Cancer Research

Second-hand smoke, also known as environmental tobacco smoke or ETS, is clearly associated with cancer, respiratory and cardiovascular disease in humans. Several studies have shown that up to 20 different carcinogens contained in tobacco smoke can be inhaled by non-smoking bystanders.

Dr. Timothy Fan, veterinary oncologist at the University of Illinois Veterinary Teaching Hospital in Urbana, explains that although associations between ETS and diseases in animals have not been as extensively researched, a handful of studies show a correlation between ETS and certain forms of cancer in pets.

The secret to the ability of a molecule critical for cell division to throw off the protein yoke that restrains its activity is the yoke itself--a disorderly molecule that seems to have a mind of its own, say investigators at St. Jude Children's Research Hospital, Innsbruck Medical University (Austria) and Max Planck Institute (Martinsried, Germany).

The researchers showed that the disorderly protein yoke, called p27, participates in its own destruction by swinging the end of its long arm up into a key side pocket of the cell division molecule called CDK2. After the end of p27 slips into the pocket, CDK2 marks p27 for destruction by tagging it with a molecule called phosphate.

Howard Hughes Medical Institute researchers have developed two strategies to reactivate the p53 gene in mice, causing blood, bone and liver tumors to self destruct. The p53 protein is called the "guardian of the genome" because it triggers the suicide of cells with damaged DNA.

Inactivation of p53 can set the stage for the development of different types of cancer. The researchers' findings show for the first time that inactivating the p53 gene is necessary for maintaining tumors. While the researchers caution that cancers can mutate to circumvent p53 reactivation, they believe their findings offer ideas for new approaches to cancer therapy.

A team led by biochemists at the University of California, San Diego has found what could be a long-elusive mechanism through which inflammation can promote cancer. The findings may provide a new approach for developing cancer therapies.

The study, published in the January 26 issue of the journal Cell, shows that what scientists thought were two distinct processes in cells—the cells’ normal development and the cells’ response to dangers such as invading organisms—are actually linked.

A provocative new model proposed by molecular biologist John Tower of the University of Southern California may help answer an enduring scientific question: Why do women tend to live longer than men?

That tendency holds true in humans and many other mammals as well as in the much-studied fruit fly Drosophila melanogaster.

In genetic studies of Drosophila, Tower and his team have shown that genes known to increase longevity always affect male and female flies differently.

"For a long time, we only did experiments in one sex or the other, depending on what was convenient," said Tower, an associate professor of biological sciences in the USC College of Letters, Arts & Sciences who has studied the genetics of aging in Drosophila for the last two decades.