Analysis of microRNA expression as a discriminatory factor between Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia

Analysis of microRNA expression as a discriminatory factor between Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 13 October 2025 V1 Latest version Share on Analysis of microRNA expression as a discriminatory factor between Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia Authors : Karla V. Maia de Queiroz 0009-0003-4073-2054 [email protected] , Eldevan da Silva Barbosa , Emerson Jhony C. Botelho , Ágatha Tereza Miranda Tavares , Lucas Brabo Rotella , Márcio Santana de Aquino , Yasmin de Souza dos Santos , Jaqueline Diniz Pinho , Bruna Claudia Meireles Khayat , and André Salim Khayat Authors Info & Affiliations https://doi.org/10.22541/au.176034619.96817178/v1 167 views 124 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Introduction: MicroRNAs (miRNAs) have been widely studied in various pathologies, especially in cancer, due to their ability to regulate the gene expression of mRNA. Evidence indicates that these biomolecules have been previously described in Acute Myeloid Leukemia (AML) and Acute Lymphoblastic Leukemia (ALL), which are malignant hematological neoplasms characterized by the excessive proliferation of blasts in the bone marrow. In this context, the aim was to identify the main miRNAs deregulated in these types of cancer, highlighting potential biomarkers capable of assisting in the differentiation between ALL and AML. Methods: To achieve this, an in silico analysis was conducted using the miR2Disease platform to identify differentially expressed miRNAs between ALL and AML. The data obtained were later validated on the miRBase platform. Additionally, a functional analysis was conducted using the STRING software and a literature review to deepen the understanding of the biological mechanisms involved in the differentiation between acute leukemias. Results: Five major miRNA families (miR-128, let-7, miR-203, miR-223, and miR-155) with expression profiles associated with leukemia were identified. These miRNAs act both as OncomiRs (with oncogenic function) and as TSmiRs (with tumor-suppressive function), playing relevant biological roles such as inducing apoptosis, inhibiting oncogenes, regulating cell proliferation, and self-renewal. Notably, the overexpression of miR-155 in both leukemias, which is associated with an unfavorable prognosis, is highlighted. Conclusion: The differential expression of specific miRNAs emerges as an important discriminative factor between ALL and AML, contributing to more accurate diagnoses, more reliable prognoses, and the enhancement of therapeutic strategies. INTRODUCTION Leukemias are types of blood neoplasms that originate from abnormalities in hematopoietic stem cells in the bone marrow in precursors of the myeloid and lymphoid lineages, which lead to excessive proliferation and interruption of cell death of such cells [1]. These malignancies are classified into: acute myeloid leukemia (AML), chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL), and chronic lymphocytic leukemia (CLL). Acute leukemias are characterized by the rapid proliferation of immature and undifferentiated hematopoietic cells, called blasts, which accumulate in the bone marrow and interfere with the production of erythrocytes and platelets in the blood [2]. In recent years, it has become evident that this dysregulated proliferation and impaired differentiation are not solely the result of genetic mutations, but also involve epigenetic and post-transcriptional regulatory mechanisms. Among these, microRNAs (miRNAs) have gained particular attention, as they act as fine modulators of gene expression and can influence key cellular processes such as proliferation, apoptosis, and differentiation. Altered miRNA expression profiles have been consistently associated with the development and progression of various hematological malignancies, including acute leukemias [20]. MiRNAs are small non-coding RNAs that regulate post-transcriptional gene expression of mRNAs, functioning as essential regulators of cellular homeostasis and being linked to the pathogenesis of multiple human diseases. The complex interaction between miRNAs, their target mRNAs, and other competing endogenous RNAs highlights the dynamic and conditional nature of this regulation, still little explored by the literature; they perform essential functions during normal hematopoiesis, interfering with the self-renewal