Global, regional, and national burdens of leukemia from 1990 to 2019: A systematic analysis of the global burden of disease in 2019 based on the APC model.

BACKGROUND: Leukemia is the tenth most common cause of cancer death worldwide and one of the most important causes of disability. To understand the current status and changing trends of the disease burden of leukemia at the global, regional, and national levels, and to provide a scientific basis for the development of leukemia prevention and treatment strategies. METHODS: Based on open data from the Global Burden of Disease Study 2019 (GBD 2019), R software was used to calculate estimated annual percentage changes to estimate trends in the age-standardized incidence (ASIR) and the age-standardized disability-adjusted life years (DALY) rate due to leukemia and its major subtypes from 1990 to 2019. RESULTS: In 2019, globally, the number of incidences and DALYs of leukemia were 643.6 × 103 (587.0 × 103, 699.7 × 103) and 11,657.5 × 103 (10529.1 × 103, 12700.7 × 103), respectively. The ASIR (estimated annual percentage change (EAPC) = -0.37, 95%UI -0.46 to -0.28) and the age-standardized DALY rate (EAPC = -1.72, 95%UI -1.80 to -1.65) of leukemia showed a decreasing trend from 1990 to 2019. The APC model analysis showed that the age effect of leukemia risk was a "U"-shaped distribution of relative risk (RR) with increasing age from 1990 to 2019, globally. The time effect was an increase in incidence rate with increasing years but a decrease in DALY rate with increasing years. The cohort effects of both incidence and DALY rates tended to increase and then decrease with the development of the birth cohort. In 1990 and 2019, smoking, high body-mass index, occupational exposure to benzene, and occupational exposure to formaldehyde were risk factors for DALY in leukemia, especially in areas with high SDI. CONCLUSIONS: From 1990 to 2019, the disease burden of leukemia showed a decreasing trend, but it is worth noting that its overall severity is still very high. The disease burden of leukemia varies greatly from region to region, and exclusive strategies for the prevention and treatment of leukemia should be developed according to the economic and cultural development of each region.

The Effect of Regular Oral Care Protocol on Preventing or Decreasing Severity of Oral Mucositis in Acute Leukemia Patient: A Prospective Trail.

This article reports a study designed to evaluate the effectiveness of regular oral care protocol developed specifically for adults in intensive care to prevent mucositis. Data were collected using oral mucositis assessment scale, oral cavity assessment tool, and the National Cancer Institute Common Toxicity Criteria. The results indicated that oral mucositis can be reduced through the practice of administering oral care in accordance with oral health care guidelines. Oral care implemented in line with an evidence-based oral care guide and frequent observation of patients is the most important step in preventing oral mucositis.

Deciphering genetic and nongenetic factors underlying tumour dormancy: insights from multiomics analysis of two syngeneic MRD models of melanoma and leukemia.

BACKGROUND: Tumour dormancy, a resistance mechanism employed by cancer cells, is a significant challenge in cancer treatment, contributing to minimal residual disease (MRD) and potential relapse. Despite its clinical importance, the mechanisms underlying tumour dormancy and MRD remain unclear. In this study, we employed two syngeneic murine models of myeloid leukemia and melanoma to investigate the genetic, epigenetic, transcriptomic and protein signatures associated with tumour dormancy. We used a multiomics approach to elucidate the molecular mechanisms driving MRD and identify potential therapeutic targets. RESULTS: We conducted an in-depth omics analysis encompassing whole-exome sequencing (WES), copy number variation (CNV) analysis, chromatin immunoprecipitation followed by sequencing (ChIP-seq), transcriptome and proteome investigations. WES analysis revealed a modest overlap of gene mutations between melanoma and leukemia dormancy models, with a significant number of mutated genes found exclusively in dormant cells. These exclusive genetic signatures suggest selective pressure during MRD, potentially conferring resistance to the microenvironment or therapies. CNV, histone marks and transcriptomic gene expression signatures combined with Gene Ontology (GO) enrichment analysis highlighted the potential functional roles of the mutated genes, providing insights into the pathways associated with MRD. In addition, we compared "murine MRD genes" profiles to the corresponding human disease through public datasets and highlighted common features according to disease progression. Proteomic analysis combined with multi-omics genetic investigations, revealed a dysregulated proteins signature in dormant cells with minimal genetic mechanism involvement. Pathway enrichment analysis revealed the metabolic, differentiation and cytoskeletal remodeling processes involved in MRD. Finally, we identified 11 common proteins differentially expressed in dormant cells from both pathologies. CONCLUSIONS: Our study underscores the complexity of tumour dormancy, implicating both genetic and nongenetic factors. By comparing genomic, transcriptomic, proteomic, and epigenomic datasets, our study provides a comprehensive understanding of the molecular landscape of minimal residual disease. These results provide a robust foundation for forthcoming investigations and offer potential avenues for the advancement of targeted MRD therapies in leukemia and melanoma patients, emphasizing the importance of considering both genetic and nongenetic factors in treatment strategies.

