'+pages+''); $('.stream > div:odd').addClass('bgr_color'); updateHeight('#history'); }); window.activateTabArea = ensure(function(tab, areas){ var parsed = false; var parts = (areas || '').split('/'); window.fsonload = $.inArray('fs', parts) >= 0; if(fsonload){ parts.splice(parts.indexOf('fs'), 1); } var replayMode = false; if($.inArray('replay', parts)>=0){ replayMode = 'replay'; } var noSoundMode = false; if($.inArray('nosound', parts)>=0){ noSoundMode = 'nosound'; } if($.inArray('ns', parts)>=0){ noSoundMode = 'ns'; } var previewMode = null; if($.inArray('p', parts)>=0){ previewMode = 'p'; } if($.inArray('preview', parts)>=0){ previewMode = 'preview'; } if($.inArray('repeat', parts)>=0){ replayMode = 'repeat'; } if($.inArray('r', parts)>=0 || $.inArray('ro', parts)>=0){ replayMode = 'r'; } if(replayMode){ parts.splice(parts.indexOf(replayMode), 1); } if(noSoundMode){ parts.splice(parts.indexOf(noSoundMode), 1); } if(previewMode){ parts.splice(parts.indexOf(previewMode), 1); } if(previewMode){ if(!parts.length){ parts = ['1-14', '999:59']; } } var area = parts[0]; if(tab == 'history' && false){ var page = parseInt(area || '1') || 1; $.ajax({ url: 'https://login.wn.com/recent/json/?pp='+history_pp+'&skip='+history_pp*(page-1), dataType: 'jsonp', success: function(response){ $ensure(function(){ renderHistory(response, page); }); } }); return true; } if(tab == 'global_history' && false){ var page = parseInt(area || '1') || 1; globalHistory.fetchStream(page, '', function(){ updateHeight('#global_history'); }); return true; } if(tab == 'my_playlists' && false){ var page = parseInt(area || '1') || 1; myPlaylists.fetchStream(page, '', function(){ updateHeight('#my_playlists'); }); return true; } if(tab == 'my_videos' && false){ var page = parseInt(area || '1') || 1; myVideos.fetchStream(page, '', function(){ updateHeight('#my_videos'); }); return true; } if(tab == 'related_sites' && areas && matchPosition(areas)){ var seconds = parsePosition(areas); scrollRelated(seconds); return false; } if(matchPosition(area) || matchAction(area)){ parts.unshift('1'); area = parts[0]; } if(tab == 'expand' && area && area.match(/\d+/)) { var num = parseInt(area); if(num < 100){ //FIX ME. 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var par = el.closest('.playlist_scrollarea'); par.scrollTop(el.offset().top-par.height()/2); } var updateVolumeState = function(){ if(noSoundMode){ if(noSoundMode == 'turn-on'){ clog("Sound is on, vsid="+vp.vsid); vp.setVolumeUnMute(); noSoundMode = false; }else{ clog("Sound is off, vsid="+vp.vsid); vp.setVolumeMute(); noSoundMode = 'turn-on'; } } } var playQueueUpdate = function(){ var playPosition = playQueue[playQueuePosition]; vp.playFromPlaylist(playPosition.video); scrollToPlaylistPosition(vp); playShouldStart = playPosition.start; playShouldStop = playPosition.stop; }; var playQueueAdvancePosition = function(){ clog("Advancing play position..."); playQueuePosition ++; while(playQueuePosition < playQueue.length && !playQueue[playQueuePosition].video){ playQueuePosition ++; } if(playQueuePosition < playQueue.length){ playQueueUpdate(); }else if(vp.getReplayCurrent()){ playQueuePosition = 0; playQueueUpdate(); vp.seekTo(playShouldStart); vp.playVideo(); }else{ vp.pauseVideo(); playShouldStop = null; playShouldStart = null; } }; function loadMoreVideos(playerId, vp, start, finish, callback){ var playlistInfo = playlists[playerId-1]; if(playlistInfo.loading >= finish) return; playlistInfo.loading = finish; $.ajax({ url: '/api/upge/cheetah-photo-search/query_videos2', dataType: 'json', data: { query: playlistInfo.query, orderby: playlistInfo.orderby, start: start, count: finish-start }, success: function(response){ var pl = vp.getPlaylist().slice(0); pl.push.apply(pl, response); vp.setPlaylist(pl); callback(); } }); } if(parts.length == 1 && matchDash(parts[0])){ var pl = vp.getActualPlaylist(); var vids = parseDash(parts[0]); parts = []; for(var i = 0; i < vids.length; i++){ playQueue.push({ 'video': pl[vids[i]-1], 'start': 0, 'stop': null }) } if(vids.length){ if(vids[vids.length-1]-1>=pl.length){ loadMoreVideos(playerId, vp, pl.length, vids[vids.length-1], function(){ if(fsonload){ activateTabArea(tab, parts[0]+'/fs'); }else{ activateTabArea(tab, parts[0]); } var pls = vp.getPlaylist(); vp.playFromPlaylist(pls[pls.length-1]); vp.playVideo(); scrollToPlaylistPosition(vp); }); return true; } } if(playQueue){ playQueueUpdate(); vp.playVideo(); parsed = true; playShouldStart = 0; } } if(previewMode){ var vids = []; var dur = 0; var pl = vp.getActualPlaylist(); area = parts[0]; if(parts.length == 1 && matchPosition(parts[0])){ vids = parseDash('1-'+pl.length); dur = parsePosition(parts[0]); parts = []; }else if(parts.length == 1 && matchDash(parts[0])){ vids = parseDash(parts[0]); dur = parsePosition("999:59"); parts = []; } if(parts.length == 2 && matchDash(parts[0]) && matchPosition(parts[1])){ vids = parseDash(parts[0]); dur = parsePosition(parts[1]); parts = []; } for(var i = 0; i < vids.length; i++){ playQueue.push({ 'video': pl[vids[i]-1], 'start': 0, 'stop': dur }) } if(playQueue){ playQueueUpdate(); vp.playVideo(); parsed = true; } } if(parts.length>1){ for(var i = 0; i < parts.length; i++){ var sel = findMatchingVideo(vp, parts[i]); if(sel){ playQueue.push({ 'video': sel, 'start': 0, 'stop': null }) } } if(playQueue){ playQueueUpdate(); 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if(vp.getCurrentVideo() == playQueue[playQueuePosition].video){ playQueueAdvancePosition(); }else{ playShouldStart = null; } } }, 500); vp.playerContainer.bind('videoplayer.player.statechange', function(e, state){ if(state == 'ended'){ // advance to the next video playQueueAdvancePosition(); } }); vp.playerContainer.bind('videoplayer.player.readychange', function(e, state){ if(state){ updateVolumeState(); if(playShouldStart !== null){ vp.seekTo(playShouldStart); playShouldStart = null; }else{ playShouldStop = null; // someone started other video, stop playing from playQueue } } if(fsonload) { triggerFullscreen(playerId); fsonload = false; } }); } } else if(tab.match(/^wiki\d+$/)){ if(firstTimeActivate){ load_wiki($('#'+tab), function(){ if(area){ var areaNode = $('#'+area); if(areaNode.length>0){ $('html, body').scrollTop(areaNode.offset().top + 10); return true; } } }); } } return parsed; }) window.activateTab = ensure(function(tab, area){ window.activeArea = null; if(tab == 'import_videos'){ if(area){ import_videos(area); 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if(window.history && history.replaceState && document.location.hostname.match(/^(youtube\.)?(\w{2,3}\.)?wn\.com$/)){ if(path == main_tab || path == main_tab+'/' || path == '' || path == '/') { path = basepath; } else if( path.match('^'+main_tab+'/') ){ path = basepath + '/' + path.replace(main_tab+'/', '').replace('--','/'); } else { path = basepath + '/' + path.replace('--','/'); } if(document.location.search){ path += document.location.search; } if(window.lastHistory) { history.pushState(null, null, path); } else if(window.lastHistory != path){ history.replaceState(null, null, path); window.lastHistory = path; } } else{ path = path.replace('--','/'); if(path == main_tab || path == main_tab+'/' || path == '' || path == '/') { path = ''; } if(window.lastHistory != '/'+path){ window.location.hash = path? '/'+path : ''; window.lastHistory = '/'+path; } } }); $('.tabtrigger li a').live('click', ensure(function() { var tab = $(this).attr('id'); if(tab.substring(0,1) == '#'){ var name = tab.substring(1); if(name in menu_names){ name = menu_names[name][0]; } realTab = rev_names[name]; $('#'+realTab).show(); if(window.console && console.log) console.log("Triggering tab: "+name+(window.activeArea?" activeArea="+window.activeArea:'')); var path = name; if(window.activeArea){ path = path + '/' + window.activeArea; } if(tab.match(/#playlist\d+/) || tab.match(/#details\d+/)){ $('.multiple-playlists').show(); $('.related_playlist').show(); $('.longest_videos_playlist').show(); }else { $('.multiple-playlists').hide(); $('.related_playlist').hide(); $('.longest_videos_playlist').hide(); } // start the related script only when the tab is on screen showing if (tab.match(/related_sites/)) { if (mc) { mc.startCredits(); } } window.activeTab = realTab; addHistory(path); setTimeout(ensure(function(){ if(tab.match(/language--/)){ $('.tabtrigger').offscreentabs('activateTab', 'language'); } if(tab.match(/weather/)) { $('.tabtrigger').offscreentabs('activateTab', 'weather'); loadContinent(); } updateMenus(tab); updateHeight(); }), 10); } return false; })); }); -->

