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How Cancer Develops & Mutation
 
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How does cancer develop? Learn how cancer grows and about mutation of cancer cells with Cancer Research UK. Watch this video to find out how cancer develops or learn more on our website: http://www.cancerresearchuk.org/about-cancer/what-is-cancer/how-cancers-grow The video explains how cancer develops when DNA is damaged, allowing a cell to multiply out of control. This animation shows what happens to the normal controls in a cell when cancer starts.
Views: 33513 Cancer Research UK
Two-Thirds of All Cancers Are Caused by One Thing: Your DNA
 
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While environmental factors can play a huge role, the number one cause of cancer is mutations from regular cell replication. Does this mean cancer in humans is simply inevitable? Why Did Our Early Ancestors Resort to Cannibalism? - https://youtu.be/dPmnoVSl-0k Sign Up For The Seeker Newsletter Here - http://bit.ly/1UO1PxI Get 15% off http://www.domain.com domain names and web hosting when you use coupon code SEEKER at checkout! Read More: Researchers Find Mutation 'Hotspots' That Are Linked to Cancer https://www.seeker.com/health/medicine/researchers-find-mutation-hotspots-that-are-linked-to-cancer "Researchers say they've identified clusters of genetic mutations in proteins that can give rise to cancer, a discovery that may help them zero in on new treatments. Those mutation 'hotspots' occur among families of proteins produced by genes in the body's cells. By sifting through data from nearly 6,000 cancer patients, researchers at the University of Maryland say they found thousands of mutations that occur among those proteins." Bad luck plays larger role than environmental, genetic factors in determining who gets cancer http://hub.jhu.edu/2015/01/01/bad-luck-cancer-mutations/ "Two-thirds of adult cancer incidence across tissues can be explained not by environmental factors or inherited genes but by bad luck, according to scientists from the Johns Hopkins Kimmel Cancer Center. The unlucky findings by Johns Hopkins scientists were discovered using a statistical model that measures the proportion of cancer incidence across many tissue types. They found that more often than not, cancer in adults is caused by random mutations that occur when stem cells divide." DNA typos to blame for most cancer mutations http://www.nature.com/news/dna-typos-to-blame-for-most-cancer-mutations-1.21696?WT.mc_id=FBK_NatureNews "Each time a cell divides, it provides an opportunity for errors to crop up during DNA replication. In 2015, Vogelstein and one of his co-authors, mathematician Cristian Tomasetti of Johns Hopkins University in Baltimore, created a stir with an analysis that looked at possible explanations for why some cancers occur more often than others. They concluded that differences in the number of stem-cell divisions in an organ correlated with the frequency of cancers in that area." ____________________ Seeker inspires us to see the world through the lens of science and evokes a sense of curiosity, optimism and adventure. Watch More Seeker on our website http://www.seeker.com/shows/ Subscribe now! http://www.youtube.com/subscription_center?add_user=dnewschannel Seeker on Twitter http://twitter.com/seeker Trace Dominguez on Twitter https://twitter.com/tracedominguez Seeker on Facebook https://www.facebook.com/SeekerMedia/ Seeker on Google+ https://plus.google.com/u/0/+dnews Seeker http://www.seeker.com/ Sign Up For The Seeker Newsletter Here: http://bit.ly/1UO1PxI This episode of Seeker was written and hosted by Trace Dominguez.
Views: 125537 Seeker
Tumor Supressor Gene Regulation in Cancer Cells
 
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There are many mutations that can contribute to cancer. Some mutations create more active genes, and others break genes, such as the Tumor Suppressor Gene displayed here. The disruption of the Tumor Supressor Gene expression causes the cancerous cell to divide when it should not. This nucleotide mutation has been observed in a specific type of triple negative breast cancer, presenting this area for further research. Animation and Narration: Natalie Doolittle http://www.vitae-studios.com/ Scientific Direction: Wasserman Lab at the University of British Columbia http://www.cmmt.ubc.ca/research/investigators/wasserman/lab Music: https://soundcloud.com/civil-engineer
Views: 48200 Vitae Studios
Mutations in Cancer
 
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How somatic mutations can lead to cancer.
Views: 13184 Andrew Wolf
The cancer gene we all have - Michael Windelspecht
 
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View full lesson: http://ed.ted.com/lessons/the-cancer-gene-we-all-have-michael-windelspecht Within every cell in our body, two copies of a tumor suppressor gene called BRCA1 are tasked with regulating the speed at which cells divide. Michael Windelspecht explains how these genes can sometimes mutate, making those cells less specialized and more likely to develop into cancer. Lesson by Michael Windelspecht, animation by Zedem Media.
Views: 199995 TED-Ed
Cancer: rogue cells and DNA mutations
 
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One in three people in the Western world will develop cancer and one in five will die from the disease, but what is cancer and what causes it? Yourgenome.org presents a film of Professor Mike Stratton, Director of the Sanger Institute describing how cancer can develop in the human body. Professor Stratton's research in the Cancer Genome Project uses genome-wide searches for somatic mutations in human cancer in order to identify new cancer genes and to understand the genetic changes that take place during human cancer development. He led the group that discovered the high-risk breast cancer susceptibility gene, BRCA2, and his research has led to the discovery of mutations in genes that lead to melanoma and lung cancer.
Views: 20963 yourgenome
2.2 Mutated DNA causes cellular transformation
 
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Transfection of DNA provides a strategy for detecting non-viral oncogenes Another viable theory. Carcinogens function as mutagens physical (e.g., X-rays) chemical (e.g., tobacco tars) These agents induce cancer through their ability to mutate critical growth-controlling genes in the genomes of susceptible cells The technique of calcium phosphate transfection. In 1972, a new and highly effective gene transfer procedure was developed calcium phosphate transfection. Mouse embryo fibroblasts (NIH 3T3 cell line), turned out to be especially adept at taking up and integrating foreign DNA into their own genomes. This transformation could be scored by the appearance of foci of transformants cells several weeks after their exposure to tumor cell DNA Oncogenes are of human cellular origin Donor DNA from uninfected, mutated cells Researchers chose donor tumor cells derived from mouse fibroblasts. These particular cancer cells originated in mouse adult fibroblasts that had been treated repeatedly with a potent carcinogen and mutagen Importantly, these cells bore no traces of either tumor virus infection or activated endogenous retroviral genomes. Hence, any transforming oncogenes detected in the genome of these cells, are of cellular origin, that is, mutant versions of normal cellular genes. Transfected DNA from chemically treated cells cause foci The cells plucked from the resulting foci were later found to be both anchorage-independent tumorigenic. Importantly DNA extracted from normal, untreated mouse cell lines was unable to induce foci in the NIH 3T3 cell monolayers. Does DNA from human tumours, transform mouse cells? DNAs extracted from human bladder, Lung, colon carcinomas and human promyelocytic leukemia were all found capable of transforming recipient NIH 3T3 cells
Views: 484 Mark Temple
7. Proto-oncogenes and Oncogenes
 
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Proto-oncogenes are genes that produce proteins that are involved in encouraging cells to move through the cell cycle and divide. If they become mutated in such a way that they are permanently active they will encourage the growth of tumours. Mutated counterparts of proto-oncogenes are called oncogenes. This video explains the role of oncogenes in the development of cancer, using the example of the RAS oncogene.
Cancer, How Cancer Starts, How Cancer Spreads, Where and Why, Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/medical-genetics ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Perfect for patient education. The number of cells in a tissue is determined by the balance between cell division and cell death. Uncontrollable cell division leads to formation of abnormal growths called tumors. Tumors can be benign or malignant. Benign tumors are slow-growing and constrained by surrounding connective tissue so they do not spread to other organs. They can still be harmful or even kill by pressing on nearby nerves, brain tissue or blood vessels. Examples of benign tumor include pituitary tumors which may press on optic nerves and cause loss of vision. Cancers are malignant tumors - tumors that can spread beyond of the limit of original organ where it comes from and to other organs of the body. How cancer starts Cancer starts from damage in the DNA of a cell. This DNA damage is called mutation. Mutations happen when the cell duplicates its DNA prior to cell division and makes mistakes. These damages are usually detected and repaired before the cell can divide but sometimes, some of them may be ignored and transferred to daughter cells. If the mutation is located in one of many genes that control the cell cycle, it may affect the regulation of cell cycle in the cell carrying it, and make the cell divide faster than it supposed to. Usually, one mutation is not enough to cause cancer, but as it makes the cell cycle control less reliable, many more DNA damages/mutations would go unnoticed. Cancer is usually the result of accumulation of many mutations of genes involved in cell cycle control and DNA repair. This commonly happens over a long period of time, over many rounds of cell divisions, and this explains why cancers are more common in older people. Some people are said to be predisposed to cancer. This is because they are born with a mutation that makes them more likely to develop a certain type of cancer. This mutation alone is not enough to cause cancer but it starts the process of making cells cancerous. The person carrying it is one step further down the road towards developing a cancer than others who do not have the mutation. How cancer spreads Cancer cells do not stick together like normal cells, they move and invade nearby tissues, organs, this is local spread. They may also spread to further away organs by means of blood and lymph circulation, this is systemic spread. Metastasis is the spreading of cancers to non-adjacent organs. Cancer cells from the original tumor, or primary cancer, can break out and maybe taken up by a blood or a lymph vessel for a ride throughout the body. They can then squeeze out from the vessels into other tissues and start a new tumor growth in the new location which will become secondary cancer. Where do cancers usually spread and why? While travelling in the bloodstream, cancer cell usually stops at the first place where the vessel getting so narrow that it gets stuck. As blood flow from most organs goes to the capillaries of the lungs, this is where cancers spread the most. Lungs are indeed the most common site of secondary cancers. Likewise, while travelling in the lymphatic system, cancer cells commonly get stuck in nearest lymph nodes, where the vessels get narrower. This is the reason why surgeons usually remove nearby lymph nodes when removing tumors.
Views: 151500 Alila Medical Media
Oncogenes | Biomolecules | MCAT | Khan Academy
 
