B-cell precursor acute lymphoblastic leukaemia with IGH::CEBP rearrangement: what have we learnt over the years?

B-cell precursor acute lymphoblastic leukaemia with IGH::CEBP rearrangement: what have we learnt over the years? | bioRxiv /* */ /* */ <!-- <!-- /*! * yepnope1.5.4 * (c) WTFPL, GPLv2 */ (function(a,b,c){function d(a){return"[object Function]"==o.call(a)}function e(a){return"string"==typeof a}function f(){}function g(a){return!a||"loaded"==a||"complete"==a||"uninitialized"==a}function h(){var a=p.shift();q=1,a?a.t?m(function(){("c"==a.t?B.injectCss:B.injectJs)(a.s,0,a.a,a.x,a.e,1)},0):(a(),h()):q=0}function i(a,c,d,e,f,i,j){function k(b){if(!o&&g(l.readyState)&&(u.r=o=1,!q&&h(),l.onload=l.onreadystatechange=null,b)){"img"!=a&&m(function(){t.removeChild(l)},50);for(var d in y[c])y[c].hasOwnProperty(d)&&y[c][d].onload()}}var j=j||B.errorTimeout,l=b.createElement(a),o=0,r=0,u={t:d,s:c,e:f,a:i,x:j};1===y[c]&&(r=1,y[c]=[]),"object"==a?l.data=c:(l.src=c,l.type=a),l.width=l.height="0",l.onerror=l.onload=l.onreadystatechange=function(){k.call(this,r)},p.splice(e,0,u),"img"!=a&&(r||2===y[c]?(t.insertBefore(l,s?null:n),m(k,j)):y[c].push(l))}function j(a,b,c,d,f){return q=0,b=b||"j",e(a)?i("c"==b?v:u,a,b,this.i++,c,d,f):(p.splice(this.i++,0,a),1==p.length&&h()),this}function k(){var a=B;return a.loader={load:j,i:0},a}var l=b.documentElement,m=a.setTimeout,n=b.getElementsByTagName("script")[0],o={}.toString,p=[],q=0,r="MozAppearance"in l.style,s=r&&!!b.createRange().compareNode,t=s?l:n.parentNode,l=a.opera&&"[object Opera]"==o.call(a.opera),l=!!b.attachEvent&&!l,u=r?"object":l?"script":"img",v=l?"script":u,w=Array.isArray||function(a){return"[object Array]"==o.call(a)},x=[],y={},z={timeout:function(a,b){return b.length&&(a.timeout=b[0]),a}},A,B;B=function(a){function b(a){var a=a.split("!"),b=x.length,c=a.pop(),d=a.length,c={url:c,origUrl:c,prefixes:a},e,f,g;for(f=0;f<d;f++)g=a[f].split("="),(e=z[g.shift()])&&(c=e(c,g));for(f=0;f<b;f++)c=x[f](c);return c}function g(a,e,f,g,h){var i=b(a),j=i.autoCallback;i.url.split(".").pop().split("?").shift(),i.bypass||(e&&(e=d(e)?e:e[a]||e[g]||e[a.split("/").pop().split("?")[0]]),i.instead?i.instead(a,e,f,g,h):(y[i.url]?i.noexec=!0:y[i.url]=1,f.load(i.url,i.forceCSS||!i.forceJS&&"css"==i.url.split(".").pop().split("?").shift()?"c":c,i.noexec,i.attrs,i.timeout),(d(e)||d(j))&&f.load(function(){k(),e&&e(i.origUrl,h,g),j&&j(i.origUrl,h,g),y[i.url]=2})))}function h(a,b){function c(a,c){if(a){if(e(a))c||(j=function(){var a=[].slice.call(arguments);k.apply(this,a),l()}),g(a,j,b,0,h);else if(Object(a)===a)for(n in m=function(){var b=0,c;for(c in a)a.hasOwnProperty(c)&&b++;return b}(),a)a.hasOwnProperty(n)&&(!c&&!--m&&(d(j)?j=function(){var a=[].slice.call(arguments);k.apply(this,a),l()}:j[n]=function(a){return function(){var b=[].slice.call(arguments);a&&a.apply(this,b),l()}}(k[n])),g(a[n],j,b,n,h))}else!c&&l()}var h=!!a.test,i=a.load||a.both,j=a.callback||f,k=j,l=a.complete||f,m,n;c(h?a.yep:a.nope,!!i),i&&c(i)}var i,j,l=this.yepnope.loader;if(e(a))g(a,0,l,0);else if(w(a))for(i=0;i (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0];var j=d.createElement(s);var dl=l!='dataLayer'?'&l='+l:'';j.src='//www.googletagmanager.com/gtm.js?id='+i+dl;j.type='text/javascript';j.async=true;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-M677548'); Skip to main content Home About Submit ALERTS / RSS Search for this keyword Advanced Search New Results B-cell precursor acute lymphoblastic leukaemia with IGH::CEBP rearrangement: what have we learnt over the years? View ORCID Profile A Alqahtani , View ORCID Profile KTM Fung , View ORCID Profile L Marchetti , View ORCID Profile O Heidenreich , View ORCID Profile CJ Harrison , View ORCID Profile AV Moorman , View ORCID Profile LJ Russell doi: https://doi.org/10.1101/2025.09.29.679048 A Alqahtani 1 Biosciences Institute, Wolfson Childhood Cancer Research Centre, Brewery Lane, Newcastle University , Newcastle upon Tyne, NE1 7RU, UK Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for A Alqahtani For correspondence: Lisa.Russell{at}ncl.ac.uk Ahlam.alqahtani{at}ncl.ac.uk KTM Fung 1 Biosciences Institute, Wolfson Childhood Cancer Research Centre, Brewery Lane, Newcastle University , Newcastle upon Tyne, NE1 7RU, UK Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for KTM Fung L Marchetti 1 Biosciences Institute, Wolfson Childhood Cancer Research Centre, Brewery Lane, Newcastle University , Newcastle upon Tyne, NE1 7RU, UK Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for L Marchetti O Heidenreich 2 Princess Máxima Center for Pediatric Oncology , 3584 CS, Utrecht, The Netherlands 3 Dept. Hematology, University Medical Center Utrecht , 3584 CX, Utrecht, The Netherlands Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for O Heidenreich CJ Harrison 4 Leukaemia Research Cytogenomics Group, Centre for Cancer, Translational and Clinical Research Institute, Newcastle University , Newcastle upon Tyne, NE1 7RU, UK Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for CJ Harrison AV Moorman 4 Leukaemia Research Cytogenomics Group, Centre for Cancer, Translational and Clinical Research Institute, Newcastle University , Newcastle upon Tyne, NE1 7RU, UK Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for AV Moorman LJ Russell 1 Biosciences Institute, Wolfson Childhood Cancer Research Centre, Brewery Lane, Newcastle University , Newcastle upon Tyne, NE1 7RU, UK Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for LJ Russell For correspondence: Lisa.Russell{at}ncl.ac.uk Ahlam.alqahtani{at}ncl.ac.uk Abstract Full Text Info/History Metrics Preview PDF Abstract B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) is a haematologic malignancy marked by the rapid proliferation of immature B cells in the bone marrow. While BCP-ALL most commonly affects children aged 1-5 years, it remains the most prevalent subtype of ALL in adolescence and adulthood. Chromosomal translocations involving the immunoglobulin ( IG ) locus and partner genes are proven useful for risk stratification and guiding clinical trials for therapeutic decision. This includes translocations with CCAAT/enhancer-binding proteins (CEBP) , which are particularly rare. This rarity has limited efforts to characterise their genetic and clinical profiles, making risk stratification for IGH::CEBP -rearranged BCP-ALL challenging. In this letter, we review the clinical and demographic characteristics of all reported IGH::CEBP cases prior to 2024 and introduce new cases, with preliminary analysis to encourage further investigation into this poorly understood subtype. This study delivers new insights into the molecular and cytogenetic landscape of IGH::CEBP rearrangements in BCP-ALL, and lays a foundation for further investigation into CEBP family roles in haematopoietic development and leukemogenesis, especially in the context of Down syndrome. Finally, it introduces the ongoing international collaborative effort to assemble the largest known IGH::CEBP cohort for comprehensive risk stratification and prognostic evaluation. B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) is a haematologic malignancy characterised by the rapid growth of immature B cells in the bone marrow. Most BCP-ALL cases are associated with genetic abnormalities such as chromosomal translocations or point mutations 1 , which have prognostic significance. As a result, risk stratification based on chromosomal features plays a critical role in guiding patient management and informing prospective clinical trial protocols 2 , 3 . The identification of immunoglobulin locus (IG) translocations is proven useful for risk stratification 3 . Among these, translocations involving CCAAT enhancer binding proteins ( CEBP ) are particularly rare. The IGH::CEBP fusion was first reported in BCP-ALL by Chapiro et al. (2006) and Akasaka