Search

Molecular measurable residual disease can persist in core-binding factor acute myeloid leukemia in otherwise disease-free patients. Utilizing cell sorting followed by fluorescent in situ hybridization, we show that detection is due to mast cells.

Detection of measurable residual disease detection (MRD) by flow cytometry after the first course of chemotherapy is a standard measure of early response in patients with acute myeloid leukemia (AML). Myeloid leukemia associated with Down Syndrome (ML‐DS) is a distinct form of AML. Differences in steady‐state and regenerating hematopoiesis between patients with or without DS are not well understood. This understanding is essential to accurately determine the presence of residual leukemia in patients with ML‐DS. A standardized antibody panel defined quantitative antigen expression in 115 follow‐up bone marrow (BM) aspirates from 45 patients following chemotherapy for ML‐DS or DS precursor B‐cell acute lymphoblastic leukemia (B‐ALL‐DS) with the “difference from normal (ΔN)” technique. When possible, FISH and SNP/CGH microarray studies were performed on sorted cell fractions. 93% of BM specimens submitted post chemotherapy had a clearly identifiable CD34+CD56+population present between 0.06% and 2.6% of total non‐erythroid cells. An overlapping CD34+HLA‐DRheterogeneouspopulation was observed among 92% of patients at a lower frequency (0.04%–0.8% of total non‐erythroid cells). In B‐ALL‐DS patients, the same CD34+CD56+HLA‐DRheterogeneousexpression was observed. FACS‐FISH/Array studies demonstrated no residual genetic clones in the DS‐specific myeloid progenitor cells. Non‐malignant myeloid progenitors in the regenerating BM of patients who have undergone chemotherapy for either ML‐DS or B‐ALL‐DS express an immunophenotype that is different from normal BM of non‐DS patients. Awareness of this DS‐specific non‐malignant myeloid progenitor is essential to the interpretation of MRD by flow cytometry in patients with ML‐DS.

Myelodysplastic syndromes (MDS) are a heterogenous collection of clonal bone marrow diseases characterized by cytopenias, abnormal karyotypes, molecular abnormalities, and dysplasia by flow cytometry and/or morphology. The progression of MDS to severe cytopenias and/or overt leukemia is associated with the accumulation of additional cytogenetic abnormalities, suggesting clonal evolution. The impact of these accumulated abnormalities on myeloid maturation and the severity of the disease is poorly understood. Bone marrow specimens from 16 patients with cytogenetic abnormalities were flow cytometrically sorted into three myeloid populations: progenitors, immature myeloid cells, and mature myeloid cells. Fluorescence in situ hybridization analysis was performed on each to determine the distribution of chromosomal abnormalities during myeloid maturation. Our findings revealed three distinct distributions of cytogenetic abnormalities across myeloid maturation, each of which corresponded to specific cytogenetic abnormalities. Group 1 had continuous distribution across all maturational stages and contained patients with a single cytogenetic aberration associated with good‐to‐intermediate prognosis; Group 2 had accumulation of abnormalities in immature cells and contained patients with high‐risk monosomy 7; and Group 3 had abnormalities defining the founding clone equally distributed across maturational stages while subclonal abnormalities were enriched in progenitor cells and contained patients with multiple, non‐monosomy 7, abnormalities with evidence of clonal evolution. Our findings demonstrate that low‐risk abnormalities (e.g., del(20q) and trisomy 8) occurring in the founding clone display a markedly different disease etiology, with respect to myeloid maturation, than monosomy 7 or abnormalities acquired in subclones, which result in a disruption of myeloid cell maturation in MDS.

