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</svg> Books</a></div><div class="jr-rhead f1 flexh"><div class="head"></div><div class="body"><div class="t">CEBPA-Associated Familial Acute Myeloid Leukemia (PDQ®): Health Professional Version</div><div class="j">PDQ Cancer Information Summaries [Internet]</div></div><div class="tail"></div></div><div id="jr-tb2"><a id="jr-bkhelp-sw" class="btn wsprkl hidden" title="Help with NLM PubReader">?</a><a id="jr-help-sw" class="btn wsprkl hidden" title="Settings and typography in NLM PubReader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 512 512" preserveAspectRatio="none"><path d="M462,283.742v-55.485l-29.981-10.662c-11.431-4.065-20.628-12.794-25.274-24.001 c-0.002-0.004-0.004-0.009-0.006-0.013c-4.659-11.235-4.333-23.918,0.889-34.903l13.653-28.724l-39.234-39.234l-28.72,13.652 c-10.979,5.219-23.68,5.546-34.908,0.889c-0.005-0.002-0.01-0.003-0.014-0.005c-11.215-4.65-19.933-13.834-24-25.273L283.741,50 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id="jr-content"><article data-type="main"><div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><div class="fm-sec"><h1 id="_NBK598327_"><span class="title" itemprop="name">CEBPA-Associated Familial Acute Myeloid Leukemia (PDQ®)</span></h1><div class="subtitle whole_rhythm">Health Professional Version</div><p class="contribs">PDQ Cancer Genetics Editorial Board.</p><p class="fm-aai"><a href="#_NBK598327_pubdet_">Publication Details</a></p></div></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><div id="_abs_rndgid_" itemprop="description"><p id="CDR0000813802__2824">This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the genetics of CEBPA-associated familial AML. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.</p><p id="CDR0000813802__2825">This summary is reviewed regularly and updated as necessary by the PDQ Cancer Genetics Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).</p></div><div id="CDR0000813802__2826"><h2 id="_CDR0000813802__2826_">Introduction and Clinical Manifestations of <i>CEBPA</i>-Associated Familial Acute Myeloid Leukemia (AML)</h2><p id="CDR0000813802__2828">The <i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000045693/" class="def">gene</a> is a granulocytic <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000390290/" class="def">transcription</a> factor (C/EBPα) that serves an important role in myeloid cell differentiation. Somatic mutations in <i>CEBPA</i> occur in approximately 10% to 15% of all AML cases. The presence of two somatic mutations in <i>CEBPA</i> (also known as <i>CEBPA</i>dm) is recognized as a unique clinical entity associated with favorable outcomes, even in the event of relapse.[<a class="bibr" href="#CDR0000813802_rl_2826_1" rid="CDR0000813802_rl_2826_1">1</a>] Germline pathogenic variants in <i>CEBPA</i> were reported in 2004 in a family with hereditary, nonsyndromic AML.[<a class="bibr" href="#CDR0000813802_rl_2826_2" rid="CDR0000813802_rl_2826_2">2</a>] <i>CEBPA</i>-associated <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000460148/" class="def">familial</a> AML (also known as familial AML with a <i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000776887/" class="def">variant</a>) became the second <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000793860/" class="def">autosomal dominant</a> AML <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000754220/" class="def">predisposition syndrome</a> described (<i>RUNX1</i>-familial platelet disorder was the first).[<a class="bibr" href="#CDR0000813802_rl_2826_3" rid="CDR0000813802_rl_2826_3">3</a>]</p><p id="CDR0000813802__3752">Features of <i>CEBPA</i>-associated familial AML include the following:</p><ul id="CDR0000813802__3753"><li class="half_rhythm"><div><b>Highly <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000339344/" class="def">penetrant</a>:</b> Unlike several other myelodysplastic syndromes (MDS)/AML predisposition syndromes, germline <i>CEBPA</i> pathogenic variants appear to be highly penetrant, conferring greater than a 90% lifetime risk to develop AML.