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January 19, 2011

In Research

Richard Glor with lizard


Environmental factors limit species diversity

New research by Richard Glor, an assistant professor of biology, and Daniel Rabosky of the University of California at Berkeley suggests that species diversity is limited by geography. The pair studied patterns of species accumulation of lizards over millions of years on the Caribbean islands of Puerto Rico, Jamaica, Hispaniola, and Cuba.

Historically, biologists needed fossil records to study patterns of species diversification. But advances in molecular methodology allowed Glor and Rabosky to use DNA sequences to reconstruct evolutionary trees that show the relationships between species.

The two scientists found that species diversification of lizards on the four islands reached a  plateau millions of years ago and has essentially come to an end—a finding that refutes some recent work suggesting that species diversity never enters equilibrium.

“Geographic size correlates to diversity,” says Glor. “In general, the larger the area, the greater the number of species that can be supported.” The research was published in the journal Proceedings of the National Academy of Sciences.

“When we look at other islands and continents that vary in species richness,” Glor says, “we can’t just consider rates of accumulation; we need to look at the plateau points.”

A state of equilibrium doesn’t mean that the evolution of a species stops, Glor adds. Lizards will continue to adapt to changes in their environment, but they aren’t expected to develop in ways that increase the number of species within a habitat. Read more at www.rochester.edu/news/show.php?id=3733.

brain with tumorResearchers pinpoint origin of deadly brain tumor

Scientists have identified the type of cell at the origin of brain tumors known as oligodendrogliomas, a type of glioma—a category that defines the most common type of malignant brain tumor.

In a paper published in the December 2010 issue of the journal Cancer Cell, investigators found that the tumor originates in and spreads through cells known as glial progenitor cells—cells that are often referred to as “daughter” cells of stem cells. The work comes at a time when many researchers are actively investigating the role that stem cells which have gone awry play in causing cancer. For scientists trying to create new ways to treat brain tumors, knowing whether stem cells or progenitor cells are part of the process is crucial.

“In many ways progenitor cells are controlled by completely different signaling pathways than true stem cells,” says Steven Goldman, the Edward A. and Anna Vollertsen Rykenboer Chair in Neurophysiology and head of the laboratory where much of the genetic analysis for the study was done. “Knowing which type of cell is involved gives us a clear look at what drug approaches might be useful to try to stop these tumors. Comparing normal progenitor cells to progenitors that give rise to tumors gives us a roadmap to follow as we try to develop new treatments.”

The study was the product of a multi-institutional collaboration led by William Weiss, a neuro-oncologist at the University of California at San Francisco. The study focuses on oligodendrogliomas, a type of tumor that presents with symptoms much like other brain tumors—headaches, seizures, and cognitive changes. Treatments like surgery typically slow or stop the tumor initially, but it usually returns, often in a much more aggressive form.

The majority of patients with oligodendrogliomas ultimately die from the disease. The team used a common brain tumor drug, temozolomide, to test several types of cells from both human and mouse tumors. They found that the drug was effective against oligodendroglioma cells and normal glial progenitor cells, and much less effective against either brain stem cells or other brain tumors called astrocytomas. Read more at www.urmc.rochester.edu/news/story/index.cfm?id=3088.


Researchers find genetic target for deadly lymphoma subtype

Scientists report in the journal Nature online that they’ve discovered a new gene mutation that drives activated B cell lymphoma.

“This opens the door for targeted therapy that may not cause the type of general toxicity we usually see with chemotherapy,” says Richard Fisher, the Samuel E. Durand Chair in Medicine and director of the Wilmot Cancer Center, who coauthored the study. A consortium of scientists from around the world, led by a laboratory from the Metabolism Branch of the National Cancer Institute in Bethesda, Md., used advanced gene sequencing techniques to uncover the MYD88 mutations in the least curable form of lymphoma, known as ABC subtype (activated B cell). The mutations were observed in 29 percent of the biopsy samples involved in the study, while the mutation was rare or absent in other lymphoma subtypes. This established MYD88 as among the most frequently altered gene in this malignancy, the paper said.

ABC lymphoma is a common type of diffuse large B cell lymphoma. The ability of ABC malignant cells to survive, despite treatment with chemotherapy and a newer drug, Rituximab, results in less than a 40 percent cure rate for this particular subtype.

Scientists used high-throughput RNA sequencing—a process of obtaining the order of molecules to better understand the genetic code—to uncover the MYD88 mutations in 382 biopsy samples and 35 lymphoma cell lines.

The study demonstrated what is required at the cellular level to maintain the viability of ABC cancer cells. By identifying the location of the mutation that is apparently unique to ABC, researchers believe they also located an enticing target for treatment, and perhaps a better way to genetically identify which patients might respond to a different combination of therapies.

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