Chronic myeloid leukaemia: the evolution of gene‐targeted therapy
Chronic myeloid leukaemia (CML) was the first human cancer linked to an acquired chromosomal abnormality, subsequently shown to be a reciprocal translocation between chromosomes 9 and 22. The resulting fusion gene product, BCR‐ABL, was shown to be the causative agent of the disease. CML has an incid...
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description | Chronic myeloid leukaemia (CML) was the first human cancer linked to an acquired chromosomal abnormality, subsequently shown to be a reciprocal translocation between chromosomes 9 and 22. The resulting fusion gene product, BCR‐ABL, was shown to be the causative agent of the disease.
CML has an incidence of around 1–2 cases per 100 000; in Australia, there are probably more than 200 new cases per year and more than 1300 prevalent cases.
Treatment of CML with imatinib has been a powerful vindication of the concept of rational, gene‐targeted drug design.
Five‐year published experience with imatinib at 400 mg orally daily demonstrates 89% overall survival and an estimated 93% freedom from disease progression. Adverse effects are mostly mild and transient.
Higher doses of imatinib may be more efficacious and will be studied in upcoming clinical trials in Australia; however, imatinib is almost certainly not curative.
Up to 28% of patients may have to stop imatinib because of intolerance or disease resistance, mostly due to point mutations of BCR‐ABL. In this situation, many patients will respond to second‐ and third‐generation tyrosine kinase inhibitors.
Management of CML patients should involve close monitoring, especially in the first 2 years, with regular cytogenetics and quantitative polymerase chain reaction to optimise response and identify suboptimal responders as early as possible.
Bone marrow transplantation remains the only known cure, but is reserved for patients whose kinase inhibitor therapy has failed, or who have advanced disease (accelerated phase or blastic transformation). |
doi_str_mv | 10.5694/j.1326-5377.2008.tb02027.x |
format | Article |
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CML has an incidence of around 1–2 cases per 100 000; in Australia, there are probably more than 200 new cases per year and more than 1300 prevalent cases.
Treatment of CML with imatinib has been a powerful vindication of the concept of rational, gene‐targeted drug design.
Five‐year published experience with imatinib at 400 mg orally daily demonstrates 89% overall survival and an estimated 93% freedom from disease progression. Adverse effects are mostly mild and transient.
Higher doses of imatinib may be more efficacious and will be studied in upcoming clinical trials in Australia; however, imatinib is almost certainly not curative.
Up to 28% of patients may have to stop imatinib because of intolerance or disease resistance, mostly due to point mutations of BCR‐ABL. In this situation, many patients will respond to second‐ and third‐generation tyrosine kinase inhibitors.
Management of CML patients should involve close monitoring, especially in the first 2 years, with regular cytogenetics and quantitative polymerase chain reaction to optimise response and identify suboptimal responders as early as possible.
Bone marrow transplantation remains the only known cure, but is reserved for patients whose kinase inhibitor therapy has failed, or who have advanced disease (accelerated phase or blastic transformation).</description><identifier>ISSN: 0025-729X</identifier><identifier>EISSN: 1326-5377</identifier><identifier>DOI: 10.5694/j.1326-5377.2008.tb02027.x</identifier><identifier>PMID: 18759727</identifier><identifier>CODEN: MJAUAJ</identifier><language>eng</language><publisher>Sydney: Australasian Medical Publishing Company</publisher><subject>Antineoplastic Agents - therapeutic use ; Australia ; Benzamides ; Binding sites ; Biological and medical sciences ; Bone marrow ; Cancer therapies ; Chromosomes ; Drug Approval ; Fusion Proteins, bcr-abl - antagonists & inhibitors ; Fusion Proteins, bcr-abl - genetics ; General aspects ; Health services administration ; Hematologic and hematopoietic diseases ; Hematologic diseases ; Hematology ; Humans ; Imatinib Mesylate ; Interferon ; Kinases ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - therapy ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Piperazines - therapeutic use ; Polymerase chain reaction ; Pyrimidines - therapeutic use ; Signal transduction ; United States</subject><ispartof>Medical journal of Australia, 2008-09, Vol.189 (5), p.277-282</ispartof><rights>2008 AMPCo Pty Ltd. All rights reserved</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Australasian Medical Publishing Company Proprietary, Ltd. Sep 1, 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4327-5b14ef3ac2ae01a37af6679678af8025588afc5143df4edad2a1b879d7da352c3</citedby><cites>FETCH-LOGICAL-c4327-5b14ef3ac2ae01a37af6679678af8025588afc5143df4edad2a1b879d7da352c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.5694%2Fj.1326-5377.2008.tb02027.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.5694%2Fj.1326-5377.2008.tb02027.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20641880$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18759727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Joske, David J L</creatorcontrib><title>Chronic myeloid leukaemia: the evolution of gene‐targeted therapy</title><title>Medical journal of Australia</title><addtitle>Med J Aust</addtitle><description>Chronic myeloid leukaemia (CML) was the first human cancer linked to an acquired chromosomal abnormality, subsequently shown to be a reciprocal translocation between chromosomes 9 and 22. The resulting fusion gene product, BCR‐ABL, was shown to be the causative agent of the disease.