[<a class="bibr" href="#CDR0000813802_rl_2826_4" rid="CDR0000813802_rl_2826_4">4</a>-<a class="bibr" href="#CDR0000813802_rl_2826_6" rid="CDR0000813802_rl_2826_6">6</a>] </div></li><li class="half_rhythm"><div><b>Early-onset AML: </b>Germline <i>CEBPA</i> pathogenic variants are associated with early-onset AML that can occur in childhood.[<a class="bibr" href="#CDR0000813802_rl_2826_7" rid="CDR0000813802_rl_2826_7">7</a>] Published research on families with <i>CEBPA</i> germline pathogenic variants have reported that AML onset can occur between the ages of 1.75 to 46 years.</div></li><li class="half_rhythm"><div><b>De novo AML: </b>Inherited <i>CEBPA</i> pathogenic variants can predispose individuals to de novo AML without prior prolonged antecedent cytopenias or multilineage dysplasia.[<a class="bibr" href="#CDR0000813802_rl_2826_2" rid="CDR0000813802_rl_2826_2">2</a>]</div></li><li class="half_rhythm"><div><b>AML similar to somatic <i>CEBPA</i> variant(s): </b>The characteristics of AML arising from a germline <i>CEBPA</i> pathogenic variant are strikingly similar to the characteristics seen in patients with somatic <i>CEBPA</i> mutation(s). These include the following: normal <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000270737/" class="def">cytogenetics</a>, French-American-British (FAB) AML subtypes M1 and M2, numerous Auer rods seen in peripheral blood and bone marrow blasts, and aberrant CD7 expression detected by flow cytometry.[<a class="bibr" href="#CDR0000813802_rl_2826_8" rid="CDR0000813802_rl_2826_8">8</a>]</div></li></ul><div id="CDR0000813802_rl_2826"><h3>References</h3><ol><li><div class="bk_ref" id="CDR0000813802_rl_2826_1">Taskesen E, Bullinger L, Corbacioglu A, et al.: Prognostic impact, concurrent genetic mutations, and gene expression features of AML with CEBPA mutations in a cohort of 1182 cytogenetically normal AML patients: further evidence for CEBPA double mutant AML as a distinctive disease entity. Blood 117 (8): 2469-75, 2011. [<a href="https://pubmed.ncbi.nlm.nih.gov/21177436" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21177436</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_2">Smith ML, Cavenagh JD, Lister TA, et al.: Mutation of CEBPA in familial acute myeloid leukemia. N Engl J Med 351 (23): 2403-7, 2004. [<a href="https://pubmed.ncbi.nlm.nih.gov/15575056" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15575056</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_3">Johns Hopkins University: Online Mendelian Inheritance in Man: CCAAT/Enhancer-Binding Protein, Alpha; CEBPA. Johns Hopkins University, 2022. <a href="https://www.omim.org/entry/116897" ref="pagearea=cite-ref&targetsite=external&targetcat=link&targettype=uri">Available online.</a> Last accessed October 9, 2023.</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_4">Owen C, Barnett M, Fitzgibbon J: Familial myelodysplasia and acute myeloid leukaemia--a review. Br J Haematol 140 (2): 123-32, 2008. [<a href="https://pubmed.ncbi.nlm.nih.gov/18173751" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18173751</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_5">Pabst T, Eyholzer M, Fos J, et al.: Heterogeneity within AML with CEBPA mutations; only CEBPA double mutations, but not single CEBPA mutations are associated with favourable prognosis. Br J Cancer 100 (8): 1343-6, 2009. [<a href="/pmc/articles/PMC2676545/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC2676545</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/19277035" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 19277035</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_6">Renneville A, Roumier C, Biggio V, et al.: Cooperating gene mutations in acute myeloid leukemia: a review of the literature. Leukemia 22 (5): 915-31, 2008. [<a href="https://pubmed.ncbi.nlm.nih.gov/18288131" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18288131</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_7">Tawana K, Wang J, Renneville A, et al.: Disease evolution and outcomes in familial AML with germline CEBPA mutations. Blood 126 (10): 1214-23, 2015. [<a href="https://pubmed.ncbi.nlm.nih.gov/26162409" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 26162409</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2826_8">Nickels EM, Soodalter J, Churpek JE, et al.: Recognizing familial myeloid leukemia in adults. Ther