Category Archives: Genome

Human Genome, Original Music and Original Art by Virgo Rouge
Copyright 2015. Virgo Rouge also know as Marissa Elienne http://virgorouge.com All instrumentation by Virgo Rouge. Composition by Virgo Rouge. Visual Artwork...

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Human Genome, Original Music and Original Art by Virgo Rouge - Video

Mapping the human genome: The Eric Lander interview
Professor Eric Lander is one of the leaders of the Human Genome Project, and a member of US President Barack Obama s scientific advisory panel. In an exclusi...

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Genome editing: "completely crazy, completely futuristic"
Maria Leptin, director of the European Molecular Biology Organization, says the new CRISPR technology, which allows scientists to carry out microsurgery on genes and easily change a DNA sequence ...

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Fringe Science Baby Genome Sequencing | SYSK Internet Roundup
Josh talks about a neat website that offers the best scientific information on fringe topics like the Loch Ness Monster, and you can now have your baby #39;s gen...

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For the first time, CRISPR-Cas9 gene-editing technology has been employed in a whole organism model to systematically target every gene in the genome. A team of scientists at the Broad Institute and MIT's David H. Koch Institute for Integrative Cancer Research have pioneered the use of this technology to "knock out," or turn off, all genes across the genome systematically in an animal model of cancer, revealing genes involved in tumor evolution and metastasis and paving the way for similar studies in other cell types and diseases. The work appears online March 5 in Cell.

"Genome-scale guide RNA libraries are a powerful screening system, and we're excited to start applying it to study gene function in animal models," said co-senior author Feng Zhang, core member of the Broad Institute of MIT and Harvard, investigator at the McGovern Institute for Brain Research at MIT, and assistant professor in the MIT Departments of Brain and Cognitive Sciences and Biological Engineering. "This study represents a first step toward using Cas9 to identify important genes in cancer and other complex diseases in vivo."

"Tumor evolution is an extremely complex set of processes, or hallmarks, controlled by networks of genes," said co-senior author Phillip Sharp, Institute Professor at the Massachusetts Institute of Technology, board member at the Broad Institute, and member of the Koch Institute. "The in vivo application of gene-editing is a powerful platform for functional genomic discovery, offering a novel means to investigate each step in tumor evolution and identify the genes that regulate these hallmarks."

CRISPR-Cas9 gene-editing technology enables scientists to investigate the role of genes and genetic mutations in human biology and disease. The system can remove the function of genes at the DNA level, versus other genetic perturbations like RNA interference that "knock down" genes at the RNA level. Broad Institute scientists previously performed genome-wide screens using CRISPR-Cas9 technology in cellular models, but that approach does not capture the complex processes at play in a whole organism. For example, for cancer to metastasize, malignant cells must leave the primary tumor, enter blood vessels to travel to a distant site in the body, leave the blood vessels, and thrive in a new environment. Zhang and Sharp teamed up to search for genes involved in metastasis by applying CRISPR-Cas9 technology in a whole animal model.

In the new study, cells from a mouse model of non-small cell lung cancer (NSCLC) were treated with the Broad's pooled library of CRISPR guide RNAs targeting every gene in the mouse genome, known as the "mouse genome-scale CRISPR knockout library A" (mGeCKOa), along with the Cas9 DNA-cutting enzyme. The system introduces mutations into specific genes, disrupting their sequence and preventing the production of proteins from those genes. The approach ensured that in each cell, only a single gene was knocked out, and that all genes in the mouse genome were targeted by the heterogeneous population of cells in culture. The researchers then transplanted the cells into a mouse and found that cells treated with the knockout library formed highly metastatic tumors.

Using next-generation sequencing, the scientists were able to identify which genes were knocked out in the primary tumors and in the metastases, indicating that the genes are likely tumor suppressors that normally inhibit tumor growth but, when knocked out, promote it.

The results highlighted some well-known tumor suppressor genes in human cancer, including Pten, Cdkn2a, and Nf2, but included some genes not previously linked to cancer. Unexpectedly, the screen also implicated several microRNAs -- small RNA segments that are functional in the cell.

More experimental work remains to fully explore the genes and microRNAs uncovered in the screen. Metastatic tumors are rarely biopsied in the clinic, making samples for research scarce, but future inclusion of metastases in cancer sequencing studies will yield more insight on hits from this study.

Researchers can take the same in vivo approach described in the Cell paper to examine the effects of gene over-expression, to screen circulating tumor cells or other cell lines, and to explore other cancer phenotypes, such as cancer stem cells, host-environment interactions, and angiogenesis.

"Our work provides a proof-of-principle in vivo knockout screen for identification of genes regulating different routes and steps of tumor evolution," said Sidi Chen, co-first author and a postdoctoral fellow working in the Sharp lab.

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In vivo CRISPR-Cas9 screen sheds light on cancer metastasis, tumor evolution

Rob Phillips (Caltech): The Genome as the Modern Rosetta Stone
http://www.ibiology.org/ibiomagazine/rob-phillips-genome-modern-rosetta-stone.html Talk Overview: Despite living in the age of genomics, Rob Phillips argues ...

