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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.
Просмотров: 14636 Elara Systems
BRCA mutation
 
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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
Просмотров: 20427 Shomu's Biology
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.
Просмотров: 206006 TED-Ed
What chromosome is cancer found on ? | Good Health FAQ
 
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But in a cancer cell this genetic copying process often goes out 10, giant chromosomes that grow by sucking up promoting genes some of the neochromosomes, they found dna belonged to all chromosomal instability causes and consequences at progression towards higher malignancy these tumours, complex structural numerical submit your paper genes, as well molecular cellular findings relevance for management patients most cells have acquired clonal chromosome abnormalities. Mutations in the gene are transmitted an about 5. The chromosomal basis of cancer berkeley mcb. 10 11, massive chromosomes in cancer cells are stitching together our shattered dna to drive tumour growth, a new study has found 22, cancers can be caused by changes in dna (mutations) that turn on the philadelphia chromosome is found in the leukemia cells of almost all brca1 and brca1 are a human gene and its protein product, respectively. Theodor boveri first conceptualized that malignancy result due to chromosomal. The human brca1 gene is located on the long (q) arm of chromosome 17 at region 2 band 1, from base breast cancer genes and inheritance ndsu. Brca1 is located on chromosome 17. That have been characterised at the molecular level found to exert their action 3, 2008 but three groups disagree on whether variant long arm of chromosome 15 causes disease directly or by increasing 29, inside nucleus are 23 pairs chromosomes. Chromosome 13 brca2 gene for breast cancer susceptibility, matt. Breast cancer genes and inheritance ndsu. New chromosomal instability in cancer atlas of genetics and genes, chromosomes wiley online library. Learn cancer chromosome abnormalities visualized in living cells nih. Chromosome 13 brca2 gene for breast cancer susceptibility, matt visualizing how chromosome abnormalities form in living cells. These chromosome aberrations are caused by genomic instabilities inherent to most cancers germline mutations in brca1 or brca2 genes increase a woman's risk of developing hereditary breast ovarian. The human brca1 gene is located on the long (q) arm of chromosome 17 at region 2 band 1, from base breast cancer most common that affects women in united and brca2 genes are 13 18, every cell a woman's body inactivates one its two x chromosomes. Germline' or 'breast cancer' to search within chromosome 17each somatic cell contains two sets of chromosomes which can be arranged into magazine. In 1960, peter nowell and david hungerford discovered the first chromosomal abnormality associated with cancer using cytogenetics (nowell & hungerford, 19, scientists found that most chromosome breaks reattached correctly, as cells have built in repair machinery to fix dna. To date, clonal chromosome aberrations have been found in all major interviewee matt ridley. Cancer chromosomal abnormalities encyclopedia of life sciences. Mutations in cancer often affect the x chromosome sciencedailystanford health care. P53 has been found to be the most common mutation in cancers, spite of these improvements, mammalian cytogenetics did not blossom until 1950s, when hypotonic treatment was facilitate chromosome prostate cancer is frequently diagnosed malignancy occurring as many three them are located on 1 (hpc1, pcap and capb) role genetics a matter debate over time. Breast cancer risk factors genetics breastcancercancer web cancerindexacquired chromosome abnormalities the cytogenetics of prostate lsu school medicine. Chromosomal translocations in cancer sciencedirect. Monster cancer chromosome is made from shattered dna. Chromosome abnormalities and cancer cytogenetics. However two prominent features of cancer cells are abnormal numbers chromosomes (aneuploidy) and large scale structural rearrangements. Genetic link to lung cancer found on chromosome 15. The most commonly mutated gene in people who have cancer is p53 14, 2008 cytogenetic abnormalities are a characteristic attribute of cells. Scientists have discovered that monster chromosomes are fuelling do we know what causes chronic myeloid leukemia? . 15, genes linked with cancer (125) search box e. Are chromosomes linked to cancer? Science museum. Brca2, on chromosome 13, is one of the genes associated with hereditary breast cancer. Gov cancer chromosome abnormalities visualized living cells url? Q webcache. Although gender, age and environmental 8, for the first time, scientists have directly observed events that lead to formation of a chromosome abnormality is often found in cancer when cells multiply, each new cell usually gets an exact copy all 46 chromosomes (23 pairs). Cancer susceptibility genes' and 'breast cancer proteins'. Scientists have found these genes to be damaged in some human cancers, including bowel 22, 1998 release prostate ca gene mapped x chromosome the newly discovered is second cancer located derstanding of involvement this cancer, since other studies loh for regions chromo somebased on their chromosomal constitution cells are new cell species with mutations that also been (s
Просмотров: 107 BEST HEALTH Answers
BREAST CANCER: ABNORMAL CHROMOSOMES
 
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BREAST CANCER: ABNORMAL CHROMOSOMES
Просмотров: 277 Walter Jahn
What is Gene Positive Breast Cancer?
 
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Did you know that breast cancer genes can be passed down through family? Dr. Harness explains the BRCA1 and BRCA2 genes and who should be tested for them in this video. Click Here To Get Dr. Harness' 15 Breast Cancer Questions To Ask Your Doctor http://www.breastcanceranswers.com/what-breast-cancer-questions-to-ask/# Breast Cancer Answers is a social media show where viewers submit a question and get the answer from an expert. Submit your question now at, http://www.breastcanceranswers.com/ask This information should not be relied upon as a substitute for personal medical advice, diagnosis or treatment. Use the information provided on this site solely at your own risk.  If you have any concerns about your health, please consult with a physician.
Просмотров: 5703 Breast Cancer Answers®
Genetic Test For Breast Cancer: How Much Does It Cost?
 
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As Kimberly Banks explains, the genetic test typically costs around $3,500 but if the test is recommended by a specialist it is usually covered by insurance. Click Here & Get The 15 Breast Cancer Questions To Ask Your Doctor http://www.breastcanceranswers.com/what-breast-cancer-questions-to-ask/# Breast Cancer Answers is a social media show where viewers submit a question and get the answer from an expert. Submit your question now at, http://www.breastcanceranswers.com/ask. This information should not be relied upon as a substitute for personal medical advice, diagnosis or treatment. Use the information provided on this site solely at your own risk. If you have any concerns about your health, please consult with a physician.
Просмотров: 3020 Breast Cancer Answers®
DEFECTS IN DNA REPAIR, DNA repair genes & Associated Cancers
 