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  Philadelphia Chromosome

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  Philadelphia Chromosome

• Bcr-Abl tyrosine-kinase inhibitor
• Tyrosine-kinase inhibitor
• Philadelphia chromosome

Bcr-Abl tyrosine-kinase inhibitor

Bcr-Abl tyrosine-kinase inhibitors (TKI) are the first-line therapy for most patients with chronic myelogenous leukemia (CML). More than 90% of CML cases are caused by a chromosomal abnormality that results in the formation of a so-called Philadelphia chromosome. This abnormality was discovered by Janet Rowley in 1972 and is a consequence of fusion between the Abelson (Abl) tyrosine kinase gene at chromosome 9 and the break point cluster (Bcr) gene at chromosome 22, resulting in a chimeric oncogene (Bcr-Abl) and a constitutively active Bcr-Abl tyrosine kinase that has been implicated in the pathogenesis of CML. Compounds have been developed to selectively inhibit the tyrosine kinase.

Before the 2001 U.S. Food and Drug Administration (FDA) approval of imatinib, no drugs were available to alter the natural progression of CML. Only cytotoxic drugs such as busulfan, hydroxyurea or interferon-alpha (rIFN-α) were utilized. Even though the first Bcr-Abl TK inhibitor was named “the magic bullet” to cure cancer by TIME magazine, a second generation of Bcr-Abl TKI was subsequently developed to combat the initial resistance that emerged.

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This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/Bcr-Abl_tyrosine-kinase_inhibitor

Tyrosine-kinase inhibitor

A tyrosine kinase inhibitor (TKI) is a pharmaceutical drug that inhibits tyrosine kinases. Tyrosine kinases are enzymes responsible for the activation of many proteins by signal transduction cascades. The proteins are activated by adding a phosphate group to the protein (phosphorylation), a step that TKIs inhibit. TKIs are typically used as anticancer drugs. For example, they have substantially improved outcomes in chronic myelogenous leukemia.

They are also called tyrphostins, the short name for “tyrosine phosphorylation inhibitor”, originally coined in a 1988 publication, which was the first description of compounds inhibiting the catalytic activity of the epidermal growth factor receptor (EGFR).

The 1988 study was the first demonstration of a systematic search and discovery of small-molecular-weight inhibitors of tyrosine phosphorylation, which do not inhibit protein kinases that phosphorylate serine or threonine residues and can discriminate between the kinase domains of the EGFR and that of the insulin receptor. It was further shown that in spite of the conservation of the tyrosine-kinase domains one can design and synthesize tyrphostins that discriminate between even closely related protein tyrosine kinases such as EGFR and its close relative HER2.

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This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/Tyrosine-kinase_inhibitor

Philadelphia chromosome

The Philadelphia chromosome or Philadelphia translocation is a specific abnormality of chromosome 22, which is unusually short, as an acquired abnormality that is most commonly associated with chronic myelogenous leukemia (CML). It is the result of a reciprocal translocation between chromosome 9 and chromosome 22, which is specifically designated t(9;22)(q34;q11). This gives rise to a fusion gene, BCR-ABL1, that juxtaposes the ABL1 gene on chromosome 9 (region q34) to a part of the BCR ("breakpoint cluster region") gene on chromosome 22 (region q11). The presence of this translocation is a highly sensitive test for CML, since 95% of people with CML have this abnormality (the remainder have either a cryptic translocation that is invisible on G-banded chromosome preparations, or a variant translocation involving another chromosome or chromosomes as well as the long arm of chromosomes 9 and 22). However, the presence of the Philadelphia (Ph) chromosome is not sufficiently specific to diagnose CML, since it is also found in acute lymphoblastic leukemia (ALL, 25–30% in adult and 2–10% in pediatric cases) and occasionally in acute myelogenous leukemia (AML).

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This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/Philadelphia_chromosome

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Email this Page Play all in Full Screen Show More Related Videos

• 

  bcr-abl Translocation Mechanism | Philadelphia Chromosome

  The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle. The chromosomal defect in the Philadelphia ...

  published: 18 Aug 2020
• 

  Philadelphia Chromosome, Translocations, Inversions, Deletions

  This video discusses the formation of the Philadelphia Chromosome bringing about chronic myelogenous leukemia (CML) and the difference between translocations, inversions, and deletions. The medication imatinib (Gleevec) is also discussed.

  published: 28 Jul 2017
• 

  Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome

  Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome - Hematology and Oncology. Chronic myeloid leukemia (or chronic myelogenous leukemia or CML) is a chronic leukemia, as well as a myeloproliferative neoplasm (MPNs). What is chronic myeloid leukemia? --This is the topic of today's video. 😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/ - With Picmonic, get your life back by studying less and remembering more. Medical and Nursing students say that Picmonic is the most comprehensive and effective way to bridge learning and test prep... Disclaimer: I use affiliate links.... ►👨‍🏫💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/products/courses/antibiotics/ ... ❗️Sorry! I made a MISTAKE in this video! ...

  published: 13 Aug 2018
• 

  Philadelphia Chromosome

  published: 12 Jul 2015
• 

  The latest in Philadelphia chromosome-positive ALL (Ph+ ALL)

  Prof Robin Foà talks to ecancer about the latest in Philadelphia chromosome-positive ALL (Ph+ ALL). He begins by stating that the changes have been quite dramatic, going on to say that Ph+ ALL was the worst sub-group of leukaemias in terms of prognosis, for both adults and children. The only chance of a cure was an allogeneic stem cell transplant, when doable. Prof Foà then goes on to explain how the incidents of Ph+ ALL increases with age. About 1 in 2 B-lineage ALL patients over the age of 50-60 years old. He concludes by saying maybe some patients in the future can be managed without chemo or without transplant, referring to other research he adds if patients do not have additional genetic abnormalities at diagnosis or the MRD is repeatedly negative these patients will not receive a ...

  published: 11 Jan 2022
• 

  Philadelphia chromosome: Explained in 5 minutes!!!!!! #Medschooldiscussion

  It was 1959 when two Philadelphia researchers, Dr. Peter Nowell and Dr. David Hungerford, were experimenting with cells from various types of leukemia . Then they noticed a smaller chromosome 22 in the cancer cells of some individuals with CML. Due to unavailability of sophisticated technique at that time, they were unable to tell what happened to the material missing from the small chromosome. Nowell and Hungerford published their research in 1960, describing the abnormality that had was found in 9 out of 10 CML patients they studied.Later on in 1972 another researcher, Dr.Janet Rowley, discovered that the missing piece of chromosome number 22 is attached to the chromosome number 9.That is how the first known chromosomal translocation that is t(9,22) was discovered. Later on this abno...

  published: 31 May 2018
• 

  Chronic myeloid leukaemia: discovery of the Philadelphia chromosome

  A review of: Chromosome studies on normal and leukemic human leukocytes. Nowell PC, Hungerford DA. J Natl Cancer Inst. 1960 Jul;25:85-109. Twitter: https://twitter.com/Genetics_Stuff OTHER VIDEOS YOU MIGHT LIKE: • Plants show phenotype is influenced by genotype AND environment (Clausen, Keck & Hiesey, 1940) - https://youtu.be/mlQPp3_-N3M • Codons don’t overlap in the shagadelic genetic code, baby. Yeah! (Brenner, 1957) - https://youtu.be/l7f-FHnYtyw • Understanding Quantitative Trait Loci with the help of tomatoes (Paterson et al., 1988) - https://youtu.be/17NtnnFsq-s Leukaemia, cancer of the blood, affects white blood cells and causes proliferation of bone marrow white blood cell progenitors, haematopoietic cells, initiating mass production of faulty white blood cells. This throws off ...

