Chronic myeloid leukaemia
Summary Chronic myeloid leukaemia (CML) was the first neoplastic disease for which knowledge of the genotype led to a rationally designed therapy. As a result of its well known pathophysiology, straightforward diagnosis, well established prognostic factors, and treatment for the cause of disease, CM...
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| Veröffentlicht in: | The Lancet (British edition) 2007-07, Vol.370 (9584), p.342-350 |
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| creator | Hehlmann, Rüdiger, Prof Hochhaus, Andreas, Prof Baccarani, Michele, Prof |
| description | Summary Chronic myeloid leukaemia (CML) was the first neoplastic disease for which knowledge of the genotype led to a rationally designed therapy. As a result of its well known pathophysiology, straightforward diagnosis, well established prognostic factors, and treatment for the cause of disease, CML has been studied to an extent that far exceeds that expected from its frequency, and serves as a model disease for other cancers. Imatinib, an inhibitor of BCR-ABL tyrosine kinase, has revolutionised treatment of this disease, and is now recommended as standard treatment for chronic-phase CML. Interferon alfa is an acceptable alternative treatment in the early chronic phase for patients who do not tolerate imatinib. If imatinib treatment fails, allogeneic stem-cell transplantation, a dose increase of imatinib, or new drugs are recommended. Up to 87% of patients achieve complete cytogenetic remission, therefore we provide guidance for monitoring disease status. Many trials of new drugs and combination therapies that include imatinib are underway. |
| doi_str_mv | 10.1016/S0140-6736(07)61165-9 |
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As a result of its well known pathophysiology, straightforward diagnosis, well established prognostic factors, and treatment for the cause of disease, CML has been studied to an extent that far exceeds that expected from its frequency, and serves as a model disease for other cancers. Imatinib, an inhibitor of BCR-ABL tyrosine kinase, has revolutionised treatment of this disease, and is now recommended as standard treatment for chronic-phase CML. Interferon alfa is an acceptable alternative treatment in the early chronic phase for patients who do not tolerate imatinib. If imatinib treatment fails, allogeneic stem-cell transplantation, a dose increase of imatinib, or new drugs are recommended. Up to 87% of patients achieve complete cytogenetic remission, therefore we provide guidance for monitoring disease status. Many trials of new drugs and combination therapies that include imatinib are underway.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/S0140-6736(07)61165-9</identifier><identifier>PMID: 17662883</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Benzamides ; Binding sites ; Biological and medical sciences ; Clinical trials ; General aspects ; Hematologic and hematopoietic diseases ; Humans ; Imatinib Mesylate ; Immunization ; Immunologic Factors - therapeutic use ; Interferon-alpha - therapeutic use ; Internal Medicine ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Medical treatment ; Older people ; Piperazines - adverse effects ; Piperazines - therapeutic use ; Prognosis ; Protein Kinase Inhibitors - adverse effects ; Protein Kinase Inhibitors - therapeutic use ; Pyrimidines - adverse effects ; Pyrimidines - therapeutic use ; Randomized Controlled Trials as Topic ; Risk factors ; Signal transduction ; Stem Cell Transplantation ; Studies ; Success ; Survival Rate</subject><ispartof>The Lancet (British edition), 2007-07, Vol.370 (9584), p.342-350</ispartof><rights>Elsevier Ltd</rights><rights>2007 Elsevier Ltd</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Elsevier Limited Jul 28-Aug 3, 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-87977be28c1e04941ed37877c52615a5a3ef0adcee88aab30fedcfe6c3ff9ec63</citedby><cites>FETCH-LOGICAL-c444t-87977be28c1e04941ed37877c52615a5a3ef0adcee88aab30fedcfe6c3ff9ec63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/199130628?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000,64390,64394,72474</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18919580$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17662883$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hehlmann, Rüdiger, Prof</creatorcontrib><creatorcontrib>Hochhaus, Andreas, Prof</creatorcontrib><creatorcontrib>Baccarani, Michele, Prof</creatorcontrib><creatorcontrib>on behalf of the European LeukemiaNet</creatorcontrib><creatorcontrib>European LeukemiaNet</creatorcontrib><title>Chronic myeloid leukaemia</title><title>The Lancet (British edition)</title><addtitle>Lancet</addtitle><description>Summary Chronic myeloid leukaemia (CML) was the first neoplastic disease for which knowledge of the genotype led to a rationally designed therapy. As a result of its well known pathophysiology, straightforward diagnosis, well established prognostic factors, and treatment for the cause of disease, CML has been studied to an extent that far exceeds that expected from its frequency, and serves as a model disease for other cancers. Imatinib, an inhibitor of BCR-ABL tyrosine kinase, has revolutionised treatment of this disease, and is now recommended as standard treatment for chronic-phase CML. Interferon alfa is an acceptable alternative treatment in the early chronic phase for patients who do not tolerate imatinib. If imatinib treatment fails, allogeneic stem-cell transplantation, a dose increase of imatinib, or new drugs are recommended. Up to 87% of patients achieve complete cytogenetic remission, therefore we provide guidance for monitoring disease status. Many trials of new drugs and combination therapies that include imatinib are underway.