CEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia
Hypermethylation of the distal CEBPA promoter region has been reported to result in the downregulation of CEBPA expression in several malignancies. However, the clinical implication of CEBPA hypermethylation in acute myeloid leukemia (AML) remains unclear. To investigate the correlation between CEBP...
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| creator | Lin, T-C Hou, H-A Chou, W-C Ou, D-L Yu, S-L Tien, H-F Lin, L-I |
| description | Hypermethylation of the distal
CEBPA
promoter region has been reported to result in the downregulation of
CEBPA
expression in several malignancies. However, the clinical implication of
CEBPA
hypermethylation in acute myeloid leukemia (AML) remains unclear. To investigate the correlation between
CEBPA
hypermethylation and clinical features in AML, quantitative MassARRAY analyses for
CEBPA
methylation status were performed on a cohort of 193 patients. High
CEBPA
methylation group (
CEBPA
high-meth
,
n
=28) and low methylation group (
CEBPA
low-meth
,
n
=165) were defined by using two-way hierarchical clustering. With a median follow-up of 48 months, among the 125 patients receiving standard induction therapy,
CEBPA
high-meth
was associated with better treatment response (complete remission rate 93.3% versus 73.6%,
P
=0.116). In patients with normal karyotype and without
CEBPA
and
NPM1
mutations, the
CEBPA
high-meth
had longer overall survival (OS) than the
CEBPA
low-meth
(
P
=0.028). Multivariate analysis further supported that the
CEBPA
methylation was an independent prognostic factor for disease free-survival (hazard ratio=0.416; 95% confidence interval, 0.223–0.777,
P
=0.006) and OS (hazard ratio=0.406; 95% confidence interval, 0.166–0.996,
P
=0.050). We conclude that
CEBPA
methylation status is a useful prognostic biomarker for AML patients. |
| doi_str_mv | 10.1038/leu.2010.222 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_856785603</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A247036345</galeid><sourcerecordid>A247036345</sourcerecordid><originalsourceid>FETCH-LOGICAL-c515t-d1ccfa7a3c84beb4ee450c40ae8d95045df379d813b239dad2bfc4f842917d0b3</originalsourceid><addsrcrecordid>eNqF0strFDEYAPBBFLut3jxLUKoXZ81zHsd1qQ8o6EFPHkIm-WY3bSbZJjPK_vdm2NVaKUgIIckvz-8rimcELwlmzVsH05Li3KOUPigWhNdVKYQgD4sFbpq6rFrKT4rTlK4wnierx8UJxS2tCeOL4vv64t2XFRpg3O6dGm3wSCWk0C6GjQ9ptBp1NgwqXkNE1qNdNuDHhH7acYsMIB9-BKT0NAIa9uCCNSjf6BoGq54Uj3rlEjw9tmfFt_cXX9cfy8vPHz6tV5elFkSMpSFa96pWTDe8g44DcIE1xwoa0wrMhelZ3ZqGsI6y1ihDu17zvuG0JbXBHTsrXh_2zZe-mSCNcrBJg3PKQ5iSbERV54rZ_yVra4IprbJ88Y-8ClP0-RkZCcIoxzyjlwe0UQ6k9X0Yo9LzlnJFeY1ZxbjIanmPysXkT9LBQ2_z-J0Fr_5asAXlxm0Kbpqjk-7CNweoY0gpQi930eZY7SXBck4OmUMh5-SQOTkyf35809QNYP7g39mQwfkRqKSV66Py2qZbx1ohKl5nVx5cylN-A_H2c-49-BemBc3r</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>835132404</pqid></control><display><type>article</type><title>CEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>Nature Journals Online</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Lin, T-C ; Hou, H-A ; Chou, W-C ; Ou, D-L ; Yu, S-L ; Tien, H-F ; Lin, L-I</creator><creatorcontrib>Lin, T-C ; Hou, H-A ; Chou, W-C ; Ou, D-L ; Yu, S-L ; Tien, H-F ; Lin, L-I</creatorcontrib><description>Hypermethylation of the distal
CEBPA
promoter region has been reported to result in the downregulation of
CEBPA
expression in several malignancies. However, the clinical implication of
CEBPA
hypermethylation in acute myeloid leukemia (AML) remains unclear. To investigate the correlation between
CEBPA
hypermethylation and clinical features in AML, quantitative MassARRAY analyses for
CEBPA
methylation status were performed on a cohort of 193 patients. High
CEBPA
methylation group (
CEBPA
high-meth
,
n
=28) and low methylation group (
CEBPA
low-meth
,
n
=165) were defined by using two-way hierarchical clustering. With a median follow-up of 48 months, among the 125 patients receiving standard induction therapy,