[Chinese consensus on autologous stem cell transplantation for adult acute leukemia (2024)].

Autologous stem cell transplantation (ASCT) emerges as a therapeutic strategy following remission in adult acute leukemia (AL). It offers advantages over allogeneic hematopoietic stem cell transplantation (allo-HSCT), including independence from donor availability, absence of graft-versus-host disease (GVHD), and a reduced risk of transplant-related mortality. Furthermore, when juxtaposed with the extended regimens of consolidation chemotherapy, ASCT stands out by markedly abbreviating treatment duration, alleviating the economic strain on patients, and enhancing their overall quality of life. Despite these benefits, the adoption of ASCT among adult AL patients in China remains disproportionately low. To enhance clinical physicians' understanding of the role and position of ASCT in AL management and to improve the clinical efficacy of ASCT, it is urgent to establish a consensus among experts on ASCT for adult acute leukemia in our nation.

4-Methylthiazole triggers apoptosis and mitochondrial disruption in HL-60 cells.

BACKGROUND: Thiazole derivatives are gaining prominence in cancer research due to their potent anti-cancer effects and multifaceted biological activities. In leukemia research, these compounds are particularly studied for their ability to induce apoptosis, disrupt mitochondrial membrane potential (MMP), and modulate cell signaling pathways. METHODS AND RESULTS: This study investigates the efficacy of 4-Methylthiazole in inducing apoptosis in HL-60 leukemia cells. Apoptosis was quantified via flow cytometry using FITC Annexin V and propidium iodide staining. Mitochondrial disruption was evaluated through alterations in mitochondrial membrane potential (MMP) as measured by the JC-1 assay. The compound significantly disrupted MMP, activated Caspase-3, and induced the release of Cytochrome C, all of which are critical markers of apoptosis (****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05). Additionally, treatment with 4-Methylthiazole markedly reduced CD45 and CD123 surface markers, indicating significant phenotypic alterations in leukemia cells (****p < 0.0001). High-dose treatment with 4-Methylthiazole significantly increased ROS levels, suggesting elevated oxidative stress and the presence of intracellular free radicals, contributing to its cytotoxic effects (*p < 0.05). A significant rise in TNF-α levels was observed post-treatment, indicating a pro-inflammatory response that may further inhibit leukemia cell viability. While IL-6 levels remained unchanged, a dose-dependent decrease in IL-10 levels was noted, suggesting a reduction in immunosuppressive conditions within the tumor microenvironment (*p < 0.05). CONCLUSIONS: Overall, 4-Methylthiazole targets leukemia cells through multiple apoptotic mechanisms and modifies the immune landscape of the tumor microenvironment, enhancing its therapeutic potential. This study highlights the need for further clinical investigation to fully exploit the potential of thiazole derivatives in leukemia treatment.

Enhancer-promoter hubs organize transcriptional networks promoting oncogenesis and drug resistance.

