Correlation analysis of two-dimensional gel electrophoretic protein patterns and biological variables

Leptomeningeal infiltration in rat models for human acute myelocytic and lymphocytic leukemia

Autophagy intensity decreases in most blood malignancies, promoting cancer cell proliferation. Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are two main variants of leukemia. LC3, an important autophagy gene, and its protein, MAP1LC3B, precisely predict autophagy initiation and progression. The main objective of this systematic review is to investigate the correlation between changes in the expression of the LC3 gene in patients with ALL and AML. We performed a literature search in PubMed, Scopus, and Web of Science database in November 20, 2025, using the keywords and MeSH terms. All searches were restricted to sources in the English language, andwe focused on human case-control studies where definitive diagnosis was performed using hematological parameters. Initial identification included 1282 articles. Duplicates were removed, leaving 821 papers for screening. From these, 787 articles were removed for inappropriate titles and abstracts, leaving 34 for further review. Ultimately, 10 papers met the criteria for this systematic review. Five AML investigations demonstrated considerably lower LC3 gene expression than healthy controls. Downregulation was similar in one research. Upregulation was seen in two investigations. In two papers, ALL patients had considerably lower expression than healthy controls. Upregulation was significant in one study and non-significant in another one. The LC3 gene appears to be downregulated more consistently in AML, suggesting potential diagnostic or prognostic value. However, findings in ALL are inconsistent, and no definitive conclusion can be drawn. Further high-quality studies are required to clarify the role of LC3 in acute leukemias.

Geographic, demographic, and risk factor profiles of acute myeloid and acute lymphoblastic leukemia in the United States: Insights from the global burden of disease study 2021

Purpose: To describe and compare the pre-treatment bone marrow metagenomes of childhood acute lymphoblastic leukemia (ALL) and childhood acute myeloid leukemia (AML).Background: Leukemia is the most common cancer in children, comprised mainly of ALL (~80%) followed by AML (~17%). The role of infections and their timing in the etiology of pre B-cell ALL’s (but not AML’s) is supported by a considerable body of epidemiologic evidence developed in the past 20 years (Gilham, Peto et al. 2005, Ma, Urayama et al. 2009). There are two main infection related hypotheses. Greaves postulates that delayed infection, akin to the hygiene hypothesis, increases risk of leukemia (Greaves and Alexander 1993, Greaves 1997). The second hypothesis set forth by Kinlen is not mutually exclusive and postulates the role of a transforming yet common virus where introduction of the infectious agent to previously naive communities trigger leukemia (Kinlen 1995). While many viral agents have been investigated (reviewed in (O’Connor and Boneva 2007)) no definitive infectious agent has been identified but, until recently, broad surveys of the microbiome were not possible. Recent developments in next generation sequencing and bioinformatics now allow for unbiased investigation into the totality of organisms that inhabit the human body.Methods: Pre-treatment bone marrow specimens were collected in pre B-cell ALL and AML cases participating in the California Childhood Leukemia Study. AML’s with similar age distribution to the ALL’s were utilized as controls, to represent the infection history of an immune suppressed child. We interrogated the viral metagenomes of 60 ALL’s and 30 AML’s, pooled and reduced with ribosomal capture, then sequenced with high coverage next generation RNA sequencing on an Illumina HiSeq 2500. The resulting sequences were analyzed using a custom bioinformatics pipeline, DARK, to remove human sequences, to identify viral transcripts, and to categorize all transcripts present in the pre-treatment bone marrow. Bacterial metagenomes of the same subjects were analyzed using 16S rRNA amplicon sequencing and the QIIME pipeline.Results: We analyzed over 500 million 100bp reads and categorized human, non-human and unknown sequences. We found striking differences between the viral metagenomes of childhood ALL and AML, with ALL subjects presenting with a greater viral infection load than AML’s. Furthermore, differences in the presence of transcripts aligning to both exogenous viruses and endogenous retroviruses were observed with some viruses occurring exclusively in ALL’s. We found no difference between the bacterial metagenomes of childhood ALL and AML suggesting no differential contamination occurred during collection and analysis.Discussion: This study provides the first measurement of all identifiable infectious agents in both childhood ALL an AML. Our data suggest that bacteria do not play a role in the etiology of ALL. The greater number and frequency of viral infectious agents were observed in ALL versus AML contribute to an etiologic hypothesis of ALL involving viral infections yet require replication and additional follow up. Moreover the clinical relevance of these infections and their relation to outcome should be investigated.ReferencesGilham, C., J. Peto, J. Simpson, E. Roman, T. O. Eden, M. F. Greaves, F. E. Alexander and U. Investigators (2005). "Day care in infancy and risk of childhood acute lymphoblastic leukaemia: findings from UK case-control study." BMJ 330(7503): 1294.Greaves, M. F. (1997). "Aetiology of acute leukaemia." Lancet 349(9048): 344-349.Greaves, M. F. and F. E. Alexander (1993). "An infectious etiology for common acute lymphoblastic leukemia in childhood?" Leukemia 7(3): 349-360.Kinlen, L. J. (1995). "Epidemiological evidence for an infective basis in childhood leukaemia." Br J Cancer 71(1): 1-5.Ma, X., K. Urayama, J. Chang, J. L. Wiemels and P. A. Buffler (2009). "Infection and pediatric acute lymphoblastic leukemia." Blood Cells Mol Dis 42(2): 117-120.O’Connor, S. M. and R. S. Boneva (2007). "Infectious etiologies of childhood leukemia: plausibility and challenges to proof." Environ Health Perspect 115(1): 146-150. DisclosuresNo relevant conflicts of interest to declare.