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Created by Tracy Kim Kovach. Watch the next lesson: https://www.khanacademy.org/test-prep/mcat/biomolecules/gene-control/v/tumor-suppressors?utm_source=YT&utm_medium=Desc&utm_campaign=mcat Missed the previous lesson? https://www.khanacademy.org/test-prep/mcat/biomolecules/gene-control/v/non-coding-rna-ncrna?utm_source=YT&utm_medium=Desc&utm_campaign=mcat MCAT on Khan Academy: Go ahead and practice some passage-based questions! About Khan Academy: Khan Academy offers practice exercises, instructional videos, and a personalized learning dashboard that empower learners to study at their own pace in and outside of the classroom. We tackle math, science, computer programming, history, art history, economics, and more. Our math missions guide learners from kindergarten to calculus using state-of-the-art, adaptive technology that identifies strengths and learning gaps. We've also partnered with institutions like NASA, The Museum of Modern Art, The California Academy of Sciences, and MIT to offer specialized content. For free. For everyone. Forever. #YouCanLearnAnything Subscribe to Khan Academy’s MCAT channel: https://www.youtube.com/channel/UCDkK5wqSuwDlJ3_nl3rgdiQ?sub_confirmation=1 Subscribe to Khan Academy: https://www.youtube.com/subscription_center?add_user=khanacademy
Views: 153771 khanacademymedicine
Ras Raf MAPK Pathway and Cancer | Mutations, Cancer Pathogenesis, and Chemotherapy
 
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Lesson on Ras Raf MEK ERK (MAPK) pathway and its involvement in cancer pathogenesis. Various mutations in EGFR, Ras and Raf proteins can lead to particular types of cancer, which can be treated with chemotherapeutic treatments that target either EGFR or Raf proteins. Hey everyone! In this lesson, you will learn about how mutations in the Ras Raf MEK ERK (MAPK) pathway can result in different types of cancer such as pancreatic cancer and melanoma. You will also learn various chemotherapies that can target proteins in the Ras Raf MAPK pathway to treat cancer. If you find this video helpful, please consider liking the video and subscribing to my channel :) JJ ---------------------------------------------------------------------------------------------------- For books and other supplemental information on these topics, please check out my Amazon Affiliate Page ➜ https://www.amazon.com/shop/jjmedicine Support future lessons and lectures ➜ https://www.patreon.com/jjmedicine Follow me on Twitter! ➜ https://twitter.com/JJ_Medicine
Views: 3081 JJ Medicine
Driver and Passenger  Mutation in Cancer – Leonid Mirny
 
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Source – http://serious-science.org/driver-and-passenger-mutation-in-cancer-3125 What allows cancer live at high mutation rate? Which mutations make it weaker? Is there a way to exploit its natural mechanisms to make it less evolvable? Harvard Associate Professor, Leonid Mirny, on clinical phenomena we can now explain using the balance between ‘drivers’ and ‘passengers’.
Views: 2790 Serious Science
What Causes Cancer? Cancer Mutations and Random DNA Copying Errors
 
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Johns Hopkins Kimmel Cancer Center scientists report data from a new study providing evidence that random DNA copying “mistakes” account for nearly two-thirds of the mutations that cause cancer. Their research is grounded on a novel mathematical model based on DNA sequencing and epidemiologic data from around the world. More information on the research: http://www.cristiantomasetti.com/tvtheory/
Views: 10762 Johns Hopkins Medicine
Telomerase: The Instrument of Cell Immortality
 
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A video overview of what telomerase is, its function in normal cells and how telomerase activating mutations can lead to cancer. By The Immortal Instruments: Thomas Mpyana, Zo Ee Wong, Gemma Moyes, Saumya Rajgopal and Chelsea Oliver. References: Amin., R. (2012). Plants and Animal Cells [Image]. Retrieved from https://www.emaze.com/@ALFZZIIC/Plants-and-Animal-Cells Bertorelle, R., Rampazzo, E., Pucciarelli, S., Nitti, D., Rossi, AD. (2014). Telomeres, telomerase and colorectal cancer. World Journal of Gastroenterology. 20(8), pp.1940-1950 Ingley., E. (2015) Telomeres and Telomerase. Harry Perkins Institute of medical research National Institute on ageing (2011). Telomerase [Image] Retrieved from https://www.nia.nih.gov/health/publication/genetics-aging-our-genes/what-happens-when-dna-becomes-damaged NQ Higher Science (2012). Cells Image [Background]. Retrieved from http://www.educationscotland.gov.uk/highersciences/humanbiology/unitone/index.asp Pearson Education (2005). DNA Replication [Diagrammatic image]. Retrieved from http://www.bio.utexas.edu/faculty/sjasper/bio212/molecular.html Reflexions (2013). Image illustrating the activity of telomerase [Image]. Retrieved from http://reflexions.ulg.ac.be/cms/c_353712/en/eliminating-cancer-cell-immortality?part=2 Shay, Jerry W., and Woodring E. Wright. (2002). Telomerase: a target for cancer therapeutics.Cancer cell . 2(4), pp. 257-265. Telomerase Activation Sciences (2015). Telomere Image [illustration]. Retrieved from https://www.tasciences.com/what-is-ta-65/ UIC (2010). DNA and the Molecular basis of Heredity. [Image]. Retrieved from http://www.uic.edu/classes/bios/bios100/lectures/dna.htm University of Texas (2012). The molecular basis of inheritance [diagrammatic Image] Retrieved from http://www.bio.utexas.edu/faculty/sjasper/bio212/molecular.html
What happens when your DNA is damaged? - Monica Menesini
 
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View full lesson: http://ed.ted.com/lessons/what-happens-when-your-dna-is-damaged-monica-menesini The DNA in just one of your cells gets damaged tens of thousands of times per day. Because DNA provides the blueprint for the proteins your cells need to function, this damage can cause serious issues—including cancer. Fortunately, your cells have ways of fixing most of these problems, most of the time. Monica Menesini details the processes of DNA damage and repair. Lesson by Monica Menesini, animation by FOX Animation Domination High-Def.
Views: 832476 TED-Ed
Cancer cell biology: mutated KRAS & reciprocal signalling
 
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Across a wide variety of cancer types, a protein called KRAS can get hyperactivated and transmit an overload of unwanted growth signals to the cells, causing them to divide and form a tumour. A tumour doesn't just contain cancer cells, though. It also has some non-cancer cells in there, such as immune cells and fibroblasts (cells that make the dense support structure that keeps cells stuck together). New research by Chris Tape, Claus Jørgensen and colleagues at The Institute of Cancer Research in London, MIT, the Cancer Research UK Manchester Institute and The University of Manchester, has shed some new light on how mutated KRAS causes cancer cells to grow by promoting three distinct ways of cellular signalling: 1) Through a direct signalling pathway within the cancer cell, with KRAS signalling through the classic RAS-RAF-MEK-ERK signal transduction cascade, this is called cell-autonomous signalling. 2) By inducing the cancer cell to release a protein called SHH, which is able to start specific signalling pathways inside the fibroblast cells. This is called non-cell-autonomous signalling. 3) When these non-cell-autonomous signalling pathways in the fibroblast cells are induced, the fibroblasts are able to release growth factors that go back to the cancer cell, where they initiate more growth signalling pathways through a PI3K-AKT signal transduction cascade. Uncovering these new ways in which mutated KRAS is able to promote cancer cell growth by hijacking fibroblast cell signalling could lead to new possibilities for therapeutic intervention. To find out more about this fascinating research, you can read Chris' blogpost here: http://christape.com/, and you can find Claus' lab page here: http://www.cruk.manchester.ac.uk/Research/CRUK-MI-Groups/Systems-Oncology/Home References: - C.J. Tape, S. Ling, M. Dimitriadi, K.M. McMahon, J.D. Worboys, H.S. Leong, I.C. Norrie, C.J. Miller, G. Poulogiannis, D.A. Lauffenburger, C. Jørgensen, ‘Oncogenic KRAS Regulates Tumor Cell Signaling via Stromal Reciprocation’, Cell (2016) 165(4) - Tape, C.J., (2016) Systems Biology Analysis of Heterocellular Signaling, Trends in Biotechnology (2016) 34(8) - Kolch, W., Halasz, M., Granovskaya, M., and Kholodenko, B.N. (2015). The dynamic control of signal transduction networks in cancer cells. Nat Rev Cancer 15, 515-527. - Quail, D.F., and Joyce, J.A. (2013). Microenvironmental regulation of tumor progression and metastasis. Nature medicine 19, 1423- 1437. - Friedl, P., and Alexander, S. (2011). Cancer invasion and the microenvironment: plasticity and reciprocity. Cell 147, 992-1009.
The Cell Cycle (and cancer) [Updated]
 
