all Kenneth Anderson stories

Cancer drug activates adult stem cells

404132862 — Fri, 25 Jan 2008 10:35:29 -0500

The use of a drug used in cancer treatment activates stem cells that differentiate into bone appears to cause regeneration of bone tissue and be may be a potential treatment strategy for osteoporosis, according to a report in the February 2008 Journal of Clinical Investigation.

Scientists discover new genetic subtypes of common blood cancer

70652986 — Mon, 26 Mar 2007 06:26:07 -0400

Scientists at Dana-Farber Cancer Institute and collaborators have identified four distinct genetic subtypes of multiple myeloma, a deadly blood cancer, that have different prognoses and might be treated most effectively with drugs specifically targeted to those subtypes.

A new computational tool based on an algorithm designed to recognize human faces plucked the four distinguishing gene patterns out of a "landscape" of many DNA alterations in the myeloma genome, the researchers report in the April 2006 issue of Cancer Cell.

These results "define new disease subgroups of multiple myeloma that can be correlated with different clinical outcomes," wrote the authors, led by Ronald DePinho, MD, director of Dana- Farber's Center for Applied Cancer Science.

Novel combination overcomes drug-resistant multiple myeloma cells

70652986 — Mon, 26 Mar 2007 06:20:05 -0400

The researchers hope to move rapidly to clinical trials of the therapy, a combination of the drug Velcade and an experimental compound that was designed by researchers at the Broad Institute of the Massachusetts Institute of Technology and Harvard University.

The report demonstrates that the combination was more than twice as effective as either drug alone in killing resistant cells from patients' bone marrow.

"This is not just another drug - this is a whole new approach to treating multiple myeloma," said Kenneth Anderson, M.D., senior author of the paper.

Velcade is the first in a class of so-called proteasome inhibitors, which destroy cancer cells by blocking the proteasome, a disposal mechanism that rids the cell of abnormal proteins. Cells in which the proteasome is jammed eventually commit suicide, triggered by the accumulation of proteins, explains Anderson.

However, many cancer cells are resistant to proteasome inhibitors like Velcade. Recent studies have revealed an alternative protein-disposal complex, the aggresome, that may take over enough of the job when the proteasome falters to allow the cells to survive.

Therefore, the Dana-Farber researchers suggested that blocking both protein disposals at once might get around this resistance mechanism. Scientists led by one of the study's authors at the Broad Institute designed a drug that blocks an enzyme critical to the aggresome's ability to function.

These highly promising results, wrote the researchers, "provide the framework for clinical trials designed to enhance sensitivity and overcome resistance to bortezomib [Velcade], thereby improving patient outcome in multiple myeloma."

New cancer drug wins FDA approval

70652986 — Mon, 26 Mar 2007 05:29:58 -0400

When he was a first-year student at Harvard Medical School, Alfred Goldberg, now a professor of cell biology, wondered why the body destroys its own proteins, which are so vital to life. He wanted to know why muscles lose much of their mass with inactivity, nerve injury, or cancer. To get an answer, he started doing experiments on his own, and kept doing them as he went from graduate student to professor. By the mid-1990s, Goldberg and his colleagues had worked out the structure and the purpose of one of the most magnificent molecular machines put together by nature.