How I treat extramedullary acute myeloid leukemia
Extramedullary (EM) manifestations of acute leukemia include a wide variety of clinically significant phenomena that often pose therapeutic dilemmas. Myeloid sarcoma (MS) and leukemia cutis (LC) represent 2 well-known EM manifestations with a range of clinical presentations. MS (also known as granul...
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Veröffentlicht in: | Blood 2011-10, Vol.118 (14), p.3785-3793 |
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description | Extramedullary (EM) manifestations of acute leukemia include a wide variety of clinically significant phenomena that often pose therapeutic dilemmas. Myeloid sarcoma (MS) and leukemia cutis (LC) represent 2 well-known EM manifestations with a range of clinical presentations. MS (also known as granulocytic sarcoma or chloroma) is a rare EM tumor of immature myeloid cells. LC specifically refers to the infiltration of the epidermis, dermis, or subcutis by neoplastic leukocytes (leukemia cells), resulting in clinically identifiable cutaneous lesions. The molecular mechanisms underlying EM involvement are not well defined, but recent immunophenotyping, cytogenetic, and molecular analysis are beginning to provide some understanding. Certain cytogenetic abnormalities are associated with increased risk of EM involvement, potentially through altering tissue-homing pathways. The prognostic significance of EM involvement is not fully understood. Therefore, it has been difficult to define the optimal treatment of patients with MS or LC. The timing of EM development at presentation versus relapse, involvement of the marrow, and AML risk classification help to determine our approach to treatment of EM disease. |
doi_str_mv | 10.1182/blood-2011-04-347229 |
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Myeloid sarcoma (MS) and leukemia cutis (LC) represent 2 well-known EM manifestations with a range of clinical presentations. MS (also known as granulocytic sarcoma or chloroma) is a rare EM tumor of immature myeloid cells. LC specifically refers to the infiltration of the epidermis, dermis, or subcutis by neoplastic leukocytes (leukemia cells), resulting in clinically identifiable cutaneous lesions. The molecular mechanisms underlying EM involvement are not well defined, but recent immunophenotyping, cytogenetic, and molecular analysis are beginning to provide some understanding. Certain cytogenetic abnormalities are associated with increased risk of EM involvement, potentially through altering tissue-homing pathways. The prognostic significance of EM involvement is not fully understood. Therefore, it has been difficult to define the optimal treatment of patients with MS or LC. The timing of EM development at presentation versus relapse, involvement of the marrow, and AML risk classification help to determine our approach to treatment of EM disease.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2011-04-347229</identifier><identifier>PMID: 21795742</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Biological and medical sciences ; Chromosome Aberrations ; Drug Therapy ; Hematologic and hematopoietic diseases ; Hematopoietic Stem Cell Transplantation ; Humans ; Leukemia, Myeloid, Acute - complications ; Leukemia, Myeloid, Acute - genetics ; Leukemia, Myeloid, Acute - pathology ; Leukemia, Myeloid, Acute - therapy ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Leukemic Infiltration - complications ; Leukemic Infiltration - genetics ; Leukemic Infiltration - pathology ; Leukemic Infiltration - therapy ; Medical sciences ; Mutation ; Prognosis ; Sarcoma, Myeloid - complications ; Sarcoma, Myeloid - genetics ; Sarcoma, Myeloid - pathology ; Sarcoma, Myeloid - therapy ; Skin - pathology</subject><ispartof>Blood, 2011-10, Vol.118 (14), p.3785-3793</ispartof><rights>2011 American Society of Hematology</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-e3eab7ce644dac7b2dcbc3daf9cf73755a22c1e1fdcd98cb1edd8918a291d14a3</citedby><cites>FETCH-LOGICAL-c503t-e3eab7ce644dac7b2dcbc3daf9cf73755a22c1e1fdcd98cb1edd8918a291d14a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24595524$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21795742$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bakst, Richard L.</creatorcontrib><creatorcontrib>Tallman, Martin S.</creatorcontrib><creatorcontrib>Douer, Dan</creatorcontrib><creatorcontrib>Yahalom, Joachim</creatorcontrib><title>How I treat extramedullary acute myeloid leukemia</title><title>Blood</title><addtitle>Blood</addtitle><description>Extramedullary (EM) manifestations of acute leukemia include a wide variety of clinically significant phenomena that often pose therapeutic dilemmas. Myeloid sarcoma (MS) and leukemia cutis (LC) represent 2 well-known EM manifestations with a range of clinical presentations. MS (also known as granulocytic sarcoma or chloroma) is a rare EM tumor of immature myeloid cells. LC specifically refers to the infiltration of the epidermis, dermis, or subcutis by neoplastic leukocytes (leukemia cells), resulting in clinically identifiable cutaneous lesions. The molecular mechanisms underlying EM involvement are not well defined, but recent immunophenotyping, cytogenetic, and molecular analysis are beginning to provide some understanding. Certain cytogenetic abnormalities are associated with increased risk of EM involvement, potentially through altering tissue-homing pathways. The prognostic significance of EM involvement is not fully understood. Therefore, it has been difficult to define the optimal treatment of patients with MS or LC. The timing of EM development at presentation versus relapse, involvement of the marrow, and AML risk classification help to determine our approach to treatment of EM disease.