Home
Search results “Mutated gene in cancer cells”
Tumor Supressor Gene Regulation in Cancer Cells
 
03:21
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: 51057 Vitae Studios
How Cancer Develops & Mutation
 
01:49
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: 37655 Cancer Research UK
Two-Thirds of All Cancers Are Caused by One Thing: Your DNA
 
04:23
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: 130475 Seeker
Mutations in Cancer
 
12:57
How somatic mutations can lead to cancer.
Views: 13740 Andrew Wolf
Mutation in tumor suppressor gene leads to cancer
 
07:06
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: 7385 Shomu's Biology
Cancer cell biology: mutated KRAS & reciprocal signalling
 
02:25
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.
Cancer: rogue cells and DNA mutations
 
05:20
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: 21588 yourgenome
Mutations
 
07:03
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: 794001 Bozeman Science
The Cell Cycle (and cancer) [Updated]
 
09:19
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: 185649 Amoeba Sisters
Telomerase: The Instrument of Cell Immortality
 
03:01
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
EGFR Mutation and Cancer
 
06:02
This is an informational video summarizing the EGFR mutations associated with cancer and current direction of research.
Views: 19874 Amy Liu
P53 animation - tumor supressor gene animation
 
02:36
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
What Causes Cancer? Cancer Mutations and Random DNA Copying Errors
 
03:25
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: 15645 Johns Hopkins Medicine
Cancer, How Cancer Starts, How Cancer Spreads, Where and Why, Animation.
 
03:58
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: 169582 Alila Medical Media
How Radiation Changes Your DNA
 
04:14
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: 504688 Seeker
p53 gene: The Guardian of the genome. functions, regulation and inactivation
 
10:22
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: 46323 ilovepathology
The cancer gene we all have - Michael Windelspecht
 
03:19
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: 208949 TED-Ed
Ras Raf MAPK Pathway and Cancer | Mutations, Cancer Pathogenesis, and Chemotherapy
 
08:41
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: 5565 JJ Medicine
KRAS mutation
 
13:59
This cancer pathway lecture explains about the KRAS mutation leading to the development of cancer. Mutations of the k-Ras gene arise in over ninety% of pancreatic carcinomas. No different human tumor comes shut in mutational frequency. The ras pathway is most important within the transmission of growth-selling alerts from the telephone floor receptors, ultimately toward the nucleus where these alerts have an effect on the creation and regulation of other key proteins. It's exciting that despite the fact that most mutations in genes are expected to reason their inactivation, with the Ras genes the reverse happens - they emerge as more energetic in signalling. This is considering of the engineering design of the protein. The ras sign is became off by using a molecular switch, which depends upon an enzyme endeavor. In picturesque terms, the nucleotide GTP (guanidine triphosphate) engages the swap to maintain it within the "on" state. A component to the Ras protein has an enzyme endeavor (a GTPase) which cleaves the GTP. This turns the change "off" after the temporary "on" period. Definitely, the mutations of Ras do indeed inactivate a operate, as most mutations are anticipated to do. The GTPase is inactivated via the mutations. However this now signifies that GTP continues to interact the change, and the Ras signalling function is unable to be grew to become "off". A quantity of drug firms at the moment are investigating ways to abate the signalling perform of Ras, which might provide a rational cure for pancreatic cancer. from -http://pathology.jhu.edu/pancreas/geneticsweb/K-ras.htm 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
Views: 14867 Shomu's Biology
Cell Biology and Cancer: Genes, Mutation, and Cell Death
 
01:38:45
Roundtable discussion with Selina Chen-Kiang, James Manley, Carol Portlock, Carol Prives, Hermann Steller, and Eileen White.
Views: 10395 philoctetesctr
6. Tumour Suppressor Genes (Retinoblastoma and the two hit hypothesis, p53)
 
10:28
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.
Oncogenetics - Mechanism of Cancer (tumor suppressor genes and oncogenes)
 
11:24
Where do I get my information from: http://armandoh.org/dig Facebook: https://www.facebook.com/ArmandoHasudungan Support me: http://www.patreon.com/armando Instagram: http://instagram.com/armandohasudungan Twitter: https://twitter.com/Armando71021105 SPECIAL THANKS: Patreon members FaberCastell Australia - https://www.youtube.com/user/FaberCastellGroup What markers do I use? FaberCastellPITTartistpens1,5 FaberCastellPITTartistpensF FaberCastellPermanentmarkers FaberCastellPITTartistpensbrush
Views: 29204 Armando Hasudungan
7. Proto-oncogenes and Oncogenes
 
05:23
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.
Why Don't We All Have Cancer?
 