et al. (2007) 4 , 5 . However, the rarity of such cases has limited efforts to characterize their genetic landscape and associated clinical profiles. In this letter, we review all reported cases of IGH::CEBP in BCP-ALL up to 2024 to investigate potential correlations with cytogenetic aberrations, as well as clinical and demographic characteristics. Moreover, we report six new IGH::CEBP cases, in which we correlate their gene expression profile to the major BCP-ALL subtypes, and anticipate the interplay between CEBP family members and the affected pathways. A total of 151 cases, including six new cases from the current study, of BCP-ALL with IGH::CEBP translocations have been reported in the literature prior to 2024 ( Figure 1A ). The majority of these cases involved IGH::CEBPD (n=96), followed by IGH::CEBPA (n=25), IGH::CEBPE (n=17), and IGH::CEBPB (n=13, Figure 1B ). The white blood cell (WBC) count for these cases ranged between 1-190X10 9 /L, with median count at 16.1X10 9 /L. While the male/female ratio across all IGH::CEBP cases was similar (1:1.01, M:50.3%), there were more female cases associated with IGH::CEBPA,::CEBPB , and ::CEBPE compared to IGH::CEBPD (1:1.6, M:38%, Figure 1C ). The median age at diagnosis across all IGH::CEBP cases was 15 years (average: 19.6 years; range: 2-76 years). However, when considering the involvement of each CEBP partner gene, it was apparent that the IGH::CEBPD rearrangements were more prevalent in younger patients (median age: 13 years; average: 16 years; Figure 1D ). This difference in age distribution was statistically significant when compared to cases involving all other CEBP partners (Mann– Whitney U test, p < 0.001). In contrast, individuals with IGH::CEBPA had a median age at diagnosis of 28 years (average: 32.2 years), those with IGH::CEBPB had a median of 26.3 years (average: 24.3 years), and those with IGH::CEBPE had a median of 16 years (average: 24.4 years; Figure 1D ). Download figure Open in new tab Figure 1: Oncoplot of IGH::CEBP rearranged BCP-ALL cases reported between 1982 and 2024. A) Clinical and cytogenetic features of the reported IGH-CEBP rearrangement cases in BCP-ALL (n=151). B) Frequencies of genetic subtypes involving an IGH translocation with a member of the CEBP gene family: CEBPA (n=25), CEBPB (n=13), CEBPD (n=96), and CEBPE (n=17). C) Gender distribution across IGH::CEBP subtypes. D) Age range distribution across different IGH::CEBP gene fusion cases. The association of IGH::CEBP with Down syndrome (DS) in BCP-ALL has been previously reported and linked to poorer outcome 6 . In our analysis, 42% of cases with IGH::CEBPD occurred in individuals with DS; much higher than the overall rate of DS in ALL cohorts of <5% 7 . This percentage increased to 52% when including individuals with somatic gain of chromosome 21 (+21). As DS patients have a constitutional trisomy 21, the expected 47 chromosomes were observed in 73% of the cases and the remaining cases had either shown 48-49 chromosomes (22%) or 46 chromosomes (5%). The karyotype of these cases was referred to as normal (N), low hyperdiploid (HeL) and high hypodiploidy (HoH), respectively ( Figure 1A ). The DS-associated cases were found in individuals under 24 years of age, potentially explaining the observed enrichment of younger patients in the IGH::CEBPD subgroup. In contrast, translocations involving IGH and other CEBP family members showed lower prevalence in DS-ALL patients or patients with somatic gain of chromosome 21 - 12% in IGH::CEBPA and 18% in IGH::CEBPE . These findings suggest a possible unique role for CEBPD in the leukemogenesis of DS-associated BCP-ALL. Further investigation is required to elucidate the mechanisms by which CEBPD contributes to leukemic transformation in the context of DS. Cytogenetic aberrations, such as trisomy 6 or deletions of chromosome 6, have been observed in a subset of ALL cases 8 , 9 . In the cohort