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How Does Sendai Virus Reprogram Cells?
 
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Learn more at http://www.lifetechnologies.com/cytotune This video demonstrates how Sendai virus, found in the Cytotune®-iPS Sendai Reprogramming Kit, reprograms somatic cells to generate induced Pluripotent Stem Cells (iPSCs) How Does Sendai Virus Reprogram Cells? Induced pluripotent stem cells (iPSCs) are genetically reprogrammed somatic cells that exhibit a pluripotent stem cell state similar to embryonic stem cells. The discovery in 2006 that human and mouse fibroblasts could be reprogrammed to generate iPSCs with qualities remarkably similar to embryonic stem cells has created a valuable new source of pluripotent cells. Fibroblasts, similar to other somatic cell types, do not express high levels of the transcription factors Oct4, Sox2, Klf4, and c-Myc under normal conditions. High levels of expression of these four genes will cause reprogramming of the fibroblast and it will become pluripotent. There are multiple methods to generate iPSCs. Viruses such as retroviral vectors require integration of the viral genome into the host's chromosomes to express reprogramming genes. Normal gene transcription allows the inserted Oct4, Sox2, Klf4, and c-Myc transgenes to be expressed along with the host's genes. Integration of viral DNA into the host genome disrupts the genome of the cells. This alteration can render the iPSCs and their derivatives less safe for clinical application and can compromise compound screens or disease pathway analyses. On the other hand, Sendai virus is a single stranded negative-sense RNA virus that replicates in the cytoplasm. This means it does not integrate into the host's genome. Sendai virus replicates independent of cell cycle, unlike other approaches where the exogenous genes are expressed only as the cell divides. Using this strategy, Sendai virus produces very high copy numbers of the target gene. The Cytotune® iPS Sendai Reprogramming Kit contains four Sendai virus-based reprogramming vectors, each expressing one of the four Yamanaka factors Oct4, Sox2, Klf4, and c-Myc. These viral vectors are added to the dish of cells to be reprogrammed, incubated overnight, and the reprogramming process begins. After reprogramming, quantitative PCR testing shows that the Sendai virus does not remain in the iPSCs, allowing you to perform your research with iPSCs that have no genomic integration or viral remnants. Sendai virus is particularly useful when reprogramming patient derived blood cells, such as CD34 positive cells, T-cells, and PBMCs. With its non-integrating capabilities, the Sendai virus within the Cytotune®-iPS Sendai Reprogramming Kit allows the use of iPSCs and their derivatives in a broad range of research experiments.
Просмотров: 14205 Thermo Fisher Scientific
Time-lapse imaging of cannibalism without the cell fusion (detail)
 
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Weakened target- cell is contacted by cannibalic cell, exploited and left to die. Time-lapse video captured using Tescan Q-PHASE multimodal holographic microscope, 10x magnification Citation: Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating Balvan J, Gumulec J, Raudenska M, Krizova A, Stepka P, et al. (2015) Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating. PLoS ONE 10(12): e0145016. doi: 10.1371/journal.pone.0145016 doi:10.1371/journal.pone.0145016.s006 To read full article : http://dx.plos.org/10.1371/journal.pone.0145016 Masarik Cancer Research Lab Faculty of Medicine, Masaryk University Kamenice 5, Brno, Czech republic http://www.med.muni.cz/masariklab/ https://www.facebook.com/MasarikLab/
Просмотров: 203 Jaromír Gumulec
4J - How somatic mutations cause cancer
 
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4J_full This is Lecture 4J of the free online course Useful Genetics Part 1. All of the lectures are on YouTube in the Useful Genetics library. Register for the full course here: https://www.edx.org/course/useful-genetics-part-1-how-genes-shape-ubcx-usegen-1x
Просмотров: 655 Useful Genetics
Comparing Fusion Detection Assays Using Sarcoma Samples
 
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In this webinar, Professor Florian Haller from the University Hospital Erlangen shares data from reliable and sensitive RNA fusion detection assays. His data compare TruSight[Symbol] RNA Pan Cancer Panel (1385 target genes), TruSight RNA Fusion Panel (507 target genes), and Archer FusionPlex[Symbol] (85 target genes) assays from sarcoma samples. To learn more about Cancer Clinical Research, visit https://www.illumina.com/areas-of-interest/cancer/clinical-cancer-research.html View related video: Identification of Novel Fusion and Pharmacogenomic Targets in Cancer https://www.youtube.com/watch?v=TZLAul5qdqk&t=507s Subscribe to the Illumina video channel http://www.youtube.com/subscription_center?add_user=IlluminaInc For Research Use Only. Not for use in diagnostic procedures.
Просмотров: 658 Illumina
Identification of Novel Fusions and Pharmacogenomic Targets in Cancer
 
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This webinar describes the optimization and validation of two commercially available clinical research next-generation sequencing (NGS) assays. The first assay is aimed at identifying fusion transcripts and can identify novel fusion partners. The second assay is used to detect pharmacogenomic targets in cancers that have not responded to current standard treatment. This webinar focuses on sarcoma samples, but the approaches used are applicable to different cancer types including other solid tumors and hematological malignancies. View related videos Next generation sequencing-based analyses of hematological malignancies http://youtu.be/Lb0zyXEpquc View related information TruSight RNA Fusion Panel http://www.illumina.com/RNAFusion Cancer Cytogenetics Solutions https://www.illumina.com/areas-of-interest/cancer/clinical-cancer-research/cancer-cytogenetics.html Introduction to Cytogenomics https://www.illumina.com/techniques/popular-applications/cytogenomics.html Subscribe to the Illumina video channel http://www.youtube.com/subscription_center?add_user=IlluminaInc For Research Use Only. Not for use in diagnostic procedures.
Просмотров: 633 Illumina
Genetic Engineering Will Change Everything Forever – CRISPR
 
