Department of Biomedical Genetics
University of Rochester
601 Elmwood Ave.
Rochester, NY 14642
Main Office: MRB 2-9633
Department of Biomedical Genetics
University of Rochester
601 Elmwood Ave.
Rochester, NY 14642
Main Office: MRB 2-9633
Scientists at the James P. Wilmot Cancer Center who investigate lymphoma and leukemia were among the top presenters at the American Society of Hematology 51st Annual Meeting, Dec. 5-8, 2009, in New Orleans.
A University of Rochester Medical Center researcher sorts out the controversy and promise around a dangerous subtype of cancer cells, known as cancer stem cells.
Scientists have identified a protein in the brain that plays a key role in the function of mitochondria – the part of the cell that supplies energy, supports cellular activity, and potentially wards off threats from disease. The discovery, which was reported today in the Journal of Cell Biology, may shed new light on how the brain recovers from stroke.
Ten scientists from the University of Rochester Medical Center (URMC) have been awarded more than $6.8 million by the Empire State Stem Cell Board.The grants are for a wide range of research programs in the fields of neurological disorders, cancer, musculoskeletal diseases, the blood system, and efforts to understand the fundamental mechanics of stem cell biology.
A system of opposing genetic forces determines why mammals develop a single row of teeth, while sharks sport several, according to a study published February 26, 2009 in the journal Science. When completely understood, the genetic program described in the study may help guide efforts to re-grow missing teeth and prevent cleft palate, one of the most common birth defects.
The promise of cancer stem cell research has reached a critical point and the University of Rochester Medical Center is establishing itself as a leader in the field by creating a Cancer Stem Cell Research Program. The Medical Center's top scientists are collaborating to discover cures for cancer by closely examining the
master cells of this deadly disease. This program is one of only three formal programs in the United States. The two others are at Harvard and Stanford universities. This is a new avenue for scientists to pursue in an effort to find the underlying causes of cancer.
Oncologists have long treated cancer by attacking the tumors, but in many cases without getting at the root of the disease - the cancer stem cells - which tend to be drug resistant and a potential cause of relapse, said Craig Jordan, Ph.D., director of Translational Research for Hematologic Malignancies at the James P. Wilmot Cancer Center and associate professor of Medicine and Biomedical Genetics.
Jordan and colleagues, Monica Guzman, Ph.D., and Mark Noble, Ph.D., authored a primer on cancer stem cells in the Sept. 21 issue of The New England Journal of Medicine, outlining the data available today and challenges that are ahead for scientists and oncologists.
University of Rochester Medical Center scientists discovered a gene mutation that impairs the placenta and also is influential in cancer development, according to a study published online December 16, 2008, in the journal PLoS (Public Library of Science) Biology.
Many scientists like to discuss how each form of cancer is a distinct disease with its own causes and its own treatments. But researcher Hartmut
Hucky Land, Ph.D., takes the opposite approach: He is hunting for the most basic rules that all cancers share to make good cells go bad.
His unique, far-reaching effort to understand the disease at its roots poses a huge challenge that is matched only by the potential payoff - findings that could lead to new treatments for not just one but many forms of cancer.
The project has taken a big step forward with a $2.7 million grant from the National Cancer Institute to unravel the gene networks at the heart of colon cancer. The funding will support work for the next five years in the laboratory of Land, who is scientific director of the James P. Wilmot Cancer Center at the University of Rochester Medical Center.
A new approach to finding genes important in the onset of cancer is described in Nature. The findings could help to identify new targets for tumour therapy.
Several genes, or
oncogenes, cooperate with each other to transform normal cells into cancer cells. Hartmut Land and colleagues have now identified a list of other genes - termed
cooperation response genes (CRGs) - that are regulated downstream of these
oncogenes. By interfering with each CRG individually, the team were able to show that 14 out of 24 of them had a critical role in tumour formation. Restoring expression of these genes to the levels observed in normal cells prevented the formation of tumours. What's more, genetic perturbations of CRGs with relatively smaller effects when examined on their own show evidence of being essential when analysed in combination.
The findings represent an important step in the search for the chink in the armour in human cancer - the elusive gene that cancer cells simply cannot live without.
Pinpointing new targets for cancer treatments is as difficult as finding a needle in a haystack, yet a University of Rochester team has discovered an entire novel class of genes they believe will lead to a greater understanding of cancer cell function and the next generation of effective and less harmful therapies for patients.
Changing dendritic spines on a neuron - evidence of brain rewiring
New findings about a protein called the nogo receptor are offering fresh ways to think about keeping the brain sharp. Scientists have found that reducing the nogo receptor in the brain results in stronger brain signaling in mice, effectively boosting signal strength between the synapses, the connections between nerve cells in the brain. The ability to enhance such connections is central to the brain's ability to rewire, a process that happens constantly as we learn and remember. The findings are in the March 12 issue of the Journal of Neuroscience.
The work ties together several research threads that touch upon the health benefits of exercise. While those benefits are broadly recognized, how the gains accrue at a molecular level has been largely unknown. The new research gives scientists a way to produce changes in the brain that mirror those brought about by exercise, by reducing the effect of the nogo receptor.
The find comes as a surprise, because for much of the last decade, the nogo receptor has been a prime target of researchers trying to coax nerves in the spinal cord to grow again. They named the protein after its ability to stop neurons from growing. Its action in the brain has not been a hot topic of study.
A green glow from a fruit fly is giving researchers the green light when they are on the right path in their quest to develop compounds that help prevent cancer.