Unsuccessful Cytogenetics and Outcomes in Acute Leukemia

Using literature data on cytogenetic abnormalities in 3,612 cases of acute myeloid leukemia (AML) and 1,551-cases of acute lymphocytic leukemia (ALL), we have attempted to quantify the information value of finding the typical ALL- and AML-associated chromosome aberrations. Sensitivity, specificity, and predictive value of finding or not finding a given aberration were calculated for several diagnostic scenarios: for the differential diagnosis between ALL and AML when the patient is known to have acute leukemia, for the differential diagnosis among AML FAB subtypes in a patient with known AML, and for the differential diagnosis between ALL FAB subtypes in a patient with known ALL. The specificities were generally high, close to 1. The highest sensitivities in AML were found for +8, t(15;17)(q22;q11), t(8;21)(q22;q22), and -7 (all greater than 0.1), and in ALL for t(9;22)(q34;q11), t(4;11)(q21;q23), and +21 (again all greater than 0.1). In the AML subtypes, the highest sensitivities were 0.89 for t(15;17)(q22;q11) in M3, followed by 0.40 for t(8;21)(q22;q22) in M2, 0.30 for inv(16)(p13q22)/del(16)(q22)/t(16;16)(p13;q22) in M4, and 0.16 for t(9;11)(p21;q23) in M5. In the ALL subtypes, the highest sensitivities were 0.71 and 0.11 for t(8;14)(q24;q32) and t(8;22)(q24;q11), respectively, in L3, 0.23 for t(9;22)(q34;q11) in L2, and 0.18 and 0.13 for +21 and t(4;11)(q21;q23), respectively, in L1. The highest (1.0) positive predictive values in the AML versus ALL comparison were found for t(1;3)(p36;q21), inv(3)(q21q26), t(6;9)(p23;q34), t(7;11)(p15;p15), t(8;16)(p11;p13), t(8;21)(q22;q22), t(15;17)(q22;q11), and, as sole anomalies, for +4, +9, and +11. In the reverse comparison, ALL versus AML, positive predictive values of 1.0 were found for t(1;14)(p32-34;q11), dup(I)(q12-21q31-32), t(2;8)(p12;q24), t(8;14)(q24;q32), t/dic(9;12)(p11-12;p11-13), t(10;14)(q24;q11), and t(11;14)(p13;q11). Among the AML subgroups, the highest predictive values were: 1.0 for M3 if t(15;17), 0.91 for M2 if t(8;21), 0.86 for M4 if inv/del(16)/t(16;16), and 0.82 for M5 if t(9;11). Among the ALL subtypes, positive predictive values of greater than 0.8 were reached only for the L3-associated aberrations t(2;8) (1.0), t(8;14) (0.95), t(8;22) (0.87), and dup(I) (0.80). The highest negative predictive values were in AML 0.98 that the disease is not M3 if t(15;17) is not found, and in ALL 0.96 that the patient does not have L3 if a t(8;14) is not detected.