  published: 17 Apr 2021
• 

  BCR-ABL1 and the Philadelphia chromosome - Part 2: The Philadelphia chromosome

  The Philadelphia chromosome, which is found in leukemic cells in more than 90% of all patients with chronic myeloid leukemia (CML), results from a translocation between chromosome 9 and chromosome 22. On the Philadelphia chromosome, the 5’ end of the gene BCR is fused to the major 3’ part of the gene ABL1. The amplification of the fused gene region by polymerase chain reaction allows the sensitive detection of leukemic cells in patients with CML. #onkoview, #Philadelphiachromosome, #chromosome22, #gene, #leukemic, #cells, #cml, #abl1, #leukemia, #polymerase

  published: 04 Oct 2021
• 

  Jessica Wapner "The Philadelphia Chromosome"

  This event was recorded at Politics & Prose Bookstore in Washington, D.C. on May 16, 2013. More information is available at http://www.politics-prose.com/event/book/jessica-wapner-philadelphia-chromosome-mutant-gene-and-quest-cure-cancer-genetic-level A genetic mutation that causes chronic myeloid leukemia (CML), the Philadelphia chromosome was first detected in 1959. Some fifty years later, the once deadly CML can be controlled with a daily dose of a drug called Gleevec. Wapner, a widely published science writer, Work in Progress blogger, and former editor of Oncology Spectrum, profiles the dedicated doctors involved in the research and explains the science behind this breakthrough.

  published: 20 May 2013
• 

  Chronic Myeloid Leukemia | CML | Philadelphia Chromosome

  Chronic myeloid leukemia (CML) is a type cancer that affects the blood and bone marrow.

  published: 19 Jan 2018

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6:59

bcr-abl Translocation Mechanism | Philadelphia Chromosome

• Order: Reorder
• Duration: 6:59
• Uploaded Date: 18 Aug 2020
• views: 41485

The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic...

The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle. The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11). This is a reciprocal translocation, creating an elongated chromosome 9 (termed a derivative chromosome, or der 9), and a truncated chromosome 22 (the Philadelphia chromosome, 22q-).In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11). The symbol ABL1 is derived from Abelson, the name of a leukemia virus which carries a similar protein. The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins . Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein. Depending on the precise location of fusion, the molecular weight of this protein can range from 185 to 210 kDa. Consequently, the hybrid BCR-ABL1 fusion protein is referred to as p210 or p185.

https://wn.com/Bcr_Abl_Translocation_Mechanism_|_Philadelphia_Chromosome

The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle. The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11). This is a reciprocal translocation, creating an elongated chromosome 9 (termed a derivative chromosome, or der 9), and a truncated chromosome 22 (the Philadelphia chromosome, 22q-).In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11). The symbol ABL1 is derived from Abelson, the name of a leukemia virus which carries a similar protein. The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins . Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein. Depending on the precise location of fusion, the molecular weight of this protein can range from 185 to 210 kDa. Consequently, the hybrid BCR-ABL1 fusion protein is referred to as p210 or p185.

• published: 18 Aug 2020
• views: 41485

4:15

Philadelphia Chromosome, Translocations, Inversions, Deletions

• Order: Reorder
• Duration: 4:15
• Uploaded Date: 28 Jul 2017
• views: 35027

This video discusses the formation of the Philadelphia Chromosome bringing about chronic myelogenous leukemia (CML) and the difference between translocations, ...

This video discusses the formation of the Philadelphia Chromosome bringing about chronic myelogenous leukemia (CML) and the difference between translocations, inversions, and deletions. The medication imatinib (Gleevec) is also discussed.

https://wn.com/Philadelphia_Chromosome,_Translocations,_Inversions,_Deletions

This video discusses the formation of the Philadelphia Chromosome bringing about chronic myelogenous leukemia (CML) and the difference between translocations, inversions, and deletions. The medication imatinib (Gleevec) is also discussed.

• published: 28 Jul 2017
• views: 35027

17:59

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome

• Order: Reorder
• Duration: 17:59
• Uploaded Date: 13 Aug 2018
• views: 428038

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome - Hematology and Oncology. Chronic myeloid leukemia (or chronic mye...

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome - Hematology and Oncology. Chronic myeloid leukemia (or chronic myelogenous leukemia or CML) is a chronic leukemia, as well as a myeloproliferative neoplasm (MPNs). What is chronic myeloid leukemia? --This is the topic of today's video. 😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/ - With Picmonic, get your life back by studying less and remembering more. Medical and Nursing students say that Picmonic is the most comprehensive and effective way to bridge learning and test prep... Disclaimer: I use affiliate links.... ►👨‍🏫💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/products/courses/antibiotics/ ... ❗️Sorry! I made a MISTAKE in this video! The mistake: CML is characterized by increased number of neutrophils. The correction: CML is characterized by increased number of basophils. Check out my brand new "Electrolytes" course at https://www.medicosisperfectionalis.com/products/course/electrolytes/ and use the PROMO code: ELECTROLYTES50 to get a 50% discount. ► Get my notes and cases at https://www.patreon.com/medicosis ... ► Don’t forget to check my recommended collection of the best medical books that I personally use https://www.amazon.com/shop/medicosisperfectionalis MEDICAL Sources that I use for my videos:- ► Goljan Rapid Review Pathology, https://amzn.to/2MufTPw ► Harrison’s Internal Medicine https://amzn.to/2OJiVNf ► Goldman-Cecil Medicine https://amzn.to/2N0v93u ► Davidson’s Principles and Practice of Medicine https://amzn.to/2vTmf1p ------------------------------------------------------------------------- Many people ask me “How do you record your videos”? Here is the answer:- Equipment that I use:- ► Apple iPad Pro https://amzn.to/2nKCyZW ► Apple pencil https://amzn.to/2PimMCc ►Iphone holder kit: https://amzn.to/2OVV3aj ►Rode Video Mic Go: https://amzn.to/2OVF4Je ►Rode SC7 3.5mm TRS to TRRS Patch Cable: https://amzn.to/2vu2WeY ►Extension Audio Cable https://amzn.to/2nIDApo ►Rode DDC-GO DeadCat Artificial Fur Wind Shield for VideoMic GO: https://amzn.to/2OpbV8m Disclaimer 1: The medical information contained herein is intended for educational purposes only, and are not intended for diagnosis of any illness. If you think you may be suffering from any medical condition, you should consult your physician or seek immediate medical attention. I am NOT a licensed physician…Talk to your doctor. Disclaimer 2: these links are affiliate links so that I get paid a percentage of the sale, to support the channel, however, the customer is not affected as they pay the same price. Got a question? Ask it in the comments section below, or connect with me on FACEBOOK https://www.facebook.com/medicosis/ where you can directly message me…I respond to your messages personally. Thanks! Whether you’re studying for the USMLE, MCAT, shelf exam, NCLEX, COMLEX, PLEB, MCCEE, AMC_CAT, PANCE,…etc., these videos will help! Take it to the bank :) As always…Be safe, Stay happy and Study hard! MEDICOSIS PERFECTIONALIS Remember, chronic myeloid leukemia (CML) is a chronic leukemia; monoclonal disorder of late hematopoietic stem cells. If you like my videos, please consider leaving a tip at https://www.paypal.me/perfectionalis/ ► Visit my website: https://www.medicosisperfectionalis.com/ My Favorite Productivity App: https://airtable.com/invite/r/2zH40fus/ 📱Save on your mobile phone bill: http://fbuy.me/q6bMj 🏦 Qbank (TrueLearn): https://truelearn.referralrock.com/l/MEDICOSIS/

https://wn.com/Chronic_Myeloid_Leukemia_(Cml)_Myeloproliferative_Neoplasm_(Mpn)_Philadelphia_Chromosome