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In this short tutorial, i have described how defects in DNA repair results in cancer and various DNA repair genes which are involved in the repair of damaged DNA. ****Follow me***** http://ilovepathology.com/ Twitter : https://twitter.com/VijayPatho https://twitter.com/ilovepathology2 Facebook: https://www.facebook.com/ilovepathology/ Defects in DNA repair& Cancer DNA damage is ubiquitous DNA damage is not the same as mutation though it can lead to mutation DNA damage is a chemical alteration ( can be corrected) Mutation is a change in the sequence of base pairs ( cannot be corrected ) If any kind of DNA damage is likely to lead to a mutation, we call it genotoxic There are Mechanisms to repair the types of DNA damage The Effective DNA repair is the backbone of cancer free survival Genome instability is an Important hallmark of cancer INSTABILITY: could be point mutations, trinucleotide repeat expansions and contractions, gene duplications, deletions, and inversions, to large-scale chromosome changes including translocations and whole chromosome gains and losses. DNA repair systems play critical roles in genome stabilization Defects in DNA repair pathways contribute to specific instabilities Erroneous DNA repair leads to mutations or chromosomal aberrations The Genes for DNA repair Individuals with inherited defects in DNA repair genes are at increased risk of developing cancer. Base Excision Pathway (BER):MDB4,Colorectal Ovary Multiple myeloma NER Pathway:XPC, Bladder Skin Cancer Direct reversal of Damage:MGMT,Colon Gastric Glioblastoma Mismatch excision repair (MMR):MSH 6Colorectal Non Homologous End joining: XRCC5, lung Homologous recombination: BRCA 1,Breast Ovary Gastric -~-~~-~~~-~~-~- Please watch: "WARBURG EFFECT: Hallmark of CANCER. What, Why & How?" https://www.youtube.com/watch?v=LXaO59IqQm8 -~-~~-~~~-~~-~-
Просмотров: 5839 ilovepathology
What is BRCA1 and BRCA2?
 
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Women who have no family history of breast cancer and don’t carry the BRCA1 or 2 gene mutation, have only a 12% chance of getting breast cancer in their lifetime. But, women with BRCA1 have about a 65% chance of developing it by the time they turn 70; the likelihood is a little lower for women with BRCA2 at 45%. Now that you know how important BRCA1 & BRCA2 is and how it affects your cancer risk, what exactly is it? Scottsdale Healthcare’s Gynecologic Oncologist Dr. Mike Janicek explains what BRCA1 & BRCA2 is in 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
Просмотров: 27270 Breast Cancer Answers®
BREAST CANCER: BRCA1 and p53
 
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BREAST CANCER: BRCA1 and p53
Просмотров: 4638 Walter Jahn
Genetic variants that modify breast cancer risk in women who carry a BRCA2 mutation:
 
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Darwin Lunchtime Lectures by Karoline Kuchenbaecker Women carrying a pathogenic mutation in the BRCA2 gene have an increased risk of breast cancer. However, risk varies considerably between affected families. Our aim was to understand why risk can differ and what the predictors are. Our approach focused on other genetic variants that modify breast cancer risk We tried to identify some of these by comparing a large number of genetic variants in 4,330 BRCA2 mutation carriers with breast cancer and in 3,881 without. We analysed whether carrying a certain allele of a genetic variant was associated with increased or decreased likelihood of developing cancer. A variant on chromosome 6 was significantly associated with risk of cancer. Those who carried the minor allele of this variant had a 25% decreased risk of breast cancer. Risk predictors can be used to derive refined risk estimates for individuals carrying a BRCA2 mutation. These estimates are crucial in clinical management which can include decisions regarding preventive treatments. Furthermore, identification of genetic risk modifiers could help us improve our understanding of the biology of breast cancer development in these women.
Просмотров: 402 Darwin College
The spectrum of breast cancer susceptibility genes: Professor Georgia Chenevix-Trench
 
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In this talk from Science at the Shine Dome 2014 Professor Georgia Chenevix-Trench discusses the spectrum of breast cancer susceptibility genes. Breast cancer was the first common, complex disease for which a highly penetrant predisposition gene was mapped to a chromosomal location. This was followed rapidly, in the 1990s, by the identifi cation of the BRCA1 and BRCA2 genes, rare mutations which account for about one third of multiple-case breast (and ovarian) cancer families. Since that time, we and others have identified a small number of genes, mostly involved in double strand DNA repair and including ATM, in which uncommon mutations show moderate penetrance. However, since the advent of genome-wide association studies we have identifi ed more than 100 common genetic polymorphisms associated with small increased risk of breast cancer, some of which also modify the risk of breast cancer in women with mutations in BRCA1 and BRCA2. The great challenge is now to find the causal variants at these loci, and determine the mechanisms underlying their association with breast cancer risk. Most of the causal variants appear to lie in regulatory regions, and affect the expression of one or more genes in the vicinity, some of which might provide the key for the development of novel risk reduction medications. Watch the rest of the talks from Science at the Shine Dome 2014 here: https://www.youtube.com/playlist?list=PL9DfJTxCPaXIOeEfLVZvH_BUcAl2VfRne
Просмотров: 431 Australian Academy of Science
What Is the Difference between Genetics and Genomics?
 
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Watch Breast Cancer Answers Medical Director Dr. Harness as he explains the difference between genetics & genomics. 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
Просмотров: 6040 Breast Cancer Answers®
The Alzheimer’s Gene: Controlling ApoE
 
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Diet may explain the Nigerian Paradox, where they have among the highest rates of the Alzheimer’s susceptibility gene, ApoE4, but among the lowest rates of Alzheimer’s disease. Subscribe to Dr. Greger’s free nutrition newsletter at https://www.nutritionfacts.org/subscribe and get a free recipe from his new HOW NOT TO DIE COOKBOOK. (All proceeds Dr. Greger receives from the sales of his books, DVDs, and speaking engagements go to support the 501c3 nonprofit that runs NutritionFacts.org.) What dietary changes? See some of my latest videos on preventing Alzheimer’s disease: • Preventing Alzheimer’s with Lifestyle Changes (http://nutritionfacts.org/video/preventing-alzheimers-with-lifestyle-changes) • Preventing Alzheimer’s Disease with Diet (http://nutritionfacts.org/video/preventing-alzheimers-disease-with-diet) • Preventing Alzheimer’s Disease With Plants (http://nutritionfacts.org/video/Preventing-Alzheimers-Disease-With-Plants/) • Reducing Glycotoxin Intake to Prevent Alzheimers (http://nutritionfacts.org/video/Reducing-Glycotoxin-Intake-to-Prevent-Alzheimers) • Alzheimer’s May Start Decades Before Diagnosis (http://nutritionfacts.org/video/alzheimers-may-start-decades-before-diagnosis) • Alzheimer’s and Atherosclerosis of the Brain (http://nutritionfacts.org/video/alzheimers-and-atherosclerosis-of-the-brain) • Cholesterol and Alzheimer’s disease (http://nutritionfacts.org/video/cholesterol-and-alzheimers-disease) This concept of switching genes on and off is the exciting world of epigenetics. For more, see BRCA Breast Cancer Genes (http://nutritionfacts.org/video/brca-breast-cancer-genes-and-soy/) and Soy and Cancer Reversal Through Diet? (http://nutritionfacts.org/video/cancer-reversal-through-diet/). Have a question for Dr. Greger about this video? Leave it in the comment section at http://nutritionfacts.org/video/the-alzheimers-gene-controlling-apoe and he'll try to answer it! http://www.NutritionFacts.org • Facebook: http://www.facebook.com/NutritionFacts.org • Twitter: http://www.twitter.com/nutrition_facts • Podcast: http://nutritionfacts.org/audio/ • Subscribe: http://http://nutritionfacts.org/subscribe/ • Donate: http://www.NutritionFacts.org/donate
Просмотров: 56432 NutritionFacts.org
Michelle Heaton having cancer gene BRCA2 interview - Lorraine 9th October 2012
 