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Designer babies, the end of diseases, genetically modified humans that never age. Outrageous things that used to be science fiction are suddenly becoming reality. The only thing we know for sure is that things will change irreversibly. Support us on Patreon so we can make more videos (and get cool stuff in return): https://www.patreon.com/Kurzgesagt?ty=h Kurzgesagt merch here: http://bit.ly/1P1hQIH Get the music of the video here: soundcloud: http://bit.ly/2aRxNZd bandcamp: http://bit.ly/2berrSW http://www.epic-mountain.com Thanks to Volker Henn, James Gurney and (prefers anonymity) for help with this video! THANKS A LOT TO OUR LOVELY PATRONS FOR SUPPORTING US: Jeffrey Schneider, Konstantin Kaganovich, Tom Leiser, Archie Castillo, Russell Eishard, Ben Kershaw, Marius Stollen, Henry Bowman, Ben Johns, Bogdan Radu, Sam Toland, Pierre Thalamy, Christopher Morgan, Rocks Arent People, Ross Devereux, Pascal Michaud, Derek DuBreuil, Sofia Quintero, Robert Swiniarski, Merkt Kızılırmak, Michelle Rowley, Andy Dong, Saphir Patel, Harris Rotto, Thomas Huzij, Ryan James Burke, NTRX, Chaz Lewis, Amir Resali, The War on Stupid, John Pestana, Lucien Delbert, iaDRM, Jacob Edwards, Lauritz Klaus, Jason Hunt, Marcus : ), Taylor Lau, Rhett H Eisenberg, Mr.Z, Jeremy Dumet, Fatman13, Kasturi Raghavan, Kousora, Rich Sekmistrz, Mozart Peter, Gaby Germanos, Andreas Hertle, Alena Vlachova, Zdravko Šašek SOURCES AND FURTHER READING: The best book we read about the topic: GMO Sapiens https://goo.gl/NxFmk8 (affiliate link, we get a cut if buy the book!) – Good Overview by Wired: http://bit.ly/1DuM4zq –timeline of computer development: http://bit.ly/1VtiJ0N – Selective breeding: http://bit.ly/29GaPVS – DNA: http://bit.ly/1rQs8Yk – Radiation research: http://bit.ly/2ad6wT1 – inserting DNA snippets into organisms: http://bit.ly/2apyqbj – First genetically modified animal: http://bit.ly/2abkfYO – First GM patent: http://bit.ly/2a5cCox – chemicals produced by GMOs: http://bit.ly/29UvTbh http://bit.ly/2abeHwU http://bit.ly/2a86sBy – Flavr Savr Tomato: http://bit.ly/29YPVwN – First Human Engineering: http://bit.ly/29ZTfsf – glowing fish: http://bit.ly/29UwuJU – CRISPR: http://go.nature.com/24Nhykm – HIV cut from cells and rats with CRISPR: http://go.nature.com/1RwR1xI http://ti.me/1TlADSi – first human CRISPR trials fighting cancer: http://go.nature.com/28PW40r first human CRISPR trial approved by Chinese for August 2016: http://go.nature.com/29RYNnK – genetic diseases: http://go.nature.com/2a8f7ny – pregnancies with Down Syndrome terminated: http://bit.ly/2acVyvg ( 1999 European study) – CRISPR and aging: http://bit.ly/2a3NYAV http://bit.ly/SuomTy http://go.nature.com/29WpDj1 http://ti.me/1R7Vus9 Help us caption & translate this video! http://www.youtube.com/timedtext_cs_panel?c=UCsXVk37bltHxD1rDPwtNM8Q&tab=2
Просмотров: 10535746 Kurzgesagt – In a Nutshell
Somatic Structural Variation Discovery in Multiple Cancer Genomes
 
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Iman Hajirasouliha, Stanford University Computational Cancer Biology https://simons.berkeley.edu/talks/iman-hajirasouliha-02-02-2016
Просмотров: 283 Simons Institute
Dance your Ph.D. 2016: Cancer, mutations, and DNA modifications
 
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In my doctorate I study the role of mutations and DNA modifications on origin and development of cancer. I feel really fortunate to live in the exciting time of big-data which allow us to pursue the symbiosis of wet-lab science and bioinformatics research on a previously unthinkable scale (I am on the bioinformatics side, but enjoy working close to the wet-lab science). The ultimate goal is obviously to turn the gained knowledge into ways how to prevent origin of cancer in the first place, how detect and quantify progression of the disease, but also how to find an effective treatment for its different subtypes. If you are interested in an example of results from our research, you can read our recent article in eLife https://elifesciences.org/content/5/e17082 . But if you prefer something less formal, or have no idea what these mutations and DNA modifications are about and why it is important to understand them in the context of cancer, you can watch this video.
Просмотров: 2418 Markéta Tomková
Examining Cancer with the minION: Methylation and Structural Variation
 
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Presented at Cancer Research & Oncology 2017: https://www.labroots.com/virtual-event/cancer-research-oncology-2017 Winston Timp, Assistant Professor Department of Biomedical Engineering Johns Hopkins University Winston Timp is an assistant professor in Biomedical Engineering at Johns Hopkins University. He earned bachelor degrees in Biochemistry, Chemistry, Physics and Electrical Engineering from the University of Illinois at Urbana. He then earned his a masters and PhD in Electrical Engineering from MIT, working at the Whitehead Institute in Paul Matsudaira's lab, focusing his thesis work on the study of cellular communication in a 3D microenvironment. After receiving his doctorate, he trained as a postdoc at Johns Hopkins in the labs of Andrew Feinberg and Andre Levchenko, studying the epigenetics of cancer. My lab's focus is in the development and application of sequencing technologies to gain a deeper understanding of biology and a more accurate set of clinical tools for human disease. We integrate biophysics, molecular biology and computational biology to create new tools for exploring the epigenome and genome. Leveraging these tools, we then explore interesting questions about fundamental biological concepts using model systems. We apply our newfound knowledge and toolset to clinical samples for diagnosis, surveillance and treatment of human disease. Recent projects range from diagnosis of infectious disease using nanopore sequencing, to developing new tools to characterize the genome and epigenome of cancer, to reading the transcriptome of the hummingbird. Examining Cancer with the minION: Methylation and Structural Variation Nanopore sequencing has enormous potential for application to cancer, but specifically offers advantages into two main arenas, epigenetics and structural variation. Methylation is well-known to be altered in cancer as compared to normal tissue, but how these changes arise and what patterns they are comprised of is only recently being explored. We have demonstrated the ability to sequencing phased methylation patterns in cancer versus normal samples over 5kb fragments, illustrating the potential of this technique. Using methylation calling, we can probe the heterogeneous nature of the cancer epigenome, as well as the changes which occur between normal and cancer samples. Structural variants comprise a significant fraction of mutations in cancer, e.g. 50% of pancreatic cancer mutations. Unfortunately, limitations of conventional, short-read DNA sequencing technologies make it difficult to detect these variations which often lie in repetitive regions. Nanopore sequencing can overcome these limitations, allowing more in-depth study of SVs and phased SNVs. We applied solution-phase hybridization capture to target SV hotspots in pancreatic cancer samples with long-read sequencing. We also demonstrate that with signal level analysis, we can call SNPs and SVs in the same sample. Sponsored By: Oxford Nanopore Earn PACE: 1. Make sure you’re a registered member of LabRoots - https://www.labroots.com/virtual-event/cancer-research-oncology-2017 2. Watch the webinar on YouTube above or on the LabRoots Website - https://www.labroots.com/virtual-event/cancer-research-oncology-2017 3. Click Here to get your PACE (October 11th, 2019) - http://www.labroots.com/credit/pace-credits/2549/third-party LabRoots on Social: Facebook: https://www.facebook.com/LabRootsInc Twitter: https://twitter.com/LabRoots LinkedIn: https://www.linkedin.com/company/labroots Instagram: https://www.instagram.com/labrootsinc Pinterest: https://www.pinterest.com/labroots/ SnapChat: labroots_inc
Просмотров: 182 LabRoots
ACD RNAscope® in situ Hybridization (ISH) Technology Overview
 
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RNAscope® in situ hybridization (ISH) is a highly sensitive and specific assay. It enables researchers to visualize, localize and quantify RNA molecular expression at the cellular level, while preserving cellular relationship and tissue structure. Although introduced in 2012, RNAscope® ISH is already proven and cited in nearly 300 peer-reviewed publications. It is published in a multitude of research areas including cancer, stem cells, neuroscience, infectious diseases and many more. This technology is widely used by basic researchers and biotech pharma researchers to validate or complement IHC (antibody-based protein detection.) Additionally, RNAscope ISH is the only solution to detect and visualize noncoding RNA in the cellular context.
Просмотров: 37599 Advanced Cell Diagnostics
What is TOTIPOTENCY? What does TOTIPOTENCY mean? TOTIPOTENCY meaning, definition & explanation
 