Adv Hematol 4 (4): 254-69, 2013. [<a href="/pmc/articles/PMC3734901/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC3734901</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/23926458" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 23926458</span></a>]</div></li></ol></div></div><div id="CDR0000813802__2827"><h2 id="_CDR0000813802__2827_">Genetics and Molecular Biology of <i>CEBPA</i>-Associated Familial Acute Myeloid Leukemia (AML)</h2><p id="CDR0000813802__2829">The <i>CEBPA</i> gene is located on <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000046470/" class="def">chromosome</a> 19q13.1. Leukemia arising from an <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000809371/" class="def">inherited</a>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000460154/" class="def">germline</a>
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<i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000783960/" class="def">pathogenic variant</a> follows a two-hit mechanism of leukemogenesis. Germline <i>CEBPA</i> pathogenic <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000776887/" class="def">variants</a> cluster in the N-terminus (5’ end) of the <i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000045693/" class="def">gene</a>. The second <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000781854/" class="def">somatic variant</a> (at the C-terminus; 3’ end) is acquired on the other <i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000339337/" class="def">allele</a> (in trans) when leukemia develops.[<a class="bibr" href="#CDR0000813802_rl_2827_1" rid="CDR0000813802_rl_2827_1">1</a>,<a class="bibr" href="#CDR0000813802_rl_2827_2" rid="CDR0000813802_rl_2827_2">2</a>] Interestingly, while the same germline pathogenic variants are present in multiple family members, individuals within families acquire distinct somatic variants in the C-terminus region of <i>CEBPA</i>. In some cases, more than one C-terminus variant can be acquired, suggesting two distinct episodes of AML in one individual.[<a class="bibr" href="#CDR0000813802_rl_2827_3" rid="CDR0000813802_rl_2827_3">3</a>] Patients with <i>CEBPA</i> germline pathogenic variants often acquire <i>GATA2</i> somatic variants when they develop AML.[<a class="bibr" href="#CDR0000813802_rl_2827_4" rid="CDR0000813802_rl_2827_4">4</a>]</p><p id="CDR0000813802__3754">The prevalence of <i>CEBPA</i>-associated <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000460148/" class="def">familial</a> AML, like that of many other inherited AML <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000754220/" class="def">predisposition syndromes</a>, is unknown. However, germline <i>CEBPA</i> pathogenic variants may account for up to 1% of all AML cases, as extrapolated from somatic testing data.[<a class="bibr" href="#CDR0000813802_rl_2827_5" rid="CDR0000813802_rl_2827_5">5</a>,<a class="bibr" href="#CDR0000813802_rl_2827_6" rid="CDR0000813802_rl_2827_6">6</a>] In one series, 2 of 18 patients (11%) with AML and a somatic <i>CEBPA</i> variant (also called <i>CEBPA</i>-mutated AML) were found to carry germline pathogenic variants in the N-terminus of <i>CEBPA</i>.[<a class="bibr" href="#CDR0000813802_rl_2827_7" rid="CDR0000813802_rl_2827_7">7</a>] In a second study, 5 of 71 patients (7%) with <i>CEBPA</i>-mutated AML carried a <i>CEBPA</i> germline pathogenic variant, suggesting that approximately 10% of individuals with <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000775789/" class="def">biallelic</a>
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<i>CEBPA</i>-mutated AML harbor germline pathogenic variants in <i>CEBPA</i>.[<a class="bibr" href="#CDR0000813802_rl_2827_8" rid="CDR0000813802_rl_2827_8">8</a>] Therefore, genetic testing for <i>CEBPA</i> germline pathogenic variants is indicated in any patient who presents with AML and <i>CEBPA</i> somatic variants (particularly biallelic <i>CEBPA</i> somatic variants).