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Review

A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies

by
Sofia Chatzileontiadou
1,
Kassiani Boulogeorgou
2,
Christina Frouzaki
1,
Maria Papaioannou
1,
Triantafyllia Koletsa
2,* and
Evdoxia Hatjiharissi
1,*
1
Division of Hematology, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece
2
Department of Pathology, School of Medicine, Aristotle University of Thessaloniki, University Campus, 54124 Thessaloniki, Greece
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2025, 26(21), 10545; https://doi.org/10.3390/ijms262110545
Submission received: 27 May 2025 / Revised: 25 October 2025 / Accepted: 28 October 2025 / Published: 30 October 2025
(This article belongs to the Section Molecular Biology)
Versions Notes

Abstract

Pre-B-cell leukemia factor 1 (PBX1) is a transcription factor that plays a significant role in various physiological, developmental, and oncogenic processes in humans. The mechanisms and interactions of PBX1 in both solid and hematologic malignancies remain significant areas of study. It was initially found in pre-B-cell acute lymphoblastic leukemia as a result of the chromosomal translocation t(1;19). Over the years, its role in other blood neoplasms has been studied. PBX1 and its variant E2A::PBX1 regulate gene expression that influences cell proliferation and differentiation in hematopoietic lineages. Their interaction with oncogenic partners results in abnormal gene regulation and tumorigenesis. Research has predominantly focused on the role of these factors in leukemias and plasma cell neoplasms, whereas other hematologic neoplasms have been largely overlooked. The potential application of PBX1 as a prognostic and predictive biomarker has recently gained attention. However, further research is needed to fully understand its complex role and how it can be targeted for therapeutic purposes. This review summarizes current knowledge on PBX1’s role in the growth of both mature and immature hematologic neoplasms. Moreover, it focuses on its prospective use as a therapeutic target and to predict prognosis, especially for aggressive neoplasms that do not respond to current therapeutic approaches.

1. Introduction

PBX1, which stands for pre-B-cell leukemia homeobox transcription factor 1, is an important transcription factor that plays a role in many physiological and developmental processes in humans [1]. It was first designated as Prl, an abbreviation for “pre-B-cell leukemia” [2,3]. Later, to prevent confusion with the prolactin gene PRL, it was renamed PBX1 [4].The PBX1 gene is located at chromosome 1q23.3, spanning more than 340 kb [1]. PBX1 is a member of the TALE (Three Aminoacid Loop Extension) family, a class of homeobox transcription factors [5,6]. The TALE class consists of two families, PBC (that includes PBX1-4) and MEINOX (that includes MEIS and PREP proteins) [5,6]. The PBX1 protein consists of 430 amino acids and contains 2 domains, PBC-A and PBC-B, that are the sites through which PBX1 binds to other proteins to carry out its function, and a homeodomain, which mediates DNA binding, and interaction with other proteins [5,6].
The PBX1 protein plays a crucial role in the regulation of gene expression during embryonic development and cell differentiation [1]. It is also essential for maintaining the pluripotency and self-renewal of stem cells and thereby it influences cell fate decisions by direct regulation of the expression of the key transcription factor NANOG [5,7]. A summary on PBX1’s involvement in the regulation of the hematopoietic and immune system is presented in Table 1.
Recent studies indicate that PBX1 is integral to the progression of various cancers [1,8]. Two separate research groups found that the homeobox domain of the gene is part of the chromosomal translocation t(1;19) in pre-B-cell acute lymphoblastic leukemia (ALL) [2,3]. PBX1 and several of its transcriptional targets have been associated with the regulation of signaling pathways involved in cell growth, invasion, metastasis, angiogenesis, resistance to cell death, and alterations in cellular energy utilization [1]. Furthermore, PBX1 may influence tumor-promoting inflammation and immune evasion, although the evidence supporting these claims is less established [1].
Understanding PBX1’s function and role in oncogenesis could aid researchers in identifying biomarkers that could enhance cancer prediction and diagnosis, as well as new therapeutic targets and strategies [8].
This review summarizes the impact of PBX1 on the development of hematologic malignancies, its influence on prognosis, and its potential use as a therapeutic target.