CEBPA
high-meth
was associated with better treatment response (complete remission rate 93.3% versus 73.6%,
P
=0.116). In patients with normal karyotype and without
CEBPA
and
NPM1
mutations, the
CEBPA
high-meth
had longer overall survival (OS) than the
CEBPA
low-meth
(
P
=0.028). Multivariate analysis further supported that the
CEBPA
methylation was an independent prognostic factor for disease free-survival (hazard ratio=0.416; 95% confidence interval, 0.223–0.777,
P
=0.006) and OS (hazard ratio=0.406; 95% confidence interval, 0.166–0.996,
P
=0.050). We conclude that
CEBPA
methylation status is a useful prognostic biomarker for AML patients.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/leu.2010.222</identifier><identifier>PMID: 20927134</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/53/2422 ; 692/699/67/1990/283/1897 ; Analysis ; Biological and medical sciences ; Biomarkers ; Bone marrow ; Cancer Research ; CCAAT-Enhancer-Binding Proteins - genetics ; Chemotherapy ; Critical Care Medicine ; Disease-Free Survival ; DNA Methylation ; Drug dosages ; Epigenetics ; Genetic aspects ; Granulocytes ; Hematologic and hematopoietic diseases ; Hematology ; Hospitals ; Humans ; Intensive ; Internal Medicine ; Leukemia ; Leukemia, Myeloid, Acute - drug therapy ; Leukemia, Myeloid, Acute - genetics ; Leukemia, Myeloid, Acute - mortality ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical laboratories ; Medical prognosis ; Medical sciences ; Medicine ; Medicine & Public Health ; Methylation ; Mutation ; Nuclear Proteins - genetics ; Oncology ; original-article ; Physiological aspects ; Prognosis ; Promoter Regions, Genetic ; Remission (Medicine) ; Translocation, Genetic ; Tumor markers</subject><ispartof>Leukemia, 2011-01, Vol.25 (1), p.32-40</ispartof><rights>Macmillan Publishers Limited 2011</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2011 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c515t-d1ccfa7a3c84beb4ee450c40ae8d95045df379d813b239dad2bfc4f842917d0b3</citedby><cites>FETCH-LOGICAL-c515t-d1ccfa7a3c84beb4ee450c40ae8d95045df379d813b239dad2bfc4f842917d0b3</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/leu.2010.222$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/leu.2010.222$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23955647$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20927134$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, T-C</creatorcontrib><creatorcontrib>Hou, H-A</creatorcontrib><creatorcontrib>Chou, W-C</creatorcontrib><creatorcontrib>Ou, D-L</creatorcontrib><creatorcontrib>Yu, S-L</creatorcontrib><creatorcontrib>Tien, H-F</creatorcontrib><creatorcontrib>Lin, L-I</creatorcontrib><title>CEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>Hypermethylation of the distal
CEBPA
promoter region has been reported to result in the downregulation of
CEBPA
expression in several malignancies. However, the clinical implication of
CEBPA
hypermethylation in acute myeloid leukemia (AML) remains unclear. To investigate the correlation between
CEBPA
hypermethylation and clinical features in AML, quantitative MassARRAY analyses for
CEBPA
methylation status were performed on a cohort of 193 patients. High
CEBPA
methylation group (
CEBPA
high-meth
,
n
=28) and low methylation group (
CEBPA
low-meth
,
n
=165) were defined by using two-way hierarchical clustering. With a median follow-up of 48 months, among the 125 patients receiving standard induction therapy,
CEBPA
high-meth
was associated with better treatment response (complete remission rate 93.3% versus 73.6%,
P
=0.116). In patients with normal karyotype and without
CEBPA
and
NPM1
mutations, the
CEBPA
high-meth
had longer overall survival (OS) than the
CEBPA
low-meth
(
P
=0.028). Multivariate analysis further supported that the
CEBPA
methylation was an independent prognostic factor for disease free-survival (hazard ratio=0.416; 95% confidence interval, 0.223–0.777,