</p><div id="CDR0000813802_rl_2827"><h3>References</h3><ol><li><div class="bk_ref" id="CDR0000813802_rl_2827_1">Leroy H, Roumier C, Huyghe P, et al.: CEBPA point mutations in hematological malignancies. Leukemia 19 (3): 329-34, 2005. [<a href="https://pubmed.ncbi.nlm.nih.gov/15674366" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15674366</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_2">Kraft IL, Godley LA: Identifying potential germline variants from sequencing hematopoietic malignancies. Blood 136 (22): 2498-2506, 2020. [<a href="https://pubmed.ncbi.nlm.nih.gov/33236764" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 33236764</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_3">Sellick GS, Spendlove HE, Catovsky D, et al.: Further evidence that germline CEBPA mutations cause dominant inheritance of acute myeloid leukaemia. Leukemia 19 (7): 1276-8, 2005. [<a href="https://pubmed.ncbi.nlm.nih.gov/15902292" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15902292</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_4">Green CL, Tawana K, Hills RK, et al.: GATA2 mutations in sporadic and familial acute myeloid leukaemia patients with CEBPA mutations. Br J Haematol 161 (5): 701-705, 2013. [<a href="https://pubmed.ncbi.nlm.nih.gov/23560626" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 23560626</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_5">Pabst T, Eyholzer M, Fos J, et al.: Heterogeneity within AML with CEBPA mutations; only CEBPA double mutations, but not single CEBPA mutations are associated with favourable prognosis. Br J Cancer 100 (8): 1343-6, 2009. [<a href="/pmc/articles/PMC2676545/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC2676545</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/19277035" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 19277035</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_6">Preudhomme C, Sagot C, Boissel N, et al.: Favorable prognostic significance of CEBPA mutations in patients with de novo acute myeloid leukemia: a study from the Acute Leukemia French Association (ALFA). Blood 100 (8): 2717-23, 2002. [<a href="https://pubmed.ncbi.nlm.nih.gov/12351377" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 12351377</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_7">Pabst T, Eyholzer M, Haefliger S, et al.: Somatic CEBPA mutations are a frequent second event in families with germline CEBPA mutations and familial acute myeloid leukemia. J Clin Oncol 26 (31): 5088-93, 2008. [<a href="https://pubmed.ncbi.nlm.nih.gov/18768433" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18768433</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2827_8">Taskesen E, Bullinger L, Corbacioglu A, et al.: Prognostic impact, concurrent genetic mutations, and gene expression features of AML with CEBPA mutations in a cohort of 1182 cytogenetically normal AML patients: further evidence for CEBPA double mutant AML as a distinctive disease entity. Blood 117 (8): 2469-75, 2011. [<a href="https://pubmed.ncbi.nlm.nih.gov/21177436" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21177436</span></a>]</div></li></ol></div></div><div id="CDR0000813802__2830"><h2 id="_CDR0000813802__2830_">Management and Prognosis for <i>CEBPA</i>-Associated Familial Acute Myeloid Leukemia (AML)</h2><p id="CDR0000813802__2831"><i>CEBPA</i>-associated <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000460148/" class="def">familial</a> AML is similar to <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000339347/" class="def">sporadic AML</a> with somatic <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000775789/" class="def">biallelic</a>
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<i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000776887/" class="def">variants</a> in that both often have a favorable prognosis and preclude the need for hematopoietic stem cell transplant (HSCT). However, in individuals with AML arising from a <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000460154/" class="def">germline</a>
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<i>CEBPA</i>