Risk Factors for Outcomes of Family Haploidentical Allogeneic Stem Cell Transplantation for Adults with Acute Leukemias: A Survey on Behalf of the Acute Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT).

In-Utero Origin of Childhood Acute Leukaemias.

Preclinical Characterization of the Anti-Leukemia Activity of the CD123 Antibody-Drug Conjugate, Pivekimab Sunirine (IMGN632)

Safety, Efficacy, and PK of the BCL2 Inhibitor Venetoclax in Combination with Chemotherapy in Pediatric and Young Adult Patients with Relapsed/Refractory Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia: Phase 1 Study

MLL Gene Rearrangements in 174 Infants with Acute Leukemia.

Minimal Residual Disease following Allogeneic Hematopoietic Stem Cell Transplantation

Morphometric properties of immature reticulocytes in health and during acute lymphoblastic and acute myeloid leukemia

TERRA R-LOOPS ARE INCREASED IN ACUTE MYELOID LEUKEMIA

Introduction. Patients with hematological malignancies undergoing chemotherapy (CT) have high incidence of infections which profile is affected by various factors including neutropenia.Objective was to evaluate incidence and type of infections in patients with de novo acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) according to neutropenia duration.Materials and methods. Prospective study (2013–2015) included 110 patients (66 AML, 44 ALL) that received 480 CT cycles throughout 6 month.Results. Neutropenia with median duration of 15 (2–55) days was in 288 (60 %) of CT cycles. Infections occurred in 242 (50 %) of CT cycles and predominated in neutropenic compared to non-neutropenic patients (80 % vs 6 %, p <0.0001). Infections prevailed in patients with AML compared to ALL patients (93 % vs 18 %, p <0.0001) as in patients with neutropenia (96 % vs 45 %, p <0.0001) and without neutropenia (27 % vs 4 %, p = 0.02). Prolongation of neutropenia from 1–7 days to ≥22 days was associated with increase of infections rate from 52 to 96 % (p <0.0001). Incidence of infections in AML patients was high (92–100 %) regardless of neutropenia duration, whereas in ALL patients it increased from 25–33 to 91 % if neutropenia lengthened from 2 weeks to ≥22 days. During neutropenia the probability of fever of unknown origin was 33.9 %, clinically documented infection – 31.3 %, bacteremia – 17.2 %. They predominated in the first 2 weeks of neutropenia. Probability of invasive aspergillosis (IA) increased after 28 days of neutropenia and reached 66 % on the 55th day. First case of IA in patients with ALL was on 28th day of neutropenia whilst in AML patients – 4 (44 %) of 9 occurred more early (6–16 days of neutropenia). Nine (6 %) of 110 patients died, 4 (4 %) of them due to infection.Conclusions. Neutropenia was a predictor of infectious complications in patients with AML and ALL. Correlation between duration of neutropenia and incidence of infections was in patients with ALL, whereas in AML patients the rate of infections was high regardless of neutropenia duration. In patients with neutropenia for 2 weeks the most common types of infection were fever of unknown origin, clinically documented infection and bacteremia whilst IA predominated if neutropenia duration was ≥28 days.