processes of stem cells and the cellular differentiation of the myeloid and lymphoid lineages [1,3]. AML is more common in adults, while ALL is more common in the pediatric population; and the association of miRNAs between these subtypes may act as a discrimination factor for classification and diagnosis. As an example, it is noteworthy that miR-128a (now 128-1 ), miR-128b ( 128-2 ), and miR128-3p are highly expressed in ALL, while let-7b and miR-223 can be differentially expressed in AML [4]. Thus, the analysis of the miRNA expression profile could allow the identification of specific sets of miRNAs whose distinct expression could indicate differences between patients with ALL and AML, potentially becoming promising biomarkers and influencing the prognosis, diagnosis, and choice of the best treatment for acute leukemias. This study aimed to analyze the expression levels of miRNAs and their associated functions and impacts on the types of leukemia studied in this work. In addition, it intends to investigate miRNAs that are associated with ALL or AML, as well as to identify the impacts between miRNA families and the types of leukemia of interest and the target genes that interact with such miRNAs. MATERIALS AND METHODS 1. General Structure The methodology of this study was structured into two main stages: the identification of miRNAs associated with ALL and AML, followed by the functional analysis of the pathways in which these miRNAs are involved. 2. Identification of microRNAs Initially, a search was conducted in the miR2Disease database ([http://www.mir2disease.org/](http://www.mir2disease.org/)), aiming to identify miRNAs differentially expressed between ALL and AML, as well as those already previously associated with these hematological neoplasms. Subsequently, the data obtained were refined and deepened through the miRBase platform ([https://www.mirbase.org/](https://www.mirbase.org/)), which allowed the confirmation of the updated nomenclature of the miRNAs, as well as obtaining additional information about their biogenesis, variants, and known functions, these informations were organized in two tables. 3. Functional analysis of molecular pathways A functional analysis of the molecular pathways associated with these miRNAs was conducted using the STRING software ([https://string-db.org/](https://string-db.org/)), a tool that allows the visualization of interactions between proteins and target genes, in addition to indicating the metabolic and signaling pathways potentially regulated by the miRNAs in question. 4. Integration of findings The integrated approach enabled the identification of relevant molecular targets and contributed to the understanding of the biological mechanisms involved in the differentiation and progression of acute leukemias. 5. Validation through literature review To validate and complement the findings, a review of the scientific literature available in databases such as PubMed was carried out, including only original articles or systematic reviews from the last 10 years, using combinations of terms in the format: “ miR-128 AND ALL OR AML”, “ let-7 AND ALL OR AML”, “ miR-203 AND ALL OR AML”, “ miR-223 AND ALL OR AML”, “ miR-155 AND ALL OR AML”, in addition to complementary combinations such as “\[microRNA] AND leukemia AND pathway”, “\[microRNA] AND leukemia AND target genes” and “\[microRNA] AND leukemia AND functional analysis”. This strategy aimed to confirm the clinical and experimental relevance of the identified miRNAs, as well as to explore their biological roles in different leukemic contexts. RESULTS Following the database analysis, five families of miRNAs were identified as particularly relevant in acute leukemias: miR-128, let-7, miR-203, miR-223, and miR-155 (Table 1). Complementarily, Table 2 illustrates how these miRNAs are related to specific gene fusions, highlighting their potential role in leukemogenesis. TABLE 1 Results from in silico analysis of public databases, showing five miRNA families (miR-128, let-7, miR-203, miR-223, and miR-155) that stand out as key regulators in acute leukemias. miR-128 Higher in ALL (especially in B cells) Regulates the tumor suppressor PHF6 ; affects sensitivity to glucocorticoids Important biomarker for understanding the complexity of leukemia Potential diagnostic marker for ALL Long-term survival indicator in ALL Associated with treatment sensitivity; Higher levels restore sensitivity to glucocorticoids and prednisolone let-7 Commonly overexpressed