2. The Function of PBX1 in the Hematopoietic System

PBX1 is a proto-oncogene and developmental regulator that maintains the balance between the self-renewal and differentiation of hematopoietic stem cells (HSCs) [9]. It can modulate the growth and differentiation of myeloid progenitors, either accelerating or decelerating these processes temporarily to safeguard its pool [9].
PBX1 is specifically involved in preserving hematopoietic stem cell potential for lymphoid, erythroid, and platelet lineages, to the detriment of other myeloid cell types [10]. PBX1 expression is essential for the differentiation of B-, T-, and NK cells, as well as megakaryocytes, and its deficiency mostly hinders B-cell maturation and megakaryocyte production [11].
PBX1 affects multiple genes associated with the commitment and maturation of B-cells and megakaryocytes, including EBF1, PAX5, GATA1, and FOG1 and through complex transcriptional networks ensures their proper formation and function [10,12,13]. Moreover, through its interaction with MN1 regulates HSC maintenance and self-renewal by participating in transcriptional regulation of target genes [8]. It interacts with genes such as SMAD and Notch, which are essential for T-cell differentiation and maturation [8,14,15,16]. It also regulates the expression of other relevant genes that influence the fate of thymic hematopoietic cells [14,15,16]. It functions as a transcriptional activator of NFIL3, facilitating the formation of natural killer cells [11].
In summary, PBX1 is a multifunctional protein that plays a role in hematopoietic stem cell self-renewal and the development of megakaryocytes, erythrocytes, and B- and T-lymphocytes [10].

3. The Role of PBX1 in Hematologic Neoplasms

The dysregulation of PBX1 has been linked to the initiation and advancement of multiple cancer types via the promotion of tumor cell proliferation through interactions with specific proteins or alterations in the transcription of target genes [1,5,8]. Its significance has been acknowledged in solid tumors, including breast, ovarian, renal, esophageal, and gastric carcinomas. It has also been examined in many hematological neoplasms, specifically multiple myeloma, Hodgkin lymphoma, myeloproliferative neoplasms (MPNs), and B-acute lymphoblastic leukemia (B-ALL) [5,6,17,18,19,20,21,22,23].
PBX1 overexpression occurs for several reasons, such as chromosomal translocations, like the t(1;19) translocation in pre-B-cell leukemia, which creates an oncogenic fusion protein. Aberrant signaling pathways, including those associated with estrogen receptors in breast cancer, can enhance PBX1 expression. Additional factors encompass mutations in regulatory elements or epigenetic alterations that augment PBX1 transcription, leading to its overexpression [6,8,24].
In the context of hematological malignancies, researchers have investigated its functional importance by employing mouse models that either lack PBX1 or have an excess of it [5,20,25,26]. At least ten hematological neoplasms have been linked to its aberrant expression. A summary on PBX1 interactions, which include gene upregulation, transcriptional regulatory complexes and signaling pathways in hematologic malignancies mainly found in mice and cell line experiments is presented in Table 2.