09:23
Thanks to Cancer Research UK! http://www.cancerresearchuk.org Links to LEARN MORE and SOURCES are below. follow me: http://www.twitter.com/tweetsauce What is cancer? http://www.cancerresearchuk.org/cancer-info/cancerandresearch/all-about-cancer/what-is-cancer/ http://www.cancerresearchuk.org/cancer-info/cancerstats/keyfacts/ http://en.wikipedia.org/wiki/Hallmarks_of_cancer Visualizing the prevention of cancer: http://www.cancerresearchuk.org/cancer-info/cancerstats/causes/attributable-risk/visualisation/ 10 cancer MYTHS debunked: http://scienceblog.cancerresearchuk.org/2014/03/24/dont-believe-the-hype-10-persistent-cancer-myths-debunked/ other cancer articles: http://www.slate.com/articles/health_and_science/science/2014/02/deadliest_cancer_chart_shows_mortality_and_incidence_rates.html http://www.nytimes.com/2014/01/05/sunday-review/why-everyone-seems-to-have-cancer.html?=ref=opinion&_r=6& http://www.pbs.org/wgbh/takeonestep/cancer/interviews-demetri.html http://www.huffingtonpost.com/bill-couzens/cancer-an-inevitable-stag_b_4558325.html http://www.wired.com/2013/05/al_argcancer/ http://www.theguardian.com/environment/2011/may/06/nuclear-power-leukaemia Stirling Engine: http://www.grand-illusions.com/acatalog/Low-Temperature-Stirling-Engine-612.html Stirling Engine: VIDEO: https://www.youtube.com/watch?v=zCGTNArwJ0s dying cells: http://www.ncbi.nlm.nih.gov/pubmed/16355657 dead outer-layer of skin (the HORNY layer): http://en.wikipedia.org/wiki/Stratum_corneum human skin in dust: http://ohioline.osu.edu/hyg-fact/2000/2157.html mistakes in DNA replication: http://www.nature.com/scitable/topicpage/dna-replication-and-causes-of-mutation-409 how long it takes cells to divide: http://www.wisegeek.org/how-long-does-it-take-for-cells-to-divide.htm not all genetic mutations causes cancer: http://ghr.nlm.nih.gov/handbook/mutationsanddisorders/neutralmutations leading causes of death (in US): http://i1213.photobucket.com/albums/cc469/EternallyLearning/COD.jpg unbalanced skin damage: http://www.nejm.org/doi/full/10.1056/NEJMicm1104059 http://www.sungrubbies.com/product_index_html/UVASkinDamage.htm Giraffe tongues: http://www.noozhawk.com/article/102609_santa_barbara_zoos_male_giraffe_dies DNA repair mechanisms: http://www.abcam.com/index.html?pageconfig=resource&rid=11812 the Selection Shadow: http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 life expectancy: http://en.wikipedia.org/wiki/Life_expectancy Living after cancer diagnosis stats: http://www.cancerresearchuk.org/about-us/our-organisation/beating-cancer-sooner-our-strategy losing cells: http://www.madsci.org/posts/archives/2001-02/981770369.An.r.html Cancer and the metaphor of war: http://www.theguardian.com/society/2014/apr/25/having-cancer-not-fight-or-battle Cool image gallery: http://publications.nigms.nih.gov/biobeat/gallery/index.html extra: why do we age and die? http://www.todayifoundout.com/index.php/2014/05/age/ http://www.psychologytoday.com/blog/adventures-in-old-age/200903/problem-darwin-why-do-we-age-and-die-rather-live-forever http://en.wikipedia.org/wiki/Evolution_of_ageing
Views: 7418584 Vsauce
Mutation in growth regulatory gene leads to cancer
 
04:36
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: 2394 Shomu's Biology
Tumor suppressors | Biomolecules | MCAT | Khan Academy
 
04:44
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: 94998 khanacademymedicine
Will Gene Therapy Cure Cancer?
 