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BROWSE The Internet EASY way with The Audiopedia owned Lightina Browser Android app! INSTALL NOW - https://play.google.com/store/apps/details?id=com.LightinaBrowser_8083351 What is TOTIPOTENCY? What does TOTIPOTENCY mean? TOTIPOTENCY meaning, definition & explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license. Totipotency is the ability of a single cell to divide and produce all of the differentiated cells in an organism. Spores and zygotes are examples of totipotent cells. In the spectrum of cell potency, totipotency represents the cell with the greatest differentiation potential. Toti comes from the Latin totus which means "entirely". It is possible for a fully differentiated cell to return to a state of totipotency. This conversion to totipotency is complex, not fully understood and the subject of recent research. Research in 2011 has shown that cells may differentiate not into a fully totipotent cell, but instead into a "complex cellular variation" of totipotency. Stem cells resembling totipotent blastomeres from 2-cell stage embryos can arise spontaneously in the embryonic stem cell cultures and also can be induced to arise more frequently in vitro through down-regulation of the chromatin assembly activity of CAF-1. The human development model is one which can be used to describe how totipotent cells arise. Human development begins when a sperm fertilizes an egg and the resulting fertilized egg creates a single totipotent cell, a zygote. In the first hours after fertilization, this zygote divides into identical totipotent cells, which can later develop into any of the three germ layers of a human (endoderm, mesoderm, or ectoderm), into cells of the cytotrophoblast layer or syncytiotrophoblast layer of the placenta. After reaching a 16-cell stage, the totipotent cells of the morula differentiate into cells that will eventually become either the blastocyst's Inner cell mass or the outer trophoblasts. Approximately four days after fertilization and after several cycles of cell division, these totipotent cells begin to specialize. The inner cell mass, the source of embryonic stem cells, becomes pluripotent. Research on Caenorhabditis elegans suggests that multiple mechanisms including RNA regulation may play a role in maintaining totipotency at different stages of development in some species. Work with zebrafish and mammals suggest a further interplay between miRNA and RNA binding proteins (RBPs) in determining development differences. In September 2013, a team from the Spanish national Cancer Research Centre was able for the first time to make adult cells from mice retreat to the characteristics of embryonic stem cells, thereby achieving totipotency.
Просмотров: 16949 The Audiopedia
The Landscape of Driver Kinase Fusions in Cancer - Nicolas Stransky
 
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May 12, 2015 - The Cancer Genome Atlas 4th Annual Scientific Symposium More: http://www.genome.gov/27561703
Просмотров: 360 National Human Genome Research Institute
Mitosis in 3D - With Chromosome Bridge
 
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Video by Dr Andrew Burgess, Group Leader - Cell Division (http://www.garvan.org.au/research/cancer/cell-division), filmed using a Leica SP8 confocal microscope, images taken every 1min30sec. 3D render of a HeLa cell expressing H2B-mCherry (red) and aTubulin-GFP (green).
Просмотров: 2328 Garvan Institute of Medical Research
Large, Medium and Small Cancer Research Panels | ESHG 2015
 
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Download the poster: http://www.slideshare.net/LifeTechnologies/development-and-validation-of-the-oncomine-cancer-research-panel-ocp-eshg-2015-poster-ps12131 Kate Rhodes discusses her poster on the Oncomine Cancer Research Panel, the Oncomine Focus Panel, and the Ion AmpliSeq Colon and Lung Panel. Abstract Treating cancer effectively requires an understanding of the molecular alterations driving each patient’s tumor. Targeted sequencing efforts that characterize prevalent somatic alterations and require limited sample input may provide an effective diagnostic approach. Herein, we describe the design and characterization of the Oncomine™ Cancer Research Panel (OCP) that includes recurrent somatic alterations in solid tumors derived from the Oncomine™ cancer database. Using Ion AmpliSeq™ technology, we designed a DNA panel that includes assays for 73 oncogenes with 1,826 recurrent hotspot mutations, 26 tumor suppressor genes enriched for deleterious mutations, as well as 75 genes subject to recurrent focal copy gain or loss. A complementary RNA panel includes 183 assays for relevant gene fusions involving 22 fusion driver genes. Recommended sample inputs were 10 ng of nucleic acid per pool. Sequencing libraries were analyzed on an Ion Torrent™ Personal Genome Machine™. Initial testing revealed an average read depth of 1,500X+ with more than 95% uniformity and on target frequency. The panel was shown to reliably detect known hotspots, insertions/deletions, gene copy changes, and gene fusions in molecular standards, cell lines and formalin-fixed paraffin embedded samples. Retrospective analysis of large sample cohorts has been completed and the results of analysis of 100 lung cancer and 100 prostate cancer cases will be summarized. In addition, a prospective cohort of 100 samples from the University of Michigan Molecular Diagnostics laboratory was profiled with OCP. Overall, we achieved 95%+ sensitivity and specificity for detection of KRAS, EGFR and BRAF mutations and ALK gene fusions.
Просмотров: 326 Thermo Fisher Scientific
Treatment of advanced metastatic cancers with Sendai Virus
 
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Sendai virus has oncolytic properties. Cancer cells could be highly sensitive to destruction by this virus because of a number of factors. Among them is ability of Sendai virus to cause a formation of a syncytium (a polykaryonic structure) that allows spreading of virus infection in the tumor without an exposure of the virus to host neutralizing antibodies. Sendai virus neuraminidase (sialidase), a component of the viral envelope, can cleave sialic acids on the surface of malignant cells thereby unmasking cancer specific antigens and exposing them to the immune system. Sialic acid residues located on the cell surface serve as natural receptors for Sendai virus. As far as tumor cells generally have very abundant sialic acid containing glycans on their surface, preferential and robust association of the virus with malignant rather than with normal cells gets promoted. Sendai virus triggers a production of interferon and many other proinflammatory cytokines and chemokines. The virus elicits strong innate as well as adaptive immune responses, which efficiently activate natural killers, dendritic cells and cytotoxic T lymphocytes that attack tumor cells. In Russia in two major cities Sendai virus was tested in advanced metastatic cancer patients by Dr. Vyacheslav Senin. The tests yield encouraging responses and warrant the continued preclinical and clinical studies.
Просмотров: 979 Olga Matveeva
Digital PCR: Rare Allele Applications with QuantStudio™ 3D Digital PCR System
 
