Common alterations in gene expression and increased proliferation in recurrent acute myeloid leukemia
Recurrent disease following high-dose chemotherapy is a major problem in patients with acute myeloid leukemia (AML). To identify its characteristics, we performed expression profiling in blasts from untreated AML and relapse, using a specific cDNA microarray comprising 4128 genes generated by cDNA s...
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Veröffentlicht in: | Oncogene 2004-01, Vol.23 (4), p.894-904 |
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description | Recurrent disease following high-dose chemotherapy is a major problem in patients with acute myeloid leukemia (AML). To identify its characteristics, we performed expression profiling in blasts from untreated AML and relapse, using a specific cDNA microarray comprising 4128 genes generated by cDNA subtraction supplemented with cancer-associated genes. Expression analysis of 18 AML bone marrow specimens showed that recurrent AML is commonly associated with the mRNA expression changes in a set of 58 genes. Increased cellular proliferation was indicated by the overexpression of the transferrin receptor, proliferating cell nuclear antigen, and G1 cyclins. An immunohistochemical study for Ki-67-positive blasts in 18 paired bone marrow biopsy samples confirmed a highly significant (
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P
<0.0001) increase in the proliferation fraction at relapse. In addition, we found enhanced activation of the RAF/MEK/ERK cascade as mRNAs of MKP-1, c-
jun
, c-
fos
, and egr-1 were significantly increased at relapse. Immunohistochemistry and immunoblotting analyses for biphosphorylated ERK1/2 protein provide additional evidence for enhanced activation of the RAF/MEK/ERK pathway. The degree of increase is significantly correlated with the increased proliferation. Furthermore, the genes identified provide a rationale for further studies on predictive diagnosis and therapeutic intervention.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1207192</identifier><identifier>PMID: 14749762</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Acute Disease ; Adult ; Aged ; Apoptosis ; Biological and medical sciences ; Blotting, Western ; Bone marrow ; Cell Biology ; Cell Division ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chemotherapy ; Cloning ; DNA, Complementary ; Fundamental and applied biological sciences. Psychology ; Gene Expression ; Hematologic and hematopoietic diseases ; Human Genetics ; Humans ; Immunohistochemistry ; Internal Medicine ; Kinases ; Leukemia ; Leukemia, Myeloid - enzymology ; Leukemia, Myeloid - genetics ; Leukemia, Myeloid - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Mitogen-Activated Protein Kinases - metabolism ; Molecular and cellular biology ; Oligonucleotide Array Sequence Analysis ; Oncology ; original-paper ; Proteins ; Recurrence ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>Oncogene, 2004-01, Vol.23 (4), p.894-904</ispartof><rights>Springer Nature Limited 2004</rights><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 29, 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c586t-7b739bc0774650cd7a329a6b5b4ef28a733e3b64dde69dba56f17e560987b6263</citedby><cites>FETCH-LOGICAL-c586t-7b739bc0774650cd7a329a6b5b4ef28a733e3b64dde69dba56f17e560987b6263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1207192$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1207192$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2725,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15674319$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14749762$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Staber, Philipp Bernhard</creatorcontrib><creatorcontrib>Linkesch, Werner</creatorcontrib><creatorcontrib>Zauner, Dorothea</creatorcontrib><creatorcontrib>Beham-Schmid, Christine</creatorcontrib><creatorcontrib>Guelly, Christian</creatorcontrib><creatorcontrib>Schauer, Silvia</creatorcontrib><creatorcontrib>Sill, Heinz</creatorcontrib><creatorcontrib>Hoefler, Gerald</creatorcontrib><title>Common alterations in gene expression and increased proliferation in recurrent acute myeloid leukemia</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Recurrent disease following high-dose chemotherapy is a major problem in patients with acute myeloid leukemia (AML). To identify its characteristics, we performed expression profiling in blasts from untreated AML and relapse, using a specific cDNA microarray comprising 4128 genes generated by cDNA subtraction supplemented with cancer-associated genes. Expression analysis of 18 AML bone marrow specimens showed that recurrent AML is commonly associated with the mRNA expression changes in a set of 58 genes. Increased cellular proliferation was indicated by the overexpression of the transferrin receptor, proliferating cell nuclear antigen, and G1 cyclins. An immunohistochemical study for Ki-67-positive blasts in 18 paired bone marrow biopsy samples confirmed a highly significant (
P
<0.0001) increase in the proliferation fraction at relapse. In addition, we found enhanced activation of the RAF/MEK/ERK cascade as mRNAs of MKP-1, c-
jun
, c-
fos
