[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-329102-105":59,"doc-detail-329102-en":131},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":124,"head_meta":126,"extra_data":128,"updated_unix":130},105,"en","insights-into-existing-and-futuristic-treatment-approach-for-chronic-myeloid-leukaemia","Insights into existing and futuristic treatment approach for chronic myeloid leukaemia","","Review of chronic myeloid leukaemia (CML) outlines the central oncogenic driver BCR-ABL1 and explains how targeted therapy with tyrosine kinase inhibitors (TKIs) transformed management. The text details mechanisms of TKI-dependent and independent resistance and summarizes ongoing pursuit of next-generation therapeutics, including CRISPR/Cas9 genome editing. It also covers diagnostic and prognostic considerations, the major CML phases, and factors influencing disease burden and progression.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/insights-into-existing-and-futuristic-treatment-approach-for-chronic-myeloid-leukaemia/329102/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/insights-into-existing-and-futuristic-treatment-approach-for-chronic-myeloid-leukaemia/329102.png","ImageObject",300,407,{"name":92,"@type":93},"Rowan","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-28","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What oncogene is primarily associated with chronic myeloid leukaemia (CML)?","Question",{"text":113,"@type":114},"The text states that all pathological traits in CML are associated with the single oncogene BCR-ABL1, produced by the BCR-ABL1 fusion gene.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How do tyrosine kinase inhibitors (TKIs) change CML treatment?",{"text":118,"@type":114},"TKIs inhibit BCR-ABL1 kinase activity, shifting therapy from chemotherapy and immunotherapy to targeted therapy.",{"name":120,"@type":111,"acceptedAnswer":121},"What are the limitations of TKIs in CML, and what is being explored next?",{"text":122,"@type":114},"The inhibitory mechanism is constrained by BCR-ABL1 dependent and independent resistance mechanisms, prompting extensive clinical trials for next-generation drugs, including CRISPR/Cas9 genome editing.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},329102,1790135398,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":36},1099514067415,"https://ap-avatar.wpscdn.com/avatar/100002539d78ffe74a7?x-image-process=image/resize,m_fixed,w_180,h_180&k=1779092875211072502","Indian J Med Res 159, May 2024, pp 455-467 DOI: 10.25259/ijmr_ 1716_22  \nReview Article  \n\n| Quick Response Code: |\n| --- |\n| |\n\nInsights into existing and futuristic treatment approach for chronic myeloid leukaemia  \nSourabh Tyagi1,\\#, Anu Singh2,\\#, Naveen Sharma3, Rupesh Chaturvedi1,2 & Hemant Ritturaj Kushwaha1,2  \n1Special Centre for Systems Medicine, 2School of Biotechnology, Jawaharlal Nehru University & 3Biomedical Informatics Division, Indian Council of Medical Research, New Delhi, India  \nReceived March 9, 2024  \nOncogenes play a crucial part in human cancer development, and when particular drugs obstruct the proteins produced by these oncogenes, the tumoural process can be ceased. For instance, in chronic myeloid leukaemia (CML), all pathological traits are associated with a single oncogene, BCR-ABL1.  \nCMLis a triphasic cancerous disorder of haematopoietic stem cells, marked by a balanced translocation between chromosomes 9 and 22, leading to the genesis of a Philadelphia chromosome encompassing the BCR-ABL1 fusion gene. This fusion oncogene further produces a constitutive active tyrosine kinase protein, enhancing the downstream signalling pathways and constitutes cancer. The treatment for CML has been entirely altered from chemotherapy and immunotherapy to targeted therapy with the emergence of tyrosine kinase inhibitors (TKIs) which inhibit BCR-ABL1 kinase activity. However, the inhibitory mechanism of TKIs is constrained by BCR-ABL1 dependent and independent resistance mechanisms, prompting the exploration of novel therapeutics through extensive clinical trials to develop next-generation drugs with enhanced potency. The persistent challenges posed by CML have motivated researchers to seek innovative strategies for its eradication, such as the application of the genome editing tool CRISPR/Cas9. This review provides insights into existing CML diagnoses, treatment modalities, resistance mechanisms, drugs under trial phases and new potential therapeutic drugs. Furthermore, thereview looks ahead to a visionary perspective wherein the CRISPR/Cas9 approach holds the potential  \nto evolve into a prospective curative measure for CML.  \nKey words Chronic myeloid leukaemia-clinical trial-CRISPR/Cas-drug resistance-treatment-free resistance (TFR) -tyrosine kinase inhibitors (TKIs)  \nCancer is a rising problem worldwide, with around 19.3 million new cancer cases in addition to 10 million cancer deaths being reported in 20201. Among all 36 types of cancers, leukaemia is the 11th globally (Global Cancer Statistics, 2020) 1. Under leukaemia, the bone  \nmarrow makes an enormous number of aberrant white blood cells (WBCs) that are not entirely developed and are known as blasts. Generally, leukaemia alters the leukocytes or WBCs. One of the existing types of leukaemia is chronic myeloid leukaemia (CML) .  \n\\#Equal contribution  \n© 2024 Indian Journal of Medical Research, published by Scientific Scholar for Director-General, Indian Council of Medical Research  \nThis open access publication is protected under CC-BY-NC-SA 4.0  \n456 INDIAN J MED RES, MAY 2024  \nNORMAL NORMAL  \nCHROMOSOME 9 CHROMOSOME 22  \nBCR  \nABL1  \nSHORTER CHROMOSOME 22 (PHILADELPHIA CHROMOSOME)  \nCHANGED  \nCHROMOSOME 9  \nFig. 1. Chromosomal translocation process in CML. Source: Ref 3.  \nCML, a non-hereditary disease, typically occurs in middle-aged individuals and accounts for 15-20 percent of all leukaemia2. CML develops as a result of chromosomal translocation of the ABELSON 1 gene (ABL1, 171.74 kb) on chromosome 9 to the Breakpoint Cluster Region gene (BCR, 137.83 kb) on chromosome 22, resulting in shorter chromosome 22-Philadelphia (Ph) chromosome [t(9,22) (q34.1,q11.2)] as shown in Figure 13. The Philadelphia chromosome is present in 90 per cent ofCML cases. BCR-ABL gene acquisition initially occurs in a single haematopoietic stem cell (HSC) that attains high proliferation capacity, giving rise to an increased number of blast cells. According to WHO 2016 crit","cbCailPBKMxeqcV2","https://ap.wps.com/l/cbCailPBKMxeqcV2","pdf",444149,16,"English","# Introduction\n# Biology and disease progression\n## Oncogenic mechanism and Philadelphia chromosome\n## Stages of CML and progression factors\n# Risk factors and clinical features\n# Treatment approaches and resistance\n# Existing and next-generation therapies\n## TKIs and resistance mechanisms\n## CRISPR/Cas9 prospects","[{\"question\":\"What oncogene is primarily associated with chronic myeloid leukaemia (CML)?\",\"answer\":\"The text states that all pathological traits in CML are associated with the single oncogene BCR-ABL1, produced by the BCR-ABL1 fusion gene.\"},{\"question\":\"How do tyrosine kinase inhibitors (TKIs) change CML treatment?\",\"answer\":\"TKIs inhibit BCR-ABL1 kinase activity, shifting therapy from chemotherapy and immunotherapy to targeted therapy.\"},{\"question\":\"What are the limitations of TKIs in CML, and what is being explored next?\",\"answer\":\"The inhibitory mechanism is constrained by BCR-ABL1 dependent and independent resistance mechanisms, prompting extensive clinical trials for next-generation drugs, including CRISPR/Cas9 genome editing.\"}]","Insights into existing and futuristic treatment approach for chronic myeloid leukaemia | PDF",1789982452]