4. PBX1 in Leukemias

The translocation t(1;19) (q23; p13.3), is present in 3–5% of individuals with B-ALL and results in the creation of the E2A::PBX1 chimeric transcription factor [6]. This initial event provides the potential for self-renewal and leads to a susceptibility to further mutations in oncogenes that develop in B-ALL [5,6]. This fusion protein obstructs normal hematopoietic development, leading to the onset of ALL. The genes BMI1, an oncogene associated with lymphoid tissues, and SETDB2, a constituent of the protein lysine methyltransferase (PKMT) family that furthermore promotes the PI3K/AKT/mTOR signaling pathway, are prevalent in pre-B-cell ALL with E2A::PBX1 translocation [6,33,34,35]. In combination, these changes cause pre-B-cells to multiply. Furthermore, E2A::PBX1-mediated gene activation and leukemogenesis depend on how the fusion protein interacts with the MED1 subunit of the Mediator complex and on the coactivation of RUNX1 through direct connection to the PBX1 homeodomain [5,17,36]. This interaction renders the MED1 subunit a potential treatment objective in B-ALL with E2A::PBX1 translocation [5,17,36].
Preclinical evidence indicates that E2A::PBX1 contributes to the proliferation of T-acute lymphoblastic leukemia (T-ALL) in murine models. E2A::PBX1 appears to induce accelerated pro-T-cell proliferation, resulting in T-ALL. Since E2A::PBX1 does not attach to DNA, the process appears to rely on stem cell factors [8,37]. The interaction between E2A::PBX1 and HOX appears to facilitate the oncogenic transformation of T cells and the initiation of T-ALL in murine models [38]. Nevertheless, further investigation is necessary to comprehensively elucidate the essential connection and molecular mechanism [8,37,38].
In mixed-lineage leukemia (MLL)-rearranged ALL, the up-regulation of MEIS1 is crucial for sustaining the proliferation of leukemic cells; this homeobox transcription factor predominantly interacts with PBX1. Downregulation of MEIS1 may alter cellular responses to chemotherapy-induced apoptosis [6,39,40].
Researchers have examined the role of HOX genes (HOXA9 and HOXB3) and MEIS1 in the pathogenesis of acute myeloid leukemia (AML) in murine models. The MEIS1-PBX1 heterodimer seemingly binds to DNA, and their interaction promotes the development of AML by accelerating the leukemic transformation [27,28]. PREP1 is a homeobox protein belonging to the MEIS family that interacts with DNA by forming a heterodimer with PBX1. MEIS1-PBX1 and PREP1-PBX1 dimers can bind to DNA and form trimeric DNA-binding complexes with HOX proteins, which are essential for leukemic proliferation [27,28].
The oncogenic potential of the E2A::PBX1 fusion protein has been investigated in mice, demonstrating its involvement in the progression of AML by promoting the transformation of hematopoietic progenitor cells [41]. The oncogenic activity suggests that E2A::PBX1 interferes with normal differentiation and regulatory mechanisms in myeloid progenitors, facilitating leukemic transformation [41].
Overall, PBX1 promotes leukemogenesis by interacting with many genes, resulting in the dysregulation of self-renewal, proliferation, differentiation, and gene expression programs through epigenetic mechanisms.

5. PBX1 in Myeloproliferative Neoplasms and Myelodysplastic Syndromes

As previously stated, PBX1 is a crucial protein that regulates the equilibrium between self-renewal and differentiation in HSCs. It also influences myeloid progenitors, allowing them to sustain their population [10,23]. In certain MPN patients with the JAK2V617F mutation, an alteration in the copy number of PBX1 was seen [42], accompanied by elevated expression levels in CD34+ cells in Polycythemia Vera (PV) patients [43]. Its involvement in JAK2 signaling was shown in mouse JAK2-deficient HSCs [23,44], and its overexpression in JAK-mutated HSCs appears to contribute to the MPN phenotype in vivo [23,45].
Research on the disease in murine models demonstrated the significant function of PBX1 in JAK2V617F-mutant MPN. In the absence of PBX1, the progression of MPN in mice was attenuated, despite the persistence of JAK2 mutation [23]. Thrombocytosis and leukocytosis were absent in the absence of PBX1, although initial erythrocytosis progressively diminished, and no other MPN-related symptoms were observed [23]. Furthermore, RNA sequencing results validated that PBX1 presence modulates various metabolic pathways affected by the JAK2V617F mutation in HPSCs [23]. This study demonstrates that PBX1 is essential for the maintenance of the malignant clone rather than the initiation of the disease [23].
PBX1 appears to be a significant factor in chronic myeloid leukemia (CML) as it promotes tumor cell proliferation through its interaction with RNF6, a direct target of PBX1 [6,29]. The HNRPDL/PBX1 axis also regulates the proliferation and imatinib sensitivity of CD34+ CML cells [6,29]. Elevated PBX1 levels inhibit cell proliferation through the silencing of HNRPDL [6,29].
Notwithstanding the previously cited data indicating PBX1’s involvement in MPNs, no studies have delineated its role in myelodysplastic syndromes (MDSs). Expression studies indicate that MDSs characterized by increased frequencies of long-term hematopoietic stem cells and multipotent progenitors generally express PBX1 [46].