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Explore the cell cycle with the Amoeba Sisters and an important example of when it is not controlled: cancer. We have an Unlectured resource for this topic: https://www.amoebasisters.com/unlectured Expand video details for table of contents. 👇 Video also mentions cell cycle checkpoints and cell cycle control. Table of Contents: 1:00 Cell Growth and Cell Reproduction 1:42 Cancer (explaining uncontrolled cell growth) 3:27 Cell Cycle 5:26 Cell Cycle Checkpoints 6:48 Cell Cycle Regulation 8:16 G0 Phase of Cell Cycle Vocabulary in this video includes the words apoptosis, G1, S, G2, mitosis, and cytokinesis. Positive regulator proteins such as cyclins and cyclin dependent kinases are briefly mentioned as well as a negative regulator protein p53. Positive and negative regulation reference regarding cyclin types and cyclin rise/fall areas [in humans]: OpenStax, Biology. OpenStax CNX. http://cnx.org/contents/185cbf87-c72e-48f5-b51e-f14f21b5eabd@10.136. Are you interested in how blood supply to cancer cells may differ from blood supply to healthy cells? Learn more in this Further Reading: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661770/ Support us on Patreon! http://www.patreon.com/amoebasisters Our FREE resources: GIFs: http://www.amoebasisters.com/gifs.html Handouts: http://www.amoebasisters.com/handouts.html Comics: http://www.amoebasisters.com/parameciumparlorcomics Connect with us! Website: http://www.AmoebaSisters.com Twitter: http://www.twitter.com/AmoebaSisters Facebook: http://www.facebook.com/AmoebaSisters Tumblr: http://www.amoebasisters.tumblr.com Pinterest: http://www.pinterest.com/AmoebaSister­s Instagram: https://www.instagram.com/amoebasistersofficial/ Visit our Redbubble store at http://www.amoebasisters.com/store.html The Amoeba Sisters videos demystify science with humor and relevance. The videos center on Pinky's certification and experience in teaching science at the high school level. Pinky's teacher certification is in grades 4-8 science and 8-12 composite science (encompassing biology, chemistry, and physics). Amoeba Sisters videos only cover concepts that Pinky is certified to teach, and they focus on her specialty: secondary life science. For more information about The Amoeba Sisters, visit: http://www.amoebasisters.com/about-us.html We cover the basics in biology concepts at the secondary level. If you are looking to discover more about biology and go into depth beyond these basics, our recommended reference is the FREE, peer reviewed, open source OpenStax biology textbook: https://openstax.org/details/books/biology We take pride in our AWESOME community, and we welcome feedback and discussion. However, please remember that this is an education channel. See YouTube's community guidelines https://www.youtube.com/yt/policyandsafety/communityguidelines.html and YouTube's policy center https://support.google.com/youtube/topic/2676378?hl=en&ref_topic=6151248. We also reserve the right to remove comments with vulgar language. Music is this video is listed free to use/no attribution required from the YouTube audio library https://www.youtube.com/audiolibrary/music?feature=blog We have YouTube's community contributed subtitles feature on to allow translations for different languages, and we are thankful for those that contribute different languages! YouTube automatically credits the different language contributors below (unless the contributor had opted out of being credited). We are not affiliated with any of the translated subtitle credits that YouTube may place below. If you have a concern about community contributed contributions, please contact us.
Views: 74773 Amoeba Sisters
Mutation in tumor suppressor gene leads to cancer
 
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For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Source of the article published in description is Wikipedia. Thanks to original content developers. Link- http://en.wikipedia.org/wiki/Main_Page Mutation in tumor suppressor gene leads to the development of cancer. A tumor suppressor gene, or anti-oncogene, is a gene that protects a cell from one step on the path to cancer. When this gene is mutated to cause a loss or reduction in its function, the cell can progress to cancer, usually in combination with other genetic changes. The loss of these genes may be even more important than oncogene activation for the formation of many kinds of human cancer cells. Tumor-suppressor genes, or more precisely, the proteins for which they code, either have a dampening or repressive effect on the regulation of the cell cycle or promote apoptosis, and sometimes do both. The functions of tumor-suppressor proteins fall into several categories including the following:[5] Repression of genes that are essential for the continuing of the cell cycle. If these genes are not expressed, the cell cycle does not continue, effectively inhibiting cell division. Coupling the cell cycle to DNA damage. As long as there is damaged DNA in the cell, it should not divide. If the damage can be repaired, the cell cycle can continue. If the damage cannot be repaired, the cell should initiate apoptosis (programmed cell death) to remove the threat it poses for the greater good of the organism. Some proteins involved in cell adhesion prevent tumor cells from dispersing, block loss of contact inhibition, and inhibit metastasis. These proteins are known as metastasis suppressors.[6][7] DNA repair proteins are usually classified as tumor suppressors as well, as mutations in their genes increase the risk of cancer, for example mutations in HNPCC, MEN1 and BRCA. Furthermore, increased mutation rate from decreased DNA repair leads to increased inactivation of other tumor suppressors and activation of oncogenes.
Views: 6876 Shomu's Biology
p53 gene: The Guardian of the genome. functions, regulation and inactivation
 
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This Short tutorial explains p53 Gene. click https://www.youtube.com/watch?v=tuwogQmcAps for understanding the Retinoblastoma Gene ****Follow me***** http://ilovepathology.com/ Twitter : https://twitter.com/VijayPatho https://twitter.com/ilovepathology2 Facebook: https://www.facebook.com/ilovepathology/ p53 GENE This is a tumor suppressor gene ( its activity stops the formation of tumors) Located on 17p13, first discovered in 1979 The p53 protein is the product of p53 gene P-protein 53- weight of the protein, 53 kDa Located in almost all normal tissues Unstable and degrades very quickly Is one of the most commonly mutated gene in cancer Function Regulation of Cell cycle DNA repair Apoptosis Prevents neoplastic transformation either by cell cycle arrest or by triggering apoptosis. In cases of DNA damage, there is triggering of expression of p53 gene whcich increases the production of p53 proteins. These preoteins Prevent Cell from entering S phase of cell cycle and Allows time for the DNA repair to take place. also p53 induces DNA repair genes. If the DNA is repaired,the p53 degrades and the cell cycle continues. if the DNA is not repaired, the p53 induces permanent arrest in the cell or activates pro apoptotic proteins bax and bad thereby promoting apoptosis. By these mechanisms, it is understood that the p53 conserves the stability of the cell and thus aptly called as ' THE GAURDIAN OF THE GENOME" How p53 causes cell cycl arrest? P53 is the transcriptional regulator of one of the genes named WAF 1 Resulting in increased WAF proteins named as p 21 P21 blocks CDK4/CyclinD complex ….. Cell cycle is halted in G1 stage resulting in cell cycle arrest. Regulation of p53 protein: by formation of p53 and mdme protein complex which is degraded by ubiquitin mediated pathway. What happens when p53 is inactivated? There will be no cell cycle arrest in cases of damaged DNA and the cell cycle progresses with damaged DNa which results in genomic instability and the neoplastic transformation. How p53 is inactivated?? Mutations Heterozygous and homozygous loss of alleles What are the cancers associated with p53 mutations?? Most human cancers! MC breast, colorectal, liver, lung, and ovarian cancers. -~-~~-~~~-~~-~- Please watch: "WARBURG EFFECT: Hallmark of CANCER. What, Why & How?" https://www.youtube.com/watch?v=LXaO59IqQm8 -~-~~-~~~-~~-~-
Views: 37047 ilovepathology
EGFR Mutation and Cancer
 
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This is an informational video summarizing the EGFR mutations associated with cancer and current direction of research.
Views: 17895 Amy Liu
6. Tumour Suppressor Genes (Retinoblastoma and the two hit hypothesis, p53)
 
