Stop And Prevent Hereditary, Cancer

This Yeas Concert Tour Purpose is To Stop And Prevent Hereditary, Cancer Houston Society And MD Anderson, Herman Hospital Get Ready: Austin Hybrid Media ( AP ) —-The mixture of the social scene to educate the public on how Genomics And Life Science can add the average of twenty years

to a college students life. Kicking this year in Houston Texas at the House Of Blues …. Looking to find students looking to have careers in Robotics , Informatic, and Genomics, To help find the next cancer fighting Drug. Moonshot Cancer & Diabetes Concert Tour by BMJSports Is Taking Giants Steps a

In A Next Generation Tour: To Prevent Hereditary, Cancer, Health, Risk Using Robots For Laboratory Automation : #LifeScience Drug Discovery Looking For Interns To Build Operate Robots That Can Handle Around The Clock Experiments To Create The Next Generation Cancer Drug: Ex Twitter Executives Like katie Jacobs Stanton & Brandless Tina Sharkey … Bringing On New Partners Like El Lilly Pharm GSK life-threatening diseases are caused or exacerbated by a mere change of a single nucleotide building block in the universal genetic DNA code. Such “point mutations” can turn single cell in the human body into a cancerous cell that goes on to grow into a tumor, or they can turn antibiotic-sensitive into antibiotic-resistant bacteria that cause untreatable infections. In an ideal world, clinicians would be able to remove cells with such deleterious point mutations right after they are created to fight diseases much more effectively. A research team at the Wyss Institute for Biologically Inspired Engineering reports now in the Proceedings of the National Academy of Sciences (PNAS) that it has accomplished the first step toward this goal by converting the CRISPR/Cas9 genome engineering system into a genome surveillance tool.

The researchers, led by Wyss Institute Core Faculty members George Church and James Collins, developed an in vivo mutation prevention method that enables the DNA-cleaving Cas9 enzyme to discriminate between genomic target sites differing by a single nucleotide and to exclusively cut the unwanted one. In proof-of-concept studies performed in bacterial E. coli strains grown in culture or the mouse gastrointestinal tract, the approach can prevent the survival of antibiotic resistant variants. The Cas9 enzyme is guided to its genomic target sequence by a small guide RNA with a complementary sequence. Once brought into position on the gene of interest, Cas9 acts like a molecular pair of scissors, cutting the target sequence at a defined site. If repaired, this deliberately introduced damage allows biologists to edit the genome of cells, but if left unrepaired, it will cause cells to die. Yet, despite the system’s effectiveness in finding and cutting target sequences in the genome of many organisms, unspecific activity that lets Cas9 randomly cut at secondary, not completely identical sites still poses a problem to genome engineers. This also means that a target sequence carrying an undesired point mutation often cannot be sufficiently discriminated by Cas9 from its normal counterpart and selectively removed. Even designer Cas9 enzymes engineered to be more specific are thus far not able to completely solve this problem. “Our method not only offers a more efficient and precise way to perform high-throughput “functional genomics” in yeast than what was possible with previous methods. It will also allow us to model and test subtle human gene variations in yeast cells that have been loosely associated with certain traits or disorders, and find out which ones may actually be relevant,” said Church, Ph.D., who also is Professor of Genetics at Harvard Medical School (HMS) and of Health Sciences and Technology at Harvard and the Massachusetts Institute of Technology (MIT). Variations in human genes normally do not occur as perfect deletions of their sequences from the genome, but rather consist of small point mutations — substitutions of single A, T, C, or G base units in the DNA code for one of the other ones — or the insertion or deletion of a few base units. To recreate such variations in the yeast genome in the absence of other potentially interfering variations, the team leveraged CRISPR-Cas9,

which can be precisely targeted to pre-selected sequences in the DNA with the help of a small guide RNA (sgRNA). After the Cas9 enzyme has cut its target sequence, a process known as homology-directed recombination (HDR) can repair the gene by using information from an additionally supplied donor template sequence that carries a variation of interest. “We have developed a strategy that physically links the blueprints for sgRNA and donor template in one stable and heritable extra-chromosomal DNA molecule (guide+donor).

This enabled us to construct large libraries of variants in one reaction, deliver multiple corresponding sgRNAs and donor templates en masse to yeast cells, and identify those that stimulate a certain cell behavior by next-generation sequencing,” said Postdoctoral Fellow Xiaoge Guo, Ph.D., one of the study’s first authors.