Humans normally have 46 chromosomes in each cell, divided into 23 pairs. Two copies of chromosome 6, one copy inherited from each parent, form one of the pairs. Chromosome 6 spans about 171 million base pairs (the building blocks of DNA) and represents between 5.5 percent and 6 percent of the total DNA in cells.
Identifying genes on each chromosome is an active area of genetic research. Because researchers use different approaches to predict the number of genes on each chromosome, the estimated number of genes varies. Chromosome 6 likely contains between 1,100 and 1,600 genes.
Genes on chromosome 6 are among the estimated 20,000 to 25,000 total genes in the human genome.
The Muscular Dystrophy Association today heralds a landmark muscular dystrophy advance by an international study team of scientists and physicians from the Netherlands, United States, France and Spain. Led by MDA-grantee Silvère van der Maarel, Ph.D., at Leiden University Medical Center in the Netherlands, the collaborative study of more than 2,300 people found that two distinct genetic changes on chromosome 4 must be present to cause facioscapulohumeral muscular dystrophy (FSHD).
Tasigna (nilotinib) capsules have been approved with conditions in Canada as a new therapy for patients with CML, in the chronic phase (first phase) of the disease. Patients must be resistant to or intolerant of at least one prior therapy, including (Pr)Gleevec (imatinib mesylate), an established standard of care.
Researchers at the University of North Carolina at Chapel Hill School of Medicine have uncovered the genetic architecture controlling the growth of the collateral circulation - the "back-up" blood vessels that can provide oxygen to starved tissues in the event of a heart attack or stroke.
Nearly two decades after they identified the specific genetic flaw that causes a common type of muscular dystrophy, scientists believe they have figured out how that flaw brings about the disease. The finding by an international team of researchers settles a longstanding question about the roots of facioscapulohumeral muscular dystrophy or FSHD.
Researchers at Massachusetts General Hospital found that patients with nonalcoholic fatty liver disease (NAFLD) who carry an allele of the PNPLA3 gene have an increased risk of developing advanced disease, including nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. A second study supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) validates these findings and further concludes that in pediatric patients, the same allele is associated with earlier disease presentation.
Researchers at Massachusetts General Hospital found that patients with nonalcoholic fatty liver disease (NAFLD) who carry an allele of the PNPLA3 gene have an increased risk of developing advanced disease, including nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. A second study supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) validates these findings and further concludes that in pediatric patients, the same allele is associated with earlier disease presentation. Both studies are available in the September issue of Hepatology, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases (AASLD).
Using a new, rapid and less expensive DNA sequencing strategy, scientists have discovered genetic alterations that account for most cases of Kabuki syndrome, a rare disorder that causes multiple birth defects and mental retardation. Instead of sequencing the entire human genome, the new approach sequences just the exome, the 1-2 percent of the human genome that contains protein-coding genes.
Scientists have identified a genetic variant which increases susceptibility to tuberculosis (TB) in African populations using a technique known as a genome-wide association (GWA) study. This is the first novel disease variant to be identified using this technique in Africans and demonstrates that such studies are viable in African populations, which have a high degree of genetic diversity.
Alnylam Pharmaceuticals, Inc. a leading RNAi therapeutics company, announced today the publication of new research findings in the journal Nature describing the discovery and validation of the role of the gene Sort1 in the development of cardiovascular disease, including myocardial infarction (MI). This work was done with collaborators at University of Pennsylvania (UPenn) School of Medicine, Massachusetts General Hospital (MGH), and the Broad Institute. The collaborative effort combined genome-wide association studies (GWAS) and RNAi technology to identify and validate novel genes as targets for new therapies for heart disease.
A group of scientists has identified a genetic variant that substantially increases the risk for developing schizophrenia in Ashkenazi Jewish and other populations. The study, published by Cell Press on August 5th in the American Journal of Human Genetics, associates a deletion on chromosome 3 with increased incidence of schizophrenia.
Researchers at the Hebrew University of Jerusalem and elsewhere have succeeded in identifying for the first time a gene associated with susceptibility to chronic pain caused by nerve injury in humans, signaling a significant step toward better understanding and treating of the condition.
Researchers at the Hebrew University of Jerusalem and elsewhere have succeeded in identifying for the first time a gene associated with susceptibility to chronic pain caused by nerve injury in humans, signalling a significant step toward better understanding and treating of the condition.
ARIAD Pharmaceuticals, Inc. today reported financial results for the second quarter and six months ended June 30, 2010 and provided an update on corporate developments.
The true power of genomic research lies in its ability to help scientists understand biological processes, particularly those that - when altered - can lead to disease. This power is demonstrated dramatically in a pair of papers published today in the journal Nature. In the first, a global team of researchers describes 95 different variations across the genome that contribute in different degrees to alterations in blood cholesterol and triglyceride levels in multiple human populations. In the second report, close examination of just one of these common variants not only reveals the involvement of an unexpected genetic pathway in lipid metabolism but also provides a blueprint for using genomic findings to unravel biological connections between lipid levels and coronary heart disease.
Some people find quinine to be bitter while others can drink it like water. Now, scientists from the Monell Center and collaborators report that individual differences in how people experience quinine's bitterness are related to underlying differences in their genes.The findings, published online in the journal Human Molecular Genetics, demonstrate that genetic variation in regions of DNA that encode bitter taste receptors predicts a person's perception of bitterness from quinine.
A genetics research team based at The Children's Hospital of Philadelphia continues to discover recurrent translocations—places in which two chromosomes exchange pieces of themselves. As many as 1 in 600 persons carry balanced chromosome translocations, which involve no loss or gain of DNA. Most such people appear healthy, but may have a child with abnormal chromosome composition and disabilities resulting from disrupted, extra or missing copies of genes.
Bio-Path Holdings, Inc.,, a biotechnology company with drug development operations in Houston, Texas, announced today that the first patient has been dosed in a Phase I study of its cancer drug candidate, Liposomal Grb-2 (L-Grb-2 or BP-100-1.01), in patients with Acute Myeloid Leukemia (AML), Chronic Myelogenous Leukemia (CML), Acute Lymphoblastic Leukemia (ALL) or Myelodysplastic Syndrome (MDS).
Scientists at deCODE genetics and colleagues at Radboud University in the Netherlands today describe how the impact of a single letter variation in the sequence of the human genome conferring risk of kidney disease varies with age and with the onset of other diseases. The study provides independent confirmation of the association made in an earlier study between a version of the the SNP, located on chromosome 16p12, and risk of chronic kidney disease. It also confirmed the link between the SNP and concentrations of serum creatinine, a key indicator of kidney function.
Scientists at the Buck Institute for Age Research have discovered that a particular family of enzymes are involved in the breakdown of proteins that modify the production of toxic fragments that lead to the pathology of Huntington's disease. These enzymes, matrix metalloproteinases, provide new targets for drug therapies for the disease - targets that have already been shown to respond to cancer drugs currently in clinical development.
A novel approach detects genetically abnormal cells in the blood of non-small cell lung cancer patients that match abnormalities found in tumor cells and increase in number with the severity of the disease, a research team led by scientists at The University of Texas MD Anderson Cancer Center report in the journal Clinical Cancer Research.
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