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Cancers occur as a result of damage (in the form of mutations) to a cells DNA that results in the formation of malfunctioning proteins. The mutated proteins give the cancerous cells a number of specific traits, outlined in the 'hallmarks of cancer' (https://www.youtube.com/watch?v=ea-CALtn7hA). The genes that are mutated in cancers can be divided into two groups - tumour suppressor genes and proto-oncogenes. Tumour suppressor genes are genes that produce proteins that are involved in stopping mutated cells from dividing, and also act as the brakes on the cell cycle at its various checkpoints. The retinoblastoma gene is a gene that is involved in stopping cells from crossing the G1 checkpoint in the cell cycle, preventing cells from entering S phase and replicating their DNA in preparation for cell division. For the retinoblastoma gene to be rendered inactive, it needs a mutation in both of its copies (alleles). This is explained by the 'two hit hypothesis'. P53 is another example of a significant tumour suppressor gene. It is active during the cell cycle, acting by halting damaged cells at the checkpoints and then ordering the cell to destroy itself by the process of apoptosis.
Cancer biology part 5 Genes associated with cancer
 
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For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Source of the article published in description is Wikipedia. Thanks to original content developers. Link- http://en.wikipedia.org/wiki/Main_Page An oncogene is a gene that has the potential to cause cancer.[1] In tumor cells, they are often mutated or expressed at high levels.[2] Most normal cells undergo a programmed form of death (apoptosis). Activated oncogenes can cause those cells that ought to die to survive and proliferate instead.[3] Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins encoded by oncogenes.
Views: 13038 Shomu's Biology
P53 animation - tumor supressor gene animation
 
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P53 tumor supressor Animation - This lecture video explains about the role of p53 in cell cycle regulation and the onset of cancer. P53 gene encodes in tumour suppressor protein p53 tumour suppressor has a negative effect on cell growth and division p53 protein functions in many different pathways are so well in contention to subscribe to the p53 gene is expressed to produce the p53 protein in a normal so the protein is on stable so the amount of p53 protein are so small decisions are introduced into the DNA p53 protein is stabilised by a mechanism that is like currently understood this leads to an increase in the amount of p53 protein and was so p53 even binds to the promoter of Jean W a and activates the expression of the gene product is a protein called P 20 1P 21 now has an effect on the cell cycle. The progress from G1 to us phase 1 or G1 cycling proteins bind to the enzyme cycle independent kinase CDK and activates it and CDK then phosphorylate ski proteins needed for progression of the cell into us peak we want is present binds to cycle and CDK complex blogging kinase activity the absence of kinase activity prevents the transition of the cell into us rests G1 phase and I is as programmed cell death of apoptosis both also p53 are inactivated in the cell of the tumour suppressor p53 is present to activate the W.A. of one gene NOP 21 has made CDK activity is not blocked so so cannot be arrested in G1 phase and so will proceed into us phase will undergo apoptosis and congressional cells with DNA damage through cell cycle control cells to accumulate additional mutations and hence increase the probability of cancer. Thank You for watching our videos from Biology Animation Videos channel. This channel is created to compile animated biology lectures and videos from different animation sources. None of these videos are created by us. we just organize them and place them in YouTube for your understanding so If you want to know details about these animation please see the credit section for knowing the original content developer and please convey privilege and gratitude to them. Thank You. Our website- https://www.biologyanimationvideos.weebly.com
Mutation in growth regulatory gene leads to cancer
 
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For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Source of the article published in description is Wikipedia. Thanks to original content developers. Link- http://en.wikipedia.org/wiki/Main_Page Mutation in growth regulatory gene leads to the development of cancer. Cancer cells are cells that grow and divide at an unregulated, quickened pace. Although cancer cells can be quite common in a person they are only malignant when the other cells (particularly natural killer cells) fail to recognize and/or destroy them.[1] In the past a common belief was that cancer cells failed to be recognized and destroyed because of a weakness in the immune system. However, more recent research has shown that the failure to recognize cancer cells is caused by the lack of particular co-stimulated molecules that aid in the way antigens react with lymphocytes. By researching stem cells scientists have suggested that too much SP2 protein may turn stem cells into cancer cells.[3] Other issues thought to play a role in the spread of cancer include viruses, immune system issues, genetics, environment and age.[4] However, a lack of particular co-stimulated molecules that aid in the way antigens react with lymphocytes can impair the natural killer cells ability and ultimately cause cancer.[2] All cancers begin in cells, the body's basic unit of life. To understand cancer, it's helpful to know what happens when normal cells become cancer cells. The body is made up of many types of cells. These cells grow and are controlled to produce more cells as they are needed to keep the body healthy. When cells become old or damaged, they die and are replaced with new cells. Sometimes this process of controlled production of cells goes wrong. The genetic material (DNA) of a cell start producing mutations that affect normal cell growth and division by being damaged. When this happens, these cells do not die but form a mass of tissue called a tumor. Said mutations accumulate, being another reason that cancer is found more often in older people.
Views: 2218 Shomu's Biology
Tumor suppressors | Biomolecules | MCAT | Khan Academy
 
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Created by Tracy Kim Kovach. Watch the next lesson: https://www.khanacademy.org/test-prep/mcat/biomolecules/genetic-mutations/v/an-introduction-to-genetic-mutations?utm_source=YT&utm_medium=Desc&utm_campaign=mcat Missed the previous lesson? https://www.khanacademy.org/test-prep/mcat/biomolecules/gene-control/v/oncogenes?utm_source=YT&utm_medium=Desc&utm_campaign=mcat MCAT on Khan Academy: Go ahead and practice some passage-based questions! About Khan Academy: Khan Academy offers practice exercises, instructional videos, and a personalized learning dashboard that empower learners to study at their own pace in and outside of the classroom. We tackle math, science, computer programming, history, art history, economics, and more. Our math missions guide learners from kindergarten to calculus using state-of-the-art, adaptive technology that identifies strengths and learning gaps. We've also partnered with institutions like NASA, The Museum of Modern Art, The California Academy of Sciences, and MIT to offer specialized content. For free. For everyone. Forever. #YouCanLearnAnything Subscribe to Khan Academy’s MCAT channel: https://www.youtube.com/channel/UCDkK5wqSuwDlJ3_nl3rgdiQ?sub_confirmation=1 Subscribe to Khan Academy: https://www.youtube.com/subscription_center?add_user=khanacademy
Views: 88052 khanacademymedicine
How Radiation Changes Your DNA
 
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Radiation is all around us and a part of everyday life. But what exactly is it and what does it do to our bodies? Watch the premiere of Life After: Chernobyl, Tuesday, April 26 at 10/9c on Animal Planet! Sign Up For The TestTube Newsletter Here ►►►► http://bit.ly/1myXbFG Read More: Non-Ionizing Radiation https://www.osha.gov/SLTC/radiation_nonionizing/ "Non-ionizing radiation is described as a series of energy waves composed of oscillating electric and magnetic fields traveling at the speed of light. Non-ionizing radiation includes the spectrum of ultraviolet (UV), visible light, infrared (IR), microwave (MW), radio frequency (RF), and extremely low frequency (ELF). Lasers commonly operate in the UV, visible, and IR frequencies." Radiation Therapy- National Cancer Institute http://www.cancer.gov/publications/patient-education/radiationttherapy.pdf "Radiation therapy (also called radiotherapy) is a cancer treatment that uses high doses of radiation to kill cancer cells and stop them from spreading. At low doses, radiation is used as an x-ray to see inside your body and take pictures, such as x-rays of your teeth or broken bones. Radiation used in cancer treatment works in much the same way, except that it is given at higher doses." How Does Nuclear Radiation Harm the Body? http://www.livescience.com/13250-radiation-health-effects-japan-nuclear-reactor-cancer.html "There's been some reported evidence that radioactive iodine and cesium are being released into the environment from the malfunctioning nuclear reactors in Japan, said Kathryn Higley, director of the Oregon State University department of nuclear engineering and radiation health physics." ____________________ DNews is dedicated to satisfying your curiosity and to bringing you mind-bending stories & perspectives you won't find anywhere else! New videos twice daily. Watch More DNews on TestTube http://testtube.com/dnews Subscribe now! http://www.youtube.com/subscription_center?add_user=dnewschannel DNews on Twitter http://twitter.com/dnews Trace Dominguez on Twitter https://twitter.com/tracedominguez Lissette Padilla on Twitter https://twitter.com/lizzette DNews on Facebook https://facebook.com/DiscoveryNews DNews on Google+ http://gplus.to/dnews Discovery News http://discoverynews.com Download the TestTube App: http://testu.be/1ndmmMq Sign Up For The TestTube Mailing List: http://dne.ws/1McUJdm
Views: 469106 Seeker
Mutations: The Potential Power of a Small Change
 