, and egr-1 were significantly increased at relapse. Immunohistochemistry and immunoblotting analyses for biphosphorylated ERK1/2 protein provide additional evidence for enhanced activation of the RAF/MEK/ERK pathway. The degree of increase is significantly correlated with the increased proliferation. Furthermore, the genes identified provide a rationale for further studies on predictive diagnosis and therapeutic intervention.</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Bone marrow</subject><subject>Cell Biology</subject><subject>Cell Division</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chemotherapy</subject><subject>Cloning</subject><subject>DNA, Complementary</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid - enzymology</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemia, Myeloid - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Molecular and cellular biology</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oncology</subject><subject>original-paper</subject><subject>Proteins</subject><subject>Recurrence</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc2LFDEQxYMo7uzq1ZvSCOutZ_OdznEZ_IIFL3oO6XT1kDGdjEk37P73ZpiGEUEkh0DV771U5SH0huAtway7K4dtim5LKFZE02doQ7iSrRCaP0cbrAVuNWX0Cl2XcsAYK43pS3RVIa6VpBsEuzRNKTY2zJDt7FMsjY_NHiI08HjMUIo_teNQyy6DLTA0x5yCH1f-hGdwS84Q58a6ZYZmeoKQ_NAEWH7C5O0r9GK0ocDr9b5BPz59_L770j58-_x1d__QOtHJuVW9Yrp3WCkuBXaDsoxqK3vRcxhpZxVjwHrJhwGkHnor5EgUCIl1p3pJJbtBH86-dcJfC5TZTL44CMFGSEsxHSZUUMH_C9a_lB2WJ8f3f4GHtORYlzCUKiYo1aJC2zO0twGMj2Oas3X1DHV5lyKMvtbvSaex1pr_IXA5lZJhNMfsJ5ufDMHmlKspB1NzNWuuVfBuHWPpJxgu-BpkBW5XwBZnw5htdL5cOCEVZ0RX7u7MldqKe8iXff759NuzItp5yXCxXPu_Abm7xcw</recordid><startdate>20040129</startdate><enddate>20040129</enddate><creator>Staber, Philipp Bernhard</creator><creator>Linkesch, Werner</creator><creator>Zauner, Dorothea</creator><creator>Beham-Schmid, Christine</creator><creator>Guelly, Christian</creator><creator>Schauer, Silvia</creator><creator>Sill, Heinz</creator><creator>Hoefler, Gerald</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20040129</creationdate><title>Common alterations in gene expression and increased proliferation in recurrent acute myeloid leukemia</title><author>Staber, Philipp Bernhard ; Linkesch, Werner ; Zauner, Dorothea ; Beham-Schmid, Christine ; Guelly, Christian ; Schauer, Silvia ; Sill, Heinz ; Hoefler, Gerald</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c586t-7b739bc0774650cd7a329a6b5b4ef28a733e3b64dde69dba56f17e560987b6263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Bone marrow</topic><topic>Cell Biology</topic><topic>Cell Division</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Chemotherapy</topic><topic>Cloning</topic><topic>DNA, Complementary</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid - enzymology</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemia, Myeloid - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Molecular and cellular biology</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Oncology</topic><topic>original-paper</topic><topic>Proteins</topic><topic>Recurrence</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Staber, Philipp Bernhard</creatorcontrib><creatorcontrib>Linkesch, Werner</creatorcontrib><creatorcontrib>Zauner, Dorothea</creatorcontrib><creatorcontrib>Beham-Schmid, Christine</creatorcontrib><creatorcontrib>Guelly, Christian</creatorcontrib><creatorcontrib>Schauer, Silvia</creatorcontrib><creatorcontrib>Sill, Heinz</creatorcontrib><creatorcontrib>Hoefler, Gerald</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 Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Staber, Philipp Bernhard</au><au>Linkesch, Werner</au><au>Zauner, Dorothea</au><au>Beham-Schmid, Christine</au><au>Guelly, Christian</au><au>Schauer, Silvia</au><au>Sill, Heinz</au><au>Hoefler, Gerald</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Common alterations in gene expression and increased proliferation in recurrent acute myeloid leukemia</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2004-01-29</date><risdate>2004</risdate><volume>23</volume><issue>4</issue><spage>894</spage><epage>904</epage><pages>894-904</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Recurrent disease following high-dose chemotherapy is a major problem in patients with acute myeloid leukemia (AML). To identify its characteristics, we performed expression profiling in blasts from untreated AML and relapse, using a specific cDNA microarray comprising 4128 genes generated by cDNA subtraction supplemented with cancer-associated genes. Expression analysis of 18 AML bone marrow specimens showed that recurrent AML is commonly associated with the mRNA expression changes in a set of 58 genes. Increased cellular proliferation was indicated by the overexpression of the transferrin receptor, proliferating cell nuclear antigen, and G1 cyclins. An immunohistochemical study for Ki-67-positive blasts in 18 paired bone marrow biopsy samples confirmed a highly significant (
P
<0.0001) increase in the proliferation fraction at relapse. In addition, we found enhanced activation of the RAF/MEK/ERK cascade as mRNAs of MKP-1, c-
jun
, c-
fos
, and egr-1 were significantly increased at relapse. Immunohistochemistry and immunoblotting analyses for biphosphorylated ERK1/2 protein provide additional evidence for enhanced activation of the RAF/MEK/ERK pathway. The degree of increase is significantly correlated with the increased proliferation. Furthermore, the genes identified provide a rationale for further studies on predictive diagnosis and therapeutic intervention.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>14749762</pmid><doi>10.1038/sj.onc.1207192</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acute Disease Adult Aged Apoptosis Biological and medical sciences Blotting, Western Bone marrow Cell Biology Cell Division Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chemotherapy Cloning DNA, Complementary Fundamental and applied biological sciences. Psychology Gene Expression Hematologic and hematopoietic diseases Human Genetics Humans Immunohistochemistry Internal Medicine Kinases Leukemia Leukemia, Myeloid - enzymology Leukemia, Myeloid - genetics Leukemia, Myeloid - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Medicine Medicine & Public Health Middle Aged Mitogen-Activated Protein Kinases - metabolism Molecular and cellular biology Oligonucleotide Array Sequence Analysis Oncology original-paper Proteins Recurrence Reverse Transcriptase Polymerase Chain Reaction |
title | Common alterations in gene expression and increased proliferation in recurrent acute myeloid leukemia |
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