6. PBX1 in Lymphomas

There is a paucity of data regarding the role of PBX1 in the development of lymphomas. However, the principal finding of PBX1 overexpression in Hodgkin lymphoma (HL) was noted in cell lines, especially in SUP-HD1 cells, a neoplastic Hodgkin-type cell line that secretes IFN-γ [5,22,47]. This overexpression is generally induced by duplication [5]. Biopsy tissue samples from patients with active disease have also been investigated, albeit to a lesser extent [22]. PBX1 stimulates NFIB, an oncogene linked to several neoplasms, in HL cell lines, as demonstrated by elevated NFIB expression levels in the presence of PBX1 and diminished expression following PBX1 knockdown, thereby demonstrating PBX1’s direct regulatory effect on NFIB transcription [22,30]. The upregulation of all four members of the NFI family (NFIA, NFIB, NFIC, and NFIX) in patients with HL suggests their potential influence on disease progression [22]. Further research indicated that TLX2, a member of the NKL homeobox gene family, is an additional target gene of PBX1 in individuals with HL [22]. TLX2 expression in HL cell lines is activated by PBX1, as evidenced by the correlation observed when PBX1 is present and the diminished expression following PBX1 knockdown [22]. The homeobox gene TLX2 belongs to the transcription factor superfamily and is implicated in neural crest differentiation [48]. PBX1 expression is inhibited in progenitor cells of the lymphocytic lineage and is downregulated during B-cell maturation. Thus, the continued presence of PBX1 positivity in mature B-cells may promote lymphoma formation [22].
The dysregulation of PBX1, independently or in combination with the HOXB9 gene, leads to aberrant expression that disturbs B-cell maturation, thereby facilitating malignancy development [22,49]. Modifications of the PBX1 gene have been verified in non-Hodgkin B-cell lymphomas, particularly Burkitt lymphoma and diffuse large B-cell lymphoma (DLBCL). A significant number of instances demonstrate PBX1 fusion with TCF3 [50]. This oncogenic translocation results in aberrant WNT signaling and an increased incidence of hematological neoplasia, impacting EBF3 and the WNT family members RORB and WNT16B [50]. In contrast, the role of PBX1 in the advancement of DLBCL remains predominantly unexamined. A limited group of individuals with DLBCL and bone marrow involvement exhibited the 1q23-q25 translocation and the associated PBX1 genetic mutation [51]. Regarding nodal disease, we are aware of only one documented case of a patient diagnosed with DLBCL and Langerhans cell histiocytosis of the inguinal lymph node [52]. Genetic analyses indicated that the patient exhibited a tetrasomy of PBX1. This genetic abnormality was probably linked to a poor outcome [52]. Finally, research utilizing murine models demonstrated that the E2A::PBX1 translocation is crucial to the pathogenesis of T-cell lymphoma, which differs from T-cell leukemia [8].

