EPR22-104: A Comparison of the Burden of Leukemia Amongst Various Regions of the World, 1990-2019

Ahmed, Alaaeldin; Jani, Chinmay; Bhatt, Padmanabh; Singh, Harpreet; Jani, Ruchi; Shalhoub, Joseph; Marshall, Dominic C; Lam, Prudence; Salciccioli, Justin D.

doi:10.6004/jnccn.2021.7211

Cited by 3 publications

(4 citation statements)

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“…However, in leukemias, these cells stop responding to external factors within the bone marrow microenvironment and, consequently, disordered growth in the bone marrow contributes to immature cells being found in the peripheral blood [19]. Ahmed et al [20] showed that the incidence and mortality of acute myeloid leukemia is increasing globally for males and females, from 1990 to 2019, and that disabilityadjusted life years (DALYs) increased for males. Plant lectins have been demonstrated to be potential antitumor drugs, including against leukemia [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Effects of Lectins from Alpinia purpurata Inflorescence (ApuL) and Schinus terebinthifolia Leaf (SteLL) on Human Leukemic Cell Lines and Mesenchymal Stem Cells

et al. 2023

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Lectins (carbohydrate-binding proteins) are able to distinguish different patterns of glycosylation on cell surfaces. This study investigated the effects of lectins from Alpinia purpurata inflorescence (ApuL) and Schinus terebinthifolia leaf (SteLL) on the viability of human leukemia cells (K562, chronic myeloid leukemia; JURKAT, acute lymphoblastic leukemia) and mesenchymal stem cells (MSCs) from human umbilical cords. In addition, possible immunomodulatory effects of ApuL and SteLL on MSCs were assessed by determining cytokine levels in cultures. ApuL reduced the viability of JURKAT cells (IC50: 12.5 μg/mL), inducing both apoptosis and necrosis. For K562 cells, ApuL at 50 µg/mL caused a decrease in viability, but of only 8.8%. Conversely, SteLL exerted a cytotoxic effect on K562 (IC50: 6.0 μg/mL), inducing apoptosis, while it was not cytotoxic to JURKAT. ApuL and SteLL (0.19–100 μg/mL) did not decrease MSCs viability. Treatment with ApuL strongly suppressed (99.5% reduction) the release of IL-6 by MSCs. SteLL also reduced the levels of this cytokine in culture supernatant. In conclusion, ApuL and SteLL showed potential to reduce the viability of leukemia cells, as well as immunomodulatory effect on MSCs without being toxic to them. These biological properties can be explored biomedically and biotechnologically in the future.

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Section: Introductionmentioning

confidence: 99%

Effects of Lectins from Alpinia purpurata Inflorescence (ApuL) and Schinus terebinthifolia Leaf (SteLL) on Human Leukemic Cell Lines and Mesenchymal Stem Cells

et al. 2023

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“…AML accounts for ~80% of all leukemia cases in adults. Although it only accounts for 1% of all cancers, AML shows a low 5‐year survival rate especially for elderly patients, and the burden of the incidence and AML‐related deaths is increasing worldwide 2,3 . Chemotherapy is the standard treatment for AML, and BM or stem cell transplants may be another option for patients with chemoresistance.…”

Section: Introductionmentioning

confidence: 99%

“…Although it only accounts for 1% of all cancers, AML shows a low 5‐year survival rate especially for elderly patients, and the burden of the incidence and AML‐related deaths is increasing worldwide. 2 , 3 Chemotherapy is the standard treatment for AML, and BM or stem cell transplants may be another option for patients with chemoresistance. Novel medications, such as targeted drugs, are being investigated to further improve the therapeutic effects.…”

Section: Introductionmentioning

confidence: 99%

Circadian clock protein Bmal1 accelerates acute myeloid leukemia by inhibiting ferroptosis through the EBF3/ALOX15 axis