of cases with IGH::CEBPA , we identified two instances with trisomy 6 and two additional instances with chromosome 6 deletion, distributed among IGH::CEBPD and::CEBPE cases ( Figure 1A ). The gain of chromosome 6 in one IGH::CEBPA case was associated with high hyperdiploid (HeH) karyotype, a feature that has been linked to favourable prognosis in ALL 8 . However, the deletions of 6q21, which includes several known tumour-suppressor genes, could contributed to malignant transformation or proliferation 9 . In addition, chromosome 8 abnormalities were identified in 14 IGH::CEBP cases. Of these, 6 showed gain of chromosome 8 (in which two were associated with HeH, another two with HeL, one with HoH and one with normal diploidy), another 6 had complete deletion of chromosome 8, and 2 exhibited either an isochromosome i(8)(q10) or isodicentric chromosome idic(8)(p11). These alterations were distributed across IGH::CEBPA (n=3), :: CEBPB (n=4), and ::CEBPD (n=7) cases ( Figure 1A ). Many of these cases (n=10/14) occurred in adults, similar to the previously reported cases of chromosome 8q24 aberrations being more frequent in adult ALL 10 . Somatic gain of chromosome 14 or trisomy 14 is relatively common in hyperdiploid BCP-ALL. In our cohort, we noted trisomy 14 presence in 7 cases, primarily associated with IGH::CEBPD and occurring in the context of a HeL karyotype (n=6/7, Figure1A ). Moreover, in 16 IGH::CEBPD cases, the translocation between chromosomes 14 and CEBPD resulted in a derivative chromosome 14. This indicates that the centromere of chromosome 14 was retained, placing CEBPD under the regulatory control of the IGH super-enhancers, and leading to overexpression of CEBPD ( Figure 1A ). These findings highlight the need for further investigation to elucidate the biological and clinical implications of these chromosomal alterations in IGH::CEBP driven BCP-ALL. The Philadelphia chromosome, resulting from the reciprocal translocation, t(9;22)(q34;q11), and generating the BCR::ABL1 fusion, was identified in 7% of all reported IGH::CEBP cases (n=10/151). This was most prominent in IGH::CEBPD , where it occurred in 8% of cases (n=8/96, Figure 1A ). Interestingly, all these cases were exclusive from DS and in patients under the age of 15 years old, which appeared to be higher than the reported percentage (3-5%) for BCR::ABL1 fusion in paediatric ALL 11 . The coexistence of BCR::ABL1 and IGH::CEBP rearrangements remains largely unknown and may have significant implications for both disease pathogenesis and prognosis. The BCR::ABL1 fusion leads to persistently enhanced tyrosine kinase activity, whereas CEBP gene fusions result in aberrant overexpression of transcription factors critical for hematopoietic differentiation. Together, these alterations may synergistically disrupt normal B-cell development and function, contributing to the initiation and progression of BCP-ALL. In this preliminary study, we analysed the transcriptome of 7 cases with IGH::CEBP rearrangements from a larger cohort of 188 BCP-ALL cases, including 182 cases from EGAS00001001795 12 and 6 new cases we collected ( Figure 1A ). RNA sequencing was performed on diagnostic samples, and molecular subtyping was conducted based on gene expression profiling with reference to Li et al. (2018) 13 . In total, we identified eight distinct molecular subtypes of BCP-ALL, visualized using uniform manifold approximation and projection (UMAP; Figure 2A ). The IGH::CEBP cases were distributed across two clusters, including one associated with hyperdiploid expression profile. The hyperdiploid cluster included cases with HeL, HeH, and TT karyotypes. To further explore molecular changes among the IGH::CEBP cases, we performed hierarchical clustering based on the top 300 differentially expressed genes (DEGs). This analysis revealed that the five cases of IGH::CEBPB (n=1), ::CEBPD (n=3), and ::CEBPE (n=1), exhibited a