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome - Hematology and Oncology. Chronic myeloid leukemia (or chronic myelogenous leukemia or CML) is a chronic leukemia, as well as a myeloproliferative neoplasm (MPNs). What is chronic myeloid leukemia? --This is the topic of today's video. 😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/ - With Picmonic, get your life back by studying less and remembering more. Medical and Nursing students say that Picmonic is the most comprehensive and effective way to bridge learning and test prep... Disclaimer: I use affiliate links.... ►👨‍🏫💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/products/courses/antibiotics/ ... ❗️Sorry! I made a MISTAKE in this video! The mistake: CML is characterized by increased number of neutrophils. The correction: CML is characterized by increased number of basophils. Check out my brand new "Electrolytes" course at https://www.medicosisperfectionalis.com/products/course/electrolytes/ and use the PROMO code: ELECTROLYTES50 to get a 50% discount. ► Get my notes and cases at https://www.patreon.com/medicosis ... ► Don’t forget to check my recommended collection of the best medical books that I personally use https://www.amazon.com/shop/medicosisperfectionalis MEDICAL Sources that I use for my videos:- ► Goljan Rapid Review Pathology, https://amzn.to/2MufTPw ► Harrison’s Internal Medicine https://amzn.to/2OJiVNf ► Goldman-Cecil Medicine https://amzn.to/2N0v93u ► Davidson’s Principles and Practice of Medicine https://amzn.to/2vTmf1p ------------------------------------------------------------------------- Many people ask me “How do you record your videos”? Here is the answer:- Equipment that I use:- ► Apple iPad Pro https://amzn.to/2nKCyZW ► Apple pencil https://amzn.to/2PimMCc ►Iphone holder kit: https://amzn.to/2OVV3aj ►Rode Video Mic Go: https://amzn.to/2OVF4Je ►Rode SC7 3.5mm TRS to TRRS Patch Cable: https://amzn.to/2vu2WeY ►Extension Audio Cable https://amzn.to/2nIDApo ►Rode DDC-GO DeadCat Artificial Fur Wind Shield for VideoMic GO: https://amzn.to/2OpbV8m Disclaimer 1: The medical information contained herein is intended for educational purposes only, and are not intended for diagnosis of any illness. If you think you may be suffering from any medical condition, you should consult your physician or seek immediate medical attention. I am NOT a licensed physician…Talk to your doctor. Disclaimer 2: these links are affiliate links so that I get paid a percentage of the sale, to support the channel, however, the customer is not affected as they pay the same price. Got a question? Ask it in the comments section below, or connect with me on FACEBOOK https://www.facebook.com/medicosis/ where you can directly message me…I respond to your messages personally. Thanks! Whether you’re studying for the USMLE, MCAT, shelf exam, NCLEX, COMLEX, PLEB, MCCEE, AMC_CAT, PANCE,…etc., these videos will help! Take it to the bank :) As always…Be safe, Stay happy and Study hard! MEDICOSIS PERFECTIONALIS Remember, chronic myeloid leukemia (CML) is a chronic leukemia; monoclonal disorder of late hematopoietic stem cells. If you like my videos, please consider leaving a tip at https://www.paypal.me/perfectionalis/ ► Visit my website: https://www.medicosisperfectionalis.com/ My Favorite Productivity App: https://airtable.com/invite/r/2zH40fus/ 📱Save on your mobile phone bill: http://fbuy.me/q6bMj 🏦 Qbank (TrueLearn): https://truelearn.referralrock.com/l/MEDICOSIS/

• published: 13 Aug 2018
• views: 428038

1:23

Philadelphia Chromosome

• Order: Reorder
• Duration: 1:23
• Uploaded Date: 12 Jul 2015
• views: 33296

https://wn.com/Philadelphia_Chromosome

• published: 12 Jul 2015
• views: 33296

8:45

The latest in Philadelphia chromosome-positive ALL (Ph+ ALL)

• Order: Reorder
• Duration: 8:45
• Uploaded Date: 11 Jan 2022
• views: 1096

Prof Robin Foà talks to ecancer about the latest in Philadelphia chromosome-positive ALL (Ph+ ALL). He begins by stating that the changes have been quite drama...

Prof Robin Foà talks to ecancer about the latest in Philadelphia chromosome-positive ALL (Ph+ ALL). He begins by stating that the changes have been quite dramatic, going on to say that Ph+ ALL was the worst sub-group of leukaemias in terms of prognosis, for both adults and children. The only chance of a cure was an allogeneic stem cell transplant, when doable. Prof Foà then goes on to explain how the incidents of Ph+ ALL increases with age. About 1 in 2 B-lineage ALL patients over the age of 50-60 years old. He concludes by saying maybe some patients in the future can be managed without chemo or without transplant, referring to other research he adds if patients do not have additional genetic abnormalities at diagnosis or the MRD is repeatedly negative these patients will not receive a transplant even with a sibling donor. So, he hopes it can be proven that at least a portion of patients can be managed and possibly cured without systemic chemo or transplant. Sign up to ecancer for free to receive tailored email alerts for more videos like this. ecancer.org/account/register.php

https://wn.com/The_Latest_In_Philadelphia_Chromosome_Positive_All_(Ph_All)

Prof Robin Foà talks to ecancer about the latest in Philadelphia chromosome-positive ALL (Ph+ ALL). He begins by stating that the changes have been quite dramatic, going on to say that Ph+ ALL was the worst sub-group of leukaemias in terms of prognosis, for both adults and children. The only chance of a cure was an allogeneic stem cell transplant, when doable. Prof Foà then goes on to explain how the incidents of Ph+ ALL increases with age. About 1 in 2 B-lineage ALL patients over the age of 50-60 years old. He concludes by saying maybe some patients in the future can be managed without chemo or without transplant, referring to other research he adds if patients do not have additional genetic abnormalities at diagnosis or the MRD is repeatedly negative these patients will not receive a transplant even with a sibling donor. So, he hopes it can be proven that at least a portion of patients can be managed and possibly cured without systemic chemo or transplant. Sign up to ecancer for free to receive tailored email alerts for more videos like this. ecancer.org/account/register.php

• published: 11 Jan 2022
• views: 1096

5:01

Philadelphia chromosome: Explained in 5 minutes!!!!!! #Medschooldiscussion

• Order: Reorder
• Duration: 5:01
• Uploaded Date: 31 May 2018
• views: 6657

It was 1959 when two Philadelphia researchers, Dr. Peter Nowell and Dr. David Hungerford, were experimenting with cells from various types of leukemia . Then t...

It was 1959 when two Philadelphia researchers, Dr. Peter Nowell and Dr. David Hungerford, were experimenting with cells from various types of leukemia . Then they noticed a smaller chromosome 22 in the cancer cells of some individuals with CML. Due to unavailability of sophisticated technique at that time, they were unable to tell what happened to the material missing from the small chromosome. Nowell and Hungerford published their research in 1960, describing the abnormality that had was found in 9 out of 10 CML patients they studied.Later on in 1972 another researcher, Dr.Janet Rowley, discovered that the missing piece of chromosome number 22 is attached to the chromosome number 9.That is how the first known chromosomal translocation that is t(9,22) was discovered. Later on this abnormally shortened chromosome22 was named after the city Philadelphia where Dr. Hungerford and Dr. nowell conducted their research . . Thet Philadelphia chromosome is found in the leukemic cells of more than 95% of patients with CML......... References: 1. https://www.oncolink.org/cancers/leukemia/chronic-myelogenous-leukemia-cml/the-philadelphia-chromosome 2. https://www.cancer.org/cancer/chronic-myeloid-leukemia/causes-risks-prevention/what-causes.html 3. https://www.foxchase.org/about-us/history/discoveries-fox-chase-research/philadelphia-chromosome/philadelphia-chromosome 4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934583/ 5. https://www.medicinenet.com/script/main/art.asp?articlekey=4870 6. Pathologic basis of disease:Robins and Cotran.

https://wn.com/Philadelphia_Chromosome_Explained_In_5_Minutes_Medschooldiscussion

It was 1959 when two Philadelphia researchers, Dr. Peter Nowell and Dr. David Hungerford, were experimenting with cells from various types of leukemia . Then they noticed a smaller chromosome 22 in the cancer cells of some individuals with CML. Due to unavailability of sophisticated technique at that time, they were unable to tell what happened to the material missing from the small chromosome. Nowell and Hungerford published their research in 1960, describing the abnormality that had was found in 9 out of 10 CML patients they studied.Later on in 1972 another researcher, Dr.Janet Rowley, discovered that the missing piece of chromosome number 22 is attached to the chromosome number 9.That is how the first known chromosomal translocation that is t(9,22) was discovered. Later on this abnormally shortened chromosome22 was named after the city Philadelphia where Dr. Hungerford and Dr. nowell conducted their research . . Thet Philadelphia chromosome is found in the leukemic cells of more than 95% of patients with CML......... References: 1. https://www.oncolink.org/cancers/leukemia/chronic-myelogenous-leukemia-cml/the-philadelphia-chromosome 2. https://www.cancer.org/cancer/chronic-myeloid-leukemia/causes-risks-prevention/what-causes.html 3. https://www.foxchase.org/about-us/history/discoveries-fox-chase-research/philadelphia-chromosome/philadelphia-chromosome 4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934583/ 5. https://www.medicinenet.com/script/main/art.asp?articlekey=4870 6. Pathologic basis of disease:Robins and Cotran.