Hucky Land, Ph.D., professor and chair of the Department of Biomedical Genetics, will give a talk titled
Construction and Deconstruction of Cancer Cells, as part of a lecture series highlighting biological and biomedical research at the University of Rochester.
Land will lead a discussion at 4 p.m. on Friday, Oct. 12, in the Adolph Auditorium (1-7619). The talk is the latest installment of the
Second Fridays Science Social for faculty, staff and students at the University, although the public is welcome to attend. The lectures are free. More information is available at: http://www.urmc.edu/sss/index.html
Cancer-causing genes can work in more powerful and sneaky ways than has been realized. Scientists have shown that a gene named JAK that is closely related to a common cancer-causing gene in people tips the scales toward cancer in an unexpected manner. JAK disrupts the activity of an organism's DNA on a broad scale, thwarting a critical molecular event very early on in an embryo's development.
University of Rochester scientists, while investigating the two most frequent types of mutations in cancer, discovered a possible new route to treatment that would take advantage of the mutations instead of trying to repair them. The research is reported online this week in the journal Nature Structural & Molecular Biology.
In experiments with rodent and human cells, co-authors Mingxuan Xia, Ph.D., and Hartmut Land, Ph.D., explored how the Rho family of proteins, which are involved in cell movement, and thus in the progression from benign to malignant cancer, are controlled by two well-known cancer genes, p53 and Ras. By closing in on this deadly collaboration, researchers showed for the first time why some molecules such as Rho are targeted by cancer genes - and how they might lead to a promising way to intervene against cancer.
We have very little understanding of how Ras and p53 or any other potent gene mutations cooperate to cause malignant tumors, said Land, who is professor and chair of the Department of Biomedical Genetics and scientific director of the James P. Wilmot Cancer Center at the University of Rochester.
But we have suspected for a long time that the way to develop rational searches for new drug targets is to first understand how these oncogenes cooperate. And in this study we've shown for the first time that this idea might work.
As far as Mark Noble is concerned, the
next medical revolution arrived more than 30 years ago. That's when the Rochester professor of biomedical genetics and scientists like him at academic medical centers across the country first began to grasp the potential of stem cells.
In Noble's lab and in the labs of scientists across the Medical Center, Rochester scientists have been exploring that potential for several years, helping lead research projects focused on new cancer treatments, the role nutrition plays in early development, and in understanding how to repair damage to the brain and nervous system.
Chris Proschel, Mark Noble, and Margot Mayer-Proschel have worked together as a team since 1990. They played key roles in identifying—and are considered to be among the best in the world at handling—the four known progenitor cells for the various cells found in the central nervous system.
Researchers believe they have identified a new way, using an advance in stem-cell technology, to promote recovery after spinal cord injury of rats, according to a study published in today's Journal of Biology. Scientists from the New York State Center of Research Excellence in Spinal Cord Injury showed that rats receiving a transplant of a certain type of immature support cell from the central nervous system (generated from stem cells) had more than 60 percent of their sensory nerve fibers regenerate. Just as importantly, the study showed that more than two-thirds of the nerve fibers grew all the way through the injury sites eight days later, a result that is much more promising than previous research. The rats that received the cell transplants also walked normally in two weeks.
These studies provide a way to make cells do what we want them to do, instead of simply putting stem cells into the damaged area and hoping the injury will cause the stem cells to turn into the most useful cell types, explains Mark Noble, Ph.D., co-author of the paper, professor of Genetics at the University of Rochester, and a pioneer in the field of stem cell research.
It really changes the way we think about this problem.
The breakthrough is based on many years of stem cell biology research led by Margot Mayer-Proschel, Ph.D., associate professor of Genetics at the University of Rochester. In the laboratory, Mayer-Proschel and colleagues took embryonic glial stem cells and induced them to change into a specific type of support cell called an astrocyte, which is known to be highly supportive of nerve fiber growth. These astrocytes, called glial precursor-derived astrocytes or GDAs, were then transplanted into the injured spinal cords of adult rats. Healing and recovery of the GDA rats was compared to other injured rats that received either no treatment at all or treatment with undifferentiated stem cells.
Many drivers feel the urge to floor the accelerator on a crisp sunny day when the highway ahead seems to stretch straight to eternity. But only the most foolish would cut the brake line while pushing the pedal to the metal. Yet one of the body's most potent cancer-causing genes does precisely that inside a cell, scientists at the University of Rochester Medical Center have found. The result of the unfettered molecular joy ride is, oftentimes, cancer. Details of the research are in the October issue of the Journal of the European Molecular Biology Organization (EMBO).
Scientists have long recognized that the protein produced by a gene known as myc spurs a cell to grow. Just like pushing the accelerator makes a car move forward, producing more myc makes a cell grow and divide. Too much myc spells an invitation to cancer, where cells grow uncontrollably and invade other tissues.
Now scientists have found that myc is even more powerful than they anticipated: The gene also has a role in disabling the molecular signals, the
brakes, that cells rely on to slow growth. When myc is out of control, not only is the accelerator floored but the brakes are out. It's no wonder that the gene plays a role in many human cancers, including those in the lung, colon, breast, bladder, and brain.
Myc is central to our cells' ability to grow, divide, and even die when they should, says Hartmut Land, Ph.D., director of the University's Center for Cancer Biology and lead investigator of the EMBO study.
Basically, myc is like the starter of an engine; it's responsible for making the whole cell go. It's a very potent gene, but one that's been slow to yield its secrets. Myc has been a conundrum.