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Tag Archives: DNA repair

Friday Science Review: February 19, 2010

Hunks and pigs highlight this week’s research wrap-up…

HUNKs Stop Cancer Metastasis: Researchers screening tumour cells found that expression of the enzyme HUNK (Hormonally Up-regulated Neu-associated Kinase) is significantly lower in cancers.  When they reconstituted HUNK into metastatic cancer cells, it decreased their metastastic potential when tested in mouse cancer models.  Its actions block the association of PP2A and cofilin-1 and prevent the formation of actin filaments, which are key skeletal proteins involved in the cell migration process.  Dr. Tak Mak led the research team at the Campbell Family Institute for Breast Cancer Research and published the study in the Proceedings of the National Academy of Sciences.

Malaria Research Gets Genomic Help: A genome-wide study on the parasite Plasmodium falciparum should help researchers in the hunt for new drugs against malaria.  The genome of 189 malaria samples from around the world were decoded and analyzed to try to identify key genes that are responsible for the parasite’s propensity to evolve and become resistant to currently available drug treatments.  These data are invaluable for the design of future therapeutic approaches.  An international team was co-led by Dr. Philip Awadalla at the Université de Montréal and reports their work in the current issue of Nature Genetics.

Genetic Clues to Diabetes: Using a genome-wide association approach, 13 SNPs concentrated in 4 genetic regions were identified to be strongly correlated with glycemic control in type 1 diabetes.  For example, SORCS1 is strongly associated with hypoglycemia (low blood glucose) and BNC2 is correlated with eye and kidney complications.  This study is a first for suggesting that there may be a genetic contribution to the individual’s ability to control blood glucose levels.  The Hospital for Sick Children’s Dr. Andrew Paterson led the study, which appears in the journal Diabetes.

Porky Pig to the Rescue: Scientists revealed a significant advantage to transplanting porcine pancreatic islet cells as a therapeutic for diabetes.  In contrast to using human islet cells, porcine derived cells do not result in the formation of islet amyloids, which allows them to continue functioning properly for the long term.  They attribute this porcine advantage to differences in the sequences of islet amyloid polypeptide (IAPP).  Dr. Bruce Verchere’s team at the University of British Columbia describes their work in the Proceedings of the National Academy of Sciences.

In (un)related news, Guelph University’s genetically engineered pigs or “Enviropigs” were given the OK by Environment Canada as being non-toxic to the environment.  Now they await Health Canada’s nod before they appear in your local supermarket.

Stem Cells Don’t Mind DNA Damage: Canadian scientists have discovered that stem cells intentionally damage their own DNA in order to regulate development… continue reading the rest of the story here at the Stem Cell Network Blog.

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Friday Science Review: October 23, 2009

A lucky find and two very different genomics projects…

Connective Tissue Disorder Linked to Defects in Ltbp4:  A McGill University researcher collaborating on two independent projects, one from Washington University School of Medicine and the other from New York University School of Medicine, made the coincidental link between the two after realizing that the tissue defects were identicalDr. Elaine Davis, an electron microscopy expert at McGill, analyzed tissue from children born with abnormally developed lungs, gastrointestinal and urinary systems, skin, skull, bones and muscles.  The underlying cause is a connective tissue disorder called cutis laxa that also causes skin to hang loosely from the body.  At the same time, Dr. Davis was analyzing tissue taken from Ltbp4 gene knockout mice from New York University when she realized that the connective tissue defects in the human and mouse samples were identical.  This connection was confirmed when they sequenced the Ltbp4 gene in human patients and discovered recessive mutations.  With this discovery, they now have a molecular target to understand the disease and to design therapeutic strategies.  The study is reported in The American Journal of Human Genetics.

A Deep-sea Microbe Genome: The microbe, SUP05, lives in the deep ocean “dead zone” where oxygenated water is minimal. It survives by using other compounds instead of oxygen, such as nitrates, sulphates and metals.  A recent surge in population suggests an expanding low-oxygen ocean ecosystem and is an indicator of global climate change.  University of British Columbia professor Dr. Steve Hallam and his research group analyzed the entire genome of SUP05 and identified a number of genes mediating carbon assimilation, sulfur oxidation, and nitrate respiration.  This study provides the first insight into the metabolism of these microbes and their effects on nutrients and gases in the deep-ocean ecosystem and will also lead to further understanding of their ecological and biogeochemical role.  The report appears in this week’s edition of Science.

Allelic Expression Genomic Map: Illumina genomics technology was used in this study to map global allelic expression differences associated with cis-acting variants.  Cis-acting elements can affect gene expression and variations due to single nucleotide polymorphisms (SNPs) explain a large percentage of the phenotypic differences in the population.  It is very informative to have this global map of the cis-acting variants and helps researchers identify variants associated with diseases.  To demonstrate this, they finely mapped cis-regulatory SNPs in a region in chromosome 8 associated with lupus.  The study was performed by Dr. Tomi Pastinen and his Genome Quebec team at McGill University and the report was published in Nature Genetics.

DNA Repair Suppresses c-Myc Lymphoma:  Overexpression of c-Myc in B cells is associated with lymphomas but requires secondary mutation events for the disease to develop.  In this study, immunologist Dr. Alberto Martin and his research team at the University of Toronto identified that the DNA repair protein, Msh2, plays an important role in mitigating c-Myc associated cancer.   To demonstrate this, they generated mice that overexpress c-Myc but with Msh2 mutations such that they are deficient in DNA mismatch repair.  These mice rapidly develop B cell lymphomas, which suggests that Msh2-dependent DNA repair actively suppresses c-Myc associated oncogenesis.  The report appears in the early edition of The Proceedings of the National Academy of Sciences.

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