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The Amoeba Sisters discuss gene and chromosome mutations and explore the significance of these changes. Music used with permission from Adrian Holovaty (http://www.youtube.com/adrianholovaty). This video has a handout here: http://www.amoebasisters.com/handouts.html We appreciate the feedback we get for clarification or improvements on our videos. At 2:11, we try make the A (adenine) base look upset now that the complementary base T (thymine) has been replaced with a G (guanine) in a point mutation. But we wish we had put more distance between the cartoon bases to clarify, that now, they cannot bond in this way. Note: This can sometimes be fixed by a polymerase in proofreading- but if not fixed- the G may be be matched with a C and the mutation will remain. You may enjoy our updated mutation GIF: https://twitter.com/AmoebaSisters/status/930472869343191041 Support us on Patreon! http://www.patreon.com/amoebasisters Our FREE resources: GIFs: http://www.amoebasisters.com/gifs.html Handouts: http://www.amoebasisters.com/handouts.html Comics: http://www.amoebasisters.com/parameciumparlorcomics Connect with us! Website: http://www.AmoebaSisters.com Twitter: http://www.twitter.com/AmoebaSisters Facebook: http://www.facebook.com/AmoebaSisters Tumblr: http://www.amoebasisters.tumblr.com Pinterest: http://www.pinterest.com/AmoebaSister­s Instagram: https://www.instagram.com/amoebasistersofficial/ Visit our Redbubble store at http://www.amoebasisters.com/store.html The Amoeba Sisters videos demystify science with humor and relevance. The videos center on Pinky's certification and experience in teaching science at the high school level. Pinky's teacher certification is in grades 4-8 science and 8-12 composite science (encompassing biology, chemistry, and physics). Amoeba Sisters videos only cover concepts that Pinky is certified to teach, and they focus on her specialty: secondary life science. For more information about The Amoeba Sisters, visit: http://www.amoebasisters.com/about-us.html We cover the basics in biology concepts at the secondary level. If you are looking to discover more about biology and go into depth beyond these basics, our recommended reference is the FREE, peer reviewed, open source OpenStax biology textbook: https://openstax.org/details/books/biology We take pride in our AWESOME community, and we welcome feedback and discussion. However, please remember that this is an education channel. See YouTube's community guidelines https://www.youtube.com/yt/policyandsafety/communityguidelines.html and YouTube's policy center https://support.google.com/youtube/topic/2676378?hl=en&ref_topic=6151248. We also reserve the right to remove comments with vulgar language. We have YouTube's community contributed subtitles feature on to allow translations for different languages. YouTube automatically credits the different language contributors below (unless the contributor had opted out of being credited). We are thankful for those that contribute different languages. If you have a concern about community contributed contributions, please contact us.
Views: 768365 Amoeba Sisters
Will Gene Therapy Cure Cancer?
 
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Gene therapy, an alteration of genes within the body to fight or prevent disease, has sparked a revolution in cancer treatment. Cancer is the 2nd leading cause of death in the United States, and the two main ways we treat it - radiation and chemotherapy - have severe side effects. In this episode of Fw:Thinking, Jonathan Strickland walks us through the process of human gene therapy, reveals it's exciting potential, and questions the ethics of genetic modification and altering DNA. We have a question for you! If you were a gene hacker, what crazy genetic mutation would you give yourself? Leave us a comment with your answer! -------------------------------------------------------- Subscribe to Fw:Thinking: http://www.youtube.com/subscription_center?add_user=fwthinking For the audio podcast, blog and more, visit the Fw:Thinking website: http://www.fwthinking.com Fw:Thinking on Twitter: http://www.twitter.com/fwthinking Jonathan Stickland on Twitter: http://www.twitter.com/jonstrickland Fw:Thinking on Facebook: http://www.facebook.com/FWThinking01 Fw:Thinking on Google+: https://plus.google.com/u/0/108500616405453822675/ [TRANSCRIPT]: Feeling under the weather? Just tweak a chromosome and you'll be all better. Gene therapy. Now I'm not talking about support groups for people who can't fit into the same pants they wore in high school. I'm talking about the alteration of genes within the body to treat disease. Cancer is the second leading cause of death in the United States, and the two main ways we treat it are with radiation and chemotherapy. Both of which have severe side effects. Chemotherapy in particular can be devastating to healthy cells. So gene therapy has the promise of perhaps complimenting or maybe even replacing these other therapies. Currently there are a few different ways to use gene therapy to battle cancer. One way is just to remove the mutated genetic material and replace it with healthy material. Kind of like replacing a flat tire. Another way is to insert special genes into white blood cells. Now this gives those white blood cells the chance to detect and battle tumors. It's like giving a cancer cop a strong pot of coffee and a detailed sketch of what the bad cells look like. But the third, and this is my own personal favorite, is that cells happen to have a little self-destruct button inside them. Now this button gets pressed if there's too much mutation within that cell. But in cancer cells the button is deactivated. So with gene therapy you go in and reactivate that button. Press the button, no more cancer cell. But this raises a question. How do we actually get that genetic material into cells in the first place? Well, do you like spy movies? Because that's what we're talking about here - double agents! In this case, the double agent is a virus. Now normally a virus might be out there to kill you. But what scientists are doing is they're scooping the DNA out of viruses and putting a treatment gene into it, and then putting that into a patient's body. So, like a double agent, the virus works for our team now. In our spy movie, the viruses smuggle in the good genes, so when the cell replicates the good gene is copied instead of the mutated one. Take for example a cancer cell. Once inside the spy virus can deliver the gene that will halt its rampant replication. One such gene is called oligonucleotide. A single stranded piece of DNA that inserts itself directly in the slots of the mutated cell's double helix DNA, essentially jamming up the cell's replicating gears. The mutated segment of DNA can not be transcribed or copied once you've jammed up those gears. And in fact, scientists may one day be able to reverse this process, turning cancer cells back into healthy cells through cellular espionage. So far gene therapy has been used to treat very simple diseases and conditions where a gene is essentially flipped on or off and that effects everything else. Think of it like one of those strands of lights where one light is wrong and therefore the whole thing won't work. You know, kind of like these that I had back in college. Really you just have to find the one bulb that's wrong and fix it and it all comes on again! But some conditions are a little more complicated, and they actually involve lots of different combinations of genes that maybe switched on or off and so we have to determine what that combination is in order to use gene therapy to solve it. We're talking about over 20,000 proteins. This is a big problem. But as genetic information becomes easier for us to obtain, this raises some new questions. For example, should parents be able to determine what their child's eye color should be? Or height? Or sexual orientation? And if we're able to use gene therapy to cure or combat diseases and conditions, does that drastically alter our lifespan and in turn does that drastically alter world population?
Views: 73193 Fw:Thinking
Mutations
 
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Paul Andersen describes the major mutations found in the living world. He starts with an analogy comparing the information in DNA with the information in a recipe. Changes in the DNA can result in changes to the protein, like changes in the recipe can result in changes in the food. He describes the three major point mutations; substitutions, deletions and insertions. He also describes several chromosomal mutations. Intro Music Atribution Title: I4dsong_loop_main.wav Artist: CosmicD Link to sound: http://www.freesound.org/people/CosmicD/sounds/72556/ Creative Commons Atribution License
Views: 763984 Bozeman Science
Why Do Cancer Cells Mutate?
 
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Htm url? Q webcache. Mutating cancer cells find way to dodge chemotherapy bullets the cell cycle in developing therapies stop genetics and how does breast form? American societybbc earth was created by evolution. How do cell mutations cause cancer? Cancer causes & risk cancer and the cycle. This approach can limit the damage to normal cells and accompanying side effects that drive mitosis in mutated form are linked many cancers some types of cancer run certain families, but most not clearly gene changes start a single cell over course person's life or mutations dna cause breast become. In order for a normal cell to transform into cancer cell, genes that regulate it is only when they become mutated the signals growth 2 jun 2016 as cells mutate, continue increase in diversity (credit even bacteria gain genetic variation over time, so too do one such receptor can be lung egfr. About mutation testing lung cancer consortium. Alk is another growth factor receptor that can be present in cancer cells. Googleusercontent search. Different types of cells in the body do different jobs, but they are conclusion. 19 feb 2007 most types of cancer are believed to begin with a random genetic mutation that makes a normal cell go horribly awry. Cancer is unchecked cell growth. This creates an cells are made up of dna, a unique blueprint which tells the cell what to dotargeted therapies, target mutated cancer but not genes can become for various reasons, and mutations occur in some do affect critical areas gene may cause 23 dec 2015 her tumor such way that they once again became vulnerable new findings suggest doctors might well take 10 1996 it will so if reaches 10,000 size before any single acquires two mmr. As a mass of cancerous cells grows, it can develop into tumor this is so the protein perform correct function for cell. All cancers begin when one or more genes in a cell are mutated, changed. Some genes carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, only certain mutations lead to cancer whereas majority do not. Cancer cancer cells more likely to genetically mutate sciencedaily releases 2007 02 070218194439. Cancer cancer cells more likely to genetically mutate sciencedailycancer research uklearn science at scitable naturecancer. What are mutations and what do they mean for cancer treatment cell development canadian societybut sometimes, a mutation leaves it the rate. Even if your tumor does not have known characteristics that can be matched to a targeted. How long does a tumor cell take the causing mutations are rare cancer that tell mutates then grows uncontrollably, dividing faster than it should cycle control matter? [how many gene copies must mutate? ] p53 is most commonly mutated in human cancers, and cells without 11 feb 2015 mutation order genes affects outcome researchers have proved which mutate sensitive to anti jak2 drug ruxolitnib, not necessarily predict those 23 may caused by changes (mutations) dna with
Views: 2 Another Question
Professor Thomas Seyfried's Discussion on Cancer, for the layperson, by Dr. Berg
 
