all Marsha Moses stories

Urine test may help monitor disfiguring birthmarks

70652986 — Mon, 26 Mar 2007 06:20:45 -0400

Vascular anomalies include both vascular malformations and vascular tumors (most commonly hemangiomas). Hemangiomas, found in about 10 percent of infants, occur when the cells lining blood vessels multiply abnormally. Hemangiomas grow rapidly in the first year of life, then usually shrink and disappear. But some grow large, causing obstruction, ulceration, and other problems. Vascular malformations occur during fetal development, usually growing in proportion to the child, but sometimes progress during adolescence or pregnancy, or after surgery or trauma, in rare instances becoming fatal.

Urine test tracks deadly birthmarks

70652986 — Mon, 26 Mar 2007 06:20:52 -0400

Although not yet approved by the Food and Drug Administration, results from simple urine tests are already being used to guide treatment of children with disfiguring birthmarks and adults with cancer. Urine tests, now given to all people as part of every physical, might someday provide doctors with valuable information difficult to obtain by other means.

"Many birthmarks, caused by abnormal growth of blood or lymphatic vessels, go away without treatment," notes Marsha Moses, associate professor of surgery at Harvard Medical School and Children's Hospital Boston. "But some grow frightfully big before they start to regress - big enough to kill a child. Also, some birthmarks grow unseen, inside the body. We can look at the urine of these children and predict the extent and activity of the abnormalities. Such a capability gives physicians data they can use to treat these patients more effectively."

The same is true for cancer. Last year, Moses and her colleagues announced discovery of ADAM 12, a protein found in the urine of breast cancer patients. Increasing amounts of this protein in urine signal that the cancer is getting worse.

Matrix-buster inhibitor has second way to throttle angiogenesis

70652986 — Mon, 26 Mar 2007 05:32:47 -0400

Matrix metalloproteinases (MMPs) and their regulators, the tissue inhibitors of metalloproteinases (TIMPs), form an intriguing partnership. MMPs work by breaking down the dense matrix surrounding cells, freeing them to wander the body during processes like metastasis and angiogenesis. TIMPs rein in the MMPs, essentially cutting off the supply of migrating cancer or endothelial cells. Given the TIMPs' anti-angiogenic action, it is no wonder that pharmaceutical companies have been rushing to develop synthetic MMP-inhibiting agents. Yet in clinical trials, these manmade versions have often performed poorly, producing serious side-effects while failing to stop angiogenesis in cancer patients. It now appears that inhibiting the MMPs is not enough to arrest the new blood vessel growth that accompanies tumors. Working in a mouse model, Marsha Moses, Cecilia Fernandez, and their colleagues found that TIMP-2, a variant known to stifle angiogenesis in vivo, owes its power to stop cancer-related angiogenesis to its unique ability to inhibit endothelial cells from proliferating, rather than its ability to bind MMP. What is more, TIMP-2's anti-proliferative power appears to be restricted to a small, easily synthesized region of the molecule, Loop 6. " "It is a new angiogenesis inhibitor, it is small, and it is bioavailable," said Moses, Harvard Medical School associate professor of surgery at Children's Hospital. The study appears in the Oct. 17, 2003 Journal of Biological Chemistry.