved much in 20 years, despite new types of treatments. With these new findings, we believe it should be possible to create an early screening and diagnostic tool to spot these cancers earlier, tell physicians which ones need the most aggressive treatments and which are most apt to recur,” said Gitali Indra, an assistant professor in the OSU College of Pharmacy.

The scientists hope that the work could lead to new therapeutic approaches.

Also they said that this genetic regulator could be involved in both skin development and these types of cancer makes some sense, as both originate from epithelial cells.

The study speculated that CTIP2 could help regulate the growth of what is believed to be a cancer “stem” or “progenitor” cell, which has a greater potential to generate tumours through the stem cell processes of self-renewal and differentiation into multiple cell types.

Therefore, targeting cancer stem cells holds promise for improvement of survival and quality of life of cancer patients.

The study is published in PLoS ONE a professional journal. (ANI)