Recent advances in high-resolution mapping of spatial interactions among regulatory elements support the existence of complex topological assemblies of enhancers and promoters known as enhancer-promoter hubs or cliques. Yet, organization principles of these multi-interacting enhancer-promoter hubs and their potential role in regulating gene expression in cancer remain unclear. Here, we systematically identify enhancer-promoter hubs in breast cancer, lymphoma, and leukemia. We find that highly interacting enhancer-promoter hubs form at key oncogenes and lineage-associated transcription factors potentially promoting oncogenesis of these diverse cancer types. Genomic and optical mapping of interactions among enhancer and promoter elements further show that topological alterations in hubs coincide with transcriptional changes underlying acquired resistance to targeted therapy in T cell leukemia and B cell lymphoma. Together, our findings suggest that enhancer-promoter hubs are dynamic and heterogeneous topological assemblies with the potential to control gene expression circuits promoting oncogenesis and drug resistance.

Paired comparisons of venetoclax concentration in cerebrospinal fluid, bone marrow, and plasma in acute leukemia patients.

Venetoclax, a small molecule inhibitor of BCL-2, has demonstrated efficacy in treating acute leukemias and has been recommended as one of the first-line anti-leukemia therapies. Although venetoclax has been suggested to probably possess the ability to penetrate the central nervous system (CNS), current data to elucidate the characteristics of venetoclax in cerebrospinal fluid (CSF), bone marrow (BM), and plasma are still lacking. This study investigated the real-world characteristics of venetoclax concentrations in CSF, BM, and plasma in acute leukemia patients. Thirteen acute leukemia patients treated with venetoclax were included, with paired samples of CSF, BM, and plasma collected and venetoclax concentrations measured using LC-MS/MS. With the results, the median venetoclax concentrations were 2030 ng/mL in plasma, 16.7 ng/mL in CSF, and 1390 ng/mL in BM. The percentages of CSF/plasma and BM/plasma were 0.74% and 70.37%, respectively. While no direct correlation was observed between CSF and plasma venetoclax levels, there was a trend toward an improved CSF/plasma percentage over time following the last administration of venetoclax. In contrast, a strong correlation was found between BM and plasma levels. This study demonstrated that venetoclax could reach its effective concentration in most patients, suggesting its potential clinical utility in the management of CNS involvement in acute leukemia.

Radiation Signature in Plasma Metabolome of Total-Body Irradiated Nonhuman Primates and Clinical Patients.

In the last decade, geopolitical instability across the globe has increased the risk of a large-scale radiological event, when radiation biomarkers would be needed for an effective triage of an irradiated population. Ionizing radiation elicits a complex response in the proteome, genome, and metabolome and hence can be leveraged as rapid and sensitive indicators of irradiation-induced damage. We analyzed the plasma of total-body irradiated (TBI) leukemia patients (n = 24) and nonhuman primates (NHPs; n = 10) before and 24 h after irradiation, and we performed a global metabolomic study aiming to provide plasma metabolites as candidate radiation biomarkers for biological dosimetry. Peripheral blood samples were collected according to the appropriate ethical approvals, and metabolites were extracted and analyzed by liquid chromatography mass spectrometry. We identified an array of metabolites significantly altered by irradiation, including bilirubin, cholesterol, and 18-hydroxycorticosterone, which were detected in leukemia patients and NHPs. Pathway analysis showed overlapping perturbations in steroidogenesis, porphyrin metabolism, and steroid hormone biosynthesis and metabolism. Additionally, we observed dysregulation in bile acid biosynthesis and tyrosine metabolism in the TBI patient cohort. This investigation is, to our best knowledge, among the first to provide valuable insights into a comparison between human and NHP irradiation models. The findings from this study could be leveraged for translational biological dosimetry.

The n-Butanol Extract Obtained from the Inner Bark of Tabebuia rosea (Bertol.) DC, Specioside, and Catalposide Induce Leukemia Cell Apoptosis in the Presence of Apicidin.