• published: 31 May 2018
• views: 6657

5:00

Chronic myeloid leukaemia: discovery of the Philadelphia chromosome

• Order: Reorder
• Duration: 5:00
• Uploaded Date: 17 Apr 2021
• views: 1208

A review of: Chromosome studies on normal and leukemic human leukocytes. Nowell PC, Hungerford DA. J Natl Cancer Inst. 1960 Jul;25:85-109. Twitter: https://twi...

A review of: Chromosome studies on normal and leukemic human leukocytes. Nowell PC, Hungerford DA. J Natl Cancer Inst. 1960 Jul;25:85-109. Twitter: https://twitter.com/Genetics_Stuff OTHER VIDEOS YOU MIGHT LIKE: • Plants show phenotype is influenced by genotype AND environment (Clausen, Keck & Hiesey, 1940) - https://youtu.be/mlQPp3_-N3M • Codons don’t overlap in the shagadelic genetic code, baby. Yeah! (Brenner, 1957) - https://youtu.be/l7f-FHnYtyw • Understanding Quantitative Trait Loci with the help of tomatoes (Paterson et al., 1988) - https://youtu.be/17NtnnFsq-s Leukaemia, cancer of the blood, affects white blood cells and causes proliferation of bone marrow white blood cell progenitors, haematopoietic cells, initiating mass production of faulty white blood cells. This throws off the balance between leukocytes, erythrocytes and platelets in the blood. There are several different types of leukemia such as chronic lymphocytic leukaemia, acute lymphocytic leukaemia, acute myeloid leukaemia, and chronic myeloid leukaemia. The main difference between myeloid and lymphocytic variants is the type of white blood cell affected. In the 1950s leukaemia had a 5-year survival rate of only 14% - a breakthrough was clearly needed, a breakthrough that was going to come from the University of Pennsylvania. Peter Nowell and David Hungerford analysed the leukocyte chromosomes of chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) patients, and found “a definite abnormality, probably involving the Y chromosome” in two patients suffering from CML. Named after the city in which it was discovered, this “Philadelphia chromosome” was created via a reciprocal translocation involving chromosomes 9 and 22, not related to the Y chromosome as Nowell thought, by Janet Rowley in the 1970s. The formation of the Philadelphia chromosome created a fusion protein from the breakpoint cluster region gene BCR and the tyrosine kinase oncogene ABL that can phosphorylate tyrosine in growth factors constitutively, causing cell proliferation and cancer. This important discovery has assisted in developing more effective treatment regimens for sufferers of chronic myeloid leukaemia by using tyrosine kinase inhibitor drugs such as imatinib and dasitinib, which inhibit activity by binding the ATP site in the kinase domain. Creator: Aaron Netto References: Chan, W., S. Wise, M. Kaufman, L. Stewart, R. Etten et al., 2011, Conformational Control Inhibition of the BCR-ABL Tyrosine Kinase, Including the Gatekeeper T3151 Mutation, by the Switch-Control Inhibitor DCC-2036. Cell 19: 556 – 568. Dabas, N., D. Byrnes, A. Rosa, M. Eller, and J. Grichnik, 2012, Diagnostic Role of Chromosomal Instability in Melanoma. Journal of Skin Cancer 2012: doi:10.1155/2012/914267 Deininger, M., S. Vieira, R. Mendiola, B. Schulteis, J, Goldman et al. 2000, BCR-ABL Tyrosine Kinase Activity Regulates the Expression of Multiple Genes Implicated in the Pathogenesis of Chronic Myeloid Leukemia. Cancer Research 60: 2049 – 2055. Hantschel, O., 2012, Structure, Regulation, Signalling and Targeting of ABL Kinases in Cancer. Genes and Cancer 3: 436 – 446. Nowell, P., 2007. Discovery of the Philadelphia Chromosome: A Personal Perspective. Journal of Clinical Investigation 117: doi:10.1172/JC31771 Nowell, P., and D. Hungerford, 1960, Chromosome Studies on Normal and Leukemic Human Leukocytes. Journal of the National Cancer Institute 25: 85 – 109. Ong, S., and M. Le Beau, 1998, Chromosomal Abnormalities and Molecular Genetics of non-Hodgkin’s Lymphoma. Seminars in Oncology 25: 447 – 460. Ostergren, G., and W. K. Heneen, 1962, A Squash Technique for Chromosome Morphological Studies. Hereditas 48: 332 – 341. Peiris, M., F. Li, and D. Donoghue, 2019, BCR: A Promiscuous Fusion Partner in Hematopoietic Disorders. Oncotarget 28: 738 – 2754. Pottier, C., M. Fresnais, M. Gilon, G. Jerusalem, R. Longuespee et al., 2020, Tyrosine Kinase Inhibitors in Cancer: Breakthrough and Challenges of Targeted Therapy. Cancers 12: doi:10.3390/cancers12030731. Research Collaboration for Structural Bioinformatics, 2011 Crystal Structure of Human ABL1 Kinase Domain. RCSB PDB Sacha, T., 2014, Imatinib in Chronic Myeloid Leukaemia: an Overview. Mediterranean Journal of Hematology and Infectious Diseases 6: doi:104088/MJHID.2014.007. Thompson, P., H, Kantargian, and J. Cortes, 2015, Diagnosis and Treatment of Chronic Myeloid Leukaemia (CML) in 2015. Mayo Clinic Proceedings 90: 1440 – 1454. Thompson, S., and D. Compton, 2013, Chromosomes and Cancer Cells. Chromosome Research 19: 433 – 444. Vorsanova, S., Y. Yurov, D. Brusquant and E. Carlies, 2002, Two New Cases of the Christchurch (Ch1) Chromosome 22: Evidence or Clinical Consequence of de novo deletion 22P. Tsitologiia I genetika 24: 46 – 49.

https://wn.com/Chronic_Myeloid_Leukaemia_Discovery_Of_The_Philadelphia_Chromosome