similar gene expression signature. In contrast, the two IGH::CEBPA cases formed a separate cluster, indicating a distinct transcriptional profile ( Figure 2B ). Furthermore, KEGG pathway analysis of the top 300 DEGs identified significant enrichment in pathways related to cancer and transcriptional deregulation in cancer ( Figure 2C ). In the three cases of IGH::CEBPD , there were two cases with DS (Asterisk in Figure 2B ). The hierarchical clustering indicated that the two DS-associated IGH::CEBPD cases shared a similar gene expression signature, while the non-DS case showed greater similarity to the IGH::CEBPE case ( Figure 2B ). Moreover, the two DS-associated IGH::CEBPD cases exhibited higher CEBPD expression levels compared to the third case without DS (asterisk in Figure 2D ). Overexpression of CEPBD in a DS mouse model was reported to alter the genetic context of B cell development, resulting in a persistent predominance of pro-B cells. In contrast, CEBPD overexpression in wild-type controls promoted increased B-lineage differentiation 6 . Hence, these findings could suggest that the combination of CEBPD overexpression and trisomy 21 may contribute to distinct gene expression patterns in DS-associated IGH::CEBPD , potentially increasing susceptibility to BCP-ALL. Further investigation is needed to elucidate the biological mechanisms underlying this interaction in human cells and to determine its potential impact on dysregulating B cell development in BCP-ALL. Download figure Open in new tab Figure 2: Transcriptomic and genomics of IGH::CEBP cases. A) Gene expression of 188 BCP-ALL cases visualized by UMAP, showing the IGH::CEBP cases (n=7, Green) distributed across different clusters. IGH::CEBPA cases were clustered separately from the other IGH::CEBP cases. The average silhouette score was used to generate this 2-dimensional UMAP. Clusters and CEBP cases are shown in different colours. B) Hierarchical clustering of the IGH::CEBP cases identified that the two IGH::CEBPA cases had a unique gene expression signature (padj > 0.01) compared to the other IGH::CEBP cases. Remarkably, the IGH::CEBPD cases with DS clustered together, separate from the IGH::CEBPD without DS. C) KEGG pathway analysis of the top 300 DEGs in IGH::CEBP cases showed enrichment for pathways involved in cancer and transcriptional dysregulation. D) Heatmap presenting differences in gene expression between IGH::CEBP cases. Interestingly, IGH::CEBPD cases with DS showed high expression of CEBPD compared to the IGH::CEBPD case without DS. Moreover, expression of CEBPG , which is involved in the tight regulation of B cell development, was high in the two IGH::CEBPA cases and this can potentially contribute to their distinct expression profile (see panel B). E) Protein–protein interaction analysis using the STRING database was performed to investigate the functional interactions among CEBP family members and their associated proteins. A maximum of 10 interactors were included, filtered by a high-confidence interaction score (>0.7). Yellow: Textmining, purple: experiments, blue: database, light purple: homology. F) KEGG pathway analysis of CEBP family members and their associated proteins revealed enrichment in pathways related to transcriptional dysregulation and acute myeloid leukaemia. B cell development involves tight regulation of CEBP family members 14 , 15 . While CEBPγ and possibly CEBPζ can act as negative regulators of other CEBP proteins— modulating their transcriptional activity through inhibitory interactions 15 , 16 — their roles in B cell development or BCP-ALL remain largely unknown. Therefore, we examined the expression of these negative regulators in IGH::CEBP cases to determine whether they might influence the unique genomic features observed in these cases. Remarkably, CEBPG was specifically overexpressed in IGH::CEBPA cases (n=2), while increased expression of CEBPZ was observed