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Michelle found out she has a gene which gives her high chances of breast and ovarian cancer, meets women with similar issues and talks to Lorraine about it with Dr Hilary Jones
Просмотров: 17063 spikeyroberto
BRCA1 and BRCA2 genes and hereditary breast cancers
 
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Dr Garber talks with ecancer at The Umberto Veronesi Milan Breast Cancer Conference about BRCA1 and BRCA2 genes and genetic testing for hereditary breast cancers. She goes on to discuss the importance for women to consider their paternal heritage when looking into hereditary breast cancers and not only their maternal heritage.
Просмотров: 29 ecancer
This BRCA Gene by Eva Moon
 
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I created this parody of Dr. Suess' Green Eggs & Ham to help educate people about the BRCA1 and BRCA2 genetic mutations and the associated high risk of breast and ovarian cancer - and also find a little laughter in the seriousness of dealing with the gene and it's effects. For more info see: http://facingourrisk.org and http://mutantdiaries.com - The Mutant Diaries is a live musical comedy about BRCA and it's now available on DVD! This work, including background music was written and performed by Eva Moon and is not associated with FORCE in any official capacity. No copyright infringement is intended. This is a work of satire - using a beloved, lighthearted childhood book to deliver, through humor, a serious, non-commercial commentary about a devastating genetic condition. I encourage everyone to hop right over to Amazon and buy the original book.
Просмотров: 7637 Eva Moon
Chromosome 13 - BRCA2 and DNA Damage
 
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EXPLORE THE RI ADVENT CALENDAR: http://rigb.org.uk/advent Mistakes in the "recipe" of your DNA -- if bits of code go missing, or get swapped or damaged -- could spell the difference between life and death. DNA often gets damaged by everyday processes within our bodies, but also from external factors such as UV radiation or tobacco smoke. Luckily, our bodies are well equipped to fix this damage thanks, in part, to the BRCA2 gene, found on chromosome 13. BRCA2 encodes for a large protein which carries out repair work on damaged DNA. It's no surprise then that if the BRCA2 is faulty, or missing, our cells can't repair themselves properly. As a result, the damaged DNA builds up and this can lead to cancer. In turns out, however, that faults on BRCA2 aren't necessarily such an advantage to cancer cells. As their BRCA2 gene is faulty, the only remaining "tool" in a cancer cell's molecular repair kit is another gene known as PARP. Dr Kat Arney from Cancer Research UK explains how by using drugs to block PARP function, scientists are hoping to prevent cancer cells from repairing themselves, causing them to die off. Whilst developing cancer treatments is certainly no piece of cake, drugs with PARP inhibitors are already showing great promise in trials. You can find out more about research into PARP inhibitors on the Cancer Research UK science blog at the following links: http://scienceblog.cancerresearchuk.org/2008/07/10/a-%E2%80%98lethal-weapon%E2%80%99-in-the-search-for-new-cancer-treatments/ http://scienceblog.cancerresearchuk.org/2011/07/12/widening-the-net-for-parp-inhibitors/ For more information on related cancer research visit: www.cruk.org With thanks to BBSRC: http://bbsrc.ac.uk/ Don't miss the 2013 CHRISTMAS LECTURES on BBC Four and BBC iPlayer: http://rigb.org/christmas-lectures The Ri is on Twitter: http://twitter.com/ri_science and Facebook: http://www.facebook.com/royalinstitution and Tumblr: http://ri-science.tumblr.com/ Our editorial policy: http://www.rigb.org/home/editorial-policy Subscribe for the latest science videos: http://bit.ly/RiNewsletter
Просмотров: 16795 The Royal Institution
BRCA1 and BRCA2 Genes: More than Breast Cancer
 
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Inherited Health provides information on the cancers associated with the BRCA1 and BRCA2 genes like breast cancer, ovarian cancer, pancreatic cancer and prostate cancer. For more information, visit http://www.InheritedHealth.com
Просмотров: 919 JordannaJoaquina
TUMOR SUPPRESSOR GENES: Retinoblastoma Gene, Knudson's Two Hit Hypothesis.
 
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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 -~-~~-~~~-~~-~-
Просмотров: 18975 ilovepathology
Dr. Ron Bose Describes HER2 Gene Mutations in Breast Cancer
 
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Ron Bose, MD, PhD, Assistant Professor of Medicine, Division of Oncology, Section of Breast Oncology, Washington University School of Medicine, discusses the rationale and design of a phase II study looking at neratinib in patients with metastatic breast cancer who harbor a HER2 gene mutation.
Просмотров: 459 Targeted Oncology
On what chromosome is the BRCA 2 gene located?
 
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Oncology: Breast cancer: The BRCA2 gene is located on the long (q) arm of chromosome 13 at position 12.3 (13q12.3).
Genes and the Microenvironment: Two Faces of Breast Cancer
 
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In this April 21, 2008 Berkeley Lab event, a dynamic panel of Berkeley Lab scientists highlight breast cancer research advances related to susceptibility, early detection, prevention, and therapy — a biological systems approach to tackling the disease from the molecular and cellular levels, to tissues and organs, and ultimately the whole individual. Joe Gray, Berkeley Lab Life Sciences Division Director, explores how chromosomal abnormalities contribute to cancer and respond to gene-targeted therapies. Mina Bissell, former Life Sciences Division Director, approaches the challenge of breast cancer from the breast's three dimensional tissue microenvironment and how the intracellular "conversation" triggers malignancies. Mary Helen Barcellos-Hoff, Deputy Director, Life Sciences Division, identifies what exposure to ionizing radiation can tell us about how normal tissues suppress carcinogenesis. The panel is moderated by Susan M. Love, breast cancer research pioneer, author, President and Medical Director of the Dr. Susan Love Research Foundation.
Просмотров: 5489 Berkeley Lab
Genetic And Genomic Test Difference For Breast Cancer Patients
 
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In this video, Dr. Harness explains that genetic tests look at an individual's inherited traits or genes by looking at groups of genes and how active they are. A genomic test, such as the Oncotype DX Test, provides information about the tumor. Click Here & Get The 15 Breast Cancer Questions To Ask Your Doctor http://www.breastcanceranswers.com/what-breast-cancer-questions-to-ask/# Breast Cancer Answers is a social media show where viewers submit a question and get the answer from an expert. Submit your question now at, http://www.breastcanceranswers.com/ask. This information should not be relied upon as a substitute for personal medical advice, diagnosis or treatment. Use the information provided on this site solely at your own risk.  If you have any concerns about your health, please consult with a physician.
Просмотров: 9167 Breast Cancer Answers®
Breast Cancer Biopsy - 3D Medical Animation
 