P
=0.006) and OS (hazard ratio=0.406; 95% confidence interval, 0.166–0.996,
P
=0.050). We conclude that
CEBPA
methylation status is a useful prognostic biomarker for AML patients.</description><subject>692/53/2422</subject><subject>692/699/67/1990/283/1897</subject><subject>Analysis</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Bone marrow</subject><subject>Cancer Research</subject><subject>CCAAT-Enhancer-Binding Proteins - genetics</subject><subject>Chemotherapy</subject><subject>Critical Care Medicine</subject><subject>Disease-Free Survival</subject><subject>DNA Methylation</subject><subject>Drug dosages</subject><subject>Epigenetics</subject><subject>Genetic aspects</subject><subject>Granulocytes</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - drug therapy</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Leukemia, Myeloid, Acute - mortality</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical laboratories</subject><subject>Medical prognosis</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methylation</subject><subject>Mutation</subject><subject>Nuclear Proteins - genetics</subject><subject>Oncology</subject><subject>original-article</subject><subject>Physiological aspects</subject><subject>Prognosis</subject><subject>Promoter Regions, Genetic</subject><subject>Remission (Medicine)</subject><subject>Translocation, Genetic</subject><subject>Tumor markers</subject><issn>0887-6924</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0strFDEYAPBBFLut3jxLUKoXZ81zHsd1qQ8o6EFPHkIm-WY3bSbZJjPK_vdm2NVaKUgIIckvz-8rimcELwlmzVsH05Li3KOUPigWhNdVKYQgD4sFbpq6rFrKT4rTlK4wnierx8UJxS2tCeOL4vv64t2XFRpg3O6dGm3wSCWk0C6GjQ9ptBp1NgwqXkNE1qNdNuDHhH7acYsMIB9-BKT0NAIa9uCCNSjf6BoGq54Uj3rlEjw9tmfFt_cXX9cfy8vPHz6tV5elFkSMpSFa96pWTDe8g44DcIE1xwoa0wrMhelZ3ZqGsI6y1ihDu17zvuG0JbXBHTsrXh_2zZe-mSCNcrBJg3PKQ5iSbERV54rZ_yVra4IprbJ88Y-8ClP0-RkZCcIoxzyjlwe0UQ6k9X0Yo9LzlnJFeY1ZxbjIanmPysXkT9LBQ2_z-J0Fr_5asAXlxm0Kbpqjk-7CNweoY0gpQi930eZY7SXBck4OmUMh5-SQOTkyf35809QNYP7g39mQwfkRqKSV66Py2qZbx1ohKl5nVx5cylN-A_H2c-49-BemBc3r</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Lin, T-C</creator><creator>Hou, H-A</creator><creator>Chou, W-C</creator><creator>Ou, D-L</creator><creator>Yu, S-L</creator><creator>Tien, H-F</creator><creator>Lin, L-I</creator><general>Nature Publishing Group UK</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>7QL</scope><scope>7RV</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</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>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20110101</creationdate><title>CEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia</title><author>Lin, T-C ; Hou, H-A ; Chou, W-C ; Ou, D-L ; Yu, S-L ; Tien, H-F ; Lin, L-I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-d1ccfa7a3c84beb4ee450c40ae8d95045df379d813b239dad2bfc4f842917d0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>692/53/2422</topic><topic>692/699/67/1990/283/1897</topic><topic>Analysis</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Bone marrow</topic><topic>Cancer Research</topic><topic>CCAAT-Enhancer-Binding Proteins - genetics</topic><topic>Chemotherapy</topic><topic>Critical Care Medicine</topic><topic>Disease-Free Survival</topic><topic>DNA Methylation</topic><topic>Drug dosages</topic><topic>Epigenetics</topic><topic>Genetic aspects</topic><topic>Granulocytes</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Intensive</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - drug therapy</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemia, Myeloid, Acute - mortality</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical laboratories</topic><topic>Medical prognosis</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methylation</topic><topic>Mutation</topic><topic>Nuclear Proteins - genetics</topic><topic>Oncology</topic><topic>original-article</topic><topic>Physiological