Using a method called genomic qPCR able to identify specific DNA sequences, they found four genes in the amplified region, two of which, GOLPH3 and SUB1, were expressed at high levels, reflecting an increase in gene copy. To determine whether either or both of these genes are involved in cancer, conducted a loss of function test, where they have abandoned the activity of each gene in a set of tumor cells grown in the laboratory. When we knocked ?GOLPH3 expression [or activity] by 95 %, significantly inhibited the ability of these cell lines to grow in a semi-solid, high-quality cancer than normal cells do not usually share, said Chin .Intriguing finding was that there was barely enough to prove that GOLPH3 is an oncogene ? a contributor to cancer when overexpressed in a cell. Demonstrate that require some experimenting to ensure that GOLPH3 itself, and not a shadow neighbor gene, is responsible for the effects. And ?in the mouse and human cells.
Co-authors include Omar Kabbarah, Mei-Chih Liang, PhD, Joyce Wu, Sabin Dhakal, Min Wu, Ph.D., Shujuan Chen, Tamar Feinberg, Joseph Huang, Hans Widlund, PhD, and Wong Kin-Kowk, MD, Ph.D., Dana-Farber, Elena Ivanova, PhD, Yonghong Xiao, Ph.D. Fisher, MD, Ph.D., of Massachusetts General Hospital; Valsami Anagnostou, and David Rimm, MD, Ph.D., Yale University School of Medicine, Abdel Saci, PhD, Harvard Medical School.
In addition to identifying GOLPH3 as a bona fide oncogene and an indicator of rapamycin may be effective against specific tumors, the study highlights the need to follow genomic studies in a rigorous review of the biological function and operation of potential cancer genes, Chin concludes . Only then can we turn our intriguing discoveries in the cancer genome into something that is useful for cancer patients.
Many genetic tests that were done in yeast, the researchers knew that defects in the retromer complex can cause cells to be vulnerable to rapamycin, as excess GOLPH3 can. Rapamycin is known to interfere with a protein called TOR, whose job is to control the size of yeast cells. This suggests that the retromer complex in yeast is important for the chemical signals sent to and from TOR.
Previous studies have shown that Americans have a strong primary health care system in place for patients paying the dividends, and ultimately the taxpayer. For example, individuals with one or more chronic conditions experience reduces the risks, and reduced the duration and effects of acute and episodic. Similarly, they report a reduction in the risk and effects of health conditions continue,
First attempt of the team to discover the role of GOLPH3 ? with gene expression profiles to see how protein levels track with many cellular functions ? has been successful.One mate was seen as VPS35, a component of a complex structure called the retromer. The work of the complex is to recycle the antenna-like receptors that dot the surface of cells.
Discovery of the Dana-Farber Cancer Institute scientists of a gene that causes cancer in the family first to be linked to cancer shows a panoramic view of the close-up perspective, genomics and molecular biology are needed to determine which genes are involved in cancer and who are mere spectators. The results are reported on the June 25 issue of the journal Nature.
In the future, we can expect genomic studies [that show the activity of thousands of cellular genes] to generate hundreds or thousands of genetic elements of interest in cancer research, said the study?s lead author, Lynda Chin, MD, Dana-Farber. To reduce this group of genes that make cancer growth and metastasis, it is necessary to do functional studies, which focus on individual genes do to turn a cell cancerous, and mechanistic studies, which examine how the cancer cells and transformed in what context. This is a long and intensive effort that will use knowledge from different fields and different model systems.
Despite their discovery that GOLPH3 can promote cancer, the researchers did not know what role the gene in normal cells. There was literally no information about what he does, says Chin. The only clue is that the protein it encodes ? designated GOLPH3 ? is located in the Golgi.
All these results have allowed us to build a case that GOLPH3 is an oncogene, Chin said. But there was a problem. This information has not been very useful to achieve our ultimate goal, which is the translation of results into a form that is clinically useful for patients.
Chin team theorized that mammalian GOLPH3 also works with the retromer complex to control the activity of TOR in mammalian cells . To test this idea, the researchers found that the inversion GOLPH3 reduced cell size, such as rapamycin did.
Followed these experiments with biochemical studies to explore how GOLPH3 affects cell size.
Source: http://www.pcaeg.org/?p=304
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