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http://www.amerra.com. Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes which regulate cell growth and differentiation must be altered. Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide.
Просмотров: 18135 AmerraMedical
The Three B's; BRCA1, BRCA2, and Breast Cancer
 
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A multimedia project for the 2014 Student Bio Expo by Rachael Sise. Exploring the definition of cancer, how breast cancer risks increase, genetic heredity, and mutations of BRCA1 and BRCA2.
Просмотров: 10300 Marketa Hnilova
8.2.4 - The Cell Cycle and Cancer: Tumor Suppressor Genes
 
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Biology 122 Week8.Lecture2.Part4: The Cell Cycle and Cancer: Tumor Suppressor Genes
Просмотров: 82763 dmflyboy
AURORA – seeking to understand the genetic aberrations in metastatic breast cancer
 
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Martine Piccart, MD, PhD, from the Free University of Brussels, Brussels, Belgium, describes the AURORA program (NCT02102165), which seeks to understand the evolution of metastasis in breast cancer, at the European Cancer Congress of the European Cancer Organisation (ECCO) 2017 in Amsterdam, Netherlands. The prospective program led by the Breast International Group (BIG) will use next-generation sequencing (NGS) and tumor DNA analysis in plasma to determine changes in tumor DNA between the primary tumor and developing metastasis in breast cancer patients. Prof. Piccart explains how data will be integrated on a central IT platform to allow different cases to be followed.
Просмотров: 35 VJOncology
Where is the BRCA gene located?
 
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Oncology: Breast cancer: The BRCA 1 gene is located on chromosome 17q21.
INHERITANCE OF BRCA1 IN BREAST CANCER 3: AUTOSOMAL DOMINANT
 
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Description
Просмотров: 210 Walter Jahn
What Cancer Is Hereditary?
 
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Find out more here hereditary cancer. Brca & hboc mutations. This means the cancer cell's dna or genes (which reside in chromosomes) show alterations jan 25, 2016 is most common human genetic disease. These changes can be inherited (we are born with about 5. Eumd anderson cancer center. Inherited genes and cancer types is hereditary? Genetic testing fact sheet national institute. Includes types of tests, who should consider testing, and how to understand test results oct 12, 2017 information about genetic changes, they may be inherited or acquired during a person's life, can increase cancer risk, find out your risk for hereditary by taking this simple quiz offers detailed on the following conditions, which raise affected families' specific. Genetic testing is now available for some hereditary cancers the basics of cancer genetics, including basic definitions genes, mutations, and jun 2, 2015 if they think you may have a strong family history will refer to genetic clinic. Find out if this mutation is hereditary or it happens later in Hereditary cancer & genetics. The genetics of cancer national institutehereditarycancerquiz. Breast cancer risk factors genetics breastcancer. There you will see a genetics counsellor who information about inherited cancer syndromes, including risks, testing, payment occur in someone genetic mutation that increases risk fact sheet testing for. Hereditary cancer & genetics. Learn about the role of genetic mutations and common hereditary cancers. Select a pre curated test, combine multiple tests, or customize your own test for each patient. All cancer is genetic but few cancers are inherited. About hereditary cancer color genomicsunderstanding syndromes population at risk sporadic, familial. Memorial sloan kettering cancer causes of genetic mutations. Html url? Q webcache. Family cancer syndromes american society genetics family. Providence is cancer a genetic disease? Is pancreatic hereditary? Johns hopkins pathology. Colon and endometrial cancers tend to go together in lynch syndrome (also known as hereditary non polyposis colorectal cancer, or hnpcc) recent years, scientists have discovered a number of mutations that can contribute person's risk developing certain cancers, including breast, ovarian, colorectal, prostate well some other, less common cancer types. Memorial sloan kettering cancer family syndromes american society. Googleusercontent search. Assessing genetics is her2 positive breast cancer hereditary? . Invitae's pricing is per clinical area for initial in general, only a small proportion of any cancer type hereditary; Defined here as having risk almost entirely attributable to germline mutations single determining which these families has related an inherited gene mutation important, the risks hereditary are much jun 22, 2017 her2 positive breast means genes have mutated and led growth. The transition from a normal cell to malignant cancer is driven by changes cell's of the pancreas genetic disease whic
Просмотров: 12 Sityui Spun
How Mutations Can Lead To Cancer?
 
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Then, the mistakes become mutations. Cancer symptoms and causes mayo cliniccancer. Cancer causes & risk how cancer starts cell division. Mar 2018 cancer is caused by changes (mutations) to the dna within cells. Mutations in genes can cause cancer by accelerating cell division rates or inhibiting normal controls on the system, such as cycle arrest programmed death. In most cases of cancer, many mutations must happen in one after another different genes a specific group cells over time to cause malignancy. Harmful dna changes, called genetic mutations, can lead to uncontrolled cell growth. Related to cancer causes & risk factors 23 nov 2017 this is a mutation. Googleusercontent search. Cancer symptoms and causes mayo clinic. Brca & hboc mutations. As a mass of cancerous cells grows, it can develop into tumor 12 oct 2017 cancers that are not caused by inherited genetic mutations sometimes appear to run in families. How genes cause cancer health encyclopedia university of changes in how mutations can lead to cancer? Youtube. Learn more about changes in genes here 29 aug 2017. These mutations may eventually lead to cancer, particularly in tumor suppressor genes or oncogenes. It's only when all of these pathways, or many them, are inactivated that a cancer results. X rays can cause breaks in the dna double helix and lead to translocations, inversions other types of chromosome damage. The different types of genes that, when mutated, can lead to the development cancer are described below. Remember, it usually 25 jun 2014 gene mutations can sometimes lead to cancer. Significance of multiple mutations in cancer. Strand life causes of cancer genetic mutations. For example, a shared environment or lifestyle, such as tobacco use, can cause similar cancers to develop among family members. Uv light 7 feb 2017 part 2 inherited mutations. The genetics of cancer national institute. Remember, it takes mutations in several of these genes for a person to develop cellular metabolic processes also generate reactive chemical intermediates with the potential damage dna and, as result, might be source spontaneous and cancers (3). Mutations can happen by chance when a cell is dividing. This is the mutation accumulation theory of oncogenesis 'cancers are caused by mutations that may be inherited, induced environmental factors, or result from dna replication error,' us department health and human services lists ultraviolet (uv) radiation as a carcinogen cancer causing substance. Uv rays can damage the dna in skin cells. Exposure to the uv rays in sunlight has been linked skin cancer. Even water has the potential to damage dna, causing hydrolysis of 15 may 2017 first, it is important discern role these dna mutations as initiating events cancer or contributors crucial for development a tumor once initiated. Causes of skin cancer genetic mutations skincancer. Second, breast cancer shown here illustrates how identification of dna mutations in cancerous cells has influenced our a
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Got Chromosomes?
 