The cell signaling pathways involved in the antiproliferative activities of T. rosea inner bark remain unexplored. This study evaluated the apoptotic effects of two iridoids from the inner bark of T. rosea and apicidin on THP-1 cells. The cytotoxic effects of the extract and the pure compounds on THP-1 and Jurkat cells were also evaluated using the MTT assay. The apoptotic effect was determined by measuring the mitochondrial membrane potential. The expression of mRNA and MAPK kinase, Bax, and Bcl-2 proteins was detected by Western blotting and RT-qPCR, respectively. The extract and the compounds evaluated increased the percentage of apoptotic cells. Depolarization of the mitochondrial membrane was observed, and the number of cells in the G0/G1 phase increased. Catalposide and specioside significantly increased p38 protein expression, mostly in cells pretreated with apicidin. The p38 MAPK signaling pathway is at least one of the pathways by which the n-butanol extract obtained from Tabebuia rosea, catalposide, and specioside exerts its apoptotic effect on THP-1 cells, and this effect generates a response in the G0/G1 phase and subsequent cell death. In addition, there was depolarization of the mitochondrial membrane, an effect that was related to the participation of the proapoptotic protein Bax.

Leukemia detection and classification using computer-aided diagnosis system with falcon optimization algorithm and deep learning.

Leukemia is a type of blood tumour that occurs because of abnormal enhancement in WBCs (white blood cells) in the bone marrow of the human body. Blood-forming tissue cancer influences the lymphatic and bone marrow system. The early diagnosis and detection of leukaemia, i.e., the accurate difference of malignant leukocytes with little expense at the beginning of the disease, is a primary challenge in the disease analysis field. Despite the higher occurrence of leukemia, there is a lack of flow cytometry tools, and the procedures accessible at medical diagnostics centres are time-consuming. Distinct researchers have implemented computer-aided diagnostic (CAD) and machine learning (ML) methods for laboratory image analysis, aiming to manage the restrictions of late leukemia analysis. This study proposes a new Falcon optimization algorithm with deep convolutional neural network for Leukemia detection and classification (FOADCNN-LDC) technique. The main objective of the FOADCNN-LDC technique is to classify and recognize leukemia. The FOADCNN-LDC technique utilizes a median filtering (MF) based noise removal process to eradicate the image noise. Besides, the FOADCNN-LDC technique employs the ShuffleNetv2 model for the feature extraction process. Moreover, the detection and classification of the leukemia process are performed by utilizing the convolutional denoising autoencoder (CDAE) model. The FOA is implemented to select the hyperparameter of the CDAE model. The simulation process of the FOADCNN-LDC approach is performed on a benchmark medical dataset. The investigational analysis of the FOADCNN-LDC approach highlighted a superior accuracy value of 99.62% over existing techniques.

Comparison of secular trends of leukemia in China and the United States from 1990 to 2021 and their projections for the next 15 years.

Background: Leukemia imposes a large healthcare burden both in China and the United States (US). The disease burden differs greatly between the two countries, but related research is limited. We explored the differences in leukemia incidence and mortality between China and the US. Methods: Data on leukemia in China and the US from 1990 to 2021 were collected from the Global Burden of Disease 2021 database. Incidence and mortality were used to estimate the disease burden, and joinpoint regression was performed to compare their secular trends. We used an age-period-cohort model to analyze the effects of age, period, and birth cohort and project future trends in the next 15 years. Results: In 2021, the age-standardized incidence rate (ASIR) and the age-standardized death rate (ASDR) of leukemia were lower in China than in the US. However, the incidence and mortality of acute lymphoblastic leukemia (ALL) was considerably higher in China. In the past decades, the ASIR showed decreased tendency in the US, while ASIR showed stable in China. The ASDR tended to decrease in both countries from 1990 to 2021. Males have higher rates of incidence and mortality than females in two countries. The age effects showed that children and older individuals have higher RRs for incidence and mortality in China, while the RRs for incidence and mortality in the US particularly increased in the older population. The disease burden of leukemia in children is obviously greater in China. The ASIRs and ASDRs of leukemia will continue to decline in the next 15 years in China and the US, with the US experiencing a more obvious downtrend. Conclusions: Over the past decades, the ASDRs in two countries both tended to decrease. And compared to the US, China had lower leukemia incidence and mortality, However, the ASIRs in China tended toward stable, which it was showed downtrend in the US. Children have obviously greater RRs for incidence and mortality in China. The incidence and mortality will decrease continuously in two countries. Effective intervention measures are needed to reduce the burden of leukemia.