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Learn more at http://www.lifetechnologies.com/quantstudio3d Genetic mutation is a hallmark of cancer, and the ability to detect genomic DNA changes is paramount to understanding this disease at a molecular level. In many cases, genetic changes can be as small as a single base substitution, or SNP, and this rarity poses an additional challenge for researchers. Assays developed to detect oncogenic mutations need to be able to identify just a few mutant cells in a huge abundance of wild type cells. This "finding a needle in a haystack" requires an assay that delivers both high signal-to-noise and low false positive/false negative rates. Common SNP genotyping technologies, such as CE sequencing and real-time PCR, are most effective in detecting mutant cells at prevalence no lower than about 20% (or approximately 1 in 5 cells). But, by combining available real-time PCR chemistries, such as TaqMan® Assays, with digital PCR, researchers are able to detect mutant cell prevalence down to 1%—and below So how does this work? First, let's review the basics of a TaqMan SNP Genotyping Assay. These assays are designed to resolve inherited SNP markers for which 3 genetic states are possible -- homozygous for allele 1, homozygous for allele 2, or heterozygous (containing one copy of each allele). The assay utilizes two gene specific primers and two allele-specific probes labeled with VIC and FAM dyes respectively. In the example shown, the presence of allele 1 is detected by VIC signal emission due to cleavage of the allele 1 probe. Similarly, the presence of allele 2 is detected by FAM signal emission due to cleavage of the allele 2 probe. The three possible outcomes are best viewed using a two-dimensional cluster plot. Because inherited germ line SNPs are either 0%, 50%, or 100% in normal diploid samples, the assays do not require extremely high probe hybridization specificity for assigning genotypes to individuals. So how can we use an inherently low-specificity assay to detect these rare events? The answer is to subdivide our sample in a digital PCR approach. Prior to PCR cycling, digital PCR requires partitioning of the DNA sample into hundreds or even thousands of independent PCR replicates such that not all reactions receive a DNA sequence of interest. The effect of this partitioning process is to reduce the number of molecules in any given reaction and to effectively enrich for sequences of interest. For example, if a sample containing 99 wild type molecules and 1 mutant equates to the mutation being present at 1 in 100 or 1%. Using TaqMan SNP Genotyping Assays in standard real-time PCR mode, the single mutant is lost in a sea of wild type copies. But if we partition the sample, competing wild type sequences in any reaction containing a mutant are reduced, effectively decreasing background noise. If sufficient partitions are used, the reaction wells reach a point where the wild type signal no longer overwhelms the mutant signal. In practice, the total count of each allele, mutant and wild type, can be calculated and a ratio determined since each data point is generated digitally. With the advent of high-throughput next-generation sequencing platforms, screening for cancer-related somatic mutations is becoming commonplace. Digital PCR combined with TaqMan SNP Genotyping Assays offer a highly sensitive and specific solution for the confirmation of these discoveries.
Просмотров: 4838 Thermo Fisher Scientific
Embryonic and Cybrid stem cells presentation (UOSM2031)
 
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A short video about the uses of embryonic and cybrid stem cells in research for our UOSM2031 module presentation
Просмотров: 174 Ryan Kirkness
Structure-Based Vaccine Design and B-cell Ontogeny in the Modern Era of Vaccinology
 
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2016 Kinyoun Lecture - Structure-Based Vaccine Design and B-cell Ontogeny in the Modern Era of Vaccinology Air date: Thursday, December 8, 2016, 3:00:00 PM Category: Joseph J. Kinyoun - Infection and Immunity Runtime: 00:53:28 Description: 2016 Joseph J. Kinyoun Memorial Lecture Dr. John Mascola, director of the Dale and Betty Bumpers Vaccine Research Center at NIAID, will deliver the 2016 Joseph J. Kinyoun Memorial Lecture. His talk, titled “Structure-Based Vaccine Design and B-cell Ontogeny in the Modern Era of Vaccinology,” will include an overview of the challenges facing the development of effective vaccines against viruses, including HIV, respiratory syncytial virus and influenza virus. Mascola will describe how researchers can use structural information about viral proteins and antiviral antibodies to design new vaccines. He also will discuss how an understanding of antibody evolution, termed B-cell ontogeny, can inform approaches to improving vaccines. Mascola, an internationally recognized expert on HIV immunology and vaccine development, was appointed VRC director in Oct. 2013. In this role, he oversees a basic and translational research program aimed at developing and testing candidate vaccines against HIV, influenza virus, Zika virus and other infectious agents that cause diseases of global importance. He also serves as chief of the Virology Laboratory and chief of the Humoral Immunology Section at the VRC, where his research focuses on structure-based design and testing of novel vaccines for HIV/AIDS and influenza, optimization of immune responses, and identification of correlates of protection. Mascola is a fellow of the American College of Physicians and has been elected to the American Society of Clinical Investigation, the Association of American Physicians and Fellowship in the American Academy for Microbiology. Mascola obtained his medical degree in 1985 and completed training in internal medicine and infectious diseases, followed by a fellowship in retrovirology. He joined the VRC as deputy director in 2000. Prior to joining the VRC, he was head of HIV prevention research in the division of retrovirology at the Walter Reed Army Institute of Research. Since 1979, NIAID has hosted an annual public lecture in honor of Dr. Joseph J. Kinyoun, who in 1887 founded the Laboratory of Hygiene, the forerunner of NIH, and launched a new era of scientific study of infectious diseases. For more information go to https://www.niaid.nih.gov/news-events/events/kinyoun-lecture-series/2016-kinyoun-lecture Author: John Mascola, M.D., Director, Vaccine Research Center, NIAID, NIH Permanent link: https://videocast.nih.gov/launch.asp?20048
Просмотров: 1122 nihvcast
Her-2 Amplification Assessment in Breast Cancer FFPE Samples: QuantStudio 3D Digital PCR vs. ISH
 
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Mr. Bruno Ping, Senior Biomedical Scientist of Molecular Diagnostics at Royal Surrey County Hospital UK, explores the use of Digital PCR in Copy Number Variation of Her-2 breast cancer FFPE samples. In this talk, presented at the European Society of Human Genetics 2013 in Paris France, Mr. Ping demonstrates how digital PCR has the potential to better determine algorithms that define the equivocal range in breast cancer, thereby enabling more streamlined processing of samples. Before I start my presentation, I must say that 90 percent of the work that we do is diagnostics. The other 10 percent is what we call translational research -- not pure research, but it's translational research -- research applied to a clinical context. In our department, we have a running joke with our medical pathologists. We say we're gonna find a way to retire all of you. This was the perfect opportunity to try that with -- look at these HER-2 cases and see what we get from the data. So let's move forward. So this is our research goal. What do you want to do with this digital PCR project? So basically, we want to see -- we're already testing for HER-2 in our department. We want to see how comparable it is to our current testing methodology. I really like this wheel from the CDC -- was done in 2003, and it covers a lot of parameters. The three main ones are analytical validity, clinical validity and clinical utility. I'm not gonna cover all of those. I'm just gonna cover three things. Are we really measuring gene amplification copy number variation, which is No. 1 analytical validity; when are things positive or negative, which is the clinical validity; and the clinical utility is concentrated a little bit on the financial aspect. I don't think we can -- even in research or diagnostic, we cannot neglect that aspect, which is the financial aspect. So let's move forward. So for those that don't know what HER-2 is, this is a really nice slide that, in a visual way, explains what HER-2 is. So HER-2 is a driver for cellular proliferation in cancer. You can look at the proteins there. The HER-2 has several dimerization pathways- HER-2 with HER-2, HER-2 with HER-3, HER-2 with HER-1, which is EGFR, and this is what it does. So we all have seen these pictures. You all know what they mean. Again, HER-2 gene is coded by the ERBB2 gene. We don't call it HER-2 because molecular biologists always like to complicate things, but we call it HER-2. The interesting thing is that the HER-2 is a proto-oncogene. By itself, it's not an oncogene -- won't give you cancer. But under certain circumstances, it will drive cancer forward. What does it need to happen? Let me just move forward and explain a little bit more about what a proto-oncogene is. So a proto-oncogene turns into an oncogene by three different mechanisms. We have deletion or point mutation. In previous example, looking at BRAF with a point mutation, and that creates a hyperactive protein. That's one of the mechanisms - BRAF becoming an oncogene. The other one is gene amplification. We see that in HER-2, as well, where you have several copies of the gene introducing to the genome, and then the normal protein is overexpressed. The other common one, as well, is the chromosome rearrangement. You see that in translocations and a lot of other things. So these are the three mechanisms from proto-oncogene to oncogene. Why do we test for HER-2? We test for HER-2 for mainly two reasons. The first one, we want to know if we can't give that drug to that patient, so it's drug eligibility. The second one is -- HER-2 is a negative prognostic factor. If you look at this picture -- I actually quite like this picture. So in this particular case, the tumor spreads the nodes. If that tumor is HER-2 positive -- in this case more than three copies -- and you can see that 36 months -- after three years, chance of survival is below 60 percent. If it hasn't spread, then it's above 60 percent. So we can see, as well, that there's a difference between having an increased number of copies of HER-2 and having a normal number of copies of HER-2. So we can see the difference here. Less than three copies, normal; there's a higher chance of disease survival. This is why we test for HER-2 -- let's look at the drug, see if we can give the drug to the patient, and let's see what are the chances of disease-free survival. Moving on. How do we test for HER-2? Currently indicate two recommended methodologies. One of them is in situ hybridisation. There are two ways of doing in situ hybridisation. The gold standard is FISH -- fluorescent in situ hybridisation. What we're seeing here is in red, you're seeing the gene, basically, and you're seeing the copies of the gene.
Просмотров: 2445 Thermo Fisher Scientific
Asymmetric cell division of Sensory Organ Precursor cells (NeurGal4, Pon::GFP, H2A::RFP)
 