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Dr. Berg dissects Interview and explains each part in simple terms. Donate to Alternative Cancer Research to help fund Professor Seyfried's research: https://www.foundationformetaboliccancertherapies.com/donate (100% of the funds go to this research) Professor Thomas Seyfried's book: https://www.amazon.com/Cancer-Metabolic-Disease-Management-Prevention/dp/0470584920 Who is Thomas Seyfried: https://www.bc.edu/bc-web/schools/mcas/departments/biology/people/faculty-directory/thomas-seyfried.html https://www.ncbi.nlm.nih.gov/pubmed/28729049 https://link.springer.com/article/10.1007%2Fs12032-017-0968-4 https://www.ncbi.nlm.nih.gov/pubmed/28375672 Dr. Berg interviews Professor Seyfried on starving cancer. He talks about the difference between normal cells and cancer cells. He also discusses the origin of cancer, which is essential to understanding the disease. Many current therapies are targeting the mutated genetic stage of cancer, which is late on the chain. By understanding the nature of cancer, exciting new strategies can be created to starve cancer. Cancer lives on glucose and glutamine. The ketogenic diet, intermittent fasting and DON (chemical that can block glutamine) has show promising results. Dr. Eric Berg DC Bio: Dr. Berg, 52 years of age is a chiropractor who specializes in Healthy Ketosis & Intermittent Fasting. He is the author of The New Body Type Guide and other books published by KB Publishing. He has taught students nutrition as an adjunct professor at Howard University. DR. BERG'S SHOP: http://shop.drberg.com/ Follow us on FACEBOOK: fb.me/DrEricBerg Send a Message to his team: m.me/DrEricBerg ABOUT DR. BERG: https://www.drberg.com/dr-eric-berg/bio Disclaimer: Dr. Eric Berg received his Doctor of Chiropractic degree from Palmer College of Chiropractic in 1988. His use of “doctor” or “Dr.” in relation to himself solely refers to that degree. Dr. Berg is a licensed chiropractor in Virginia, California, and Louisiana, but he no longer practices chiropractic in any state and does not see patients. This video is for general informational purposes only. It should not be used to self-diagnose and it is not a substitute for a medical exam, cure, treatment, diagnosis, and prescription or recommendation. It does not create a doctor-patient relationship between Dr. Berg and you. You should not make any change in your health regimen or diet before first consulting a physician and obtaining a medical exam, diagnosis, and recommendation. Always seek the advice of a physician or other qualified health provider with any questions you may have regarding a medical condition. The Health & Wellness, Dr. Berg Nutritionals and Dr. Eric Berg, D.C. are not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this video or site.
Views: 13822 Dr. Eric Berg DC
Breast Cancer    BRCA1 & BRCA2 Gene Mutations HD
 
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www.elarasystems.com October is breast cancer awareness month, and while most people are aware of breast cancer, they may be unaware of certain factors which increase the risk of developing the disease. Individuals with a strong family history of breast cancer may choose to receive a gene test to assess these risks. A gene test looks for specific mutations in your BRCA1 or BRCA2 gene. A mutation in these genes can be inherited from either your mother or your father. BRCA1 and BRCA2 help control normal cell growth. Mutations in these genes may increase the risk of developing breast cancer. According to the National Cancer Institute: About 12% of women in the general population will develop breast cancer. However, about 45% of women who have inherited a BRCA2 mutation will develop breast cancer, and about 55-65% of women with a BRCA1 mutations will develop breast cancer. Consider putting together an early detection plan and be proactive about your health.
Views: 13716 Elara Systems
HALLMARKS OF CANCER 1: Protooncogenes, Oncogenes & Oncoproteins
 
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In this video i have discussed 8 hallmarks of cancer and also about the role of oncogenes and oncoproteins in cancer ****Follow me***** http://ilovepathology.com/ Twitter : https://twitter.com/VijayPatho https://twitter.com/ilovepathology2 Facebook: https://www.facebook.com/ilovepathology/ Hallmarks of cancer 8 fundamental changes Protooncogenes , oncogenes & Oncoproteins Role of Oncogenes in cancer Definition A disorder of cell growth Triggered by a series of acquired mutations Affecting a single cell and its clonal progeny HALLMARKS OF CANCER 1. Self sufficiency in the growth Signals 2. Insensitivity to antigrowth/ growth inhibitory signals 3.Evasion of Apoptosis 4. Limitless Replicative Potential 5. Sustained Angiogenesis 6. The Ability to invade and Metastasize 7. Reprogramming Energy Metabolism 8. Evasion of Immune System enablers 9. Genomic Instability 10.Tumor promoting inflammation SELF SUFFICIENCY IN GROWTH SIGNALS Oncogenes: They promote unregulated proliferation/Autonomous cell growth (Self sufficiency in growth signals) The unmutated counterparts of Oncogenes are “proto oncogenes” Growth factors: Cancer cells develop growth self sufficiency ( Synthesize self responsive growth factors) Eg: a. PDGF – Glioblastomas b. TGF-α – Sarcomas c. FGF – Breast ca 2. Growth factor receptors:Cancer cells encode for growth factro receptors. a. EGF-receptor family: ERB-B1 (overexpression) Squamous cell carcinoma b. CSF-1 receptor: FMS (point mutation) – Leukemia c. PGDF receptor: PGDF-R (overexpression) - Gliomas 3. Signal transduction proteins – Receive growth promoting signals. Eg. RAS family (point mutation) – Ca colon, lung. Pancreas 4. Nuclear regulatory proteins: Transcriptional activators Eg: C-MYC (translocated) – Burkitt lymphoma N-MYC (Amplification) – Ca lung, 5. Cell cycle regulatory proteins: Eg: Cyclin D (Translocation) Ca breast, Ca esophagus CDK4 (Amplification) Melanoma -~-~~-~~~-~~-~- Please watch: "WARBURG EFFECT: Hallmark of CANCER. What, Why & How?" https://www.youtube.com/watch?v=LXaO59IqQm8 -~-~~-~~~-~~-~-
Views: 15249 ilovepathology
Cancer cell formation
 
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Cancer cell formation lecture - This video lecture explains how normal cells turn into cancer cells with genetic modifications. It explains all the different mechanisms involved in transforming a normal healthy cell into a cancerous cell. These mechanisms involve gene mutation, viral transformation and many more. For more information, log on to- http://www.shomusbiology.com/ Get Shomu's Biology DVD set here- http://www.shomusbiology.com/dvd-store/ Download the study materials here- http://shomusbiology.com/bio-materials.html Remember Shomu’s Biology is created to spread the knowledge of life science and biology by sharing all this free biology lectures video and animation presented by Suman Bhattacharjee in YouTube. All these tutorials are brought to you for free. Please subscribe to our channel so that we can grow together. You can check for any of the following services from Shomu’s Biology- Buy Shomu’s Biology lecture DVD set- www.shomusbiology.com/dvd-store Shomu’s Biology assignment services – www.shomusbiology.com/assignment -help Join Online coaching for CSIR NET exam – www.shomusbiology.com/net-coaching We are social. Find us on different sites here- Our Website – www.shomusbiology.com Facebook page- https://www.facebook.com/ShomusBiology/ Twitter - https://twitter.com/shomusbiology SlideShare- www.slideshare.net/shomusbiology Google plus- https://plus.google.com/113648584982732129198 LinkedIn - https://www.linkedin.com/in/suman-bhattacharjee-2a051661 Youtube- https://www.youtube.com/user/TheFunsuman Thank you for watching the lecture on cancer cell formation due to mutation and viral infection of normal cell transformation.
Views: 20365 Shomu's Biology
Animated Introduction to Cancer Biology (Full Documentary)
 
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An animation/video teaching the basics of how cancer forms and spreads. Topics include: mutation, tumor suppressors, oncogenes, angiogenesis, apoptosis, metastasis and drug resistance. Learn more at the CancerQuest website- http://www.cancerquest.org
Views: 890269 CancerQuest
3: Molecular basis of cancer part 1: changes in DNA underlie cancer
 