Live sobre Fevereiro Laranja - cuidados com a leucemia

Genetic analysis from multiple cohorts implies causality between 2200 druggable genes, telomere length, and leukemia.

BACKGROUND: Clinical therapeutic targets for leukemia remain to be identified and the causality between leukemia and telomere length is unclear. METHODS: This work employed cis expression quantitative trait locus (eQTL) for 2,200 druggable genes from the eQTLGen Consortium and genome-wide association studies (GWAS) summary data for telomere length in seven blood cell types from the UK Biobank, Netherlands Cohort as exposures. GWAS data for lymphoid leukemia (LL) and myeloid leukemia (ML) from FinnGen and Lee Lab were used as outcomes for discovery and replication cohorts, respectively. Robust Mendelian randomization (MR) findings were generated from seven MR models and a series of sensitivity analyses. Summary-data-based MR (SMR) analysis and transcriptome-wide association studies (TWAS) were further implemented to verify the association between identified druggable genes and leukemia. Single-cell type expression analysis was employed to identify the specific expression of leukemia casual genes on human bone marrow and peripheral blood immune cells. Multivariable MR analysis, linkage disequilibrium score regression (LDSC), and Bayesian colocalization analysis were performed to further validate the relationship between telomere length and leukemia. Mediation analysis was used to assess the effects of identified druggable genes affecting leukemia via telomere length. Phenome-wide MR (Phe-MR) analysis for assessing the effect of leukemia causal genes and telomere length on 1,403 disease phenotypes. RESULTS: Combining the results of the meta-analysis for MR estimates from two cohorts, SMR and TWAS analysis, we identified five LL causal genes (TYMP, DSTYK, PPIF, GDF15, FAM20A) and three ML causal genes (LY75, ADA, ABCA2) as promising drug targets for leukemia. Univariable MR analysis showed genetically predicted higher leukocyte telomere length increased the risk of LL (odds ratio [OR] = 2.33, 95 % confidence interval [95 % CI] 1.70-3.18; P = 1.33E-07), and there was no heterogeneity and horizontal pleiotropy. Evidence from the meta-analysis of two cohorts strengthened this finding (OR = 1.88, 95 % CI 1.06-3.05; P = 0.01). Multivariable MR analysis showed the causality between leukocyte telomere length and LL without interference from the other six blood cell telomere length (OR = 2.72, 95 % CI 1.88-3.93; P = 1.23E-07). Evidence from LDSC supported the positive genetic correlation between leukocyte telomere length and LL (rg = 0.309, P = 0.0001). Colocalization analysis revealed that the causality from leukocyte telomere length on LL was driven by the genetic variant rs770526 in the TERT region. The mediation analysis via two-step MR showed that the causal effect from TYMP on LL was partly mediated by leukocyte telomere length, with a mediated proportion of 12 %. CONCLUSION: Our study identified several druggable genes associated with leukemia risk and provided new insights into the etiology and drug development of leukemia. We also found that genetically predicted higher leukocyte telomere length increased LL risk and its potential mechanism of action.

Evaluating exposure-response relationship in 1,3-butadiene and leukemia studies.