04:24
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: 74392 Fw:Thinking
Sporadic and hereditary tumours
 
03:04
Cancer is caused by the accumulation of mutations in the cell genome. Some mutations are caused by external agents, other by internal ones. Some mutations can also be inherited by our parents. What is the difference between sporadic and hereditary tumours? Series: Cancer predisposition and genetic testing. Project: Drawn to Biology.
Views: 571 IFOM
Mutations: The Potential Power of a Small Change
 
07:22
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: 837227 Amoeba Sisters
TaqMan® and castPCR™ for Somatic Mutation Detection in Cancer Genes
 
02:26
To learn more, visit http://www.lifetechnologies.com/castpcr With the new LifeTechnologies developed castPCR technology, somatic mutations now have nowhere to hide. The TaqMan® Mutation Detection Assays use this castPCR™ technology, (which refers to competitive allele-specific TaqMan® PCR) are specifically designed to detect somatic mutations that occur in cancer cells. Let's see how it works. Let's take an example of a tumor sample in which only 0.1% of the DNA contains a somatic mutation and the other 99.9% is normal, wild type DNA . A mutant allele assay based on castPCR technology contains four components: The allele specific (AS) primer is designed to be specific for a mutant allele in a target gene. A locus specific primer is designed to be specific to the target gene. This will bind to mutant and wild type allele-containing DNA. A locus specific TaqMan® probe is designed to bind to the target gene between the primers. This will also bind to both mutant and wild type allele-containing DNA. This probe will generate a fluorescent signal during the PCR reaction to monitor the target amplification. An allele specific MGB blocker oligonucleotide is designed to bind specifically to the wild type allele. The role of this blocker is to compete with the mutant allele specific primer and inhibit its binding to the wild type allele. This blocker suppresses non specific amplification of the wild type allele and improves the specificity of the reaction. Only the mutant allele is amplified and generates a florescent signal. By increasing the specificity and inhibiting the amplification of the wild type allele, this competitive allele-specific TaqMan® PCR provides a very sensitive and specific method to detect as low as 1 mutant allele in a presence of 1000 wild type alleles.
Removing the Most Common P53 Mutation in Colorectal Cancer Halts Disease Progression
 
01:31
By genetically manipulating and removing the most common mutant form of the p53 gene that promotes colorectal cancer in humans, an international team of scientists demonstrated that this therapy reduces tumor growth and tissue invasion. Led by Ute Moll, MD, Professor and cancer biologist in the Department of Pathology at Stony Brook University School of Medicine, the findings are published in "Cancer Cell".
Cancer cell formation
 
20:23
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: 24585 Shomu's Biology
PAY ATTENTION TO THE PASSENGER: A new therapeutic target in cancer cell DNA
 
07:24
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: 732 YourekaScience
Driver and Passenger  Mutation in Cancer – Leonid Mirny
 
12:04
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: 3245 Serious Science
BRCA mutation
 