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<a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000783960/" class="def">pathogenic variant,</a> the HSCT’s purpose is to both treat the AML and to replace the constitutional stem cell population that harbors the AML susceptibility.[<a class="bibr" href="#CDR0000813802_rl_2830_1" rid="CDR0000813802_rl_2830_1">1</a>] Like in all <a href="/books/n/pdqcis/glossary_gen/def-item/glossary_gen_CDR0000809371/" class="def">inherited predispositions</a> to AML, great care needs to be taken to avoid use of a stem cell donor who carries a germline <i>CEBPA</i> pathogenic variant. Donor-derived leukemia has been reported in individuals with <i>CEBPA</i>-associated familial AML who received a transplant, unknowingly, from a donor who carried a <i>CEBPA</i> germline pathogenic variant.[<a class="bibr" href="#CDR0000813802_rl_2830_2" rid="CDR0000813802_rl_2830_2">2</a>] </p><div id="CDR0000813802_rl_2830"><h3>References</h3><ol><li><div class="bk_ref" id="CDR0000813802_rl_2830_1">Stelljes M, Corbacioglu A, Schlenk RF, et al.: Allogeneic stem cell transplant to eliminate germline mutations in the gene for CCAAT-enhancer-binding protein α from hematopoietic cells in a family with AML. Leukemia 25 (7): 1209-10, 2011. [<a href="https://pubmed.ncbi.nlm.nih.gov/21455213" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21455213</span></a>]</div></li><li><div class="bk_ref" id="CDR0000813802_rl_2830_2">Xiao H, Shi J, Luo Y, et al.: First report of multiple CEBPA mutations contributing to donor origin of leukemia relapse after allogeneic hematopoietic stem cell transplantation. Blood 117 (19): 5257-60, 2011. [<a href="https://pubmed.ncbi.nlm.nih.gov/21403128" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21403128</span></a>]</div></li></ol></div></div><div id="CDR0000813802__3751"><h2 id="_CDR0000813802__3751_">Latest Updates to This Summary (11/25/2024)</h2><p id="CDR0000813802__1182">The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.</p><p id="CDR0000813802__3757">Editorial changes were made to this summary.</p><p id="CDR0000813802__disclaimerHP_3">This summary is written and maintained by the <a href="https://www.cancer.gov/publications/pdq/editorial-boards/genetics" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PDQ Cancer Genetics Editorial Board</a>, which is
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editorially independent of NCI. The summary reflects an independent review of
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the literature and does not represent a policy statement of NCI or NIH. More
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information about summary policies and the role of the PDQ Editorial Boards in
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maintaining the PDQ summaries can be found on the <a href="#CDR0000813802__AboutThis_1">About This PDQ Summary</a> and <a href="https://www.cancer.gov/publications/pdq" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PDQ® Cancer Information for Health Professionals</a> pages.
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</p></div><div id="CDR0000813802__AboutThis_1"><h2 id="_CDR0000813802__AboutThis_1_">About This PDQ Summary</h2><div id="CDR0000813802__AboutThis_2"><h3>Purpose of This Summary</h3><p id="CDR0000813802__AboutThis_3">This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about CEBPA-associated familial AML. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.</p></div><div id="CDR0000813802__AboutThis_4"><h3>Reviewers and Updates</h3><p id="CDR0000813802__AboutThis_5">This summary is reviewed regularly and updated as necessary by the <a href="https://www.cancer.gov/publications/pdq/editorial-boards/genetics" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PDQ Cancer Genetics Editorial Board</a>, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).</p><p id="CDR0000813802__AboutThis_22"> Board members review recently published articles each month to determine whether an article should:</p><ul id="CDR0000813802__AboutThis_6"><li class="half_rhythm"><div>be discussed at a meeting,</div></li><li class="half_rhythm"><div>be cited with text, or</div></li><li class="half_rhythm"><div>replace or update an existing article that is already cited.</div></li></ul><p id="CDR0000813802__AboutThis_7">Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.