in AML Regulates AML1:;ETO ; inhibits oncogenes such as c-Myc and RAS Significant correlation with AML Not specifically mentioned Prognostic biomarker in AML; Better outcomes in patients with stem cell transplantation Associated with a better treatment response in AML miR-203 Negatively regulated in ALL and AML Acts as a tumor suppressor; Inhibits cell proliferation and self-renewal Lower levels associated with low survival rates in AML Potential diagnostic marker for AML Poor prognosis with lower serum levels; Distinguishes AML from healthy controls Potential therapeutic target; restoration may inhibit leukemia growth miR-223 Negatively regulated in ALL and AML Acts as a tumor suppressor; Induces apoptosis in leukemic cells Potential therapeutic indicator Limited use in diagnosis Potential indicator of treatment response Therapeutic potential in AML and ALL; Induces apoptosis of leukemic cells miR-155 Overexpressed in ALL and AML Promotes proliferation by inhibiting ZNF238 ; Affects signaling pathways ( mTOR, WNT) Associated with aggressive disease phenotype and treatment resistance Not specifically mentioned Poor prognosis in both types of leukemia; Linked to aggressive diseases Silencing improves sensitivity to antileukemic drugs Abbreviations: miRNA, microRNA; ALL, acute lymphoblastic leukemia; AML, acute myeloid leukemia. miR-128 family The miRNAs miR-128a (currently named 128-1 ), miR-128b ( 128-2 ), and miR-128-3p are differentially expressed in ALL and AML. In ALL, especially the B-type, the three miRNAs show significantly higher expression levels compared to AML. Despite the overexpression in ALL being a common factor among the miRNAs of the 128 family, their functions differ. let-7 family The let-7 family, especially let-7b , was differentially expressed in AML compared to ALL. miR-203 and miR-223 The negative regulation of these miRNAs is present in both ALL and AML. miR-203 , specifically, proved to be a crucial factor in both neoplasms, performing several significant functions, even though the negative regulation of miR-203 in ALL is related to a specific BCR::ABL1 translocation event. miR-155 miR-155 is overexpressed in both ALL and AML. Its expression pattern is being considered as a biomarker of poor prognosis in both lineages. TABLE 2 Correlation of miRNAs with gene fusions or target genes and the type of leukemia. miR-128 MLL::AF4 ALL let-7b AML1::ETO AML miR-203 BCR::ABL1 ALL and AML miR-223 FBXW7 (induced) ALL and AML miR-155 ZNF238 (inhibited) ALL and AML Abbreviations: ALL, acute lymphoblastic leukemia; AML, acute myeloid leukemia. DISCUSSION Studies report that miR-128 expression is particularly important in ALL, as it correlates with long-term prognosis and survival data in pediatric ALL [5]. Additionally, it is directly linked to treatment sensitivity and is an important differential biomarker, as its classification helps to understand the complexity and diversity of acute leukemias, especially pediatric ones [6]. Nemes et al. [5] pointed out that changes in the expression of these miRNAs, especially miR-128b , were observed in parallel with the percentage of bone marrow blasts during remission and relapse. To elucidate, miR-128b levels may vary in response to treatment and disease state, further emphasizing its relevance in the clinical management of ALL. Moreover, another study found that miR-128-3p plays a significant role as an oncogene, as it contributes to the development of T-ALL by negatively regulating the tumor suppressor PHF6 ; that is, miR-128-3p overexpression accelerates the development of T-ALL [7]. Regarding treatment, it was observed that when miR-128b is expressed at normal levels, it can help restore glucocorticoid sensitivity in leukemic cells. Furthermore, miR-128b functions by negatively regulating certain fusion proteins, such as MLL::AF4 (Table 2), which are produced due to genetic alterations in blasts. These fusion proteins are involved in promoting the growth and survival of cancer cells. By reducing the levels of these proteins, miR-128b helps cells respond better to glucocorticoids [8]. Besides glucocorticoids, the literature also shows the role of miR-128b in treatment with prednisone: higher levels of miR-128b are associated with a better response to this treatment [5]. let-7b has been strongly associated with AML and the negative regulation of AML1::ETO , caused by the chromosomal translocation of the same name (t(8;21)). Johnson et al. [9] concluded that let-7b targets