in both IGH::CEBPB (n=1) and DS-associated CEBPD cases (n=2/3, Figure 2D ). This hence may suggest a role for these inhibitors in the modulating other CEBP family member activities. The functional protein associations of CEBP family members were analysed using the STRING database ( https://string-db.org ). This analysis revealed that CEBPα and CEBPβ were central nodes in the network, associated with each other and with other CEBP family members—including CEBPγ (for both), CEBPε (for CEBPα), and CEBPδ (for CEBPβ). However, CEBPδ and CEBPε showed no interactions with each other or with CEBPγ ( Figure 2E ). We included the top ten interacting proteins with high-confidence interaction scores (≥0.7), which encompassed factors involved in lymphoid and myeloid lineage development, such as SPI1, ATF4/5, and DDIT3 ( Figure 2E ). This network was most significantly enriched for KEGG pathways related to transcriptional dysregulation in cancer, carcinogenesis, and acute myeloid leukaemia—consistent with the pathway enrichment observed in the IGH::CEBP cases ( Figure 2F ). Therefore, the interaction profile of CEBP family members highlights their central role in transcriptional regulation pathways implicated in haematopoietic development and leukemic transformation. Altogether, this study provides new insights into the molecular and cytogenetic landscape of IGH::CEBP rearrangements in BCP-ALL. Although most reported cases lack comprehensive treatment information and outcome data, making it difficult to assess prognostic implications and inform risk stratification, we are conducting an international study to assemble a larger cohort of IGH::CEBP cases to address these gaps. In addition, our findings highlight the clinical and biological heterogeneity of IGH::CEBP fusions and emphasise on the need for further investigation into their role in B-cell development, particularly in the context of DS and co-occurring genetic alterations. Conflict of interest The authors have declared that no competing interests exist. Acknowledgements We would like to thank the Blood cancer UK (BCUK, 24012) for funding this project. Funder Information Declared Blood Cancer UK, https://ror.org/0055acf80 , BCUK, 24012 Reference 1. ↵ Purizaca , J. , Meza , I. & Pelayo , R. Early Lymphoid Development and Microenvironmental Cues in B-cell Acute Lymphoblastic Leukemia . Arch Med Res 43 , 89 – 101 ( 2012 ). OpenUrl PubMed 2. ↵ Harrison , C. J. The detection and significance of chromosomal abnormalities in childhood acute lymphoblastic leukaemia . Blood Rev 15 , 49 – 59 ( 2001 ). OpenUrl CrossRef PubMed 3. ↵ Bomken , S. et al. Molecular characterization and clinical outcome of B-cell precursor acute lymphoblastic leukemia with IG-MYC rearrangement . Haematologica 108 , 717 – 731 ( 2023 ). OpenUrl PubMed 4. ↵ Akasaka , T. et al. Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) . ( 2007 ) doi: 10.1182/blood-2006-08 . OpenUrl CrossRef 5. ↵ Chapiro , E. et al. Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia . Blood 108 , 3560 – 3563 ( 2006 ). OpenUrl Abstract / FREE Full Text 6. ↵ Li , Z. et al. Genomic landscape of Down syndrome–associated acute lymphoblastic leukemia . Blood 142 , 172 – 184 ( 2023 ). OpenUrl CrossRef PubMed 7. ↵ Maloney , K. W. et al. Down syndrome childhood acute lymphoblastic leukemia has a unique spectrum of sentinel cytogenetic lesions that influences treatment outcome: a report from the Children’s Oncology Group . Blood 116 , 1045 – 50 ( 2010 ). OpenUrl Abstract / FREE Full Text 8. ↵ Jackson , J. F. et al. Favorable prognosis associated with hyperdiploidy in children with acute lymphocytic leukemia correlates with extra chromosome 6. A pediatric oncology group study . Cancer 66 , 1183 – 1189 ( 1990 ). OpenUrl CrossRef PubMed 9. ↵ Hayashi , Y. et al. Abnormalities of the long arm of chromosome 6 in childhood acute lymphoblastic leukemia . Blood 76 , 1626 – 1630 ( 1990 ). OpenUrl Abstract / FREE Full Text 10. ↵ Davey , F. R. et al. Morphologic characteristics of acute lymphoblastic leukemia (ALL) with abnormalities of chromosome 8, band q24 . Am J Hematol 40 , 183 – 191 ( 1992 ). OpenUrl PubMed 11. ↵ Cario , G. et al. BCR-ABL1-like acute lymphoblastic leukemia in childhood and targeted therapy . Haematologica 105 , 2200 – 2204 ( 2020 ). OpenUrl PubMed 12. ↵ Lilljebjörn , H. et al. Identification of ETV6-RUNX1-like and DUX4-rearranged subtypes in paediatric B-cell precursor acute lymphoblastic leukaemia . Nat Commun 7 , 11790 ( 2016 ). OpenUrl CrossRef PubMed 13. ↵ Li , J.-F. et al. Transcriptional landscape of B cell precursor acute lymphoblastic leukemia based on an international study of 1,223 cases . Proceedings of the National Academy of Sciences 115 , ( 2018 ). 14. ↵ Hu , H.-M. et al. The C/EBP bZIP Domain Can Mediate Lipopolysaccharide Induction of the Proinflammatory Cytokines Interleukin-6 and Monocyte Chemoattractant Protein-1 . Journal of Biological Chemistry 275 , 16373 – 16381 ( 2000 ). OpenUrl Abstract / FREE Full Text 15. ↵ Parkin , S. E. , Baer , M. , Copeland , T. D. , Schwartz , R. C. & Johnson , P. F. Regulation of CCAAT/Enhancer-binding Protein (C/EBP) Activator Proteins by Heterodimerization with C/EBP γ (Ig/EBP) . Journal of Biological Chemistry 277 , 23563 – 23572 ( 2002 ). OpenUrl Abstract / FREE Full Text 16. ↵ Cooper , C. , Henderson , A. , Artandi , S. , Avitahl , N. & Calame , K. Ig/EBP (C/EBP γ ) is a transdominant negative inhibitor of C/EBP family transcriptional activators . Nucleic Acids Res 23 , 4371 – 4377 ( 1995 ). OpenUrl CrossRef PubMed Web of Science View the discussion thread. Back to top Previous Next Posted October 01, 2025. Download PDF Email Thank you for your interest in spreading the word about bioRxiv. NOTE: Your email address is requested solely to identify you as the sender of this article. Your Email * Your Name * Send To * Enter multiple addresses on separate lines or separate them with commas. You are going to email the following B-cell precursor acute lymphoblastic leukaemia with IGH::CEBP rearrangement: what have we learnt over the years? Message Subject (Your Name) has forwarded a page to you from bioRxiv Message Body (Your Name) thought you would like to see this page from the bioRxiv website. Your Personal Message CAPTCHA This question is for testing whether or not you are a human visitor and to prevent automated spam submissions. Share B-cell precursor acute lymphoblastic leukaemia with IGH::CEBP rearrangement: what have we learnt over the years? A Alqahtani , KTM Fung , L Marchetti , O Heidenreich , CJ Harrison , AV Moorman , LJ Russell bioRxiv 2025.09.29.679048; doi: https://doi.org/10.1101/2025.09.29.679048 Share This Article: Copy Citation Tools B-cell precursor acute lymphoblastic leukaemia with IGH::CEBP rearrangement: what have we learnt over the years? A Alqahtani , KTM Fung , L Marchetti , O Heidenreich , CJ Harrison , AV Moorman , LJ Russell bioRxiv 2025.09.29.679048; doi: https://doi.org/10.1101/2025.09.29.679048 Citation Manager Formats BibTeX Bookends EasyBib EndNote (tagged) EndNote 8 (xml) Medlars Mendeley Papers RefWorks Tagged Ref Manager RIS Zotero Tweet Widget Facebook Like Google Plus One Subject Area Cancer Biology Subject Areas All Articles Animal Behavior and Cognition (7622) Biochemistry (17648) Bioengineering (13870) Bioinformatics (41880) Biophysics (21423) Cancer Biology (18553) Cell Biology (25458) Clinical Trials (138) Developmental Biology (13364) Ecology (19866) Epidemiology (2067) Evolutionary Biology (24290) Genetics (15589) Genomics (22475) Immunology (17711) Microbiology (40326) Molecular Biology (17145) Neuroscience (88471) Paleontology (666) Pathology (2826) Pharmacology and Toxicology (4815) Physiology (7635) Plant Biology (15114) Scientific Communication and Education (2044) Synthetic Biology (4286) Systems Biology (9815) Zoology (2268)