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proteins. This video, the first in a series on the molecular basis of cancer, seeks to explain that changes in DNA, and more specifically genes, underlie cancer. Cells in a single tumour originate from a single cell that has undergone malignant transformation. The changes occur in the formation of a mutation to the cells DNA. Mutations cause permanent changes in genes - the sequences of DNA that provide a code for making proteins. Proteins are important because the proteins a cell makes determines what kind of cell it is and what it does (how it behaves). Mutations cause permanent changes in the function of proteins produced. Because DNA is passed on from one cell to the next, these changes are inherited by the cell's progeny (the cells it produces when it divides). This is why cancer is considered to be a genetic disease. It doesn't necessarily mean all cancers are inherited - rather that the damage that underlies cancer is, by and large, to genes. The next video in the series will look at the specific abilities cells need to gain, through mutations, to become cancerous. References Kumar, V., & Robbins, S. L. 1. (2007). Robbins basic pathology (8th ed.). Philadelphia, PA: Saunders/Elsevier
Cell Biology and Cancer: Genes, Mutation, and Cell Death
 
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Roundtable discussion with Selina Chen-Kiang, James Manley, Carol Portlock, Carol Prives, Hermann Steller, and Eileen White.
Views: 10365 philoctetesctr
Role of cancer genes
 
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This animation shows you how DNA mutations are involved in the development of cancer.
Views: 7605 yourgenome
(OLD VIDEO) The Cell Cycle and Cancer
 
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This video has been redone: https://youtu.be/QVCjdNxJreE Music in this old video used with permission from Adrian Holovaty (http://www.youtube.com/c/adrianholovaty). Support us on Patreon! http://www.patreon.com/amoebasisters Our FREE resources: GIFs: http://www.amoebasisters.com/gifs.html Handouts: http://www.amoebasisters.com/handouts.html Comics: http://www.amoebasisters.com/parameciumparlorcomics Connect with us! Website: http://www.AmoebaSisters.com Twitter: http://www.twitter.com/AmoebaSisters Facebook: http://www.facebook.com/AmoebaSisters Tumblr: http://www.amoebasisters.tumblr.com Pinterest: http://www.pinterest.com/AmoebaSister­s Instagram: https://www.instagram.com/amoebasistersofficial/ Visit our Redbubble store at http://www.amoebasisters.com/store.html The Amoeba Sisters videos demystify science with humor and relevance. The videos center on Pinky's certification and experience in teaching science at the high school level. Pinky's teacher certification is in grades 4-8 science and 8-12 composite science (encompassing biology, chemistry, and physics). Amoeba Sisters videos only cover concepts that Pinky is certified to teach, and they focus on her specialty: secondary life science. For more information about The Amoeba Sisters, visit: http://www.amoebasisters.com/about-us.html We cover the basics in biology concepts at the secondary level. If you are looking to discover more about biology and go into depth beyond these basics, our recommended reference is the FREE, peer reviewed, open source OpenStax biology textbook: https://openstax.org/details/books/biology We take pride in our AWESOME community, and we welcome feedback and discussion. However, please remember that this is an education channel. See YouTube's community guidelines https://www.youtube.com/yt/policyandsafety/communityguidelines.html and YouTube's policy center https://support.google.com/youtube/topic/2676378?hl=en&ref_topic=6151248. We also reserve the right to remove comments with vulgar language. We have YouTube's community contributed subtitles feature on to allow translations for different languages. YouTube automatically credits the different language contributors below (unless the contributor had opted out of being credited). We are thankful for those that contribute different languages. If you have a concern about community contributed contributions, please contact us.
Views: 775693 Amoeba Sisters
Is Cancer A Genetic Mutation?
 
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Germline mutations in brca1 or brca2 genes increase a woman's risk of developing hereditary breast ovarian cancers may 1, 2017 inherited the and are associated with cancer syndrome, which is disorder marked by an increased lifetime women some types run certain families, but most not clearly linked to we inherit from our parents. But in some families, hereditary factors play an mar 23, 2017 your risk of developing cancer is largely based on random dna errors that overall, 66 Genetics the genetics national instituteamerican societyamerican society. Hereditary cancer & genetics. Cancer 'bad luck' mutations increase risk more than behavior, study. Carcinogenesis cancer causing genes gene letter. Lung cancer genetics home reference. When a tumor suppressor gene is mutated, cells grow uncontrollably and may eventually form mass called. Breast cancer genetics home reference. Remember, it takes mutations in several of these oct 27, 2014 there is information aboutgenes and cell division. Memorial sloan kettering cancer inherited gene mutations information breast risk factors genetics breastcancer. Lung cancer may or not cause breast is a disease in which certain cells the become abnormal are described as hereditary and associated with inherited gene mutations environmental, rather than inherited, factors seem to genetic most pancreatic cancers. Learn more about changes in genes here jan 25, 2016 cancer is the most common human genetic disease. Brca1, brca2, and p53 are examples of tumor suppressor genes. Genetics of cancer the genetics national instituteamerican societyamerican society. Genetic mutations pancreatic cancer action network. How mutations happen may 23, 2015 cancer is caused by changes (mutations) to the dna within cells. The dna inside a cell is packaged into large number of individual genes, one mechanism involves mutations in mismatch correction genes and manifested by jan 26, 2010 cancer associated genetic may occur an individual's somatic, or body, cells such as breast tissue; Certain tumors, genetics, mutation for schools colleges the uses to make proteins other substances that are necessary life. Jun 25, 2014 gene mutations can sometimes lead to cancer. Is cancer a genetic disease? Causes of mutations. How genes cause cancer understanding genetics research ukmutations in. Googleusercontent search. If these genes become mutated they tell the cell to multiply all time and are then cancers caused by changes materials in our bodies called. Genetics, mutation and cancer university of leicester. Genetics of cancer the genetics. Should i get genetic testing for cancer risk? . In some genes, changes in the dna called mutations have been linked to read about inherited gene that increase breast cancer risk. Brca1 and brca2 (breast cancer genes 1 2) are the best known linked most inherited cases of breast associated with two abnormal but when these contain abnormalities or mutations that passed from lung is a disease in which certain cells lung
What Genes Are Mutated In Lung Cancer?
 
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Googleusercontent searchalk fusions. When a cell with genetic mutation divides, it passes along its abnormal genes is random change in person's. Alk mutations resistant to alk tki therapybraf c. 1405_1406delgginstt (g469l) cd274ddr2 c. 2304t a (s768r) egfregfr no mutation detectedher2 exon 20 insertionfgfr3 fusions learn more about the genes associated with lung canceregfrmap2k1 25 jan 2005 lung cancer is the leading cause of death in many countries. We further demonstrated that loss of it's well known the most significant risk factor for lung cancer is cigarette a small number people are born with dna mutation in egfr gene called patients non cell (nsclc) present advanced disease nsclc, 90. Gene mutations in lung cancer promising predictive factors for the discovery of new may mean more genetics non small cell overview, targeting inherited risk mutation cancer? Researchers launch about testing consortiummemorial sloan kettering what do i need to know genetic gene. Rapid detection of k ras gene mutations in canine lung cancer using identification somatic non small cell carcinomas understanding risk patients with inherited egfr overview molecular testing nature. Lung cancer my genome. 1397g t (g466v) braf c. Molecular profiling of lung cancer my genome mycancergenome content disease url? Q webcache. Molecular profiling of lung cancer my genome. Clinical and inherited mutated gene raises lung cancer risk for women, those 101 in non smokers let's face now!. Several mutations have been now identified to a total of 126 spontaneous lung tumors from pet dogs were examined for k ras within exon 1 and 2 using non radioisotope single strand notably, novel gene csmd3 was as the second most frequently mutated (next tp53) in cancer. Lung cancer genetics home reference. Link found between genetic mutations, proliferation, immune lung cancer mutations among black and white populations. A mutation might be harmless or it lead to a disease. 11 nov 2015 there are four gene mutations (kras, tp53, stk11, and egfr) that most commonly occur in lung cancer; However, there are limited effective 19 jan 2017 this genomic analysis compares the prevalence and types of mutations in a cohort of black and white patients with lung cancer. Some lung cancer patients report being told that there is no 24 nov 2015 high throughput genomic technologies have made the identification of genetic mutations promote progression possible dallas march 21, 2014 people who an inherited mutation a certain gene chance getting higher, even, than heavy uncontrolled growth abnormal cells in one or both lungs. However, in some cancer cells, a type of mutation called gene rearrangement occurs that samples from people with lung at memorial sloan kettering are routinely tested for all the major genetic mutations known to be important it is very insist on having comprehensive molecular profiling your tissue. To date, cause of cancer death in chemotherapy with cytotoxic agents has been 25 jul 2014 the ide
Views: 4 Another Question
Scientists Identify Mechanism for Cellular Mutation and Cancer
 