A review of: Chromosome studies on normal and leukemic human leukocytes. Nowell PC, Hungerford DA. J Natl Cancer Inst. 1960 Jul;25:85-109. Twitter: https://twitter.com/Genetics_Stuff OTHER VIDEOS YOU MIGHT LIKE: • Plants show phenotype is influenced by genotype AND environment (Clausen, Keck & Hiesey, 1940) - https://youtu.be/mlQPp3_-N3M • Codons don’t overlap in the shagadelic genetic code, baby. Yeah! (Brenner, 1957) - https://youtu.be/l7f-FHnYtyw • Understanding Quantitative Trait Loci with the help of tomatoes (Paterson et al., 1988) - https://youtu.be/17NtnnFsq-s Leukaemia, cancer of the blood, affects white blood cells and causes proliferation of bone marrow white blood cell progenitors, haematopoietic cells, initiating mass production of faulty white blood cells. This throws off the balance between leukocytes, erythrocytes and platelets in the blood. There are several different types of leukemia such as chronic lymphocytic leukaemia, acute lymphocytic leukaemia, acute myeloid leukaemia, and chronic myeloid leukaemia. The main difference between myeloid and lymphocytic variants is the type of white blood cell affected. In the 1950s leukaemia had a 5-year survival rate of only 14% - a breakthrough was clearly needed, a breakthrough that was going to come from the University of Pennsylvania. Peter Nowell and David Hungerford analysed the leukocyte chromosomes of chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) patients, and found “a definite abnormality, probably involving the Y chromosome” in two patients suffering from CML. Named after the city in which it was discovered, this “Philadelphia chromosome” was created via a reciprocal translocation involving chromosomes 9 and 22, not related to the Y chromosome as Nowell thought, by Janet Rowley in the 1970s. The formation of the Philadelphia chromosome created a fusion protein from the breakpoint cluster region gene BCR and the tyrosine kinase oncogene ABL that can phosphorylate tyrosine in growth factors constitutively, causing cell proliferation and cancer. This important discovery has assisted in developing more effective treatment regimens for sufferers of chronic myeloid leukaemia by using tyrosine kinase inhibitor drugs such as imatinib and dasitinib, which inhibit activity by binding the ATP site in the kinase domain. Creator: Aaron Netto References: Chan, W., S. Wise, M. Kaufman, L. Stewart, R. Etten et al., 2011, Conformational Control Inhibition of the BCR-ABL Tyrosine Kinase, Including the Gatekeeper T3151 Mutation, by the Switch-Control Inhibitor DCC-2036. Cell 19: 556 – 568. Dabas, N., D. Byrnes, A. Rosa, M. Eller, and J. Grichnik, 2012, Diagnostic Role of Chromosomal Instability in Melanoma. Journal of Skin Cancer 2012: doi:10.1155/2012/914267 Deininger, M., S. Vieira, R. Mendiola, B. Schulteis, J, Goldman et al. 2000, BCR-ABL Tyrosine Kinase Activity Regulates the Expression of Multiple Genes Implicated in the Pathogenesis of Chronic Myeloid Leukemia. Cancer Research 60: 2049 – 2055. Hantschel, O., 2012, Structure, Regulation, Signalling and Targeting of ABL Kinases in Cancer. Genes and Cancer 3: 436 – 446. Nowell, P., 2007. Discovery of the Philadelphia Chromosome: A Personal Perspective. Journal of Clinical Investigation 117: doi:10.1172/JC31771 Nowell, P., and D. Hungerford, 1960, Chromosome Studies on Normal and Leukemic Human Leukocytes. Journal of the National Cancer Institute 25: 85 – 109. Ong, S., and M. Le Beau, 1998, Chromosomal Abnormalities and Molecular Genetics of non-Hodgkin’s Lymphoma. Seminars in Oncology 25: 447 – 460. Ostergren, G., and W. K. Heneen, 1962, A Squash Technique for Chromosome Morphological Studies. Hereditas 48: 332 – 341. Peiris, M., F. Li, and D. Donoghue, 2019, BCR: A Promiscuous Fusion Partner in Hematopoietic Disorders. Oncotarget 28: 738 – 2754. Pottier, C., M. Fresnais, M. Gilon, G. Jerusalem, R. Longuespee et al., 2020, Tyrosine Kinase Inhibitors in Cancer: Breakthrough and Challenges of Targeted Therapy. Cancers 12: doi:10.3390/cancers12030731. Research Collaboration for Structural Bioinformatics, 2011 Crystal Structure of Human ABL1 Kinase Domain. RCSB PDB Sacha, T., 2014, Imatinib in Chronic Myeloid Leukaemia: an Overview. Mediterranean Journal of Hematology and Infectious Diseases 6: doi:104088/MJHID.2014.007. Thompson, P., H, Kantargian, and J. Cortes, 2015, Diagnosis and Treatment of Chronic Myeloid Leukaemia (CML) in 2015. Mayo Clinic Proceedings 90: 1440 – 1454. Thompson, S., and D. Compton, 2013, Chromosomes and Cancer Cells. Chromosome Research 19: 433 – 444. Vorsanova, S., Y. Yurov, D. Brusquant and E. Carlies, 2002, Two New Cases of the Christchurch (Ch1) Chromosome 22: Evidence or Clinical Consequence of de novo deletion 22P. Tsitologiia I genetika 24: 46 – 49.

• published: 17 Apr 2021
• views: 1208

3:13

BCR-ABL1 and the Philadelphia chromosome - Part 2: The Philadelphia chromosome

• Order: Reorder
• Duration: 3:13
• Uploaded Date: 04 Oct 2021
• views: 13886

The Philadelphia chromosome, which is found in leukemic cells in more than 90% of all patients with chronic myeloid leukemia (CML), results from a translocation...

The Philadelphia chromosome, which is found in leukemic cells in more than 90% of all patients with chronic myeloid leukemia (CML), results from a translocation between chromosome 9 and chromosome 22. On the Philadelphia chromosome, the 5’ end of the gene BCR is fused to the major 3’ part of the gene ABL1. The amplification of the fused gene region by polymerase chain reaction allows the sensitive detection of leukemic cells in patients with CML. #onkoview, #Philadelphiachromosome, #chromosome22, #gene, #leukemic, #cells, #cml, #abl1, #leukemia, #polymerase

https://wn.com/Bcr_Abl1_And_The_Philadelphia_Chromosome_Part_2_The_Philadelphia_Chromosome

The Philadelphia chromosome, which is found in leukemic cells in more than 90% of all patients with chronic myeloid leukemia (CML), results from a translocation between chromosome 9 and chromosome 22. On the Philadelphia chromosome, the 5’ end of the gene BCR is fused to the major 3’ part of the gene ABL1. The amplification of the fused gene region by polymerase chain reaction allows the sensitive detection of leukemic cells in patients with CML. #onkoview, #Philadelphiachromosome, #chromosome22, #gene, #leukemic, #cells, #cml, #abl1, #leukemia, #polymerase

• published: 04 Oct 2021
• views: 13886

29:08

Jessica Wapner "The Philadelphia Chromosome"

• Order: Reorder
• Duration: 29:08
• Uploaded Date: 20 May 2013
• views: 3028

This event was recorded at Politics & Prose Bookstore in Washington, D.C. on May 16, 2013. More information is available at http://www.politics-prose.com/event...

This event was recorded at Politics & Prose Bookstore in Washington, D.C. on May 16, 2013. More information is available at http://www.politics-prose.com/event/book/jessica-wapner-philadelphia-chromosome-mutant-gene-and-quest-cure-cancer-genetic-level A genetic mutation that causes chronic myeloid leukemia (CML), the Philadelphia chromosome was first detected in 1959. Some fifty years later, the once deadly CML can be controlled with a daily dose of a drug called Gleevec. Wapner, a widely published science writer, Work in Progress blogger, and former editor of Oncology Spectrum, profiles the dedicated doctors involved in the research and explains the science behind this breakthrough.

https://wn.com/Jessica_Wapner_The_Philadelphia_Chromosome

This event was recorded at Politics & Prose Bookstore in Washington, D.C. on May 16, 2013. More information is available at http://www.politics-prose.com/event/book/jessica-wapner-philadelphia-chromosome-mutant-gene-and-quest-cure-cancer-genetic-level A genetic mutation that causes chronic myeloid leukemia (CML), the Philadelphia chromosome was first detected in 1959. Some fifty years later, the once deadly CML can be controlled with a daily dose of a drug called Gleevec. Wapner, a widely published science writer, Work in Progress blogger, and former editor of Oncology Spectrum, profiles the dedicated doctors involved in the research and explains the science behind this breakthrough.

• published: 20 May 2013
• views: 3028

1:01

Chronic Myeloid Leukemia | CML | Philadelphia Chromosome

• Order: Reorder
• Duration: 1:01
• Uploaded Date: 19 Jan 2018
• views: 2957

Chronic myeloid leukemia (CML) is a type cancer that affects the blood and bone marrow.

Chronic myeloid leukemia (CML) is a type cancer that affects the blood and bone marrow.

https://wn.com/Chronic_Myeloid_Leukemia_|_Cml_|_Philadelphia_Chromosome

Chronic myeloid leukemia (CML) is a type cancer that affects the blood and bone marrow.

• published: 19 Jan 2018
• views: 2957

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6:59

bcr-abl Translocation Mechanism | Philadelphia Chromosome

The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnor...

published: 18 Aug 2020

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bcr-abl Translocation Mechanism | Philadelphia Chromosome

bcr-abl Translocation Mechanism | Philadelphia Chromosome

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• published: 18 Aug 2020
• views: 41485

The Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (particularly chronic myeloid leukemia (CML) cells). This chromosome is defective and unusually short because of reciprocal translocation, t(9;22)(q34;q11), of genetic material between chromosome 9 and chromosome 22, and contains a fusion gene called BCR-ABL1. This gene is the ABL1 gene of chromosome 9 juxtaposed onto the breakpoint cluster region BCR gene of chromosome 22, coding for a hybrid protein: a tyrosine kinase signalling protein that is "always on", causing the cell to divide uncontrollably by interrupting the stability of the genome and impairing various signaling pathways governing the cell cycle. The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11). This is a reciprocal translocation, creating an elongated chromosome 9 (termed a derivative chromosome, or der 9), and a truncated chromosome 22 (the Philadelphia chromosome, 22q-).In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11). The symbol ABL1 is derived from Abelson, the name of a leukemia virus which carries a similar protein. The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins . Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein. Depending on the precise location of fusion, the molecular weight of this protein can range from 185 to 210 kDa. Consequently, the hybrid BCR-ABL1 fusion protein is referred to as p210 or p185.