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High definition 4D movie of Drosophila melanogaster's Sensory Organ Precursor. SOP cells are arranged in a regular array on the notum of a fly pupa. Partner of Numb fused to GFP (Pon::GFP) reveals the asymmetric segregation of cell fate determinants during asymmetric cell division. Cell fate determinants are segregated into the anterior daughter cell (PIIB) where they make that cell different from its posterior sibling (PIIA). DNA fused to RFP (H2A::RFP) reveals the genomic inheritance by both daughter cells (PIIB and PIIA). The area in between SOP cells is taken up by epithelial cells, which do not express fluorescent marker. All SOP asymmetric cell division occurs along the anterior-posterior axis of the fly pupa. For time-lapse 4D microscopy of sensory organ precursor cells, Drosophila melanogaster pupa was incubated for 15 hours prior to imaging, dissected and imaged. The GFP and RFP channel movies were acquired using a Nikon A1R 60X N.A. 1.4 oil immersion objective confocal microscope, using a 488 Argon laser for green channel and 561 Diode laser for red channel. Movies were acquired with no delay time interval in resonant mode (high-speed acquisition scanner). The 4D movies were rendered and processed for visualisation using Imaris software. Pon::GFP/H2A::RFP image stacks were acquired with no delay at intervals ranging from 0.15 to 0.5 µm, 27 to 32 steps using high-speed piezoelectric objective-positioning Z stage system. The experiment was done at the Bioimaging facility of the Institute for Research and Immunology and Cancer, Department of Pathology and Cell Biology, Université de Montreal. Researcher: Arturo Papaluca.
Просмотров: 407 Science Of Metal
Stem cells
 
01:18
Scientists have reported a simple way to turn animal cells back to a youthful, neutral state, a feat hailed as a "game-changer" in the quest to grow transplant tissue in the lab. The research, reported in the journal Nature, could be the third great advance in stem cells -- a futuristic field that aims to reverse Alzheimer's, cancer and other crippling or lethal diseases.VIDEOGRAPHIC
Просмотров: 537 AFP news agency
Target Sequencing of Cancer Samples
 
59:06
Targeted Sequencing of Cancer Samples for Clinical Testing and Functional Analysis of Tumor Subclones Dr. David Spencer discusses the performance of various targeted next-generation sequencing methods for detecting cancer-associated mutations in clinical samples. In this presentation, Targeting Sequencing of Cancer Samples for Clinical Testing and Functional Analysis of Tumor Subclones, Dr. Spencer demonstrates that cross-contamination of samples can occur during the course of multiplex sequencing and presents preliminary data on methods for detecting such admixture from sequencing data. His presentation also illustrates the use of targeted next-generation sequencing to study the functional properties of subclonal populations of cells in primary acute myeloid leukemia samples and Merkel cell carcinoma, an aggressive skin cancer that is typically driven by a common polyomavirus. David Spencer, MD, PhD Fellow, Division of Molecular Genetic Pathology Department of Laboratory and Genomic Medicine Washington University School of Medicine, St. Louis 4/30/2014
Просмотров: 750 UW Video
Mitochondrial dynamics through cell division
 
00:14
U2OS cells were transduced with CellLight® Mito-RFP and imaged every 5 minutes for 16 hours. Extensive mitochondrial motility is seen throughout mitosis and as the cell regains it's pre mitotic shape following mitosis.
Просмотров: 1770 Thermo Fisher Scientific
Nuclear Transfer Research - Elaine Fuchs (Rockefeller/HHMI)
 
10:26
The transfer of the nucleus from an adult cell into an enucleated oocyte can generate stem cells that go on to produce healthy mice. While this technology holds promise for regenerative medicine there are still many hurdles to clear.
Просмотров: 193 iBiology Techniques
Dr. Belani Discusses Driver Mutations in NSCLC
 
01:11
Chandra P. Belani, MD, Deputy Director, Penn State Hershey Cancer Institute, Miriam Beckner Distinguished Professor of Medicine, Penn State Hershey Medical Center & College of Medicine, discusses the multicenter Lung Cancer Mutation Consortium (LCMC) study that sought to detect driver mutations in patients with non-small cell lung cancer (NSCLC). The detection of various driver mutations could help compartmentalize overall NSCLC. Determining the exact mutation responsible for tumor growth could help identify the patients that are eligible to receive specific targeted agents. The LCMC study found that approximately 54% of patients with NSCLC have some form of a mutation. The major abnormalities include mutations in KRAS, EGFR, c-Met, PI3K, and the EML4-ALK rearrangement. Most of these alterations appear to be mutually exclusive; very few tumors have dual or triple abnormalities. According to Belani this research only scratches the surface of the NSCLC biology. Subsequent discoveries will show that NSCLC is heterogeneous; further aberrations will be discovered as more research is completed.
Просмотров: 217 OncLiveTV
primary cells
 
07:23
primary cell vs cell line what is primary cell and cell line?why yes primary cell instead of cell line?how primary cell are currently being used?
Просмотров: 234 Creative Bioarray
Master's Thesis Defense | Integrative Analysis of Heterogeneous Genomics Data
 