aspects</topic><topic>Prognosis</topic><topic>Promoter Regions, Genetic</topic><topic>Remission (Medicine)</topic><topic>Translocation, Genetic</topic><topic>Tumor markers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, T-C</creatorcontrib><creatorcontrib>Hou, H-A</creatorcontrib><creatorcontrib>Chou, W-C</creatorcontrib><creatorcontrib>Ou, D-L</creatorcontrib><creatorcontrib>Yu, S-L</creatorcontrib><creatorcontrib>Tien, H-F</creatorcontrib><creatorcontrib>Lin, L-I</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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>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>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>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><jtitle>Leukemia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, T-C</au><au>Hou, H-A</au><au>Chou, W-C</au><au>Ou, D-L</au><au>Yu, S-L</au><au>Tien, H-F</au><au>Lin, L-I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia</atitle><jtitle>Leukemia</jtitle><stitle>Leukemia</stitle><addtitle>Leukemia</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>25</volume><issue>1</issue><spage>32</spage><epage>40</epage><pages>32-40</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><coden>LEUKED</coden><abstract>Hypermethylation of the distal
CEBPA
promoter region has been reported to result in the downregulation of
CEBPA
expression in several malignancies. However, the clinical implication of
CEBPA
hypermethylation in acute myeloid leukemia (AML) remains unclear. To investigate the correlation between
CEBPA
hypermethylation and clinical features in AML, quantitative MassARRAY analyses for
CEBPA
methylation status were performed on a cohort of 193 patients. High
CEBPA
methylation group (
CEBPA
high-meth
,
n
=28) and low methylation group (
CEBPA
low-meth
,
n
=165) were defined by using two-way hierarchical clustering. With a median follow-up of 48 months, among the 125 patients receiving standard induction therapy,
CEBPA
high-meth
was associated with better treatment response (complete remission rate 93.3% versus 73.6%,
P
=0.116). In patients with normal karyotype and without
CEBPA
and
NPM1
mutations, the
CEBPA
high-meth
had longer overall survival (OS) than the
CEBPA
low-meth
(
P
=0.028). Multivariate analysis further supported that the
CEBPA
methylation was an independent prognostic factor for disease free-survival (hazard ratio=0.416; 95% confidence interval, 0.223–0.777,
P
=0.006) and OS (hazard ratio=0.406; 95% confidence interval, 0.166–0.996,
P
=0.050). We conclude that
CEBPA
methylation status is a useful prognostic biomarker for AML patients.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20927134</pmid><doi>10.1038/leu.2010.222</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Leukemia, 2011-01, Vol.25 (1), p.32-40 |
| issn | 0887-6924 1476-5551 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_856785603 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 692/53/2422 692/699/67/1990/283/1897 Analysis Biological and medical sciences Biomarkers Bone marrow Cancer Research CCAAT-Enhancer-Binding Proteins - genetics Chemotherapy Critical Care Medicine Disease-Free Survival DNA Methylation Drug dosages Epigenetics Genetic aspects Granulocytes Hematologic and hematopoietic diseases Hematology Hospitals Humans Intensive Internal Medicine Leukemia Leukemia, Myeloid, Acute - drug therapy Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - mortality Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical laboratories Medical prognosis Medical sciences Medicine Medicine & Public Health Methylation Mutation Nuclear Proteins - genetics Oncology original-article Physiological aspects Prognosis Promoter Regions, Genetic Remission (Medicine) Translocation, Genetic Tumor markers |
| title | CEBPA methylation as a prognostic biomarker in patients with de novo acute myeloid leukemia |
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