OBJECTIVES: 1,3-Butadiene (BD) exposure's link to leukemia is under regulatory scrutiny. The assessment methods for BD exposure risks have evolved from early animal and limited human studies to advanced exposure-response modelling with comprehensive quantitative data. The objec- tive of this study is to explore the nuances of exposure-response modelling, investigating how various statistical methods have influenced the quan- tification of exposure-response relationships. MATERIAL AND METHODS: Although this study was not conducted as a formal systematic review, a search was performed in Medline/Pubmed to identify all human studies on leukemia risk assessment for BD exposure. This search included articles written in English. The electronic search spanned from inception of records until July 23, 2023, using the search term: "butadiene AND (leukaemia OR leukemia OR myeloid OR lymphoid)" and was restricted to human species. Focusing on the synthetic styrene-butadiene rubber (SBR) industry cohort study conducted by the University of Alabama at Birmingham, USA, this review evaluates various statistical models and factors influenc- ing exposure-response modelling. RESULTS: Peak exposures to BD may be more influential in the dose-response relationship than cumulative or long-term exposure. The authors recommend utilizing ß-coefficients derived from the latest SBR study update, employing Cox proportional hazard modelling, non-lagged and non-transformed cumulative BD exposure, and adjusting for age and peak BD exposure. The study reveals that statistical model selection has a limited impact on the calculated dose-response effects. The significant variation in estimated cancer mortality values arises from additional assumptions needed for metrics like the excess leukemia risk or the occupational BD effective concentration. CONCLUSIONS: In con- clusion, this study provides insights into exposure-response modelling for BD exposure and leukemia mortality, highlighting the importance of peak exposures. The recommended statistical approach offers a reliable basis for regulatory risk assessment and public health population metrics. Int J Occup Med Environ Health. 2024;37(3):300-10.

Understanding the role of B cells in CAR T-cell therapy in leukemia through a mathematical model.

Chimeric antigen receptor T (CAR T) cell therapy has been proven to be successful against a variety of leukemias and lymphomas. This paper undertakes an analytical and numerical study of a mathematical model describing the competition of CAR T, leukemia, tumor, and B cells. Considering its significance in sustaining anti-CD19 CAR T-cell stimulation, a B-cell source term is integrated into the model. Through stability and bifurcation analyses, the potential for tumor eradication, contingent on the continuous influx of B cells, has been revealed, showing a transcritical bifurcation at a critical B-cell input. Additionally, an almost heteroclinic cycle between equilibrium points is identified, providing a theoretical basis for understanding disease relapse. Analyzing the oscillatory behavior of the system, the time-dependent dynamics of CAR T cells and leukemic cells can be approximated, shedding light on the impact of initial tumor burden on therapeutic outcomes. In conclusion, the study provides insights into CAR T-cell therapy dynamics for acute lymphoblastic leukemias, offering a theoretical foundation for clinical observations and suggesting avenues for future immunotherapy modeling research.

[Antibody-Drug Conjugate for Treating Leukemia and Lymphoma-The Present Status, Problems, and Future Development].

Antibody-drug conjugate(ADC)contain monoclonal antibodies that target-specific tumor antigens, cytotoxic payloads, and linkers. ADCs use antibodies to selectively act on tumors, making them more effective and less toxic. In Japan, 4 drugs are approved as ADCs for leukemia and lymphoma: gemtuzumab ozogamicin(GO)consists of an anti-CD33 monoclonal antibody bound to calicheamicin via a linker, approved for relapsed/refractory acute myeloid leukemia. Brentuximab vedotin (BV)has anti-CD30 antibodies bound to MMAE via a linker and is approved for CD30-positive Hodgkin's lymphoma, peripheral T-cell lymphoma, and cutaneous T-cell lymphoma. BV, in combination with multi-agent chemotherapy, resulted in significantly prolonged progression-free survival(PFS)in classical Hodgkin's lymphoma and peripheral T-cell lymphoma compared to the control group. Inotuzumab ozogamicin(IO)has an anti-CD22 antibody bound to calicheamicin via a linker, approved for relapsed/refractory CD22-positive B-cell acute lymphoblastic leukemia. In relapsed/refractory B-cell acute lymphoblastic leukemia, IO showed a higher complete remission rate than the control group. Polatuzumab vedotin(PV)has an anti-CD79b monoclonal antibody bounds to MMAE via a linker, approved for diffuse large B-cell lymphoma(DLBCL). In DLBCL patients with an international prognostic index score(IPI score)of 2 or higher, the combination of PV plus rituximab, cyclophosphamide, doxorubicin, and prednisone(PV+R-CHP)extended PFS at 2 years compared with R-CHOP(rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone), which has long been the standard of care. As shown, ADCs exhibit high therapeutic efficacy in leukemia and lymphoma treatment, but many aspects of their resistance mechanisms remain unclear and require further research.