</p><p>The lead reviewers for CEBPA-Associated Familial Acute Myeloid Leukemia are:</p><ul><li class="half_rhythm"><div>Julia Cooper, MS, CGC (Ohio State University)</div></li><li class="half_rhythm"><div>Courtney DiNardo, MD, MSC (University of Texas, M.D. Anderson Cancer Center)</div></li><li class="half_rhythm"><div>Marcin Wlodarski, MD, PhD (St. Jude Children's Research Hospital)</div></li></ul><p id="CDR0000813802__AboutThis_9">Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's <a href="https://www.cancer.gov/contact/email-us" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Email Us</a>. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.</p></div><div id="CDR0000813802__AboutThis_10"><h3>Levels of Evidence</h3><p id="CDR0000813802__AboutThis_11">Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Cancer Genetics Editorial Board uses a <a href="/books/n/pdqcis/CDR0000685387/?report=reader">formal evidence ranking system</a> in developing its level-of-evidence designations.</p></div><div id="CDR0000813802__AboutThis_12"><h3>Permission to Use This Summary</h3><p id="CDR0000813802__AboutThis_13">PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”</p><p id="CDR0000813802__AboutThis_14">The preferred citation for this PDQ summary is:</p><p id="CDR0000813802__AboutThis_15">PDQ® Cancer Genetics Editorial Board. PDQ CEBPA-Associated Familial Acute Myeloid Leukemia. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: <a href="https://www.cancer.gov/publications/pdq/information-summaries/genetics/cebpa-hp-pdq" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">https://www.cancer.gov/publications/pdq/information-summaries/genetics/cebpa-hp-pdq</a>. Accessed <MM/DD/YYYY>. [PMID: 38113348]</p><p id="CDR0000813802__AboutThis_16">Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in <a href="https://visualsonline.cancer.gov/" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Visuals Online</a>, a collection of over 2,000 scientific images.
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</p></div><div id="CDR0000813802__AboutThis_17"><h3>Disclaimer</h3><p id="CDR0000813802__AboutThis_19">The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the <a href="https://www.cancer.gov/about-cancer/managing-care" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Managing Cancer Care</a> page.</p></div><div id="CDR0000813802__AboutThis_20"><h3>Contact Us</h3><p id="CDR0000813802__AboutThis_21">More information about contacting us or receiving help with the Cancer.gov website can be found on our <a href="https://www.cancer.gov/contact" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Contact Us for Help</a> page. Questions can also be submitted to Cancer.gov through the website’s <a href="https://www.cancer.gov/contact/email-us" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Email Us</a>.</p></div></div></div></div><div class="fm-sec"><h2 id="_NBK598327_pubdet_">Publication Details</h2><h3>Author Information and Affiliations</h3><p class="contrib-group"><h4>Authors</h4><span itemprop="author">PDQ Cancer Genetics Editorial Board</span>.</p><h3>Publication History</h3><p class="small">Published online: November 25, 2024.</p><p class="small">Created: <span itemprop="datePublished">December 14, 2023</span>.</p><h3>Version History</h3><ul class="simple-list" style="padding:0"><li><span class="bk_col_itm">NBK598327.2</span> November 25, 2024 (Displayed Version)</li><li><span class="bk_col_itm"><a href="/books/NBK598327.1/?report=reader">NBK598327.1</a></span> December 14, 2023</li></ul><h3>Copyright</h3><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright Notice</a></div></div><h3>Publisher</h3><p><a href="http://www.cancer.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Cancer Institute (US)</a>, Bethesda (MD)</p><h3>NLM Citation</h3><p>PDQ Cancer Genetics Editorial Board. CEBPA-Associated Familial Acute Myeloid Leukemia (PDQ®): Health Professional Version. 2024 Nov 25. In: PDQ Cancer Information Summaries [Internet]. Bethesda (MD): National Cancer Institute (US); 2002-. <span class="bk_cite_avail"></span></p></div><div class="small-screen-prev"></div><div class="small-screen-next"></div></article></div><div id="jr-scripts"><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/libs.min.js"> </script><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.min.js"> </script></div></div>
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