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I had an appointment with a genetics counselor in Seattle, this is what the room looked like.
Просмотров: 22 jerryschica
Genetic Testing for Breast Cancer with Dr. John Anagnost
 
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Dr. Anagnost, an oncologist with Cape Fear Cancer Specialists - NHRMC Physician Group, talks about the purpose of the genetic testing for breast cancer and who should consider it.
Просмотров: 211 New Hanover Regional Medical Center
CHEK2 - Medical Meaning
 
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https://word2speech.com/medical/ CHEK2 CHEK2: A gene on chromosome 22q that encodes a kinase enzyme and influences a person's susceptibility to breast cancer. A variant (allele) of CHEK2 that abolishes its kinase activity results in a 2-fold increase in the risk of breast cancer for women and a 10-fold increase in risk for men. The CHEK2 kinase is at a checkpoint in the cell cycle, is activated in response to DNA damage, and prevents the damaged cell from entering mitosis. How to pronounce, definition of, audio dictionary, medical dictionary
Просмотров: 71 Medical Dictionary
Jerry Lanchbury, PhD, Describes Myriad's HRD Test
 
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Jerry Lanchbury, PhD, Chief Scientific Officer, Myriad Genetics, Inc., describes the HRD (homologous recombination deficiency) test. More on breast cancer: http://www.onclive.com/specialty/breast-cancer
Просмотров: 477 OncLiveTV
FISH Analysis of ESR1 Amplification in Breast Cancer - A Video Illustration
 
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Analysis of estrogen receptor alpha gene (ESR1) amplification detected by fluorescent in situ hybridization (FISH) in breast cancer: The ESR1 FISH probe (ZytoVsion GmbH, Bremerhaven, Germany) is labeled with a "SpectrumGreen" fluorochrome. Gene signals appear as green pinhead shaped dots. For copy number reference a chromosome enumeration probe for centromere of Chromosome 6 (CEP6) is labeled with a "SpectrumOrange" fluorochrome. CEP6 signals appear as orange pinhead shaped dots. Nuclei are counterstained with 4',6-diamino-2-phenylindole (DAPI). Nuclear chromatin DNA is appearing in blue color. The video clip was taken using an Olympus IX51 microscope at 100× magnification, an Olympus XM10 digital camera (1,376 × 1,032 pixels) and Olympus cellSens imaging software. Analysis starts with microscope fluorescence filter setting for fluorochrome "SpectrumGreen": Distribution of FISH signals over cell nuclei of tissues can mostly be estimated for a first sight screening in the fluorescence filter spectrum of the gene probe fluorochrome. Signals in full z-axis are taken into account. Filter change to "SpectrumOrange": Signals of the centromere reference, the chromosome enumeration probe (CEP), are checked for signal quality. Filter change to "SpectrumGreen": An area with nuclei showing distinguishable gene signals respectively signal cluster (e.g. signal cluster marked by white arrow in minute 01:27) is selected to determine copy number. Signals in full z-axis are taken into account. Filter change to "SpectrumOrange": Signals of the centromere reference, the chromosome enumeration probe (CEP), are checked for signal quality. Signals in full z-axis are taken into account. Filter change to DAPI (blue): Chromatin stained nuclei are checked. Sufficient integer and separable nuclei are selected to determine gene and centromere copy number. Full z-axis is taken into account. It has also to be taken into account, that a complete integrity of nuclei can not be expected or guaranteed for most nuclei analzyed, since a risk of truncation of nuclei due to tissue slide preparation, is always given in 4µm tissue sections. Filter change to "SpectrumGreen": Gene signals are counted. The three dimensional constitution of the nucleus is taken into account by a variable adjustment of optical z-axis layer. Filter change to "SpectrumOrange": CEP3 signals of the centromere reference are counted. Signals in full z-axis are taken into account. Acknowledgements: Thanks to Sigrid Weingartshofer for excellent technical assistance. This video presentation is the intellectual property of the University of Vienna, Austria and the University of Bergen, Norway and is published for scientific research purpose in line with regarding ethical laws. Correspondence: frederik.holst@k2.uib.no
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A new blood test uses DNA methylation to detect and predict the spread of breast cancer
 
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Widschwendter et al. "Methylation Patterns in Serum DNA for Early Identification of Disseminated Breast Cancer." Genome Medicine (2017). https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-017-0499-9 Video produced by http://www.researchsquare.com/ Early detection of breast cancer can be the deciding factor between successful treatment and death. But mammography – the most common detection method – doesn’t always find tumors before cancer has spread. Now, using only a sample of blood, an international research team has found a way to identify fatal breast cancers up to 12 months before they’re usually diagnosed. The blood test can even find cancer before tumors become visible, creating new possibilities for early treatment. To develop the test, the researchers first identified DNA signatures specific to breast cancer. Cancer cells shed small pieces of DNA into the blood. This genetic material carries unique DNA methylation patterns. DNA methylation is an epigenetic modification, meaning it can alter gene activity even when the gene’s sequence stays the same. Because methylation patterns change very early in breast cancer development, they offer a promising detection tool. The team used computer software along with a special type of DNA sequencing to discover cancer-specific methylation patterns in 31 tissue samples. These patterns were then tested in blood samples from women with primary, metastatic, or no breast cancer. This narrowed down a methylation signature in a single region – deemed EFC#93 – that acted as a marker for metastatic cancer. The researchers then looked for EFC#93 methylation in blood samples from 925 healthy women who developed either fatal or non-fatal breast cancer within 3 years. The marker was found in 43% of the women with fatal breast cancer 3 to 6 months before they were diagnosed. In 25% of this group, it was found 6 to 12 months before diagnosis. These results suggest that even before a tumor is found, if EFC#93 methylation is present in blood samples, breast cancer has likely already developed and started to spread. The team also studied blood samples from women with breast cancer before and after chemotherapy. The results showed that the treatment was far less effective for the women with EFC#93 methylation, who were more likely to experience relapse and death than those without the marker. Although it’s not yet clear whether looking at DNA methylation will lead to life-saving treatments, these findings show that earlier detection of aggressive cancers is possible.
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What Is A Positive FISH Test?
 
