HMS/HSDM Class Day
2005
The Doctor’s Advice: Talk to Strangers
Faculty Symposium
Profs Tell Tales of Molecular Medicine
HSPH Class Day
UN Official Sees Women’s Health Crisis in Africa
Alumni Day
How Doctors Speak to the Public
Class Symposium
For Class of ’80, Risk and Reward Mark a Productive 25 Years
DMS Symposium
Integration Key to Student Success in Life Sciences
Student Speakers
Students Recount Lessons Learned
Scenes From Alumni Week
Pictures from Commencement and Alumni Week activities
Student and Faculty Awards
Honors Given to Faculty and Students During Commencement
Growth Factor May Aid in Crohn’s Disease Treatment
Bench Science Advances Against Cancer
Dental School Dedicates New Building on Longwood
Faculty Health Survey Being Conducted
Awards Recognize Advancement of Women
BLAST Resource Available to HMS Faculty
The July Effect: How Hospitals Cope with Intern Turnover
FACULTY SYMPOSIUM
Profs Tell Tales of Molecular Medicine
Unveiling promiscuous oncogenes, fighting breast and ovarian cancer with the Y chromosome, detoxifying cellular neighborhoods to save eyesight, and regenerating tissues from embryonic stem cells were all subjects of this year’s HMS Faculty Symposium during Alumni Week.
The symposium showcased the process of creating molecular ap-proaches to medicine. “Assuming that you would get in again, this is some of the science you would be hearing,” moderator Daniel Federman told the audience. Federman is the Carl W. Walter distinguished professor of medicine and senior dean for alumni affairs and clinical teaching at HMS.
Philip Leder opened with a synopsis of the creation of the first transgenic animal model and some of the important insights into cancer it provided. His interest in the genetic basis of cancer had been sparked by an encounter with a preleukemic patient in Minnesota at the end of medical training, said Leder, the John Emory Andrus professor of genetics and head of the HMS Genetics Department. Harnessing the powerful new tools of genomics as they emerged, he found a translocated chromosome segment that disrupted the usual sequence of amino acids in the regulatory region of an otherwise normal gene. The mutation was necessary, but not sufficient, for cancerous proliferation of B cells. Leder’s group soon identified a second gene and traced its molecular connection to the first. In an important lesson, the research showed that one drug might not be enough to target the pair of cancer genes.
It took almost as long for an embryologic observation from the 1930s to become a medical reality as it did for the Red Sox to stage their comeback as World Series champs, said Patricia Donahoe, the Marshall K. Bartlett professor of surgery at HMS and director of the pediatric surgical research laboratories at Massachusetts General Hospital.
Scientists later observed that fetuses turn into males by virtue of some genetic switch at the tip of the Y chromosome. Potent products from the early testes zap the concurrently developing female genital organs. Donahoe wondered if these substances could do the same to tumors emanating from those organs decades later. She and her colleagues isolated Mullerian-inhibiting substance (MIS) as the key protein, cloned the genes for the receptors, identified potential targets in cancers ranging from breast to prostate, tested it in animal models of ovarian cancer, and found an industry partner to begin phase I clinical testing in women. “We spent 30 years getting to this step,” Donahoe said. “We hope in a year or so to bring the product to clinical application.”
Constance Cepko, Howard Hughes investigator and HMS professor of genetics, is searching for a way to save the thin, flimsy layer of neurons at the back of the eye from the progressive destruction of macular degeneration, diabetic retinopathy, and other diseases that cause blindness. She is focusing on the five percent of photoreceptors known as cones, which are concentrated in the middle of a vast field of rods and used for seeing color, bright light, and details.
“If you’re a neighbor of dying cones, you’re more likely to die,” said Cepko. Maybe the nearby photoreceptors make something toxic, or maybe the dying cells remove some crucial supporting factor. Successful gene therapy five years ago that restored sight without side effects to a dog named Lancelot, blind from birth due to a genetic defect, has made researchers optimistic about therapeutic possibilities.
“What genes should we deliver when we don’t know the cause of the disease?” Cepko said. “That’s what we’re trying to figure out.”
George Daley, HMS associate professor of biological chemistry and molecular pharmacology at Children’s Hospital Boston, studies how to use stem cells to treat disease. The highly versatile embryonic stem cells hold promise for creating better animal models of human disease, to provide assays for drug development and toxicity testing, and to repair or replace diseased tissues, such as the insulin-producing beta cells lost in diabetes and midbrain dopamine neurons in Parkinson’s disease.
Some day, a child with a genetic disease, such as sickle cell anemia, may benefit from cellular microsurgery. The patient’s mother or sister will donate an egg. After removing the egg’s DNA with tiny microneedles, scientists will insert the nucleus from one of the patient’s cells into the egg, Daley said. Scientists will use electricity or calcium to trick the egg into thinking it was fertilized, so it will divide into a tiny blob of undifferentiated embryonic stem cells. The defective gene that causes sickle cell anemia will be repaired in these cells. They then will be coaxed into blood cells and transplanted into patients to treat the incurable disease.