[Aberrant Expression of Small Nucleolar RNA SNORA63 and Its Clinical Significance in Patients with Acute Leukemia].

OBJECTIVE: To investigate the expression level of small nucleolar RNA (snoRNA) SNORA63 in bone marrow of patients with acute leukemia (AL) and its significance in the clinical diagnosis, treatment and prognosis of AL patients. METHODS: Bone marrow samples of 53 newly diagnosed AL patients and 29 healthy subjects in the Affiliated Hospital of Guangdong Medical University from March 2018 to December 2021 were collected. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression level of SNORA63 in bone marrow mononuclear cells of the two groups. The median expression level of SNORA63 in AL patients was used as the boundary value to divide the patients into SNORA63 high and low expression groups, and the relationship between the expression level of SNORA63 and the clinical characteristics, clinical indicators and prognosis of AL patients was analyzed and discussed. RESULTS: The relative expression level of SNORA63 in AL patients was significantly lower than that in healthy control group [0.3018 (0.0244-1.2792) vs 1.0882 (0.2797-1.9889)] (P < 0.01). The expression level of SNORA63 in AL patients without remission after initial treatment was significantly lower than that in healthy controls and the patients who received complete remission (CR) (P < 0.01), while there was no statistical difference in the expression level of SNORA63 between AML and ALL groups (P >0.05). The abnormal low expression of SNORA63 was closely related to fever, hemorrage, poor prognosis, efficacy, platelets (PLT), lactate dehydrogenase (LDH), albumin (ALB), and molecular biological abnormalities of AL patients (P < 0.05), but not significantly correlated with sex, age, AL subtype, pallor, fatigue, extramedullary infiltration, white blood cell count (WBC), hemoglobin (HGB), C-reactive protein (CRP), procalcitonin (PCT), fibrinogen (FIB) or chromosome karyotype (P >0.05). Meanwhile, overall survival (OS) and event-free survival (EFS) of AL patients in SNORA63 high-expression group were significantly higher than those in SNORA63 low-expression group (P < 0.05). Univariate Cox regression analysis showed that SNORA63, molecular biological abnormalities, fever, PLT and LDH were the factors influencing OS and EFS in AL patients (P < 0.05). Multivariate Cox regression analysis indicated that fever, molecular biological abnormalities and LDH were independent factors associated with OS and EFS in AL patients (P < 0.05). CONCLUSION: SNORA63 is significantly down-expressed in AL patients, which is a molecular marker of great clinical value for disease monitoring and prognosis evaluation in AL patients.

[Comparison of Blood Oxygen Saturation Detection Methods in Patients with Hyperleukocytic Acute Leukemia].

OBJECTIVE: To investigate which indicator is more advantageous when using arterial oxygen saturation (SaO2) and fingertip pulse oxygen saturation (SpO2) for blood oxygen detection in patients with hyperleukocytic acute leukemia (HAL). METHODS: In this prospective research, the difference between SaO2 and SpO2 of 18 HAL patients (observation group) and 14 patients (control group), as well as the relationship between the difference and white blood cell (WBC) counts were analyzed. RESULTS: SaO2 was lower than SpO2 in the observation group (P <0.05), and SpO2-SaO2 difference was positively correlated with WBC counts (r =0.47). However, there was no statistical difference between SaO2 and SpO2 in the control group. SaO2 and PO2 showed a downward trend with the prolongation of detection time after arterial blood was collected in the observation group, but there was no statistical difference. There was no downward trend of SaO2 and PO2 in the control group. CONCLUSION: HAL patients have a phenomenon where SaO2 is lower than SpO2, that is pseudohypoxemia, and this phenomenon may be caused by excessive consumption of oxygen by the leukemia cells in vitro SpO2 can be monitored bedside in real time and is non-invasive, it is a better way to detect the blood oxygen status of HAL patients.