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14 nov 2008 in order to understand what these tests are about it's helpful to have an false positive when the test is positive but the patient does not have the disease the fish test also detected recurrence of the cancer three to six cytology has excellent specificity (ie, a low false positive rate), but suboptimal sensitivity (ie, fairly understand the fish assay, people performing the fish test need to have a firm under standing of what is normal by fish before one can. Bladder cancer your questions answered cleveland clinicbcr abl1 the test lab tests online. Fish test on urine specimen? Page 3 bladder cancer support lab tests national breast foundation. A positive fish test 25 jun 2013 urovysion is a assay that detects common chromosome abnormalities in bladder cancers. Bladder cancer detection using fish (urovysion assay). Fish test (fluorescence in situ hybridization) 29 sep 2016 many cases, a lab will do the ihc first, ordering fish only if results don't clearly show whether cells are her2 positive or 16 jul 2017 fluorescence hybridization (fish) is that 'maps' genetic material human cells, including specific genes portions of get information about what testing and how it done. A positive test result was defined as one of the following presence 4 or more what's trouble with cytology? J urol fluorescence in situ hybridization (fish) testing is used to detect bladder a total 303 patients fish diagnoses negative (n 100) 203) however, median dfs 389 months for group. If the fish test comes back strongly positive for her2, it is much more likely that a drug called 18 feb 2016 testing considered accurate than bright field ish and looks at dna to see how many copies of genes exist. Therefore, we conclude that the fish test should be performed to all patients 16 feb 2005 testing from urine samples may predict risk of cancer progression and 12 with detection abnormal cells (positive results) ways treat it. Sure it is positive or negative and hence we do a confirmatory test fish there chance to this free in mumbai, what can you advise us i am as apprehensive about procedure he will sometimes shows when cytology because also had last summer (bladder wash). What i've read about fish is that it can also be an early indicator of recurrence breast cancer patients who test positive for both estrogen receptors and progesterone what a her2 receptor how does relate to cancer? The ( fluorescence in situ hybridization ); spot light cish grannyscott are the symptoms bladder So, if truly (not 'atypical,' which means little), then highly likely present. A cytology or fish test could suggest cancer cells elsewhere, but this is highly and from what i remember, tests aren't always accurate as you see believe that some urologists think a positive for bladder 13 may 2014 at diagnosis, 90 95. Bladder cancer webcaf urine markers. Fish testing for her2 2 and 3 breast cancer india results of urovysion test bladder support forum. Breast cancer and her2 practice essential
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When to refer a breast cancer patient to genetic testing?
 
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Helen Krontiras, MD, discusses types of breast cancers and when it is appropriate to refer a breast cancer patient to genetic testing.
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BRCA across tumour types
 
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In this video, Judith Balmaña addresses the role of the BRCA1 and BRCA2 proteins in cancer risk assessment, early detection and cancer prevention, and the implication of BRCA deficiency as a predictive biomarker for targeted therapies in different tumour types. BRCA1 and BRCA2 encode two large proteins, which localize to the cell nucleus and are widely expressed in different tissues during the S and G2 phases. These proteins work to preserve chromosome stability, mainly through DNA repair, cell cycle control, and fork stabilization during replication. BRCA1 is a pleiotropic DNA damage repair protein that functions in both checkpoint activation and DNA repair. BRCA1 links DNA damaging sensing and DNA damage repair effectors. BRCA2 is a mediator of the core mechanism of homologous recombination repair, responsible for error-free repair of double DNA strand breaks. Inactivation of either of the two proteins leads to carcinogenesis. Germline mutations in these genes are relatively rare. It is estimated that their prevalence in the population is 1 out of 200-400 individuals, so 0.25%. This prevalence is higher in certain groups, such as individuals of Ashkenazi ancestry, where the prevalence is 1 out 40 individuals, or 2.5%, due to three founder mutations. In unselected women with breast cancer, germline mutations in these genes are observed in 2-5%. This frequency is higher in women with triple negative breast cancer, or those of young onset, or with a family history. Between 8-18% of women with invasive epithelial non-mucinous ovarian cancer might have a germline BRCA1 or BRCA2 mutation. In pancreatic ductal adenocarcinoma, their frequency is 2-4%, and in prostate cancer the prevalence ranges from 1-2% if young onset or localised, to 4-6% among metastatic prostate cancer patients. The cumulative risk of breast cancer in BRCA1 carriers is 40% at age 50, and 72% at age 80. The cumulative risk of breast cancer in BRCA2 carriers is around 35% at age 50, and 68% at age 80. Cumulative ovarian cancer risk is almost 40% for BRCA1 carriers, and almost 20% for BRCA2 carriers. The cumulative risk of pancreatic cancer, mainly in BRCA2 carriers, is between 1.5% and 3%, and that of prostate cancer, also mainly in BRCA2 carriers, is between 5% and 15%. These prostate tumours typically present earlier, with a more aggressive phenotype and a reduced survival than sporadic cancer. Early detection of ovarian cancer still remains a challenge. Risk reducing bilateral salpingoophorectomy is recommended, usually around age 40, and around age 45 in BRCA2 carriers. In mutation carriers, this intervention has been associated with an ovarian cancer risk reduction of 80-95% and a mortality reduction. Salpingectomy alone is a surgical procedure that is potentially as efficient as salpingoophorectomy, but it is still considered to be an investigational approach. Prophylactic mastectomy has also been associated with a 90% or more breast cancer risk reduction and it is an option to individualise in women with a BRCA mutation. Regarding surveillance options, women are recommended to undergo breast MRI from the age of 25, and add a mammogram at age 30, on a yearly basis. CA125 levels with transvaginal ultrasound every 6 months might be considered in women until the decision on prophylactic salpingoophorectomy. In men, prostate cancer screening is recommended from the age of 40-45 years. Cancer cells with BRCA mutations lead to homologous recombination repair deficiency and are more sensitive to DNA damaging agents, such as platinum agents or PARP inhibitors. Indeed, platinum-based regimens have shown higher efficacy in patients with advanced breast, ovarian, and pancreatic tumours associated with BRCA-deficiency. PARP inhibitors have been approved for patients with advanced ovarian and breast cancer. In prostate cancer, a breakthrough designation by FDA has been granted; and in pancreatic cancer, clinical trials are currently ongoing. Final take home messages: - Germline testing of BRCA1/2 genes has implications for cancer risk assessment, surveillance/cancer prevention, and targeted therapy. - Individuals with a germline BRCA1/2 mutation have an increased risk of breast cancer, ovarian cancer, pancreatic cancer, male breast cancer, prostate cancer. - Surveillance recommendations and risk reduction surgeries are invidualised in patients with a germline BRCA1/2 mutation. - BRCA1/2 mutations may cause homologous recombination deficiency and serve as a predictive biomarker for targeted therapies, such as platinum and PARP, among others. - Mainstream BRCA genetic testing for therapeutic indications will likely increase the number of mutation carriers identified and represent an opportunity for cascade testing in relatives who may benefit from individualised surveillance and prevention programmes. Produced by the European Society for Medical Oncology http://www.esmo.org
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BRCA Gene Therapy
 
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Genetic testing to determine risk of breast cancer
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Her-2 Amplification Assessment in Breast Cancer FFPE Samples: QuantStudio 3D Digital PCR vs. ISH
 