the 3′UTR pathway of AML1::ETO, causing protein reduction, significant inhibition of cell proliferation, and an increase in differentiation markers, suggesting that let-7b can neutralize the effects of AML1::ETO . Additionally, this miRNA is capable of restoring certain genes that are targets of AML1::ETO , such as CEBPA and RASSF2 , which are normally repressed by it. This indicates that let-7b can partially reverse the transcriptional repression caused by AML1::ETO (Table 2) [9]. Other studies report that let-7a-2-3p regulates oncogenes such as c-MYC and RAS ; by inhibiting these oncogenes, let-7a-2-3p helps control the growth and spread of leukemic cells, thus improving patient survival chances, serving as a prognostic biomarker. Furthermore, this miRNA has a significant impact on treatment response, as it was observed that patients undergoing stem cell transplantation who had overexpression of let-7a-2-3p obtained beneficial outcomes, with good response to therapeutic measures [10]. Thus, the let-7 family has a strong correlation with AML, as an important discriminatory factor between lymphoid and myeloid lineages and as a prognostic biomarker, in addition to being an important component in the treatment approach. As previously noted, miR-203 is negatively regulated in both ALL and AML, which has a direct meaning in leukemia progression. In AML, for example, it was observed that miR-203 levels were significantly lower in leukemic stem cells (LSCs), compared to non-stem cells and normal blood samples. This negative regulation is crucial for the proliferation and self-renewal of such cells, indicating that miR-203 acts as a tumor suppressor in this context. In the same study, when miR-203 was reintroduced into LSCs, there was a sharp decrease in cell proliferation and self-renewal [11]. This suggests that by restoring miR-203 levels, leukemic stem cell growth may be inhibited [11]. A study by Zheng et al. [12] supported the argument of negative regulation of miR-203 . The research found that serum levels of miR-203 were significantly lower in 134 patients with AML compared to 70 healthy controls; that is, lower serum miR-203 levels were associated with lower overall survival rates and relapse-free survival rates among patients with AML. This reinforces that miR-203 may play a crucial role in disease pathology. Moreover, the study indicated that miR-203 could effectively distinguish between AML cases and normal controls [12]. This highlights its potential as a diagnostic biomarker for AML. In ALL, it was reported that miR-203 is negatively regulated by genetic and epigenetic mechanisms where there is expression of ABL1 or BCR::AB L; this silencing can lead to increased levels of these oncogenes, which promote cancer cell growth. It was observed that restoring miR-203 expression in these cases can reduce the levels of such proteins, decreasing or inhibiting cell proliferation. This finding shows the potential of miR-203 as a therapeutic target and its overexpression as a good prognostic marker in leukemias [13]. In AML, miR-223 is significantly negatively regulated compared to healthy individuals. Xiao et al. [14] showed that when miR-223 was overexpressed in AML cell lines (specifically HL-60 and K562), it inhibited cell proliferation, showing that this miRNA acts in the myeloid lineage as a tumor suppressor. Additionally, it was analyzed that miR-223 induces apoptosis of leukemic cells through the negative regulation of the FBXW7 gene, reducing luciferase activity in the cells [14]. In ALL, miR-223 was also negatively regulated; however, when overexpressed in the CCRF::CEM and NALM-6 cell lines, a decrease in proliferation, migration, and cell invasion was observed. From a different perspective, miR-223 inhibition resulted in increased cell growth and movement, indicating that miR-223 also plays a tumor suppressor role in ALL. Furthermore, it also induces leukemic cell apoptosis, but this time by targeting a different gene: FOXO1 , where when this gene is negatively regulated, there is a reduction in cell proliferation [15]. Despite its low expression in both leukemia lineages, making it not very effective as a discriminatory diagnostic biomarker between AML and ALL, miR-223 has significant potential in the therapeutic approach of patients and also as a prognostic indicator. miR-155 is overexpressed in both ALL and AML. Studies indicate that this miR-155 overexpression is an indicator of poor prognosis, as it is associated with