Seborrheic Dermatitis

Jun. 14 - A new gene associated with a variant of psoriasis and
seborrheic dermatitis has been identified by a research group led by
Dr. Ohad Birk at the Morris Kahn Laboratory of Human Genetics at Ben
Gurion University and Soroka Medical Center. The gene discovered by
the Israeli researchers is of much interest as it allows the first
major molecular insight into why the specific skin cells proliferate
excessively, causing these two common skin diseases. Psoriasis and
seborrheic dermatitis affect 2-3% of the population worldwide and 85%
of AIDS patients. Both skin diseases are caused by excessive
proliferation of specific cells (keratinocytes) in the skin. To date,
there is only very limited understanding as to the molecular
mechanisms causing these two common disorders. The two-and-a-half-year
study examined an Israeli Moroccan Jewish family with 44 members over
five generations who showed signs characteristic of psoriasis and
seborrheic dermatitis. By using advanced techniques to analyze DNA

samples of the affected members of the family and comparing them to
normal, unmutated DNA, Ramon Birnbaum, a doctoral student at Birk’s
laboratory, has succeeded in pinning the beginning of the molecular
pathway on a mutation in a gene that is normally expressed, or "turned
on" in the keratinocytes. The gene is believed to suppress or regulate
cell proliferation and is thought to be a transcription factor,
meaning that it switches on other genes, which may also play a role in
the disease. When mutated, this regulation malfunctions, enabling
excessive proliferation of skin cells and calling in cells of the
immune system. The findings, to be reported in this month’s issue of
Nature Genetics, allow new insights into the mechanism of disease in
psoriasis and seborrheic dermatitis. In turn, these insights are
likely to assist pharmaceutical companies in developing "smart drugs"
for these two common skin diseases.

This entry was posted on Friday, November 17th, 2006 at 7:05 pm and is filed under Uncategorized. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.