CML has an incidence of around 1–2 cases per 100 000; in Australia, there are probably more than 200 new cases per year and more than 1300 prevalent cases.
Treatment of CML with imatinib has been a powerful vindication of the concept of rational, gene‐targeted drug design.
Five‐year published experience with imatinib at 400 mg orally daily demonstrates 89% overall survival and an estimated 93% freedom from disease progression. Adverse effects are mostly mild and transient.
Higher doses of imatinib may be more efficacious and will be studied in upcoming clinical trials in Australia; however, imatinib is almost certainly not curative.
Up to 28% of patients may have to stop imatinib because of intolerance or disease resistance, mostly due to point mutations of BCR‐ABL. In this situation, many patients will respond to second‐ and third‐generation tyrosine kinase inhibitors.
Management of CML patients should involve close monitoring, especially in the first 2 years, with regular cytogenetics and quantitative polymerase chain reaction to optimise response and identify suboptimal responders as early as possible.
Bone marrow transplantation remains the only known cure, but is reserved for patients whose kinase inhibitor therapy has failed, or who have advanced disease (accelerated phase or blastic transformation).</description><subject>Antineoplastic Agents - therapeutic use</subject><subject>Australia</subject><subject>Benzamides</subject><subject>Binding sites</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Cancer therapies</subject><subject>Chromosomes</subject><subject>Drug Approval</subject><subject>Fusion Proteins, bcr-abl - antagonists & inhibitors</subject><subject>Fusion Proteins, bcr-abl - genetics</subject><subject>General aspects</subject><subject>Health services administration</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematologic diseases</subject><subject>Hematology</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Interferon</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - therapy</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Piperazines - therapeutic use</subject><subject>Polymerase chain reaction</subject><subject>Pyrimidines - therapeutic use</subject><subject>Signal transduction</subject><subject>United States</subject><issn>0025-729X</issn><issn>1326-5377</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkM1O3DAQx62qCLbAK1QRUrkl-COOHW6rVb8QqBeQuFmzzgSyTeKtnRT21kfoM_ZJ6nQjKvXW08zIv_H89SPkjNFMFmV-scmY4EUqhVIZp1Rnw5pyylX2_IosXp5ekwWlXKaKl_dH5E0ImzgyydUhOWJayVJxtSCr1aN3fWOTboeta6qkxfErYNfAZTI8YoLfXTsOjesTVycP2OOvHz8H8A84YDUBHra7E3JQQxvwdK7H5O7D-9vVp_T6y8fPq-V1anPBVSrXLMdagOWAlIFQUBeFKgulodYxqdSxsZLloqpzrKDiwNZalZWqQEhuxTE53_-79e7biGEwXRMsti306MZgohud57SM4Nk_4MaNvo_ZDBcyHhSlitDlHrLeheCxNlvfdOB3hlEzeTYbM8k0k0wzeTazZ_Mcl9_OF8Z1h9Xf1VlsBN7NAAQLbe2ht0144TgtcqY1jdxyzz01Le7-I4K5uVryP734DZfcm60</recordid><startdate>200809</startdate><enddate>200809</enddate><creator>Joske, David J L</creator><general>Australasian Medical Publishing Company</general><general>Australasian Medical Publishing Company Proprietary, Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>200809</creationdate><title>Chronic myeloid leukaemia: the evolution of gene‐targeted therapy</title><author>Joske, David J L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4327-5b14ef3ac2ae01a37af6679678af8025588afc5143df4edad2a1b879d7da352c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Antineoplastic Agents - therapeutic use</topic><topic>Australia</topic><topic>Benzamides</topic><topic>Binding sites</topic><topic>Biological and medical sciences</topic><topic>Bone marrow</topic><topic>Cancer therapies</topic><topic>Chromosomes</topic><topic>Drug Approval</topic><topic>Fusion Proteins, bcr-abl - antagonists & inhibitors</topic><topic>Fusion Proteins, bcr-abl - genetics</topic><topic>General aspects</topic><topic>Health services administration</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematologic diseases</topic><topic>Hematology</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Interferon</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - therapy</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Piperazines - therapeutic use</topic><topic>Polymerase chain reaction</topic><topic>Pyrimidines - therapeutic use</topic><topic>Signal transduction</topic><topic>United States</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Joske, David J L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Medical journal of Australia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Joske, David J L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic myeloid leukaemia: the evolution of gene‐targeted therapy</atitle><jtitle>Medical journal of Australia</jtitle><addtitle>Med J Aust</addtitle><date>2008-09</date><risdate>2008</risdate><volume>189</volume><issue>5</issue><spage>277</spage><epage>282</epage><pages>277-282</pages><issn>0025-729X</issn><eissn>1326-5377</eissn><coden>MJAUAJ</coden><abstract>Chronic myeloid leukaemia (CML) was the first human cancer linked to an acquired chromosomal abnormality, subsequently shown to be a reciprocal translocation between chromosomes 9 and 22. The resulting fusion gene product, BCR‐ABL, was shown to be the causative agent of the disease.
CML has an incidence of around 1–2 cases per 100 000; in Australia, there are probably more than 200 new cases per year and more than 1300 prevalent cases.
Treatment of CML with imatinib has been a powerful vindication of the concept of rational, gene‐targeted drug design.
Five‐year published experience with imatinib at 400 mg orally daily demonstrates 89% overall survival and an estimated 93% freedom from disease progression. Adverse effects are mostly mild and transient.
Higher doses of imatinib may be more efficacious and will be studied in upcoming clinical trials in Australia; however, imatinib is almost certainly not curative.
Up to 28% of patients may have to stop imatinib because of intolerance or disease resistance, mostly due to point mutations of BCR‐ABL. In this situation, many patients will respond to second‐ and third‐generation tyrosine kinase inhibitors.
Management of CML patients should involve close monitoring, especially in the first 2 years, with regular cytogenetics and quantitative polymerase chain reaction to optimise response and identify suboptimal responders as early as possible.
Bone marrow transplantation remains the only known cure, but is reserved for patients whose kinase inhibitor therapy has failed, or who have advanced disease (accelerated phase or blastic transformation).</abstract><cop>Sydney</cop><pub>Australasian Medical Publishing Company</pub><pmid>18759727</pmid><doi>10.5694/j.1326-5377.2008.tb02027.x</doi><tpages>6</tpages></addata></record> |
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subjects | Antineoplastic Agents - therapeutic use Australia Benzamides Binding sites Biological and medical sciences Bone marrow Cancer therapies Chromosomes Drug Approval Fusion Proteins, bcr-abl - antagonists & inhibitors Fusion Proteins, bcr-abl - genetics General aspects Health services administration Hematologic and hematopoietic diseases Hematologic diseases Hematology Humans Imatinib Mesylate Interferon Kinases Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Leukemia, Myelogenous, Chronic, BCR-ABL Positive - therapy Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Piperazines - therapeutic use Polymerase chain reaction Pyrimidines - therapeutic use Signal transduction United States |
title | Chronic myeloid leukaemia: the evolution of gene‐targeted therapy |
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