an aggressive disease phenotype and treatment resistance. Wang et al . [16] performed miR-155 silencing in the AML MV411 cell line using CRISPR/Cas9 technology. It was observed that when the miRNA was silenced, there was a significant increase in cell sensitivity to anti-FLT3-ITD+ drugs, such as doxorubicin, quizartinib, and midostaurin. Additionally, it was observed that after the knockout, the mTOR and WNT signaling pathways were also inhibited, suggesting that miR-155 has activity on these pathways [16]. Furthermore, it was observed that miR-155 negatively affects the PIK3R1 pathway, which also influences cell sensitivity to drugs [17]. In ALL, miR-155 is also significantly positively regulated and is also an indicator of poor prognosis for the patient with cancer, as it promotes the proliferation of leukemic cells through inhibition of the ZNF238 gene, which plays a role in growth regulation and cell differentiation. By inhibiting ZNF238, miR-155 can disrupt normal cellular functions, further increasing the proliferation of leukemic cells [18]. Thus, miR-155 has the same level of expression in both ALL and AML, but, like miR-223 , it serves as a major prognostic indicator in both neoplasms, and its silencing may help with future therapeutic approaches. The results obtained in this study highlight the relevance of specific miRNAs as discriminatory factors between ALL and AML, especially miR-128, let-7 , miR-203 , miR-223 , and miR-155 . miR-128 , significantly overexpressed in ALL, especially in the B lineage, was shown to be related to crucial hematopoiesis and oncogenesis genes, such as PHF6 and MLL::AF4 , suggesting its function as a tumor suppressor. Alternatively, miR-155 , associated with overexpression in AML and ALL, has been recognized as a promising biomarker for early diagnosis, despite its dose-dependent function in disease progression, indicating a poor prognosis. Meanwhile, miR-203 and miR-223 are negatively regulated in both types of leukemia; however, miR-203 plays a central role in modulating the expression of oncogenes such as ABL1 and the BCR::ABL1 gene fusion, frequently observed in ALL with poor prognosis, indicating its potential as a therapeutic target and epigenetic regulator. let-7 also acts as a tumor suppressor, negatively regulating AML1::ETO. The functional analysis of the involved pathways confirmed that these miRNAs regulate genes associated with proliferative processes, cell differentiation, and therapy resistance, consolidating their value as diagnostic, prognostic, and therapeutic tools. Therefore, the need for future investigations exploring the molecular mechanisms mediated by these miRNAs is reinforced, as well as their clinical application in personalized medicine strategies for the treatment of acute leukemias. DECLARATION OF CONFLICT OF INTEREST The authors declare no conflicts of interest. ACKNOWLEDGMENTS The authors express their sincere gratitude to the Federal University of Pará (UFPA) for the technical assistance and infrastructure provided throughout the course of this research. We are indebted to St. Jude Cloud platform for their valuable collaboration in supplying both the data to the public. The authors gratefully acknowledge the National Council for Scientific and Technological Development (CNPq) (QUEIROZ, KVM; KHAYAT, AS) for the funding granted, which provided essential financial support and enabled the dedication necessary to carry out this study. DATA AVAILABILITY STATEMENT REFERENCES 1. A. Turk, G. A. Calin, and T. Kunej, ”MicroRNAs in Leukemias: A Clinically Annotated Compendium,” International Journal of Molecular Sciences 23, no. 7 (2022): 3469.] 2. C. K. Tebbi, ”Etiology of Acute Leukemia: A Review,” Cancers 13, no. 9 (2021): 2256. 3. J. Shu, B. V. R. E. Silva, T. Gao et al., ” Dynamic and modularized MicroRNA regulation and its implication in human cancers,” Scientific Reports 7, no. 1 (2017): 13356. 4. Y. Wang, Z. Li, C. He, D. Wang, et al., ”MicroRNAs Expression Signatures Are Associated with Lineage and Survival in Acute Leukemias,” Blood Cells, Molecules & Diseases 44, no. 3 (2010): 191-197. 5. K. Nemes, M. Csóka, N. Nagy, et al., ”Expression of Certain Leukemia/Lymphoma Related MicroRNAs and Its Correlation with Prognosis in Childhood Acute Lymphoblastic Leukemia,” Pathology & Oncology Research 21, no. 3 (2015): 597–604. 6. J. Szczepanek, ”Role of MicroRNA Dysregulation in Childhood Acute Leukemias: Diagnostics, Monitoring and Therapeutics: A Comprehensive Review,” World Journal of Clinical Oncology 11, no. 6 (2020): 348–369. 