7. PBX1 in Multiple Myeloma

Multiple myeloma (MM) is a disease characterized by genetic and clinical heterogeneity [53]. Molecular abnormalities, primarily detected using FISH, are present in the majority of MM patients and are highly suggestive of prognosis [54]. Multiple myeloma often displays the t(4;14) translocation, a chromosomal anomaly linked to an unfavorable prognosis [54]. Previous studies have underscored the pivotal involvement of PBX1 in the pathogenesis of MM, especially in cases involving the t(4;14) translocation [54,55]. In particular, the t(4;14) is associated with the overexpression of PBX1, which in complex with MEIS2 is suggested to be involved in transcriptional regulation mediated by the KLF4 gene, which is specifically overexpressed in t(4;14) patients. [54,55]. This implies that PBX1 is involved in the transcriptional circuits that are linked to this particular molecular lesion in MM [6,54,55].
The genetic amplification of chromosome 1q21, the most prevalent copy number variation in MM, is well recognized as being related with a high disease burden, treatment resistance and dismal prognosis [20]. In addition to the various chr1q21 genes associated with a poor prognosis, other genes located on chr1q have recently been linked to the biology and prognosis of MM [20]. This discovery led to the hypothesis that the impact of chromosome 1q amplification in myeloma could be influenced by different regions along chromosome 1 [20]. A large-scale integrative analysis of clinical and multi-omics datasets revealed novel genes in the chr1q22 and chr1q23.3 regions that predict adverse prognosis for MM patients [20]. For instance, in myeloma cells displaying amplification of chromosome 1, ectopic expression of PBX1, situated at 1q23.3, has been documented [20]. The process involved genetic amplification and epigenetic activation across the entire domain [20]. The PBX1-FOXM1 axis controls critical oncogenic pathways or a transcriptional program that requires FOXM1 to promote cell proliferation [20]. PBX1 increases FOXM1 expression and its target genes, causing treatment resistance and poor prognosis [20]. The decrease in cell viability and cell cycle arrest after this axis disruption shows that it promotes the proliferative phenotype in MM and 1q amplification [20].
Recent research on a single-cell multiomics dataset from MM patients at different stages found proliferative states associated with high-risk cytogenetic events [31]. PHF19, an epigenetic regulator involved in gene expression control and chromatin remodeling, is particularly regulated by PBX1 [31]. PHF19 expression in myeloma cell lines is greatly reduced by PBX1 silencing, although PBX1 amplification on 1q greatly enhances PHF19 levels [31]. The positive regulation of PHF19 by PBX1 affects cell proliferation and contributes to MM development [31]. High PHF19 levels are linked to aggressive disease characteristics such as enhanced proliferation and treatment resistance [31]. Thus, PBX1 and PHF19 may identify high-risk myeloma subtypes, necessitating more intensive treatment [20,31].
Recent studies have focused on the immunological evasion of MM cells from natural killer (NK) cells, specifically exosome-mediated lncRNA NEAT1 [32]. IncRNAs are RNA molecules that engage in biological processes but cannot transcribe into proteins [32]. Multiple myeloma exhibits lncRNA NEAT1 overexpression [32]. In a restricted study, exosomal NEAT1 by downregulating PBX1 via the EZH2/PBX1 pathway, decreases NK-cell activity and lets MM cells avoid immunological detection [32].