</description><subject>Benzamides</subject><subject>Binding sites</subject><subject>Biological and medical sciences</subject><subject>Clinical trials</subject><subject>General aspects</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Immunization</subject><subject>Immunologic Factors - therapeutic use</subject><subject>Interferon-alpha - therapeutic use</subject><subject>Internal Medicine</subject><subject>Leukemia</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Medical treatment</subject><subject>Older people</subject><subject>Piperazines - adverse effects</subject><subject>Piperazines - therapeutic use</subject><subject>Prognosis</subject><subject>Protein Kinase Inhibitors - adverse effects</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Pyrimidines - adverse effects</subject><subject>Pyrimidines - therapeutic use</subject><subject>Randomized Controlled Trials as Topic</subject><subject>Risk factors</subject><subject>Signal transduction</subject><subject>Stem Cell Transplantation</subject><subject>Studies</subject><subject>Success</subject><subject>Survival Rate</subject><issn>0140-6736</issn><issn>1474-547X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkMtKAzEUQIMotlY_wIVSBEEXozeTTB4bRYovKLhQwV1IM3cw7XSmJh2hf-_0gQU3rrI59-TeQ8gJhSsKVFy_AuWQCMnEBchLQanIEr1DupRLnmRcfuyS7i_SIQcxjgGAC8j2SYdKIVKlWJccDz5DXXnXny6wrH3eL7GZWJx6e0j2CltGPNq8PfL-cP82eEqGL4_Pg7th4jjn80RJLeUIU-UoAtecYs6kktJlqaCZzSzDAmzuEJWydsSgwNwVKBwrCo1OsB45W3tnof5qMM7NuG5C1X5pqNaUQbtpC2VryIU6xoCFmQU_tWFhKJhlD7PqYZbHGpBm1cPodu50I29GU8y3U5sALXC-AWx0tiyCrZyPW05pqjMFLXe75rBN8e0xmOg8Vg5zH9DNTV77f1e5-WNwpW_L23KCC4zbo01MDawlSwfIlUGzH69Wj-I</recordid><startdate>20070728</startdate><enddate>20070728</enddate><creator>Hehlmann, Rüdiger, Prof</creator><creator>Hochhaus, Andreas, Prof</creator><creator>Baccarani, Michele, Prof</creator><general>Elsevier Ltd</general><general>Lancet</general><general>Elsevier Limited</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>0TT</scope><scope>0TZ</scope><scope>0U~</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88C</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8C2</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K6X</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>KB~</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>S0X</scope></search><sort><creationdate>20070728</creationdate><title>Chronic myeloid leukaemia</title><author>Hehlmann, Rüdiger, Prof ; Hochhaus, Andreas, Prof ; Baccarani, Michele, Prof</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-87977be28c1e04941ed37877c52615a5a3ef0adcee88aab30fedcfe6c3ff9ec63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Benzamides</topic><topic>Binding sites</topic><topic>Biological and medical sciences</topic><topic>Clinical trials</topic><topic>General aspects</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Immunization</topic><topic>Immunologic Factors - therapeutic use</topic><topic>Interferon-alpha - therapeutic use</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Medical treatment</topic><topic>Older people</topic><topic>Piperazines - adverse effects</topic><topic>Piperazines - therapeutic use</topic><topic>Prognosis</topic><topic>Protein Kinase Inhibitors - adverse effects</topic><topic>Protein Kinase Inhibitors - therapeutic use</topic><topic>Pyrimidines - adverse effects</topic><topic>Pyrimidines - therapeutic use</topic><topic>Randomized Controlled Trials as Topic</topic><topic>Risk factors</topic><topic>Signal transduction</topic><topic>Stem Cell Transplantation</topic><topic>Studies</topic><topic>Success</topic><topic>Survival Rate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hehlmann, Rüdiger, Prof</creatorcontrib><creatorcontrib>Hochhaus, Andreas, Prof</creatorcontrib><creatorcontrib>Baccarani, Michele, Prof</creatorcontrib><creatorcontrib>on behalf of the European LeukemiaNet</creatorcontrib><creatorcontrib>European 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of the genotype led to a rationally designed therapy. As a result of its well known pathophysiology, straightforward diagnosis, well established prognostic factors, and treatment for the cause of disease, CML has been studied to an extent that far exceeds that expected from its frequency, and serves as a model disease for other cancers. Imatinib, an inhibitor of BCR-ABL tyrosine kinase, has revolutionised treatment of this disease, and is now recommended as standard treatment for chronic-phase CML. Interferon alfa is an acceptable alternative treatment in the early chronic phase for patients who do not tolerate imatinib. If imatinib treatment fails, allogeneic stem-cell transplantation, a dose increase of imatinib, or new drugs are recommended. Up to 87% of patients achieve complete cytogenetic remission, therefore we provide guidance for monitoring disease status. Many trials of new drugs and combination therapies that include imatinib are underway.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>17662883</pmid><doi>10.1016/S0140-6736(07)61165-9</doi><tpages>9</tpages></addata></record> |
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| subjects | Benzamides Binding sites Biological and medical sciences Clinical trials General aspects Hematologic and hematopoietic diseases Humans Imatinib Mesylate Immunization Immunologic Factors - therapeutic use Interferon-alpha - therapeutic use Internal Medicine Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Medical treatment Older people Piperazines - adverse effects Piperazines - therapeutic use Prognosis Protein Kinase Inhibitors - adverse effects Protein Kinase Inhibitors - therapeutic use Pyrimidines - adverse effects Pyrimidines - therapeutic use Randomized Controlled Trials as Topic Risk factors Signal transduction Stem Cell Transplantation Studies Success Survival Rate |
| title | Chronic myeloid leukaemia |
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