Hope for a new sunscreen that can prevent and treat UV light “induced skin cancers has been provided by a new study in a mouse model of the disease by Mohammad Athar and colleagues at Columbia University College of Physicians and Surgeons, New York.

Mutations in the p53 gene that result in the production of mutant forms of p53 protein unable to do their job are associated with cancer in various tissues in mice and humans. An agent known as CP-31398 has previously been shown to bind mutant forms of p53 and restore their function. In the study, applying CP-31398 to the skin of mice reduced skin cancer (in terms of the size and number of tumors) induced by exposure to UVB light. In addition, treating mice already carrying UVB light “induced skin cancers with CP-31398 reduced tumor growth and volume. These effects were associated with increased p53 function. The clinical relevance of these observations was highlighted by the demonstration that CP-31398 increased p53 function in a human skin cancer cell line expressing a mutant form of p53. However, as Wafik S. El-Deiry from the University of Pennsylvania School of Medicine, Philadelphia, notes in his accompanying commentary, this study raises a number of questions that need to be addressed before these promising findings lead to new sunscreens for the prevention and treatment of UV light “induced skin cancer.

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While other studies have found disorganized white matter in the general population of people with dyslexia, these individuals often struggle with several aspects of reading, making it "hard to know exactly what the role of white-matter integrity is in isolation," says Chang. By demonstrating white-matter problems in PNH patients, who have an isolated reading fluency problem, and correlating that with reading fluency scores, the researchers were able to conclude that white-matter integrity and organization may be the structural basis in the brain for reading fluency.

"This makes sense," says Chang. "When we read, we need to take in information visually, hook it up with our inner dictionary of what letters and words mean, and when we're reading aloud, connect that with the region that gives us our ability to speak." For smooth, automatic reading, "the white matter is there to connect different regions of gray matter and allow them to function seamlessly." When reading fluency is the primary problem, "it may be that the areas of the brain that are important for reading are not connected efficiently," says Chang.

Most people with dyslexia who have trouble reading fluently don't have misplaced gray matter or PNH. But Walsh and Chang believe that disorganized white matter could similarly alter brain function in both groups. Their next study will examine how faulty white-matter connections alter brain patterns, comparing brain activation during reading in PNH patients and in dyslexic readers with poor fluency, who do not have PNH.

Pinpointing the brain structures responsible for fluent reading may eventually help researchers and educational specialists develop and use techniques that help improve the automatic nature of reading in children and adults with these kinds of difficulties, the researchers note.

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