The Sylvester Comprehensive Cancer Center is fortunate to be the beneficiary of this year’s Glam-A-Thon event to be held on Saturday, October 10 along Las Olas Boulevard in Fort Lauderdale. Sophie Loiseau, senior research associate, is leading a team for the Glam Doll Strut, and the team is  reaching out to all faculty, staff, friends, and family interested in getting involved in the event. To participate, click here.

Glam-A-Thon consists of three exciting events to raise awareness and funding for UM Sylvester breast cancer research studies (Braman Family Breast Cancer Institute). The first is the Little Rock Star Play Day from 11 a.m. to 2 p.m. This new, free event for children and their families will offer a variety of activities, crafts, and entertainment staged in the grassy park area on Las Olas Boulevard and Southeast Eighth Avenue.

At 3 p.m. the Glam Doll Strut will begin. South Florida’s fabulous divas (and dudes) will bring the sizzle to Las Olas as glamorous teams assemble in their sassiest stilettos and prettiest pumps to kick off the first-ever Glam Doll Strut to benefit breast cancer initiatives and research at UM Sylvester-Comprehensive Cancer Center. Elvis made “Viva Las Vegas” famous, but South Florida’s divas will make “Diva Las Olas” famous!

The main event is the walk, scheduled from 4 to 6 p.m. (with registration starting at 3 p.m.). It is only four blocks long, so participants can wear their heels comfortably. There will be pink champagne, cupcakes, makeover booths (including manicures) and lots of other fun stops along the walk route. Children are welcome.

For some time, researchers have known that the protein p27 is an important inhibitor of the cell division that spreads cancer. Understanding the full mechanism and extent of that role has taken much longer. Now, scientists at the Braman Family Breast Cancer Institute at the Sylvester Comprehensive Cancer Center have solved part of the puzzle, discovering that p27 can severely misbehave when in bad company. In fact, it can lose its restraining action on cell growth and bind to other molecules to promote cell motility, one of the first steps in the spread of cancer. In other words, Dr. Jeckyl becomes Mr. Hyde.

Joyce M. Slingerland, director of the Braman Family Breast Cancer Institute at Sylvester at the University of Miami Miller School of Medicine, led a team of researchers in collaboration with David Helfman, professor of cell biology and anatomy at Sylvester. Their findings were published in the May 19 issue of the Proceedings of the National Academy of Sciences (PNAS) journal.

The growth inhibitor p27 is a key regulator of cell division and motility, and resides in the nucleus. In that position, it regulates cell cycle progression. However, when p27 localization is shifted out into the cell’s cytoplasm, it takes on a different role, promoting cell motility and tumor spread. ”Earlier work showed that p27 can play a role in cell motility,” says Slingerland, “but how this happened was really not clear.”

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New findings just published in the Proceedings of the National Academy of Sciences by University of Miami Miller School of Medicine researchers suggest that antioxidant therapy could help prevent and treat Kaposi’s sarcoma, a major AIDS-related malignancy. Even though the number of cases has gone down with the use of highly active antiretroviral therapy, Kaposi’s sarcoma still has a high death rate, particularly in Sub-Saharan Africa.

Recently it has been found that the human herpesvirus 8 (HHV8) is responsible for the development of Kaposi’s hallmark skin and mucosal lesions, making it a class of tumors induced by a viral infection. While the human herpesvirus 8 causes the disease, the molecular mechanisms responsible for the tumors have remained an enigma.

Scientists at the University of Miami Miller School of Medicine’s Sylvester Comprehensive Cancer Center and other collaborating universities have been able to reproduce Kaposi’s sarcoma in mice by overexpressing a single protein from the Rac1 gene. The researchers found that as mice age, overexpression of Rac1, in a form that is constitutively activated, triggers the development of a tumor that has all the scientific characteristics of human Kaposi’s sarcoma.

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