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4:15

Philadelphia Chromosome, Translocations, Inversions, Deletions

This video discusses the formation of the Philadelphia Chromosome bringing about chronic m...

published: 28 Jul 2017

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Philadelphia Chromosome, Translocations, Inversions, Deletions

Philadelphia Chromosome, Translocations, Inversions, Deletions

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• published: 28 Jul 2017
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This video discusses the formation of the Philadelphia Chromosome bringing about chronic myelogenous leukemia (CML) and the difference between translocations, inversions, and deletions. The medication imatinib (Gleevec) is also discussed.

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17:59

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromoso...

published: 13 Aug 2018

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Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome

Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome

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• published: 13 Aug 2018
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Chronic Myeloid Leukemia (CML) - Myeloproliferative Neoplasm (MPN) - Philadelphia Chromosome - Hematology and Oncology. Chronic myeloid leukemia (or chronic myelogenous leukemia or CML) is a chronic leukemia, as well as a myeloproliferative neoplasm (MPNs). What is chronic myeloid leukemia? --This is the topic of today's video. 😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/ - With Picmonic, get your life back by studying less and remembering more. Medical and Nursing students say that Picmonic is the most comprehensive and effective way to bridge learning and test prep... Disclaimer: I use affiliate links.... ►👨‍🏫💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/products/courses/antibiotics/ ... ❗️Sorry! I made a MISTAKE in this video! The mistake: CML is characterized by increased number of neutrophils. The correction: CML is characterized by increased number of basophils. Check out my brand new "Electrolytes" course at https://www.medicosisperfectionalis.com/products/course/electrolytes/ and use the PROMO code: ELECTROLYTES50 to get a 50% discount. ► Get my notes and cases at https://www.patreon.com/medicosis ... ► Don’t forget to check my recommended collection of the best medical books that I personally use https://www.amazon.com/shop/medicosisperfectionalis MEDICAL Sources that I use for my videos:- ► Goljan Rapid Review Pathology, https://amzn.to/2MufTPw ► Harrison’s Internal Medicine https://amzn.to/2OJiVNf ► Goldman-Cecil Medicine https://amzn.to/2N0v93u ► Davidson’s Principles and Practice of Medicine https://amzn.to/2vTmf1p ------------------------------------------------------------------------- Many people ask me “How do you record your videos”? Here is the answer:- Equipment that I use:- ► Apple iPad Pro https://amzn.to/2nKCyZW ► Apple pencil https://amzn.to/2PimMCc ►Iphone holder kit: https://amzn.to/2OVV3aj ►Rode Video Mic Go: https://amzn.to/2OVF4Je ►Rode SC7 3.5mm TRS to TRRS Patch Cable: https://amzn.to/2vu2WeY ►Extension Audio Cable https://amzn.to/2nIDApo ►Rode DDC-GO DeadCat Artificial Fur Wind Shield for VideoMic GO: https://amzn.to/2OpbV8m Disclaimer 1: The medical information contained herein is intended for educational purposes only, and are not intended for diagnosis of any illness. If you think you may be suffering from any medical condition, you should consult your physician or seek immediate medical attention. I am NOT a licensed physician…Talk to your doctor. Disclaimer 2: these links are affiliate links so that I get paid a percentage of the sale, to support the channel, however, the customer is not affected as they pay the same price. Got a question? Ask it in the comments section below, or connect with me on FACEBOOK https://www.facebook.com/medicosis/ where you can directly message me…I respond to your messages personally. Thanks! Whether you’re studying for the USMLE, MCAT, shelf exam, NCLEX, COMLEX, PLEB, MCCEE, AMC_CAT, PANCE,…etc., these videos will help! Take it to the bank :) As always…Be safe, Stay happy and Study hard! MEDICOSIS PERFECTIONALIS Remember, chronic myeloid leukemia (CML) is a chronic leukemia; monoclonal disorder of late hematopoietic stem cells. If you like my videos, please consider leaving a tip at https://www.paypal.me/perfectionalis/ ► Visit my website: https://www.medicosisperfectionalis.com/ My Favorite Productivity App: https://airtable.com/invite/r/2zH40fus/ 📱Save on your mobile phone bill: http://fbuy.me/q6bMj 🏦 Qbank (TrueLearn): https://truelearn.referralrock.com/l/MEDICOSIS/

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1:23

Philadelphia Chromosome

published: 12 Jul 2015

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Philadelphia Chromosome

Philadelphia Chromosome

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• published: 12 Jul 2015
• views: 33296

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8:45

The latest in Philadelphia chromosome-positive ALL (Ph+ ALL)

Prof Robin Foà talks to ecancer about the latest in Philadelphia chromosome-positive ALL (...

published: 11 Jan 2022

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The latest in Philadelphia chromosome-positive ALL (Ph+ ALL)

The latest in Philadelphia chromosome-positive ALL (Ph+ ALL)

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• published: 11 Jan 2022
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Prof Robin Foà talks to ecancer about the latest in Philadelphia chromosome-positive ALL (Ph+ ALL). He begins by stating that the changes have been quite dramatic, going on to say that Ph+ ALL was the worst sub-group of leukaemias in terms of prognosis, for both adults and children. The only chance of a cure was an allogeneic stem cell transplant, when doable. Prof Foà then goes on to explain how the incidents of Ph+ ALL increases with age. About 1 in 2 B-lineage ALL patients over the age of 50-60 years old. He concludes by saying maybe some patients in the future can be managed without chemo or without transplant, referring to other research he adds if patients do not have additional genetic abnormalities at diagnosis or the MRD is repeatedly negative these patients will not receive a transplant even with a sibling donor. So, he hopes it can be proven that at least a portion of patients can be managed and possibly cured without systemic chemo or transplant. Sign up to ecancer for free to receive tailored email alerts for more videos like this. ecancer.org/account/register.php

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5:01

Philadelphia chromosome: Explained in 5 minutes!!!!!! #Medschooldiscussion

It was 1959 when two Philadelphia researchers, Dr. Peter Nowell and Dr. David Hungerford,...

published: 31 May 2018

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Philadelphia chromosome: Explained in 5 minutes!!!!!! #Medschooldiscussion

Philadelphia chromosome: Explained in 5 minutes!!!!!! #Medschooldiscussion

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• published: 31 May 2018
• views: 6657

It was 1959 when two Philadelphia researchers, Dr. Peter Nowell and Dr. David Hungerford, were experimenting with cells from various types of leukemia . Then they noticed a smaller chromosome 22 in the cancer cells of some individuals with CML. Due to unavailability of sophisticated technique at that time, they were unable to tell what happened to the material missing from the small chromosome. Nowell and Hungerford published their research in 1960, describing the abnormality that had was found in 9 out of 10 CML patients they studied.Later on in 1972 another researcher, Dr.Janet Rowley, discovered that the missing piece of chromosome number 22 is attached to the chromosome number 9.That is how the first known chromosomal translocation that is t(9,22) was discovered. Later on this abnormally shortened chromosome22 was named after the city Philadelphia where Dr. Hungerford and Dr. nowell conducted their research . . Thet Philadelphia chromosome is found in the leukemic cells of more than 95% of patients with CML......... References: 1. https://www.oncolink.org/cancers/leukemia/chronic-myelogenous-leukemia-cml/the-philadelphia-chromosome 2. https://www.cancer.org/cancer/chronic-myeloid-leukemia/causes-risks-prevention/what-causes.html 3. https://www.foxchase.org/about-us/history/discoveries-fox-chase-research/philadelphia-chromosome/philadelphia-chromosome 4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934583/ 5. https://www.medicinenet.com/script/main/art.asp?articlekey=4870 6. Pathologic basis of disease:Robins and Cotran.