50:01
Thesis Title: Integrative Analysis of Heterogeneous Genomics Data for Triple Negative Breast Cancer and High Grade Serous Ovarian Cancer Abstract: The human body is made up of trillions of cells. Although all the human body cells contain the same DNA sequence inside their nuclei, each one carries out its own function. Normally, human cells grow and divide to form daughter cells as the body needs them. When cells grow old, or lose their ability to function properly, they die (in a very organized way called apoptosis or programmed cell death) and new cells take their role. Cancer is a disease that is caused by uncontrolled division of abnormal cells in some part of the body, breaking the natural process of growing. Old or damaged cells survive when they should die, and new (abnormal) cells form when they are not needed. Some types of cancer form solid tumors, which are masses of tissue. Others, such as leukemias, do not form solid tumors. It is widely believed that cancer is caused by the accumulation of detrimental variation in the genome over the course of a lifetime. Variations can take several forms. Single Nucleotide Polymorphism (SNP) is a mutation in a single base of the DNA. Indels describe insertions or deletions of bases in the genome. Copy Number Variation (CNV) represents multiplied and deleted segments in a genome. Most of the time, one type of mutation is not sufficient to induce cancer formation. In this study, we have investigated genomic datasets of a phase-1 clinical trial on triple-negative breast cancer and ovarian cancer patients. The goal is to identify genes that drive drug resistance. We have developed data analysis pipelines to obtain genomics variations (somatic mutations and copy number variations) from the Whole Exome Sequencing (WES) raw data of 35 triple-negative breast cancer (TNBC) and ovarian cancer patients. In addition, we have analyzed the gene expression levels and gene fusion from the RNA-Seq raw reads data for a subset of 16 patients. This study is an effort toward optimizing the integrative analysis of genomic datasets under certain limitations. The main limitation is the small number of samples in the clinical trial (as is the case in most clinical trials). Another challenge is to find an abstract way to analyze the raw sequencing data given its large size and heterogeneity. The novelty of our work comes in following a data science approach in answering such research questions. The unbiased and data-driven approach was successful in identifying genes that are most likely related to the drug resistance. Our results will guide clinicians toward having an in-depth study of the driver genes. For full thesis manuscript, contact me at: http://www.abdelrahmanhosny.me
Просмотров: 288 Abdelrahman Hosny
Enabling CNV Studies from Single Cells Using Whole Genome Amplification and Low Pass Sequencing
 
09:11
DNA copy number variations (CNVs) play an important role in the pathogenesis and progression of cancer. While array comparative genomic hybridization (aCGH) has generally been used to identify CNVs in the whole genome, next-generation sequencing (NGS) provides an opportunity to characterize CNVs genome-wide with unprecedented resolution, even at the single cell level. However, CNV detection in single cells is faced with various challenges, such as incomplete genome coverage, introduction of sequence errors, GC bias and false positives.
Просмотров: 679 QIAGEN
Stem Cells: Division in the Ovaries and Testes
 
03:00
Sophia Ladyzhets' Presenters Application for the CT State Junior Science and Humanities Symposium Works Cited: Chang, Y.-J., Pi, H., Hsieh, C.-C., et. al (2013). Smurf-mediated differential proteolysis generates dynamic BMP signaling in germline stem cells during Drosophila testes development. Developmental Biology. Retrieved from http://www.elsevier.com/locate/developmentalbiology Inaba, M., Buszczak, M., & Yamashita, Y. M. (2015). Nanotubes mediate niche-stem-cell signalling in the Drosophila testis. Nature, 523(7560), 329-332. Inaba, M., & Yamashita, Y. M. (2016). Evaluation of the asymmetric division of Drosophila male germline stem cells. In M. Buszczak (Ed.), Methods in Molecular Biology: Germline stem cells (pp. 49-62). https://doi.org/10.1007/978-1-4939-4017-2_3 Kawase, E., Wong, M. D., Ding, B. C., Xie, T., (2004). Gbb/Bmp signaling is essential for maintaining germline stem cells and for repressing bam transcription in the Drosophila testes. Development, 131, (pp. 1365-1375). King, F. J., Szakmary, A., Cox, D. N., and Lin, H. (2001). Yb modulates the divisions of both germline and somatic stem cells through piwi- and hh-mediated mechanisms in the Drosophila ovary. Mol. Cell 7, (pp. 497-508). Korolchuk, V. I., Menzies, F. M., & Rubinsztein, D. C. (2010). Mechanisms of cross‐talk between the ubiquitin‐proteasome and autophagy‐lysosome systems. FEBS letters, 584(7), 1393-1398. Nishikawa, S. I., Osawa, M., Yonetani, S., Torikai-Nishikawa, S., and Freter, R. (2008). Niche required for inducing quiescent stem cells. Cold Spring Harb. Symp. Quant. Biol. 73, (pp. 67-71). Xia, L., Jia, S., Huang, S., et. al (2010). The fused/smurf complex controls the fate of Drosophila germline stem cells by generating a gradient BMP response. Cell. https://doi.org/10.1016/j.cell.2010.11.022 Yamashita, M., Ying, S. X., Zhang, G. M., Li, C., Cheng, S. Y., Deng, C. X., Zhang, Y. E., (2005). Ubiquitin ligase Smurf1 controls osteoblast activity and bone homeostasis by targeting MEKK2 for degradation. Cell 121, (pp. 101-113).
Просмотров: 141 Sophia Ladyzhets
TCGA: Genomic Characterization of Cancer-Adjacent Tissue - Melissa Troester
 
18:30
November 27-28, 2012 - The Cancer Genome Atlas' 2nd Annual Scientific Symposium: Enabling Cancer Research Through TCGA More: http://www.genome.gov/27551851
Просмотров: 785 National Human Genome Research Institute
TaqMan Gene Fusion Assays as a NGS data validation tool? | AACR 2015
 
02:05
Similar to other Thermo Fisher Scientific Taqman Gene Espression Assays, the Taqman Gene Fusison Assay consists of an unlabeled PCR primer and a flourescent probe, but the Taqman Gene Fusion Assays are designed to span the fusion breakpoint.
Просмотров: 165 Thermo Fisher Scientific
What is Cell Senescence in Aging, Telomeres, & its Purpose - Part 2
 
06:24
In this video, I will explain what cell senescence is, the significance of cell senescence, its purpose, the loss of function that comes with cell senescence, and its connection to telomeres. You can learn about it more from my article: https://therevisionist.org/reviews/how-telomere-length-limits-cell-replication-life-span-senescence/ Telomere Playlist: https://www.youtube.com/watch?v=uSjvSL9Yzq0&list=PLOK2VRNQNad9ivOOgL28lhOJVks9Doca5 --- High Quality Web Hosting ➝ https://www.siteground.com/go/biohacking My Bio Hacking Subreddit ➝ https://www.reddit.com/r/Bio_Hacking/ My Bio Hacking Articles ➝ https://therevisionist.org/bio-hacking/ My Bio Hacking Newsletter ➝ http://eepurl.com/cw1X81 --- Follow me ┴┬┴┤( ͡° ͜ʖ├┬┴┬ ✪ Facebook: https://www.facebook.com/profile.php?id=100010037778391 ✪ Twitter: https://twitter.com/raqib_zaman ✪ Google+: https://plus.google.com/+RaqibZaman --- Cellular senescence is one phenomenon by which normal cells cease to divide. In their seminal experiments from the early 1960's, Leonard Hayflick and Paul Moorhead discovered that normal human fetal fibroblasts in culture reach a maximum of approximately 50 cell population doublings before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit. Hayflick's discovery that normal cells are mortal overturned a 60-year-old dogma in cell biology that maintained that all cultured cells are immortal. Hayflick found that the only immortal cultured cells are cancer cells. Mechanistically, replicative senescence is triggered by a DNA damage response which results from the shortening of telomeres during each cellular division process. Cells can also be induced to senesce independent of the number of cellular divisions via DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes and cell-cell fusion. The number of senescent cells in tissues rises substantially during normal aging. Although senescent cells can no longer replicate, they remain metabolically active and commonly adopt an immunogenic phenotype consisting of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE) and stain positive for senescence-associated β-galactosidase activity. Senescence-associated beta-galactosidase, along with p16Ink4A, is regarded to be a biomarker of cellular senescence. This results in false positives for maturing tissue macrophages and senescence-associated beta-galactosidase as well as for T-cells p16Ink4A. A Senescence Associated Secretory Phenotype (SASP) consisting of inflammatory cytokines, growth factors, and proteases is another characteristic feature of senescent cells. SASP is associated with many age-related diseases, including type 2 diabetes and atherosclerosis. This has motivated researchers to develop senolytic drugs to kill and/or eliminate senescent cells in an effort to improve health in the elderly. Whether or not this approach will prove effective is debatable. The nucleus of senescent cells is characterized by senescence-associated heterochromatin foci (SAHF) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS). Senescent cells affect tumour suppression, wound healing and possibly embryonic/placental development and a pathological role in age-related diseases. Cellular senescence is not observed in some organisms, including perennial plants, sponges, corals, and lobsters. In those species where cellular senescence is observed, cells eventually become post-mitotic when they can no longer replicate themselves through the process of cellular mitosis; i.e., cells experience replicative senescence. How and why some cells become post-mitotic in some species has been the subject of much research and speculation, but it has been suggested that cellular senescence evolved as a way to prevent the onset and spread of cancer. Somatic cells that have divided many times will have accumulated DNA mutations and would therefore be in danger of becoming cancerous if cell division continued. As such, it is becoming apparent that senescent cells undergo conversion to an immunogenic phenotype that enables them to be eliminated by the immune system. The DNA damage response (DDR) arrests cell cycle progression until damages, such as double-strand breaks (DSBs), are repaired. Senescent cells display persistent DDR foci that appear to be resistant to endogenous DNA repair activities. Such senescent cells in culture and tissues from aged mammals retain true DSBs associated with DDR markers. It has been proposed that retained DSBs are major drivers of the aging process.
Просмотров: 393 Raqib Zaman
Discovery and Functional Characterization of Recurrent Gene Fusions... - Chai Bandlamudi
 