As the most common cancer disease in the world, breast cancer is the main cause of death of female cancer patients. The number of women in China is far greater than that in other countries. Therefore, the absolute death toll is often high. Even a small increase in incidence rate will lead to a severe increase in deaths. Therefore, accurate preoperative diagnosis of benign and malignant breast cancer and the status prediction of various clinical indicators are urgently needed in clinical practice. Deep learning based on neural network has been widely used in diagnosis. Therefore, this paper attempts to explore the influence of deep learning on the auxiliary diagnosis technology of small tumor in mammography. In this paper, 200 cases of breast disease patients in a hospital of our city were taken as the research object, and the artificial neural network model was established. Through the experimental simulation, the results showed that the diagnostic sensitivity, specificity and overall accuracy of BP neural network for test set samples were 95.3%, 96.7 and 96.2%, respectively. The experimental results confirmed its generalization ability. In this paper, the core idea of multi feature kernel hash, combined with a variety of features and deep kernel hash network framework, constructs a new multi feature based deep learning network, which can effectively express the image features of breast tumor, and complete the task of breast micro tumor detection with good performance.

Introduction: Core binding factor acute myeloid leukemia (CBF-AML) accounts for 30% of pediatric and 15% adult AMLs and is defined by fusions involving RUNX1or CBFB. RT-PCR is commonly used to monitor measurable residual disease (MRD) in patients with CBF-AML. However, it has been reported that these fusions can be detected in patients during complete remission (CR) or after hematopoietic cell transplant (HCT). This raises the question of if these patients should be considered MRD positive, given they appear otherwise disease free. We utilized flow cytometric cell sorting and fluorescent in situhybridization (FISH) to determine the source of persistent CBF fusions.

Sustainable development is one of the themes of the world today. Considering growing urban traffic problems and urban environmental problems, developing sustainable transport is particularly important. Based on the urban traffic sustainable development theory, an evaluation index system of traffic sustainable development is built using analysis method and testing methods of index system. Then an improved entropy method is used to define the weight of index of traffic sustainable evaluation index system, and an evaluation model is built, which provides a new perspective for urban sustainable development research.

Induced pluripotent stem cells (iPSCs) hold great promise for modeling human hematopoietic diseases. However, intrinsic variability in the capacities of different iPSC lines for hematopoietic development complicates comparative studies and is currently unexplained. We created and analyzed 3 separate iPSC clones from fibroblasts of 3 different normal individuals using a standardized approach that included excision of integrated reprogramming genes by Cre-Lox mediated recombination. Gene expression profiling and hematopoietic differentiation assays showed that independent lines from the same individual were generally more similar to one another than those from different individuals. However, one iPSC line (WT2.1) exhibited a distinctly different gene expression, proliferation rate, and hematopoietic developmental potential relative to all other iPSC lines. This “outlier” clone also acquired extensive copy number variations (CNVs) during reprogramming, which may be responsible for its divergent properties. Our data indicate how inherent and acquired genetic differences can influence iPSC properties, including hematopoietic potential.

Induced pluripotent stem cells (iPSCs) hold great promise for modeling human hematopoietic diseases. However, intrinsic variability in the capacities of different iPSC lines for hematopoietic development complicates comparative studies and is currently unexplained. We created and analyzed 3 separate iPSC clones from fibroblasts of 3 different normal individuals using a standardized approach that included excision of integrated reprogramming genes by Cre-Lox mediated recombination. Gene expression profiling and hematopoietic differentiation assays showed that independent lines from the same individual were generally more similar to one another than those from different individuals. However, one iPSC line (WT2.1) exhibited a distinctly different gene expression, proliferation rate, and hematopoietic developmental potential relative to all other iPSC lines. This “outlier” clone also acquired extensive copy number variations (CNVs) during reprogramming, which may be responsible for its divergent properties. Our data indicate how inherent and acquired genetic differences can influence iPSC properties, including hematopoietic potential.

Programmed cell death, or apoptosis, is a highly conserved cellular process that has been intensively investigated in nematodes, flies, and mammals. The genetic conservation, the low redundancy, the feasibility for high-throughput genetic screens and the identification of temporally and spatially regulated apoptotic responses make Drosophila melanogastera great model for the study of apoptosis. Here, we review the key players of the cell death pathway in Drosophila and discuss their roles in apoptotic and non-apoptotic processes.