8. Clinical Implications and Therapeutic Challenges

PBX1 acts as a major regulator in cancer by orchestrating many oncogenic signaling pathways that facilitate tumor formation and progression [1,6]. In neoplasms, it plays a pivotal role in several processes, including angiogenesis, metastasis, apoptosis, and cellular proliferation and survival [1]. Moreover, PBX1 modulates gene expression and enhances chemoresistance and malignant stem cell characteristics by interacting with other transcription factors [1,6].
Several hematologic malignancies are linked to PBX1. It has been predominantly examined in ALL, a disorder that significantly contributes to leukemogenesis through the formation of the E2A::PBX1 fusion protein [5,6,8]. This protein arises from chromosomal translocation and acts as a powerful oncogene, facilitating the proliferation and survival of leukemic cells [5,6,8]. Information concerning the role of PBX1 in adult lymphomas remains limited, requiring further research [5,21,22]. PBX1 in MM patients with 1q amplification is a subject of considerable interest [19,20]. The overexpression of PBX1 induces FOXM1 upregulation, thereby influencing the biologic behavior of the disease and the proliferation of myeloma cells [19,20]. The PBX1 level may also function as a biomarker in many malignancies. Nonetheless, further standardization and validation of the optimal measuring method are necessary for its application in clinical practice [1,5,6,8].
PBX1 could serve as a therapeutic target due to its interaction with various genes and pathways that facilitate cancer development [6]. This can be accomplished by modifying its activity or focusing on the unique PBX1-mediated pathway [6]. Numerous efforts have been undertaken to target PBX1 in a preclinical context, yielding promising outcomes thus far [6]. The therapeutic strategy of targeting HOX/PBX dimers was advantageous in AML [56]. Cases of B-ALL exhibiting translocation t(1;19) can be also treated with agents that diminish E2A::PBX1 expression [57]. Additionally, drugs that interfere with the PBX1-FOXM1 axis or PBX1 small-molecule inhibitors have been proposed as potential treatment alternatives for chr1q-amp myeloma [19]. T417 is a small molecule that inhibits the transcriptional activity of PBX1 [58]. The compound effectively interferes with PBX1-DNA interactions and thereby destabilizing them and thus reducing the expression of PBX1 target genes [58]. Its potential benefit has been previously reported in other types of cancers [58] and most recently, its selective activity against chr1q21 amplified MM cells has been reported in a preclinical setting [20]. To fully understand the therapeutic potential of PBX1 interactions, further research and clinical studies are necessary [6,8].

9. Conclusions

In conclusion, PBX1 and its variant E2A::PBX1 function as transcription factors, engaging with several proteins, including HOX, MEIS, and PREP, to modulate gene expression. PBX1 is crucial for the regulation of cell proliferation and differentiation in hematopoietic lineages. The complexity of PBX1 makes it a compelling subject for further research to thoroughly elucidate the specific mechanisms by which this molecule governs cellular processes, its influence on the development of both mature and immature hematologic neoplasms, and its viability as a biomarker. Furthermore, to translate initial findings into viable antineoplastic treatments, further clinical studies of PBX1-targeted medicines are necessary. We assert that the development of targeted therapeutics for malignancies associated with PBX1 and E2A::PBX1 will gain significance as research on their oncogenic mechanisms advances.

Author Contributions

S.C. wrote the first draft of the manuscript, contributed to the review design, and edited the final manuscript; K.B. and C.F. assisted in writing sections of the manuscript; M.P. and T.K. contributed to the conception of the review and revised the manuscript; E.H. conceptualized the theme, wrote sections of the manuscript, revised it, and supervised all co-authors in preparing their contributions. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

Not applicable.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
ALLAcute lymphoblastic leukemia
B-ALLB-Acute lymphoblastic leukemia
CMLChronic myeloid leukemia
DLBCLDiffuse large B-cell lymphoma
EBFEarly B-cell factor
FOG1Forkhead box G1
FOXM1Forkhead box protein M1
HLHodgkin lymphoma
HNRPDLHeterogeneous nuclear ribonucleoprotein D-like
HOXHomeobox
HSCsHematopoietic stem cells
lncRNALong noncoding RNAs
MDSMyelodysplastic syndromes
MEIS1Myeloid ecotropic viral integration site 1
MLLMixed lineage leukemia
MMMultiple myeloma
MPNMyeloproliferative neoplasm
NFINuclear factor I
NFIL3Nuclear factor interleukin 3 regulated
NKNatural Killer
PAX5Paired box 5
PBX1Pre-B-cell leukemia factor 1
PHF19PHD finger protein 19
PKMTProtein lysine methyltransferase
PREP1PBX-regulating protein 1
PVPolycythemia vera
RNF6Ring finger protein 6
RORBRAR-related orphan receptor beta
RT-qPCRReal time quantitative polymerase chain reaction
TALEThree amino acid loop extension
T-ALLT-Acute lymphoblastic leukemia
TLX2T-cell leukemia homeobox 2