Wang

Zhang

et al. 2023

Cancer Science

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Acute myeloid leukemia (AML) is a major leukemia with high mortality. Ferroptosis is an important regulator of cancers. However, the role of ferroptosis and its regulatory mechanisms in AML remain largely unknown. In this study, we reported elevated brain and muscle ARNT-Like protein-1 (Bmal1) expression in AML patients and cell lines, and its upregulation indicated the poor survival of patients. The correlation analysis showed that Bmal1 expression was closely correlated with cytogenetics and the French-American-British subtypes, but was not correlated with age, gender and white blood cells. RSL3 reduced Bmal1 expression in HL-60 and NB4 cells. Malondialdehyde, total iron, Fe 2+ , glutathione and lipid peroxidation were examined to evaluate ferroptosis. Overexpression of Bmal1 repressed RSL3-induced ferroptosis in AML cells. Bmal1 recruited Enhancer of zeste homolog 2 (EZH2) to the Early B cell factor 3 (EBF3) promoter and enhanced its methylation, thus suppressing EBF3 expression. Moreover, the knockdown of Bmal1 sensitized AML cells to RSL3-induced ferroptosis, and it was counteracted by EBF3 knockdown. Furthermore, EBF3 bound to the Arachidonate 15-pipoxygenase (ALOX15) promoter to enhance its expression, and overexpression of EBF3 enhanced RSL3-induced ferroptosis dependent on ALOX5. We established a subcutaneous AML xenograft tumor model and reported that knockdown of Bmal1 and overexpression of EBF3 restrained AML growth by promoting ALOX15-mediated ferroptosis in vivo. Collectively, Bmal1 inhibits RSL3induced ferroptosis by promoting EZH2-mediated EBF3 methylation and suppressing the expression of EBF3 and ALOX15, thus accelerating AML.

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“…According to recent studies, the total number of AML cases reported between 1990 and 2019 is 16,328,147 with total death cases accounting for 8,769,413 in the US alone [3]. Agestandardized mortality rates (ASMR) increased by 11.7% in males and 1.5% in females and age-standardized incidence rate (ASIR) increased by 34.6% in males and 7.9% in females globally [3]. In India, the incidence of AML is estimated to be around 8,000-10,000 new cases per year [4].…”

Section: Introductionmentioning

confidence: 99%

AMLdb: A comprehensive multi-omics platform to understand the pathogenesis and discover biomarkers for acute myeloid leukemia

Kumar,

Kundal

et al. 2023

Preprint

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Acute myeloid leukemia (AML) is one of the leading leukemic malignancies in adults. The heterogeneity of the disease makes the diagnosis and treatment extremely difficult. Despite the significant developments and the rapid advancements in finding new medication targets, the treatment for AML remains a challenge. With the advent of next-generation sequencing (NGS) technologies, exploration at the molecular level for the identification of biomarkers and drug targets has been the main focus for the researchers to come up with novel therapies for better prognosis and survival outcomes of AML patients. However, the massive amounts of data generated from the NGS platforms demands the necessity to create a comprehensive platform on AML to save the time invested in mining literature. To facilitate this, we developed AMLdb, an interactive multi-omics platform that allows users to query, visualize, retrieve and analyze AML-related multi-omics data. It provides a diverse collection of data resourced from various repositories allowing for a more comprehensive analysis. AMLdb contains 86 datasets for gene expression profiles, 15 datasets for methylation profiles, CRISPR-Cas9 knockout screens of 26 AML cell lines, sensitivity of 26 AML cell lines to 288 drugs, mutations in 41 unique genes in 23 AML cell lines and information on 27 experimentally validated biomarkers. The data provided can be used for deriving conclusions on potential targets for therapies, sensitivity of these targets towards the drugs, patient classification, prediction of treatment strategies and outcomes, chances of relapse etc. In this study, we have reported five genes i.e., CBFB, ENO1, IMPDH2, SEPHS2 and MYH9 identified via our analysis using AMLdb as potential targets. Amongst this, CBFB, IMPDH2, SEPHS2 and MYH9 have been previously validated as targets by experimental studies which is in par with our results. However, ENO1 is a novel target identified using AMLdb which needs further investigation. We anticipates that, AMLdb can be a valuable resource to aid the research community accelerate the development of effective therapies for AML. AMLdb is freely accessible at https://project.iith.ac.in/cgntlab/amldb/ without any restrictions.

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EPR22-104: A Comparison of the Burden of Leukemia Amongst Various Regions of the World, 1990-2019

Cited by 3 publications

References 0 publications

Effects of Lectins from Alpinia purpurata Inflorescence (ApuL) and Schinus terebinthifolia Leaf (SteLL) on Human Leukemic Cell Lines and Mesenchymal Stem Cells

Effects of Lectins from Alpinia purpurata Inflorescence (ApuL) and Schinus terebinthifolia Leaf (SteLL) on Human Leukemic Cell Lines and Mesenchymal Stem Cells

Circadian clock protein Bmal1 accelerates acute myeloid leukemia by inhibiting ferroptosis through the EBF3/ALOX15 axis

AMLdb: A comprehensive multi-omics platform to understand the pathogenesis and discover biomarkers for acute myeloid leukemia

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