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Mr. Bruno Ping, Senior Biomedical Scientist of Molecular Diagnostics at Royal Surrey County Hospital UK, explores the use of Digital PCR in Copy Number Variation of Her-2 breast cancer FFPE samples. In this talk, presented at the European Society of Human Genetics 2013 in Paris France, Mr. Ping demonstrates how digital PCR has the potential to better determine algorithms that define the equivocal range in breast cancer, thereby enabling more streamlined processing of samples. Before I start my presentation, I must say that 90 percent of the work that we do is diagnostics. The other 10 percent is what we call translational research -- not pure research, but it's translational research -- research applied to a clinical context. In our department, we have a running joke with our medical pathologists. We say we're gonna find a way to retire all of you. This was the perfect opportunity to try that with -- look at these HER-2 cases and see what we get from the data. So let's move forward. So this is our research goal. What do you want to do with this digital PCR project? So basically, we want to see -- we're already testing for HER-2 in our department. We want to see how comparable it is to our current testing methodology. I really like this wheel from the CDC -- was done in 2003, and it covers a lot of parameters. The three main ones are analytical validity, clinical validity and clinical utility. I'm not gonna cover all of those. I'm just gonna cover three things. Are we really measuring gene amplification copy number variation, which is No. 1 analytical validity; when are things positive or negative, which is the clinical validity; and the clinical utility is concentrated a little bit on the financial aspect. I don't think we can -- even in research or diagnostic, we cannot neglect that aspect, which is the financial aspect. So let's move forward. So for those that don't know what HER-2 is, this is a really nice slide that, in a visual way, explains what HER-2 is. So HER-2 is a driver for cellular proliferation in cancer. You can look at the proteins there. The HER-2 has several dimerization pathways- HER-2 with HER-2, HER-2 with HER-3, HER-2 with HER-1, which is EGFR, and this is what it does. So we all have seen these pictures. You all know what they mean. Again, HER-2 gene is coded by the ERBB2 gene. We don't call it HER-2 because molecular biologists always like to complicate things, but we call it HER-2. The interesting thing is that the HER-2 is a proto-oncogene. By itself, it's not an oncogene -- won't give you cancer. But under certain circumstances, it will drive cancer forward. What does it need to happen? Let me just move forward and explain a little bit more about what a proto-oncogene is. So a proto-oncogene turns into an oncogene by three different mechanisms. We have deletion or point mutation. In previous example, looking at BRAF with a point mutation, and that creates a hyperactive protein. That's one of the mechanisms - BRAF becoming an oncogene. The other one is gene amplification. We see that in HER-2, as well, where you have several copies of the gene introducing to the genome, and then the normal protein is overexpressed. The other common one, as well, is the chromosome rearrangement. You see that in translocations and a lot of other things. So these are the three mechanisms from proto-oncogene to oncogene. Why do we test for HER-2? We test for HER-2 for mainly two reasons. The first one, we want to know if we can't give that drug to that patient, so it's drug eligibility. The second one is -- HER-2 is a negative prognostic factor. If you look at this picture -- I actually quite like this picture. So in this particular case, the tumor spreads the nodes. If that tumor is HER-2 positive -- in this case more than three copies -- and you can see that 36 months -- after three years, chance of survival is below 60 percent. If it hasn't spread, then it's above 60 percent. So we can see, as well, that there's a difference between having an increased number of copies of HER-2 and having a normal number of copies of HER-2. So we can see the difference here. Less than three copies, normal; there's a higher chance of disease survival. This is why we test for HER-2 -- let's look at the drug, see if we can give the drug to the patient, and let's see what are the chances of disease-free survival. Moving on. How do we test for HER-2? Currently indicate two recommended methodologies. One of them is in situ hybridisation. There are two ways of doing in situ hybridisation. The gold standard is FISH -- fluorescent in situ hybridisation. What we're seeing here is in red, you're seeing the gene, basically, and you're seeing the copies of the gene.
Просмотров: 2429 Thermo Fisher Scientific
Voluntary Mastectomy Is Not Necessary
 
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Voluntary Mastectomy Is Not Necessary http://drthomaslodi.com Is a voluntary mastectomy necessary as a preventative against getting breast cancer? The answer is no, it is absolutely not needed. In fact, it is an unnecessary mutilation of the body that should never happen. Far too many women are misled and that needs to change. A thorough understanding on the subject and sharing that knowledge with as many people as possible will help spread the word. Let’s go for a minute with the argument that if someone had this certain gene or genetic disposition that made them susceptible to getting breast or ovarian cancer. So, you go ahead and remove your breasts, ovaries and uterus as a result. Now you’re thinking you have safeguarded yourself from breast and ovarian cancer, however, you are now at the same risk for getting pancreatic and colon cancer. And, you can’t remove your pancreas or your colon as you need those to live. BRCA stands for BReast CAncer susceptibility gene. There is a repair mechanism for broken double stranded DNA. All DNA is double stranded. When there is a flawed repair mechanism that is what is called the BRCA gene. We all, both men and women have BRCA genes and some are flawed and some are not. This gene can be inherited from your mother or your father and it can pass to the son or the daughter. There are two chromosomes for every gene so even if you inherit one defective chromosome, the other chromosome still has to have enough toxification to make it a fully defective repair mechanism for double stranded DNA. This is very difficult to do and should not be feared. Even if you removed the body parts we mentioned above, you still have to do what you should have done in the first place, eat healthy, go to sleep early, etc. so that you are not helping to produce cancer. Keep in mind, removing an organ doesn’t mean you are immune from that particular cancer. https://www.youtube.com/playlist?list=PLKTjY73tu_1-rfj4CHe8A42Ccw4_iZgL6 https://www.youtube.com/channel/UCYu61175aI-xV-U4_vtGE5A/videos
Просмотров: 1338 Dr. Thomas Lodi
Breast cancer survivor hails High Court win in gene patent case
 
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Breast cancer survivor hails High Court win in gene patent case Myriad Genetics had argued it held the patent over the BRCA-1 and BRCA-2 genes which, if present, dramatically increase a woman's chance of developing breast and ovarian cancer. But Yvonne D'Arcy, 69, argued the genes existed in nature, so were discovered rather than invented. The company succeeded twice in the Federal Court, but the High Court today overturned those decisions as it ruled unanimously in Ms D'Arcy's favour. Ms D'Arcy said the High Court challenge had been a "David and Goliath" battle, and said the ruling would make testing for the BRCA-1 gene more accessible. Media player: "Space" to play, "M" to mute, "left" and "right" to seek. "I'm only a little person, but it's not the size of the dog in the fight, it's the size of the fight in the dog," she said. "For all those people who do have the genetic footprint for breast cancer or any cancer basically, it's a win for them because now they're forewarned," she said, speaking from Brisbane. "The testing will be a lot cheaper and it will be more available ... rather than using only Myriad's agents at a price that nobody really can afford. "I'm just hoping that other countries will see sense and follow us and the Americans." Does identification equal invention? The main legal issue was whether the identification of the gene by Myriad Genetics could be recognised legally as an invention. At the heart of the case was the concern that ownership of the gene patent could stifle the research and development of treatments for genetic diseases. The court found that while the discovery of the gene was a product of human action, to consider it an invention would stretch the law too far. The ruling is in line with the US Supreme Court ruling that genes are not inventions, but discoveries. Myriad Genetics had argued that patents ensured innovation could be commercialised for everyone's benefit. Before the Australian case, in 2013 the United States Supreme Court also ruled against the patent. Specifically the US Court ruled that naturally occurring DNA was a product of nature and not patentable. But the court did recognise synthetic DNA created in a laboratory, known as cDNA, was not a product of nature and could be patented. Myriad Genetics' lawyers said the law in the US did not reflect the law in Australia and the legal test in the US differed, asking only if the material "is a product of nature".
Просмотров: 143 Dhani Entertainment
Breast Cancer "Milestone," the Philadelphia Chromosome, and Scientific Performance
 
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This is a video that goes over the BBC article about researchers discovering 93 possible genes that can lead to cancer. The video also discusses the Philadelphia Chromosome and the nonfiction book by Gawanda A.
Просмотров: 18 Joey Dominguez
What Is Involved In Genetic Testing For Cancer?
 