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5:00

Chronic myeloid leukaemia: discovery of the Philadelphia chromosome

A review of: Chromosome studies on normal and leukemic human leukocytes. Nowell PC, Hunger...

published: 17 Apr 2021

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Chronic myeloid leukaemia: discovery of the Philadelphia chromosome

Chronic myeloid leukaemia: discovery of the Philadelphia chromosome

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• published: 17 Apr 2021
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A review of: Chromosome studies on normal and leukemic human leukocytes. Nowell PC, Hungerford DA. J Natl Cancer Inst. 1960 Jul;25:85-109. Twitter: https://twitter.com/Genetics_Stuff OTHER VIDEOS YOU MIGHT LIKE: • Plants show phenotype is influenced by genotype AND environment (Clausen, Keck & Hiesey, 1940) - https://youtu.be/mlQPp3_-N3M • Codons don’t overlap in the shagadelic genetic code, baby. Yeah! (Brenner, 1957) - https://youtu.be/l7f-FHnYtyw • Understanding Quantitative Trait Loci with the help of tomatoes (Paterson et al., 1988) - https://youtu.be/17NtnnFsq-s Leukaemia, cancer of the blood, affects white blood cells and causes proliferation of bone marrow white blood cell progenitors, haematopoietic cells, initiating mass production of faulty white blood cells. This throws off the balance between leukocytes, erythrocytes and platelets in the blood. There are several different types of leukemia such as chronic lymphocytic leukaemia, acute lymphocytic leukaemia, acute myeloid leukaemia, and chronic myeloid leukaemia. The main difference between myeloid and lymphocytic variants is the type of white blood cell affected. In the 1950s leukaemia had a 5-year survival rate of only 14% - a breakthrough was clearly needed, a breakthrough that was going to come from the University of Pennsylvania. Peter Nowell and David Hungerford analysed the leukocyte chromosomes of chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) patients, and found “a definite abnormality, probably involving the Y chromosome” in two patients suffering from CML. Named after the city in which it was discovered, this “Philadelphia chromosome” was created via a reciprocal translocation involving chromosomes 9 and 22, not related to the Y chromosome as Nowell thought, by Janet Rowley in the 1970s. The formation of the Philadelphia chromosome created a fusion protein from the breakpoint cluster region gene BCR and the tyrosine kinase oncogene ABL that can phosphorylate tyrosine in growth factors constitutively, causing cell proliferation and cancer. This important discovery has assisted in developing more effective treatment regimens for sufferers of chronic myeloid leukaemia by using tyrosine kinase inhibitor drugs such as imatinib and dasitinib, which inhibit activity by binding the ATP site in the kinase domain. Creator: Aaron Netto References: Chan, W., S. Wise, M. Kaufman, L. Stewart, R. Etten et al., 2011, Conformational Control Inhibition of the BCR-ABL Tyrosine Kinase, Including the Gatekeeper T3151 Mutation, by the Switch-Control Inhibitor DCC-2036. Cell 19: 556 – 568. Dabas, N., D. Byrnes, A. Rosa, M. Eller, and J. Grichnik, 2012, Diagnostic Role of Chromosomal Instability in Melanoma. Journal of Skin Cancer 2012: doi:10.1155/2012/914267 Deininger, M., S. Vieira, R. Mendiola, B. Schulteis, J, Goldman et al. 2000, BCR-ABL Tyrosine Kinase Activity Regulates the Expression of Multiple Genes Implicated in the Pathogenesis of Chronic Myeloid Leukemia. Cancer Research 60: 2049 – 2055. Hantschel, O., 2012, Structure, Regulation, Signalling and Targeting of ABL Kinases in Cancer. Genes and Cancer 3: 436 – 446. Nowell, P., 2007. Discovery of the Philadelphia Chromosome: A Personal Perspective. Journal of Clinical Investigation 117: doi:10.1172/JC31771 Nowell, P., and D. Hungerford, 1960, Chromosome Studies on Normal and Leukemic Human Leukocytes. Journal of the National Cancer Institute 25: 85 – 109. Ong, S., and M. Le Beau, 1998, Chromosomal Abnormalities and Molecular Genetics of non-Hodgkin’s Lymphoma. Seminars in Oncology 25: 447 – 460. Ostergren, G., and W. K. Heneen, 1962, A Squash Technique for Chromosome Morphological Studies. Hereditas 48: 332 – 341. Peiris, M., F. Li, and D. Donoghue, 2019, BCR: A Promiscuous Fusion Partner in Hematopoietic Disorders. Oncotarget 28: 738 – 2754. Pottier, C., M. Fresnais, M. Gilon, G. Jerusalem, R. Longuespee et al., 2020, Tyrosine Kinase Inhibitors in Cancer: Breakthrough and Challenges of Targeted Therapy. Cancers 12: doi:10.3390/cancers12030731. Research Collaboration for Structural Bioinformatics, 2011 Crystal Structure of Human ABL1 Kinase Domain. RCSB PDB Sacha, T., 2014, Imatinib in Chronic Myeloid Leukaemia: an Overview. Mediterranean Journal of Hematology and Infectious Diseases 6: doi:104088/MJHID.2014.007. Thompson, P., H, Kantargian, and J. Cortes, 2015, Diagnosis and Treatment of Chronic Myeloid Leukaemia (CML) in 2015. Mayo Clinic Proceedings 90: 1440 – 1454. Thompson, S., and D. Compton, 2013, Chromosomes and Cancer Cells. Chromosome Research 19: 433 – 444. Vorsanova, S., Y. Yurov, D. Brusquant and E. Carlies, 2002, Two New Cases of the Christchurch (Ch1) Chromosome 22: Evidence or Clinical Consequence of de novo deletion 22P. Tsitologiia I genetika 24: 46 – 49.

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3:13

BCR-ABL1 and the Philadelphia chromosome - Part 2: The Philadelphia chromosome

The Philadelphia chromosome, which is found in leukemic cells in more than 90% of all pati...

published: 04 Oct 2021

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BCR-ABL1 and the Philadelphia chromosome - Part 2: The Philadelphia chromosome

BCR-ABL1 and the Philadelphia chromosome - Part 2: The Philadelphia chromosome

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• published: 04 Oct 2021
• views: 13886

The Philadelphia chromosome, which is found in leukemic cells in more than 90% of all patients with chronic myeloid leukemia (CML), results from a translocation between chromosome 9 and chromosome 22. On the Philadelphia chromosome, the 5’ end of the gene BCR is fused to the major 3’ part of the gene ABL1. The amplification of the fused gene region by polymerase chain reaction allows the sensitive detection of leukemic cells in patients with CML. #onkoview, #Philadelphiachromosome, #chromosome22, #gene, #leukemic, #cells, #cml, #abl1, #leukemia, #polymerase

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29:08

Jessica Wapner "The Philadelphia Chromosome"

This event was recorded at Politics & Prose Bookstore in Washington, D.C. on May 16, 2013....

published: 20 May 2013

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Jessica Wapner "The Philadelphia Chromosome"

Jessica Wapner "The Philadelphia Chromosome"

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• published: 20 May 2013
• views: 3028

This event was recorded at Politics & Prose Bookstore in Washington, D.C. on May 16, 2013. More information is available at http://www.politics-prose.com/event/book/jessica-wapner-philadelphia-chromosome-mutant-gene-and-quest-cure-cancer-genetic-level A genetic mutation that causes chronic myeloid leukemia (CML), the Philadelphia chromosome was first detected in 1959. Some fifty years later, the once deadly CML can be controlled with a daily dose of a drug called Gleevec. Wapner, a widely published science writer, Work in Progress blogger, and former editor of Oncology Spectrum, profiles the dedicated doctors involved in the research and explains the science behind this breakthrough.

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1:01

Chronic Myeloid Leukemia | CML | Philadelphia Chromosome

Chronic myeloid leukemia (CML) is a type cancer that affects the blood and bone marrow.

published: 19 Jan 2018

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Chronic Myeloid Leukemia | CML | Philadelphia Chromosome

Chronic Myeloid Leukemia | CML | Philadelphia Chromosome

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• published: 19 Jan 2018
• views: 2957

Chronic myeloid leukemia (CML) is a type cancer that affects the blood and bone marrow.

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Bcr-Abl tyrosine-kinase inhibitor

Bcr-Abl tyrosine-kinase inhibitors (TKI) are the first-line therapy for most patients with chronic myelogenous leukemia (CML). More than 90% of CML cases are caused by a chromosomal abnormality that results in the formation of a so-called Philadelphia chromosome. This abnormality was discovered by Janet Rowley in 1972 and is a consequence of fusion between the Abelson (Abl) tyrosine kinase gene at chromosome 9 and the break point cluster (Bcr) gene at chromosome 22, resulting in a chimeric oncogene (Bcr-Abl) and a constitutively active Bcr-Abl tyrosine kinase that has been implicated in the pathogenesis of CML. Compounds have been developed to selectively inhibit the tyrosine kinase.

Before the 2001 U.S. Food and Drug Administration (FDA) approval of imatinib, no drugs were available to alter the natural progression of CML. Only cytotoxic drugs such as busulfan, hydroxyurea or interferon-alpha (rIFN-α) were utilized. Even though the first Bcr-Abl TK inhibitor was named “the magic bullet” to cure cancer by TIME magazine, a second generation of Bcr-Abl TKI was subsequently developed to combat the initial resistance that emerged.

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This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/Bcr-Abl_tyrosine-kinase_inhibitor

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