Homologous Recombination Can Cause More Breaks As It Fixes Them
The traditional view of cancer is that a cell has to sustain a series of hits to its DNA before its defenses break down enough for it to turn cancerous. But cancer researchers have also found that cells can experience very rapid and widespread DNA damage that could quickly lead to cancer or developmental defects.
Now researchers at the University of California, Davis, have found that these complex chromosomal rearrangements can be triggered in a single event when a process used to repair DNA breaks, homologous recombination, goes wrong. The work is published Aug. 10 in the journal Cell.
By Kathy Keatley Garvey
Researchers in Professor Bruce Hammock’s laboratory at UC Davis are studying mechanisms involved in blocking angiogenesis — the formation of new blood vessels. The findings may lead to new methods for preventing cancer growth and targeting other diseases, the researchers report.
Postdoc Amy Rand is studying how certain fats can affect growth of blood vessels in tumors.
A recently-published study from Hammock’s lab describes a novel lipid-signaling molecule that can change fundamental biological processes involved in human health and disease. It builds on landmark research by the Judah Folkman laboratory of Harvard Medical School, which earlier showed that cutting off blood vessels that feed a cancerous tumor could stop its growth.
Where would we be without meiosis and recombination? For a start, none of us sexually reproducing organisms would be here, because that’s how sperm and eggs are made. And when meiosis doesn’t work properly, it can lead to infertility, miscarriage, birth defects and developmental disorders.
Neil Hunter’s laboratory at the UC Davis College of Biological Sciences is teasing out the complex details of how meiosis works. In a new paper published online Jan. 6 in the journal Science, Hunter’s group describes new key players in meiosis, proteins called SUMO and ubiquitin and molecular machines called proteasomes. Ubiquitin is already well-known as a small protein that “tags” other proteins to be destroyed by proteasomes (wood chippers for proteins). SUMO is a close relative of ubiquitin.
Full post: New Steps in the Meiosis Chromosome Dance
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“Gnothi seauton” or “Know thyself,” said the Ancient Greeks; but they might have also said, “eat yourself.” For biologists, autophagy or “self-eating” is the process that cells use to recycle material inside the cell. It breaks down defective proteins and molecules, disposes of invading viruses and bacteria, provides an energy source when food is lacking and generally keeps cells fit and healthy. Problems in autophagy are implicated in cancer, aging, infectious disease and degenerative disorders.
Yoshinori Ohsumi after hearing he had been awarded the 2016 Nobel Prize in Physiology or Medicine.
Photo: Mari Honda
Full post: Nobel Medicine Prize for “self-eating”
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UC Davis researchers have developed a way to use the empty shell of a Hepatitis E virus to carry vaccines or drugs into the body. The technique has been tested in rodents as a way to target breast cancer, and is available for commercial licensing through UC Davis Office of Research.
Hepatitis E virus is feco-orally transmitted, so it can survive passing through the digestive system, said Marie Stark, a graduate student working with Professor Holland Cheng in the UC Davis Department of Molecular and Cell Biology.
Some of the world’s leading experts in how DNA is protected and repaired from damage will meet at UC Davis Feb. 12-13 for a symposium in honor of Stephen Kowalczykowski, distinguished professor of microbiology and molecular genetics at the UC Davis College of Biological Sciences. Registration information is available here.
“Genome maintenance” is essential to life, said Frederic Chedin, Professor of Molecular and Cellular Biology, who is co-organizer of the symposium with Professors Wolf-Dietrich Heyer and Neil Hunter, Department of Microbiology and Molecular Genetics. Every second of the day, our DNA sustains damage for example from chemicals, radiation or just natural processes inside the cell. Breaks and lesions in DNA can lead to cancer, disease and developmental defects. Living things, from bacteria to plants to people, have evolved a fundamentally similar set of tools and processes that constantly defend and repair DNA.
By Holly Ober
Thermal ablation with magnetic resonance–guided focused ultrasound surgery (MRgFUS) is a noninvasive technique for treating fibroids and cancer. New research from UC Davis shows that combining the technique with chemotherapy can allow complete destruction of tumors in mice.
MRgFUS combines an ultrasound beam that heats and destroys tissue with a magnetic resonance imaging to guide the beam and monitor the effects of treatment. The effectiveness of the treatment can be limited by the need to spare normal tissue or critical structures on the tumor margins, as well as the need to eliminate micrometastases.
“Terrific,” “Amazing news,” “Excellent choice,” were some of the terms two UC Davis experts in DNA repair used to describe the award of the 2015 Nobel Prize for Chemistry to three pioneers of the field this morning. The recipients are: Tomas Lindal, Francis Crick Institute, London; Paul Modrich, Howard Hughes Medical Institute and Duke University; and Aziz Sancar of the University of North Carolina Chapel Hill.
“They discovered that DNA in your body, which suffers from millions of DNA damaging events from every day due to normal chemical processes, is repaired efficiently by remarkably complex and disparate sets of repair machineries and mechanisms,” said Stephen Kowalczykowski, distinguished professor of microbiology and molecular genetics in the UC Davis College of Biological Sciences.
Fanconi anemia is a rare, inherited disorder that affects about one in 350,000 births. It affects the blood and bone marrow and many other organs, can cause physical abnormalities and vulnerability to cancer. Recently, the case of a child with serious Fanconi-like symptoms has helped researchers at The Rockefeller University in New York and UC Davis better understand the causes of the disease, and discover a new role for a protein already known to be involved in DNA repair and protection from cancer. The work was published recently in the journal Molecular Cell.
Full post: Fanconi anemia gene poisons DNA repair
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Despite decades of warnings about smoking, lung cancer is still the second-most common cancer and the leading cause of death from cancer in the U.S. Patients are often diagnosed only when their disease is already at an advanced stage and hard to treat. Researchers at the West Coast Metabolomics Center at UC Davis are trying to change that, by identifying biomarkers that could be the basis of early tests for lung cancer.
“Early diagnosis is the key to fighting lung cancer,” said Oliver Fiehn, director of the metabolomics center and a professor of molecular and cellular biology at UC Davis.