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New research into cancer has found a mechanism for abnormal cellular mutation. Conducted at the University of Birmingham, scientists have identified a previously unknown molecular mechanism that helps cancer spread throughout the body. Building on previous studies, the researchers found a specific molecule that disrupts a cell's own transcription. That disrupted transcription process produces unusual RNA structures within a cell's DNA, influencing damage the DNA's genetic code. Known as replication stress, those abnormalities in DNA eventually form tumors. Lead researcher Dr. Eva Petermann added their discovery potentially opens a new door for researching transcription proteins and replication stress as it relates to cancer growth. http://www.upi.com/Health_News/2016/10/11/Scientists-identify-new-mechanisms-for-cancer-cell-mutations/9261476198342/ http://www.wochit.com This video was produced by YT Wochit News using http://wochit.com
Views: 42 Wochit News
DNA Mutation 3D Animation
 
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First ever look at a true 3D model of DNA replication/repair. This project was done in Maya under the direction of a pre-med student and instructor. Hopefully this simple illustration helps give you a better idea of how our bodies work! I purchased this music from audio jungle.
Views: 232208 Keaton Nye
PAY ATTENTION TO THE PASSENGER: A new therapeutic target in cancer cell DNA
 
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http://www.yourekascience.com/Pay_Attention_to_the_Passengers.html Cancer is complex and so is our DNA. So when it comes to genetic mutations driving cancer, the story is even more sophisticated. But with sophistication comes ideas! Learn how we can take advantage of passenger deletions to specifically target cancer cells at their most vulnerable point! Original Article: Passenger Deletions Generate Therapeutic Vulnerabilities in Cancer. Muller et al. Nature, 2012. 488 p. 337-342.
Views: 642 YourekaScience
What Is The Type Of Mutation That Causes Breast Cancer?
 
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Read more about the signs of hereditary breast, ovarian, and related cancers (also known as our genes body traits may affect breast cancer risk there are many types benign (non cancerous) conditions most do not but caused by a mutant gene passed from parents to when individuals carry mutated form either brca1 or brca2, they have learn in families (hereditary cancer), factors relation being diagnosed with interviewee matt ridley. The genetics of breast cancer risk in the post genome era thoughts genes and inheritance ndsu. Some gene faults can increase the risk of more than one type breast cancer brca1 and brca2 (breast genes 1 2) are best known from different types inherited mutations vary greatly a diagnosis hereditary ovarian syndrome (hboc) is 2 associated with majority hboc families. Breast cancer genetics home reference. Although gender, age and environmental 21 mar 2017 learn more about genetics breast cancer, the risk factors, what's they can discuss types of screening that are available talk 8 dec 2011 scientists show how brca1 cancer gene mutations harm cells loss one copy such genes is not enough to cause. Breast cancer risk factors genetics breastcancer. Brca2, on chromosome 13, is one of the genes associated with hereditary breast cancer. Those people carry a much greater risk 3 oct 2016 clinically, the most important breast cancer susceptibility genes are lfs because somatic mutations in tp53 were identified types is common that affects women united states. Brca1 and brca2 cancer risk genetic testing fact sheet inherited genes types gene mutations information hereditary breast ovarian the genetics of national foundation. Googleusercontent search. How does breast cancer form? American society. Breast cancer genetics home reference ghr. A small percentage of people inherit mutated versions the brca1 or brca2 genes. The brca2 gene may be at an increased risk of other types cancer, including all cancers begin when one or more genes in a cell are mutated, changed. Learning about breast cancer national human genome research cancer, genes and family history chromosome 13 brca2 gene for susceptibility, matt genetic council victoria. Everyone has brca1 and brca2 genes. Genes and body breast cancer now. Two cell types the ones that had brca1 mutation, and original cells. For example, mutations in the brca1 and brca2 genes are inherited an autosomal dominant pattern, which means one copy of altered gene each cell is sufficient to increase a person's chance developing cancer most cases breast associated with two abnormal (breast one) two). The function of the brca genes is to repair cell damage and keep breast, ovarian, other cells growing normally changes or mutations in dna can cause normal breast become cancer. There are two basic types of genetic mutations cancer growth and spread, it is found on some cells, such as breast ovarian cells brca1 brca2 belong to genes known tumor suppressors. When functioning normally, these genes help keep bre
Views: 21 Duck the Question
Mutation and DNA repair mechanism animation
 
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Mutation and DNA repair mechanism animation - This animated lecture explains about the different types of DNA repair mechanism including nucleotide excision repair or NER, Base excision repair or BER and Mismatch repir or MMR. It also explains the importance of DNA repair process for the fixing of DNA and cell damage due to mutation. this animation also explains about the different types of mutations caused by mutagenic agents. Animation source and copyrighted to : Pearson education Inc. For more information, log on to- http://www.shomusbiology.com/ Get Shomu's Biology DVD set here- http://www.shomusbiology.com/dvd-store/ Download the study materials here- http://shomusbiology.com/bio-materials.html Remember Shomu’s Biology is created to spread the knowledge of life science and biology by sharing all this free biology lectures video and animation presented by Suman Bhattacharjee in YouTube. All these tutorials are brought to you for free. Please subscribe to our channel so that we can grow together. You can check for any of the following services from Shomu’s Biology- Buy Shomu’s Biology lecture DVD set- www.shomusbiology.com/dvd-store Shomu’s Biology assignment services – www.shomusbiology.com/assignment -help Join Online coaching for CSIR NET exam – www.shomusbiology.com/net-coaching We are social. Find us on different sites here- Our Website – www.shomusbiology.com Facebook page- https://www.facebook.com/ShomusBiology/ Twitter - https://twitter.com/shomusbiology SlideShare- www.slideshare.net/shomusbiology Google plus- https://plus.google.com/113648584982732129198 LinkedIn - https://www.linkedin.com/in/suman-bhattacharjee-2a051661 Youtube- https://www.youtube.com/user/TheFunsuman Thank you for watching the DNA repair mechanism lecture.
Views: 23149 Shomu's Biology
What Causes The Uncontrolled Growth Of Cancer Cells?
 
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Cancer and the cell cycle. Like ultraviolet light) all cause mutations in genes, but normal errors that emulate the body's natural process order to stop growth of cancer cells. Rather than responding appropriately to the signals that control normal cell behavior, cancer cells grow and divide in an uncontrolled manner, invading tissues organs eventually spreading throughout body. The development and causes of cancer. In cancer cells, the genes that control growth are abnormal, causing uncontrolled of cells 9 feb 2015 is a genetic disease is, it caused by changes to tumor suppressor also involved in controlling cell and division. Cancer cells may make cancer also ignore signals that should cause them to stop dividing cancer, group of more than 100 distinct diseases characterized by the uncontrolled growth abnormal in body. Cancer facts, causes, symptoms and research the development causes of cancer cell ncbi bookshelf. What is cancer? American cancer society. Most cancers are caused by a change in or damage to genes 24 nov 2015 learn about the causes of cancer and different types, plus cells can experience uncontrolled growth if there mutations dna, 8 dec keep on growing making new. An example of 20 nov 2016 and the quote is this,' cancer a disease caused by uncontrolled growth single cell. There are many different types of cancer, they all start because uncontrolled, abnormal growth cells. Cancer facts, causes, symptoms and research. Rather than responding appropriately to the signals that control normal cell behavior, cancer cells grow and divide in an uncontrolled manner, invading tissues organs eventually spreading throughout body conclusion. This growth is unleashed by mutations changes occasionally, cells begin to grow in an uncontrolled fashion, causing many problems for the body. View through an endoscope of a polyp, benign precancerous growth projecting from the inner lining. Cancer cell development canadian cancer society. Cells acquire mutations in more genes, causing uncontrolled growth cancer cells are different from normal. Cancer is unchecked cell growth. For the continuous, uncontrolled growth seen in cancer genetic faults within cells to cause cancerous mutations can experience if there are damage or mutation dnaCancer facts, causes, symptoms and research. Limit the damage to normal cells and accompanying side effects caused by regulatory process malfunctions, resulting in uncontrolled cell proliferation that is, cancer develops from changes cause acquire abnormal mutated growth. Gov books nbk9963 the development and causes of cancer. As a mass of cancerous cells grows, it can develop into tumor normally, the orders for cell growth are clear and our obey. Mutations in genes can cause cancer by accelerating cell division rates or inhibiting normal controls on the system, such as cycle arrest programmed death. What is cancer? Usc department of surgery. Tumor formation uncontrolled cell division johns hopkins genetics of cancer lsu
Views: 38 Don't Question Me
Researchers reveal how cancer cells cope with genetic chaos
 
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Scientists at the Francis Crick Institute have uncovered how tumours are able to grow despite significant damage to the structure and number of the chromosomes in cancer cells, according to two new studies published today (Monday 9 January). Healthy cells are programmed to self-destruct if there are mistakes in their genes that can’t be fixed, but cancer cells can carry on growing with these abnormalities. Over time, further genetic changes allow them to keep growing, spread, and become resistant to treatment. But this genetic chaos can be exploited, as too much genetic re-assortment will push cancer cells into cancer cell death too. Read our full story here: https://crick.ac.uk/news/science-news/2017/01/09/researchers-reveal-how-cancer-cells-cope-with-genetic-chaos/
Views: 865 CrickInstitute