16:51
May 13, 2014 - The Cancer Genome Atlas 3rd Annual Scientific Symposium More: http://www.genome.gov/27557040
Просмотров: 372 National Human Genome Research Institute
These Monkeys Were Successfully Cloned
 
01:04
Chinese scientists just cloned these monkeys. Subscribe to Gizmodo: https://goo.gl/YTRLAE Visit us at: http://www.gizmodo.com/ Like us at: https://www.facebook.com/gizmodo Follow us at: https://twitter.com/gizmodo View us: https://www.instagram.com/gizmodo/ Watch more from Fusion friends: Fusion: http://fus.in/subscribe Splinter: https://goo.gl/BwuJiy F-Comedy: https://goo.gl/Q27Mf7 Fusion TV: https://goo.gl/1IbZ1B Kotaku: https://goo.gl/OcnXv7 Deadspin: https://goo.gl/An7N8g Jezebel: https://goo.gl/XNsnCJ Lifehacker: https://goo.gl/3rNmzw io9: https://goo.gl/ismnzP Jalopnik: https://goo.gl/u7sDEk Sploid: https://goo.gl/4yq2UY The Root: https://goo.gl/QMOjBE Earther: https://goo.gl/nxgn48
Просмотров: 9549 Gizmodo
A John Iafrate - Clinically actionable gene fusions, CNVs and SNVs detected by NGS based comprehensi
 
01:09:45
Watch on LabRoots at http://labroots.com/webinar/id/140 Driver mutations are causally implicated in tumorigenesis and disease progression, and they are defined by molecular abnormalities such as gene fusions, copy number variations (CNVs), single-nucleotide variants (SNVs) and insertions/deletions (indels). Driver mutations vary by gene and cancer type, and the ability to accurately, rapidly and economically characterize all of the driver mutations in a single sample in a clinical setting has been untenable. Anchored Multiplex PCR (AMP™) is a target enrichment chemistry for next-generation sequencing (NGS). AMP is used by Archer FusionPlex assays to detect known and novel gene fusions, SNVs and indels from RNA and by Archer VariantPlex assays to detect CNVs, SNVs and indels from DNA. In this webinar, Dr. Iafrate outlines the limitations of current methods of mutation detection and shares data demonstrating the effective use of AMP chemistry for multiplex NGS-based mutation calling in the clinic. Dr. Iafrate also describes the concomitant use of AMP-based assays using RNA and DNA from a single sample, respectively, to generate a comprehensive tumor mutation profile with minimal sample input. Objectives: 1. Describe the limitations of detecting mutations using standard molecular pathology 2. Demonstrate accurate multiplex mutation calling using AMP chemistry 3. Introduce comprehensive tumor mutation profiling from a single sample
Просмотров: 440 LabRoots
What is CELLULAR SENESCENCE? What does CELLULAR SENESCENCE mean? CELLULAR SENESCENCE meaning
 
04:52
What is CELLULAR SENESCENCE? What does CELLULAR SENESCENCE mean? CELLULAR SENESCENCE meaning - CELLULAR SENESCENCE definition - CELLULAR SENESCENCE explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license. Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit. Replicative senescence is the result of telomere shortening that ultimately triggers a DNA damage response. Cells can also be induced to senesce via DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes and cell-cell fusion, independent of telomere length. As such, cellular senescence represents a change in "cell state" rather than a cell becoming "aged" as the name confusingly suggests. Nonetheless, the number of senescent cells in tissues rises substantially during normal aging. Although senescent cells can no longer replicate, they remain metabolically active and commonly adopt an immunogenic phenotype consisting of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE) and stain positive for senescence-associated ß-galactosidase activity. Senescence-associated beta-galactosidase, along with p16Ink4A, is regarded to be a biomarker of cellular senescence. Nonetheless, false positives exist for maturing tissue macrophages and senescence-associated beta-galactosidase as well as for T-cells p16Ink4A. Senescent cells that grow attached to a solid substrate such as glass or plastic surface assume flattened appearance being thinner and having greater cellular and nuclear area. After staining nuclear DNA with a fluorescent dye the cellular imaging reveals a dramatic decrease in maximum pixel of the nuclear DNA-associated fluorescence accompanied by an increase in nuclear area; thus even a more remarkable decrease in maximal pixel to nuclear area ratio A Senescence Associated Secretory Phenotype (SASP) consisting of inflammatory cytokines, growth factors, and proteases is another highly characteristic feature of senescent cells. SASP contributes to many age-related diseases, including type 2 diabetes and atherosclerosis. The damaging effects of SASP have motivated researchers to develop senolytic chemicals that would kill and eliminate senescent cells to improve health in the elderly. Healthy mice treated with senolytics have shown improved cardiac and vascular, function. Removal of senescent cells in normal mice increased healthspan as well as life expectancy, The nucleus of senescent cells is characterized by senescence-associated heterochromatin foci (SAHF) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS). Senescent cells affect tumour suppression, wound healing and possibly embryonic/placental development and a pathological role in age-related diseases. The experimental elimination of senescent cells from transgenic progeroid mice and non-progeroid, naturally-aged mice led to greater resistance against aging-associated diseases. Moreover, cellular senescence is not observed in several organisms, including perennial plants, sponges, corals, and lobsters. In those species where cellular senescence is observed, cells eventually become post-mitotic when they can no longer replicate themselves through the process of cellular mitosis; i.e., cells experience replicative senescence. How and why some cells become post-mitotic in some species has been the subject of much research and speculation, but (as noted above) it is sometimes suggested that cellular senescence evolved as a way to prevent the onset and spread of cancer. Somatic cells that have divided many times will have accumulated DNA mutations and would therefore be in danger of becoming cancerous if cell division continued. As such, it is becoming apparent that senescent cells undergo conversion to an immunogenic phenotype that enables them to be eliminated by the immune system.
Просмотров: 2255 The Audiopedia
Evolutionary biology and CLL therapy
 