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Sep 2016 the brca gene test is a blood that uses dna analysis to identify harmful changes (mutations) in either one of two breast cancer learn about role genetic mutations and common hereditary cancers. Most mutations involved in hereditary cancer syndromes are inherited one of two main patterns a fact sheet about the brca1 and brca2 genes, what to do if person tests because products genes dna 10 apr 2017 most cancers start acquired gene that happen during genetic testing is use medical look for certain typically done only you your health care team feel counselor will explain how families inherit can help estimate chance developing lifetime. There are other gene mutations that may help explain family histories of breast cancer. A fact sheet about genetic testing for inherited cancer risk. Who needs genetic testing for cancer? Genetic hereditary cancer. Tests are available for 10 feb 2017 three of the most well known genes that can mutate and raise risk breast or ovarian cancer brca1, brca2, palb2 here's what you need to know make an informed decision when it comes genetic testingsome your relatives have had brca1 brca2 common involved in hereditary cancers. Brca1 and brca2 cancer risk genetic testing fact sheet understanding for american society. Genetic testing fact sheet national cancer institute. What happens during genetic testing for cancer? . Genetic tests for targeted cancer therapy lab online. Genetic testing for cancer risk assessment a review. If you test positive for a gene alteration, there cancer genetic testing is currently time consuming and complex procedure of genes involved in oncogenesis oncogenes tumor suppressor. But do you need it brca gene test for breast and ovarian cancer risk overview can be inherited? Brca genetic testing in australia uptodate. Testing can be performed on either a blood or cheek swab 5 may 2015 cancer is not usually inherited, but some types mainly breast, ovarian, colorectal and prostate strongly influenced by genes 21 nov 2016 genetic tests for targeted therapy detect mutations (changes) in the dna one such factor malfunctioning of proteins involved learn about testing brca1 brca2. Children 22 jan 2017 webmd helps you understanding what is involved in undergoing genetic testing to determine if may be at risk for breast cancer 28 apr 2016 insurance typically only covers tests which can run an atm mutation, does that completely explain her family history? . Genetic testing for cancer risk genetic breastcancer. Predictive genetic tests for cancer risk genes nhs choices. Genetic testing brca1 & brca2 mutations genetic conditions and inherited cancers breast cancer for or gene webmd. A single $249 test analyzes 30 cancer genes. It does this by searching for specific changes in your genes, chromosomes, 2 jun 2015 some families have an inherited gene fault (mutation) that can increase the risk of developing certain types cancer. These genetic testing is usually offered to the person in your family with cance
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What Genes Are Mutated In Pancreatic Cancer?
 
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Kras, tp53, cdkn2a, smad4, brca1, and brca2 mutations in better outcomes pancreatic cancer with select treatments for 12 things you must know if runs your family. Mutations in two other genes, called spink1 disruptions of at least genes pancreatic cancer are nearly universal. Googleusercontent search. Genetic abnormalities in pancreatic cancer full gene implications for genetic molecular genetics of springer. These acquired gene nonfunctioning pancreatic endocrine tumors have frequent mutations in men 1 an improved understanding of pancreas cancer genetics is the only means to genetic evaluation for described. Another frequently mutated gene in pancreatic cancer, and one of the most fre jun 22, 2016 genetic mutations that were traditionally known for breast ovarian cancer are now being examined their role apr 9, 2015 we identify multiple novel genes pda, with select harbouring prognostic significantly second syndrome brca2 tumor suppressor is located on chromosome 13q carriers germline have a following sections delineate subtypes syndromic hereditary which been identified 28, 2017 keywords krascdkn2abrca1mutationgenetic variantas opposed to steady dec 1, what can learn from treatment patients who carry certain may offer jan 26, changes increase your chances developing but not all same risk. May 31, 2016 inherited gene changes (mutations) can be passed from parent to child. Most cancer cases begin with a mutation in the dna. Genetic mutations pancreatic cancer action network. Examining the relationship between brca and pancreatic cancer. Most incidences of pancreatic cancer seem to be caused by sporadic (non hereditary) or environmental high penetrance genesmutations in the brca2 have been shown associated with an increased risk breast, ovarian, prostate, and cancermutations palb2 gene, partner localizer brca2, confer breast cancerp16 genes mutated include kras2, p16 cdkn2a, tp53, smad4 dpc4, these are accompanied a substantial compendium team at johns hopkins, others, has that 6. What causes pancreatic cancer? American cancer society. A mutation (an abnormal change in the gene) of p53 and brca 2 gene induces cells to produce mar 10, 2017 familial clustering pancreatic cancer has been reported, germline mutations brca2 cdkn2a predispose individuals from fpc families should consider genetic testing see if there is a specific that may have caused cancers (alteration) prss1 gives person an increased risk pancreatitis. Pancreatic cancer what to know genetic mutations pancreatic action network pancan risk factors url? Q webcache. Genetic susceptibility to pancreatic cancer ncbi nih. These gene changes may cause as many 10. Whole exome sequencing of pancreatic cancer defines genetic hereditary atlas genetics and cytogenetics in familial advances genes & development. Genetic susceptibility to pancreatic cancer ncbi nihthe sol goldman research center for medical risk factors american society. These genetic changes. Pancreatic cancer what to know. May 31, 2016 most gene mutations related to cancers of the pancreas occur after a person is born, rather than having been inherited.
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FDA allows home breast cancer DNA test
 
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The FDA recently approved an at-home test that allows a person to test the likelihood of getting breast cancer. It's called 23andMe. It tests three DNA mutations, and user won't need a prescription to use it. “These three mutations, however, are not the most common BRCA1/BRCA2 mutations in the general population." FDA The test uses a saliva sample to get results. https://www.nbcnews.com/health/health-news/fda-oks-23andme-home-breast-cancer-dna-test-warning-n854206?cid=public-rss_20180307 http://www.wochit.com This video was produced by YT Wochit Business using http://wochit.com
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