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Protein 'chatter' linked to cancer activation
August 14, 2007Scientists have found the existence of cross-talk between human chromosome ends and the protein complexes central to the stability of the entire human genome, a "chat" that contributes to cancer development.
The research, published today in Nature Structural & Molecular Biology, sheds new light on the pathology of three related but non-curable cancer-predisposed human disorders: ataxia telangiectasia, ataxia telangiectasia-like disorder, and Nijmegen breakage syndrome.
"The proteins whose deficiency is responsible for these three human disorders have the job of ensuring that chromosome ends are maintained and protected," says Xu-Dong Zhu, assistant professor of biology and the lead author on the study. "As we age, our chromosome ends become shorter. Individuals whose ends deteriorate faster are at a higher risk of developing cancer because short chromosome ends are a serious threat to the stability of our genome. When the genome becomes unstable, it puts our bodies at greater risk of cancer."
Zhu adds that patients with ataxia telangiectasia, ataxia telangiectasia-like disorder, and Nijmegen breakage syndrome experience an accelerated rate of loss of DNA from chromosome ends. "We didn't know why this happens; now we have found that the communication link between these proteins and a protein crucial for maintenance of chromosome ends is either missing or nonfunctional in these patients."
Zhu further explains that lack of this cross talk in normal cells promotes short chromosome ends and as a result promotes cancer formation. A key difference between cancer cells and normal cells is that the former maintain their chromosome ends and have the unlimited potential to grow. Disruption of this communication in cancer cells induces shortening of chromosome ends and may restrict their potential to grow.
Zhu says that the discovery will help researchers understand the onset and progression of these diseases as well as help them find a cure for cancer.
McMaster University
Zhu adds that patients with ataxia telangiectasia, ataxia telangiectasia-like disorder, and Nijmegen breakage syndrome experience an accelerated rate of loss of DNA from chromosome ends. "We didn't know why this happens; now we have found that the communication link between these proteins and a protein crucial for maintenance of chromosome ends is either missing or nonfunctional in these patients."
Zhu further explains that lack of this cross talk in normal cells promotes short chromosome ends and as a result promotes cancer formation. A key difference between cancer cells and normal cells is that the former maintain their chromosome ends and have the unlimited potential to grow. Disruption of this communication in cancer cells induces shortening of chromosome ends and may restrict their potential to grow.
Zhu says that the discovery will help researchers understand the onset and progression of these diseases as well as help them find a cure for cancer.
McMaster University
Chromosome Current Events and Chromosome News RSSGene mismatch influences success of bone marrow transplants
A commonly inherited gene deletion can increase the likelihood of immune complications following bone marrow transplantation, an international team of researchers reports in the November 22 advance online issue of Nature Genetics.
New map of variation in maize genetics holds promise for developing new varieties
A new study of maize has identified thousands of diverse genes in genetically inaccessible portions of the genome. New techniques may allow breeders and researchers to use this genetic variation to identify desirable traits and create new varieties that were not easily possible before.
New Down syndrome treatment suggested by Stanford/Packard study in mice
At birth, children with Down syndrome aren't developmentally delayed. But as they age, these kids fall behind. Memory deficits inherent in Down syndrome hinder learning, making it hard for the brain to collect experiences needed for normal cognitive development.
Cognitive dysfunction reversed in mouse model of Down syndrome
A study by neuroscientist William C. Mobley, MD, PhD, chair of the Department of Neurosciences at the University of California, San Diego School of Medicine, and colleagues at Stanford University Medical School has demonstrated a possible new approach to slowing the inevitable progression of cognitive decline found in Down's syndrome.
Chromosomes dance and pair up on the nuclear membrane
Meiosis - the pairing and recombination of chromosomes, followed by segregation of half to each egg or sperm cell - is a major crossroads in all organisms reproducing sexually.
Largest gene study of childhood IBD identifies 5 new genes
In the largest, most comprehensive genetic analysis of childhood-onset inflammatory bowel disease (IBD), an international research team has identified five new gene regions, including one involved in a biological pathway that helps drive the painful inflammation of the digestive tract that characterizes the disease.
CSHL study shows that some malignant tumors can be shut down after all
Oncologists have had their hands tied because more than half of all human cancers have mutations that disable a protein called p53.
Possible help in fight against muscle-wasting disease
A compound already used to treat pneumonia could become a new therapy for an inherited muscular wasting disease, according to researchers at the University of Oregon and the University of Rochester School of Medicine and Dentistry in New York.
Developmental delay could stem from nicotinic receptor deletion
The loss of a gene through deletion of genetic material on chromosome 15 is associated with significant abnormalities in learning and behavior, said a consortium of researchers led by Baylor College of Medicine (www.bcm.edu) in a report that appears online today in the journal Nature Genetics.
Autism Consortium symposium draws record number of researchers, advocates, parents for autism update
The Autism Consortium, an innovative collaboration of researchers, clinicians, funders and families dedicated to catalyzing research and enhancing clinical care for autism spectrum disorders (ASDs), held its fourth annual symposium on October 28th, 2009, at Harvard Medical School in Boston.
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