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Rob Phillips (Caltech): The Genome as the Modern Rosetta Stone - Video

Cobalt Cry - "Genome" Official Music Video
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Cobalt Cry - "Genome" Official Music Video - Video

The more copies of an organism's genome in its cells, the more those cells seem to benefit in terms of growth and adaptation.

So says a study completed with the help of Creighton University microbiologist Anna Selmecki, Ph.D., which will be published in the journal Nature this month. Using populations of yeast, Selmecki and a team of researchers from around the country determined that polyploidy -- having more than two copies of an organism's genome in one cell -- greatly aids in the cells' ability to adapt to their environments. The study may have implications for the study of cancer cells, which are often polyploid and aneuploid (having an abnormal chromosome number).

"Having extra copies of the genome does seem to allow for faster adaptation in yeast," said Selmecki, who began this research as a postdoctoral fellow at the Dana-Farber Cancer Institute and Harvard Medical School. "It seems like such a simple study, but we were able to compare the rate of adaptation of diploid cells, like those which make up most of the human body, to genetically identical polyploid cells, and then sequence the entire genome of about 75 individuals to see how they adapted during the experiment."

Selmecki said she was fascinated by the multiplicity she observed in the yeast populations that started out polyploid. In cancer, she said many tumor cells undergo a genome doubling, and become tetraploid (having four copies of the genome). From there, many mutations can manifest, often with irregularities that develop quickly. Getting a handle on those adaptations could help in cancer diagnosis and treatments.

Using genomics, cell biology, evolutionary theory, and mathematical modeling, Selmecki's research captured the attention of the American Cancer Society, which helped fund a portion of the present project through a postdoctoral fellowship. Selmecki's long-term scientific goal is to continue researching genome evolution to aid in finding new treatments for cancer and other diseases.

"It's very interesting to see the diversity that unfolds in our experiment," she said. "There are still many questions out there: Why has evolution seen fit for mammals to be mostly diploid and other species, like plants, to become polyploid? How often does genome doubling occur in other organisms and what are the consequences? We're continuing to take this research into that next series of explorations."

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The above story is based on materials provided by Creighton University. Note: Materials may be edited for content and length.

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Genome replication may hold clues to cancer evolution

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Newswise (MEMPHIS, Tenn. March 4, 2015) The St. Jude Childrens Research HospitalWashington University Pediatric Cancer Genome Project found that melanoma in some adolescent and adult patients involves many of the same genetic alterations and would likely respond to the same therapy. The research appears in the March issue of the Journal of Investigational Dermatology.

The similarities involved adolescents with conventional melanoma tumors and included the first genetic evidence that sun damage contributes to melanoma in children and adolescents as well as adults. The findings stem from the most comprehensive analysis yet of the genetic alterations responsible for pediatric melanoma, which is the most common skin cancer in children and adolescents.

This study shows that unlike many cancers, conventional melanoma is essentially the same disease in children and adults. That means we need to make it easier for adolescents to access promising therapeutic agents being tried in adults, said co-corresponding author Alberto Pappo, M.D., a member of the St. Jude Department of Oncology. These results also underscore the importance of starting sun protection early and making it a habit for life.

Researchers also identified distinct genetic alterations associated with other pediatric melanoma subtypes, including those associated with large congenital nevi (CNM) and spitzoid tumors. The alterations include a mutation that might help identify spitzoid patients who would benefit from aggressive therapy as well as those who could be cured with less intensive treatment.

Until now the genetic basis of pediatric melanoma has been a bit of a mystery, said co-corresponding author Armita Bahrami, M.D., an assistant member of the St. Jude Department of Pathology. With this study, we have established the molecular signatures of the three subtypes of this cancer, signatures that have implications for diagnosis and treatment.

The National Cancer Institute (NCI) estimates that melanoma is diagnosed in 425 U.S. residents age 19 and younger each year. While the cancer remains rare in young people, the incidence has risen about 2 percent annually in recent decades, primarily in those ages 15 to 19. That age group makes up the majority of current pediatric melanoma patients. For the 75 percent of pediatric patients whose disease has not spread, long-term survival rates now exceed 90 percent.

We were surprised to see that so many of the pediatric melanomas had genetic changes linked to UV damage, said co-author Richard K. Wilson, Ph.D., director of The Genome Institute at Washington University School of Medicine in St. Louis. This in-depth look at the genomics of pediatric melanoma is extraordinarily important for diagnosis and for selecting treatments that give young patients the best chances of a cure.

This study included 23 melanoma patients ranging in age from 9 months to 19 years old. Researchers used whole genome sequencing and other techniques to compare the normal and tumor genomes of patients with three different types of melanoma for clues about the genetic alterations that underlie their disease. The genome is the blueprint for life that is encoded in the DNA found in almost every cell.

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Sun Damage Causes Genetic Changes That Predispose Children and Adolescents to Melanoma

Yijun Ruan 3D Genome Organization
A New Frontier of Genomics, 3D Genome Organization and Transcription Regulation Dr. Yijun Ruan, Professor, The Jackson Laboratory for Genomic Medicine Presen...

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