17:32
This breast cancer lecture explains about the brca gene (brca1 and brca2 mechanism) mutation which leads to the development of breast cancer. A BRCA mutation is a mutation in both of the genes BRCA1 and BRCA2. Detrimental mutations in these tumor suppressor genes produce a hereditary breast-ovarian melanoma syndrome in affected families. Mutations in BRCA1 and BRCA2 are distinctive, and breast cancer is relatively original, so these mutations consequently account for only five to ten percent of all breast cancer cases in women. 1000s of distinctive types of mutations in these genes have been recognized. Excessive-danger mutations, which disable an primary error-free DNA repair procedure (homology directed repair), tremendously develop the character's threat of setting up breast cancer, ovarian melanoma and specific different cancers. Why BRCA1 and BRCA2 mutations lead preferentially to cancers of the breast and ovary is not identified, but lack of BRCA1 function seems to result in non-useful x-chromosome inactivation. No longer all mutations are excessive-chance; some show up to be harmless editions. The cancer hazard related to any given mutation varies greatly and depends on the distinctive variety and area of the mutation and in all probability different person reasons. Ladies with unsafe mutations in either BRCA1 or BRCA2 have risk of breast melanoma that is about five occasions the average chance, and a hazard of ovarian cancer that's about ten to thirty occasions common. BRCA1 mutations typically confer a higher danger of breast and ovarian melanoma in females than BRCA2 mutations. Having a high-threat mutation does no longer guarantee that the girl will increase any sort of cancer, or warranty that any melanoma that appears was once genuinely induced through the mutation, alternatively than every other element, like alcohol consumption. 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
Views: 21200 Shomu's Biology
1.4 Colon cancer pathogenesis - gene mutations
 
12:02
Increasing numbers of mutant genes accumulate in cells as they evolve from a more benign to a more malignant growth state. We know so much about the genetic basis of tumor progression in the colon because the colonic epithelium is relatively accessible through colonoscopy They examined the genomes of sizable groups of small colonic adenomas, mid-sized adenomas, large adenomas, and carcinomas It was plausible that as colonic tissues advanced progressively from normalcy to a high-grade malignancy The epithelial cells in these various tissues would accumulate increasing numbers of mutations in various genes. (NOTE: the identities of the tumor suppressor genes that participate in colon cancer pathogenesis were not known when they began their work, so they searched instead for chromosomal regions that suffered loss of heterozygosity (LOH) during tumor progression) Landmark research: Colon Cancer Early-stage adenomas often showed loss of heterozygosity in the long arm of Chromosome 5 Almost half of slightly larger adenomas showed in addition, a mutant K- ras oncogene. Even larger adenomas tended to showed high rates of LOH on the long arm of Chromosome 18 LOH on the short arm of Chromosome 17 These observations support the idea that epithehial cells acquire increasingly neoplastic phenotypes during the course of tumor progression Increasingly neoplastic phenotypes during the course of tumor progression Tumor progression Involves the activation of one proto-oncogene into an oncogene and the inactivation of at least three tumor suppressor genes This was the first suggestion of a phenomenon that is now recognized to be quite common in human tumor cell genomes. The most obvious way to rationalize the steps in colon cancer development involves an ordered succession of genetic changes that strike the genomes of colonic epithelial cells as they evolve progressively toward malignancy Colon cancer pathogenesis. Most colon cancers will begin with a Chromosome 5 alteration, but then will take alternative genetic paths on the road toward full-fledged malignancy The loss of heterozygosity on Chromosome 5q is almost always the first in the progression the precise order of the subsequent changes may vary from tumor to tumor. Some of these mutations appear to confer growth advantages at an early stage of tumor development Other mutations promote the later stages, including invasion and metastasis, which are required for the malignant phenotype
Views: 699 Mark Temple
Tumor Suppressor Genes - p53, pten, p21, pRB
 
12:20
This lecture explains about the different types of tumour suppressor genes including p53,p21,p10, pRB and so on. Tumor suppressor genes are constitutively produced in cell that regulates cell cycle stages and make the decision to either fix any DNA damage or to kill the cell with apoptosis pathway. Tumor suppressor genes are normal genes that slow down cell division, repair DNA mistakes, or tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes don't work properly, cells can grow out of control, which can lead to cancer. 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
Views: 60073 Shomu's Biology
Animated Introduction to Cancer Biology (Full Documentary)
 
12:08
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: 950494 CancerQuest
Breast Cancer    BRCA1 & BRCA2 Gene Mutations HD
 
01:16
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: 14864 Elara Systems
Role of cancer genes
 
02:50
This animation shows you how DNA mutations are involved in the development of cancer.
Views: 8549 yourgenome
TUMOR SUPPRESSOR GENES: Retinoblastoma Gene, Knudson's Two Hit Hypothesis.
 