7. E. Mets, G. Van Peer, J. Van der Meulen, et al., ”MicroRNA-128-3p Is a Novel OncomiR Targeting PHF6 in T-Cell Acute Lymphoblastic Leukemia,” Haematologica 99, no. 8 (2014): 1326–1333. 8. A. Kotani, D. Ha, D. Schotte, et al., ”A Novel Mutation in the miR-128b Gene Reduces miRNA Processing and Leads to Glucocorticoid Resistance of MLL-AF4 Acute Lymphocytic Leukemia Cells,” Cell Cycle 9, no. 6 (2010): 1037–1042. 9. D. T. Johnson, A.G. Davis, J.H. Zhou, et al., ”MicroRNA Let-7b Downregulates AML1-ETO Oncogene Expression in t(8;21) AML by Targeting Its 3′UTR,” Experimental Hematology & Oncology 10, no. 1 (2021): 8. 10. H. Chen, J. Wang, H. Wang, et al., ”Advances in the Application of Let-7 microRNAs in the Diagnosis, Treatment and Prognosis of Leukemia,” Oncology Letters 23, no. 1 (2021): 1. 11. Y. Zhang, S.Y. Zhou, H.Z. Yan, et al., ”miR-203 Inhibits Proliferation and Self-Renewal of Leukemia Stem Cells by Targeting Survivin and Bmi-1,” Scientific Reports 6, no. 1 (2016): 19995. 12. Z. Zheng, G. Rong, G. Li, et al., ”Diagnostic and Prognostic Significance of Serum miR-203 in Patients with Acute Myeloid Leukemia,” International Journal of Clinical and Experimental Pathology 12, no. 5 (2019): 1548. 13. S. Ultimo, A.M. Martelli, G. Zauli, et al., ”Roles and Clinical Implications of MicroRNAs in Acute Lymphoblastic Leukemia,” Journal of Cellular Physiology 233, no. 8 (2018): 5642–5654. 14. Y. Xiao, C. Su, and T. Deng, ”miR-223 Decreases Cell Proliferation and Enhances Cell Apoptosis in Acute Myeloid Leukemia via Targeting FBXW7,” Oncology Letters 12, no. 5 (2016): 3531–3536. 15. C. Li, T. Zhao, L. Nie, et al., ”MicroRNA-223 Decreases Cell Proliferation, Migration, Invasion, and Enhances Cell Apoptosis in Childhood Acute Lymphoblastic Leukemia via Targeting Forkhead Box O 1,” Bioscience Reports 40, no. 10 (2020): BSR20200485. 16. L. Y. Wang, P.F. Jiang, J.Z. Li, et al., ”Correlation of miR-155 Expression with Drug Sensitivity of FLT3-ITD+ Acute Myeloid Leukemia Cell Line and Its Mechanism,” Zhongguo Shi Yan Xue Ye Xue Za Zhi 32, no. 2 (2024): 395–401. 17. L. Wang, P. Jiang, J. Li, et al., ”Loss of MiR-155 Sensitizes FLT3-ITD+AML to Chemotherapy and FLT3 Inhibitors via Glycolysis Blocking by Targeting PIK3R1,” Journal of Cancer 14, no. 1 (2023): 99–113. 18. C. Liang, Y. Li, L.N. Wang, et al., ”Up-Regulated miR-155 Is Associated with Poor Prognosis in Childhood Acute Lymphoblastic Leukemia and Promotes Cell Proliferation Targeting ZNF238,” Hematology 26, no. 1 (2020): 16–25. 19. S. Mi, J. Lu, M. Sun, et al., ”MicroRNA Expression Signatures Accurately Discriminate Acute Lymphoblastic Leukemia from Acute Myeloid Leukemia,” Proceedings of the National Academy of Sciences of the United States of America 104, no. 50 (2007): 19971–19976. 20. Turk A, Calin GA, Kunej T. MicroRNAs in Leukemias: A Clinically Annotated Compendium. Int J Mol Sci. 2022 Mar 23;23(7):3469. doi: 10.3390/ijms23073469. PMID: 35408829; PMCID: PMC8998245. LEGENDS The manuscript did not contain figures, therefore there was no list of legends. Information & Authors Information Version history V1 Version 1 13 October 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords all aml cancer genetics hematology/oncology leukemia molecular diagnosis & therapy Authors Affiliations Karla V. Maia de Queiroz 0009-0003-4073-2054 [email protected] Universidade da Amazonia View all articles by this author Eldevan da Silva Barbosa Universidade Federal do Maranhao View all articles by this author Emerson Jhony C. Botelho Universidade Federal do Para View all articles by this author Ágatha Tereza Miranda Tavares Universidade Federal do Para View all articles by this author Lucas Brabo Rotella Universidade Federal do Para View all articles by this author Márcio Santana de Aquino Universidade Federal do Para View all articles by this author Yasmin de Souza dos Santos Universidade Federal do Para View all articles by this author Jaqueline Diniz Pinho Universidade Federal do Maranhao View all articles by this author Bruna Claudia Meireles Khayat Universidade Federal do Para View all articles by this author André Salim Khayat Universidade Federal do Para View all articles by this author Metrics & Citations Metrics Article Usage 167 views 124 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Karla V. Maia de Queiroz, Eldevan da Silva Barbosa, Emerson Jhony C. Botelho, et al. 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