</description><subject>Biological and medical sciences</subject><subject>Chromosome Aberrations</subject><subject>Drug Therapy</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Humans</subject><subject>Leukemia, Myeloid, Acute - complications</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemia, Myeloid, Acute - therapy</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Leukemic Infiltration - complications</subject><subject>Leukemic Infiltration - genetics</subject><subject>Leukemic Infiltration - pathology</subject><subject>Leukemic Infiltration - therapy</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>Prognosis</subject><subject>Sarcoma, Myeloid - complications</subject><subject>Sarcoma, Myeloid - genetics</subject><subject>Sarcoma, Myeloid - pathology</subject><subject>Sarcoma, Myeloid - therapy</subject><subject>Skin - pathology</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0EoqXwBwhlg1gFPH408QYJIV5SJTawtpzxRDIkDdgJj78npQV2rGZz7sydw9gh8FOAUpxVTdf5XHCAnKtcqkIIs8WmoEWZcy74Nptyzue5MgVM2F5KT5yDkkLvsomAwuhCiSmD2-49u8v6SK7P6KOPriU_NI2Ln5nDoaes_aSmCz5raHimNrh9tlO7JtHBZs7Y4_XVw-Vtvri_ubu8WOSouexzkuSqAmmulHdYVMJjhdK72mBdyEJrJwQCQe3RmxIrIO9LA6UTBjwoJ2fsZL33JXavA6XetiEhjdWW1A3JlmZeSimVGEm1JjF2KUWq7UsM7fiBBW5Xruy3K7tyZbmya1dj7GhzYKjGp39DP3JG4HgDuISuqaNbYkh_nNJGa6FG7nzN0ajjLVC0CQMtkXyIhL31Xfi_yReF9oh2</recordid><startdate>20111006</startdate><enddate>20111006</enddate><creator>Bakst, Richard L.</creator><creator>Tallman, Martin S.</creator><creator>Douer, Dan</creator><creator>Yahalom, Joachim</creator><general>Elsevier Inc</general><general>Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope></search><sort><creationdate>20111006</creationdate><title>How I treat extramedullary acute myeloid leukemia</title><author>Bakst, Richard L. ; Tallman, Martin S. ; Douer, Dan ; Yahalom, Joachim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-e3eab7ce644dac7b2dcbc3daf9cf73755a22c1e1fdcd98cb1edd8918a291d14a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Biological and medical sciences</topic><topic>Chromosome Aberrations</topic><topic>Drug Therapy</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematopoietic Stem Cell Transplantation</topic><topic>Humans</topic><topic>Leukemia, Myeloid, Acute - complications</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemia, Myeloid, Acute - therapy</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Leukemic Infiltration - complications</topic><topic>Leukemic Infiltration - genetics</topic><topic>Leukemic Infiltration - pathology</topic><topic>Leukemic Infiltration - therapy</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>Prognosis</topic><topic>Sarcoma, Myeloid - complications</topic><topic>Sarcoma, Myeloid - genetics</topic><topic>Sarcoma, Myeloid - pathology</topic><topic>Sarcoma, Myeloid - therapy</topic><topic>Skin - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bakst, Richard L.</creatorcontrib><creatorcontrib>Tallman, Martin S.</creatorcontrib><creatorcontrib>Douer, Dan</creatorcontrib><creatorcontrib>Yahalom, Joachim</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>MEDLINE - Academic</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bakst, Richard L.</au><au>Tallman, Martin S.</au><au>Douer, Dan</au><au>Yahalom, Joachim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>How I treat extramedullary acute myeloid leukemia</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2011-10-06</date><risdate>2011</risdate><volume>118</volume><issue>14</issue><spage>3785</spage><epage>3793</epage><pages>3785-3793</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Extramedullary (EM) manifestations of acute leukemia include a wide variety of clinically significant phenomena that often pose therapeutic dilemmas. Myeloid sarcoma (MS) and leukemia cutis (LC) represent 2 well-known EM manifestations with a range of clinical presentations. MS (also known as granulocytic sarcoma or chloroma) is a rare EM tumor of immature myeloid cells. LC specifically refers to the infiltration of the epidermis, dermis, or subcutis by neoplastic leukocytes (leukemia cells), resulting in clinically identifiable cutaneous lesions. The molecular mechanisms underlying EM involvement are not well defined, but recent immunophenotyping, cytogenetic, and molecular analysis are beginning to provide some understanding. Certain cytogenetic abnormalities are associated with increased risk of EM involvement, potentially through altering tissue-homing pathways. The prognostic significance of EM involvement is not fully understood. Therefore, it has been difficult to define the optimal treatment of patients with MS or LC. The timing of EM development at presentation versus relapse, involvement of the marrow, and AML risk classification help to determine our approach to treatment of EM disease.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>21795742</pmid><doi>10.1182/blood-2011-04-347229</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Chromosome Aberrations Drug Therapy Hematologic and hematopoietic diseases Hematopoietic Stem Cell Transplantation Humans Leukemia, Myeloid, Acute - complications Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - pathology Leukemia, Myeloid, Acute - therapy Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Leukemic Infiltration - complications Leukemic Infiltration - genetics Leukemic Infiltration - pathology Leukemic Infiltration - therapy Medical sciences Mutation Prognosis Sarcoma, Myeloid - complications Sarcoma, Myeloid - genetics Sarcoma, Myeloid - pathology Sarcoma, Myeloid - therapy Skin - pathology |
title | How I treat extramedullary acute myeloid leukemia |
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