11:24
This short tutorial explains the general concepts of tumor suppressor genes and a detailed explaination of Retinoblastoma gene ****Follow me***** http://ilovepathology.com/ Twitter : https://twitter.com/VijayPatho https://twitter.com/ilovepathology2 Facebook: https://www.facebook.com/ilovepathology/ Tumor suppression genes- general aspects Retinoblastoma gene Knudson’s two Hit Hypothesis Role of RB in regulation of cell cycle Mechanism of inactivation of RB Tumors associated with RB gene mutations Tumor suppressor proteins( products of TSG) Regulate cell growth by applying brakes to cell proliferation ( Growth Inhibition) Failure of growth inhibition is seen in carcinogenesis Loss of function of these genes is a key event in carcinogenesis Retinoblastoma Gene ( RB Gene) First discovered Tumor suppressor gene Chromosome 13q14 Retinoblastoma: is a childhood tumor with inactivation of this gene. Knudson’s two-hit hypothesis Two mutations ( hits) involving both the alleles of TSG ( here RB gene) is a basic requisite for the development of tumor Retinoblastoma can occur as hereditary or sporadic form Explanation for the same is given by Knudson’s two-hit hypothesis RB protein- product of RB gene Key role in regulation of the cell cycle “Governor” of the cell cycle So, How does RB gets inactivated ?OrHow does the Antiproliferative activity of RB is nullified? 1. Germline & somatic Loss of function Mutations of RB Gene 2. Gene Amplifications of CDK 4 and Cyclin D genes 3. Functional inactivation of RB Tumors associated with RB Gene mutations Retinoblastoma Osteosarcoma Glioblastomas Small cell carcinomas of lung Breast cancers & Bladder cancers -~-~~-~~~-~~-~- Please watch: "WARBURG EFFECT: Hallmark of CANCER. What, Why & How?" https://www.youtube.com/watch?v=LXaO59IqQm8 -~-~~-~~~-~~-~-
Views: 20434 ilovepathology
2.2 Mutated DNA causes cellular transformation
 
10:54
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: 705 Mark Temple
How Does a BRCA Gene Mutation Affect Your Cancer Risk?
 
03:56
If you’re a breast cancer patient, you’ve probably heard the term BRCA being used. There are two BRCA (Breast Cancer Susceptibility) tumor suppressor genes that are either BRCA1 or BRCA2. Everyone has BRCA gene, one of each from your mother and one from your father. When these genes work correctly, these inherited BRCA genes can actually help your body prevent cancer. Although when changes and mutations in the BRCA genes occur, cells are at risk of dividing and changing rapidly. This can lead to cancer developing. According to SHARE Cancer Support Board Member and Genetic Counselor, it’s been said that if you had a BRCA mutation, you had a 75% chance of getting breast cancer. In time, we have learned that your risk may be significantly less. Find out what your likelihood of getting cancer is if you have BRCA gene abnormalities by watching the video below. SUBSCRIBE FOR MORE EXPERT INFORMATION AND BREAKING BREAST CANCER NEWS http://www.youtube.com/user/drjayharness VISIT BREASTCANCERANSWERS.com FOR THE LATEST IN BREAKING BREAST CANCER NEWS http://www.breastcanceranswers.com/news SUBMIT A QUESTION http://www.breastcanceranswers.com/ DOWNLOAD DR. HARNESS' 15 QUESTIONS TO ASK YOUR DOCTOR http://www.breastcanceranswers.com/ CONNECT WITH US! Google+: http://bit.ly/16nhEnr Facebook: https://www.facebook.com/BreastCancerAnswers Twitter: https://twitter.com/BreastCancerDr
Cancer Genes and the Cell Cycle
 
08:59
Ms. Parrott teaches about how mutations in specific genes involved in the cell cycle can result in cancer. She also analyzes the mode of inheritance of the BRCA1 gene and the role of carcinogens in development of cancer.
Views: 510 Danielle Parrott