02:44
Dan Landau, MD, PhD, of Weill Cornell Medical College and the NYGC, New York, NY, discusses his work focusing on the process of evolutionary biology. His research looks specifically at how cells within our body evolve continuously throughout our lifetime. Cancer represents an accelerated form of this process, the cells start to evolve independently. Dr Landau expresses being very excited about this, particularly chronic lymphocytic leukemia (CLL), which offers a chance to study this directly in patients. Samples can be taken longitudinally over time, categorizing the process of somatic evolution, in very fine detail. He mentions how this type of information can be utilized, to think about better therapeutic approaches. Evolution is one of the central challenges that we have today, in terms of cancer therapy. Despite the fact that good therapies are being developed, the cancer is able to evolve and adapt, therefore experts need to start thinking about how to directly anticipate this evolutionary process. Dr Landau believes CLL is a good area to explore those questions, as multiple effective therapies are starting to be applied, thereby bringing up questions such as, how they can be combined and what the quantitative frameworks are that can be leveraged to help make those kinds of decisions. Recorded at the 2016 International Workshop of the German CLL Study Group (GCLLSG) in Cologne, Germany.
TCGA: The Somatic Genomic Landscape of Glioblastoma Multiforme - Roel Verhaak
 
13:35
November 27-28, 2012 - The Cancer Genome Atlas' 2nd Annual Scientific Symposium: Enabling Cancer Research Through TCGA More: http://www.genome.gov/27551851
Просмотров: 1761 National Human Genome Research Institute
04 19 2018 Prostate Cancer Update
 
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City Wide Grand Rounds 04-19-2018 Prostate Cancer Update Dr. G. Chatta The information included herein should never be used as a substitute for clinical judgment and does not represent an official position of UB Internal Medicine Residency Program. Board review questions are Copyright © 2015 American College of Physicians. All Rights Reserved. 190 North Independence Mall West, Philadelphia, PA 19106-1572 Toll Free: (800) 523.1546 - Local: (215) 351.2400
Просмотров: 119 UB IM Residency Program
Uncovering the Pseudo-Subclonal Structure of Tumor Sample With... - Yi Qiao
 
17:27
November 17-18, 2011 - The Cancer Genome Atlas' 1st Annual Scientific Symposium More: http://www.genome.gov/27546242
Просмотров: 372 National Human Genome Research Institute
Algorithms for Automated Discovery of Mutated Pathways in Cancer - Ben Raphael
 
17:20
November 17-18, 2011 - The Cancer Genome Atlas' 1st Annual Scientific Symposium More: http://www.genome.gov/27546242
Просмотров: 944 National Human Genome Research Institute
TCGA: Status Report and Insights From Leadership - Kenna Shaw
 
15:27
November 27-28, 2012 - The Cancer Genome Atlas' 2nd Annual Scientific Symposium: Enabling Cancer Research Through TCGA More: http://www.genome.gov/27551851
Просмотров: 1224 National Human Genome Research Institute
Medical vocabulary: What does Artificial Gene Fusion mean
 
00:17
What does Artificial Gene Fusion mean in English?
Просмотров: 13 botcaster inc. bot
Anthony Wynshaw-Boris: Chromosome Therapy - Rescue of Ring Chromosomes by Cellular Reprogramming
 
25:05
Hanna Symposium "Chromosome Therapy: Rescue of Ring Chromosomes by Cellular Reprogramming" Anthony Wynshaw-Boris, PhD September 9, 2015 Presented by the CWRU Institute of Origins, Department of Genetics and Genome Sciences, Cancer Center, Program in Cell Biology
Просмотров: 288 case
TCGA: Structural Variant Detection in Colorectal Cancer - Evert van den Broek
 
13:52
November 27-28, 2012 - The Cancer Genome Atlas' 2nd Annual Scientific Symposium: Enabling Cancer Research Through TCGA More: http://www.genome.gov/27551851
Просмотров: 800 National Human Genome Research Institute
TCGA Samples + Laser Capture Microdissection (LCM) | #LabChat w/ Dr. Chip Petricoin
 
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What is #LabChat? https://www.youtube.com/watch?v=zlCKPGTHHlM Learn more about the Center for Applied Proteomics and Molecular Medicine: http://capmm.gmu.edu Read Chip's paper: http://cancerres.aacrjournals.org/content/74/3/818.long Learn more about the Arcturus LCM system: http://www.lifetechnologies.com/us/en/home/life-science/gene-expression-analysis-genotyping/laser-capture-microdissection/overview-arcturus-laser-capture-microdissection-lcm-system.html Dr. Chip Petricoin’s team at the Center for Applied Proteomics and Molecular Medicine at George Mason University had a hunch that the highly pure tumor samples from The Cancer Genome Atlas project (TCGA) were affected by the unknown and unknowable amounts of stroma and other cells. To get to the bottom of this, Chip’s team decided to employ laser capture microdissection (LCM) for their sample prep to see if it made a difference in final output. It turns out that even with TCGA tumor samples that were high in purity (as high as 90%), the phosphoprotein and protein measurements from the microdissected samples showed better statistical concordance with expected genomic arrangements. These results were often entirely lost in undissected sample material. Not only does Chip’s team feel LCM is essential for sample prep, but they’re big fans of the Arcturus laser capture microdissection system and its infrared laser beam. Other platforms solely use a UV laser, which can leave your samples extra crispy, destroying vital RNA and proteins.
Просмотров: 902 Thermo Fisher Scientific
The 2017 Jeffrey M. Trent Lecture in Cancer Research - Katherine A. Janeway
 
01:03:21
September 6, 2017 Lecture Title: Bringing Genomics to the Pediatric Oncology Clinic: Diagnosis, Treatment Selection and Rational Clinical Trial Design More: https://www.genome.gov/27568937
Просмотров: 335 National Human Genome Research Institute
Nicola Normanno - Building an Ion AmpliSeq Colon and Lung Cancer Panel Consortium development...
 
39:27
Watch on LabRoots at: http://labroots.com/user/webinars/details/id/83 The knowledge of molecular alterations involved in colon carcinoma (CRC) and non-small-cell lung carcinoma (NSCLC) has significantly increased in the past few years. Molecular subgroups of tumors carrying mutations in druggable genes have been identified in CRC and NSCLC. In this respect, the availability of approaches that are compatible with small amounts of input DNA from FFPE tissue and that allow a rapid screening of a large number of somatic mutations is definitely needed. Ion AmpliSeq technology introduces a groundbreaking workflow enabling the rapid sequencing of hundreds of mutations with low allele frequency using as little as 10ng of DNA per reaction. The OncoNetwork Consortium is a European collaborative effort of 8 Cancer Translational Research Institutions to evaluate a custom panel targeting hotspots mutations in 22 genes implicated in CRC and NSCLC. In particular, 7 labs will test the gene panel in 3 phases using 180 retrospective FFPE samples previously tested with orthogonal technologies, and 1 lab will perform confirmatory testing on novel SNPs.
Просмотров: 245 LabRoots