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Table 1. PBX1’s involvement in the regulation of hematopoietic and immune systems [8].
Table 1. PBX1’s involvement in the regulation of hematopoietic and immune systems [8].
SystemSignaling PathwayFunction
Hematopoietic systemRegulation of EF1, PAX5,
GATA1, FOG1, MN1		Supports HSC self-renewal and differentiation
B-cell and megakaryocyte expansion and maturation
Immune systemUpregulation of the AKT1 pathway via activation by ILT2 receptor
Direct activation of Rtkn2 expression
Direct regulation of CD44 expression		Maturation and function of several immune cells
(NK cells, T reg cells, T cells)
ThymusRegulates PAX1 expression
Interactions with SMAD, Notch		Regulates the proliferation of thymocytes
SpleenUpregulation of Nkx2-5
Downregulation of p15Ink4b		Splenic cell development and function
Table 2. A summary of the main PBX1 interactions in hematologic neoplasms.
Table 2. A summary of the main PBX1 interactions in hematologic neoplasms.
Hematologic NeoplasmGene Upregulation,
Transcriptional Regulators
and Signaling Pathways		Function
Acute lymphoblastic leukemiaE2A::PBX1Impedes normal hematopoiesis [6]
Acute myeloid leukemiaMEIS1-PBX1 interaction
(transcriptional regulatory complex)		Binds to DNA and facilitates leukemic
transformation [27,28]
PREP-PBX1 interactionBinds to DNA and creates complexes with HOX proteins inducing leukemic cell
proliferation [27,28]
Mixed-lineage leukemiaMEIS1 upregulationPrimarily interacts with PBX1 and promotes proliferation of leukemic cells [6]
Philadelphia-negative MPNPBX1 upregulationSustain malignant clone of MPN [23]
Chronic myeloid leukemiaHNRPDL/PBX1 axisControls growth and imatinib sensitivity of CD34+ CML cells [6,29]
Hodgkin lymphomaNFIB upregulationActivated by PBX1 [22,30]
TLX2 upregulationActivated by PBX1 [22,30]
Multiple myelomaPBX1-FOXM1 signaling axisDrives proliferative phenotype in 1q amp MM [20]
PHF19 upregulationPBX1 is a positive regulator of PHF19, which
affects cell proliferation in MM [31]
lncRNA NEAT1 overexpressionInhibits NK-cell activity and therefore
promotes immune escape [32]
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Chatzileontiadou, S.; Boulogeorgou, K.; Frouzaki, C.; Papaioannou, M.; Koletsa, T.; Hatjiharissi, E. A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies. Int. J. Mol. Sci. 2025, 26, 10545. https://doi.org/10.3390/ijms262110545

AMA Style

Chatzileontiadou S, Boulogeorgou K, Frouzaki C, Papaioannou M, Koletsa T, Hatjiharissi E. A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies. International Journal of Molecular Sciences. 2025; 26(21):10545. https://doi.org/10.3390/ijms262110545

Chicago/Turabian Style

Chatzileontiadou, Sofia, Kassiani Boulogeorgou, Christina Frouzaki, Maria Papaioannou, Triantafyllia Koletsa, and Evdoxia Hatjiharissi. 2025. "A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies" International Journal of Molecular Sciences 26, no. 21: 10545. https://doi.org/10.3390/ijms262110545

APA Style

Chatzileontiadou, S., Boulogeorgou, K., Frouzaki, C., Papaioannou, M., Koletsa, T., & Hatjiharissi, E. (2025). A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies. International Journal of Molecular Sciences, 26(21), 10545. https://doi.org/10.3390/ijms262110545

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