Publications by authors named "Jing-Xin Pan"

Purpose: N6-methyladenosine (m6A) is reported to play a critical role in cancer through various mechanisms. We aimed to construct and validate an m6A RNA methylation regulators-based prognostic signature for Esophageal cancer (ESCA).

Materials And Methods: The RNA sequencing transcriptome data of 13 m6A RNA methylation regulators as well as clinical data were obtained from The Cancer Genome Atlas (TCGA) ESCA database.

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Objective: To determine the clinical features and survival difference of HBV related and Non-HBV related diffuse large B-cell lymphoma (DLBCL) and to evaluate the occurrence of HBV reactivation in DLBCL patients and related risk factors for HBV reactivation after R-CHOP therapy.

Methods: A total of 246 patients diagnosed with CD20+ DLBCL were enrolled from June 2010 to June 2015. The medical records and survival data were analysed.

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Objective: To study whether chlorambucil has apoptotic effect on the B cell lymphoma A20 cells and its exact mechanisms in apoptotic signaling pathway.

Methods: The experimental cells were treated with 20 μmol/L chlorambucil, the control cells were treated with PBS. Annexin V-FITC Cell Apoptosis Detection Kit was used to examine cell apoptosis.

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To simulate the concept acquisition and binding of different senses in the brain, a biologically inspired neural network model named perception coordination network (PCN) is proposed. It is a hierarchical structure, which is functionally divided into the primary sensory area (PSA), the primary sensory association area (SAA), and the higher order association area (HAA). The PSA contains feature neurons which respond to many elementary features, e.

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Objective: To investigate the clinical characteristics and outcome of parhents with EBV infection conbined with hemophagocytic syndrome and Hodgkin's lymphoma.

Methods: The morphotogy of bone marrow cells was observed by bone marrow smear and light microscopy, the pathologic changes of bone marrow ware analyzed by bone marrow biopsy and immunohistochemistry methord, the pathologic changes of lymphonudes ware detected by immunohistochemical methord, the paticnts were treated with ABVD (epirubicin, bleomycin, vincristine and dacarbazine) chemotherapeutic regimen.

Results: Fever complicatid with pancytopenia, obvious increase of ferritin and sCD25, hypofibrinogenemia, hemophogocytic phenomen of bone marrow, increase of EBV-DNA copy number ware observed, which all accorded with the criteria EBV righted hemophagocytic syndrome.

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Objective: To study the clinical characteristics and prognosis of patients with variant Ph chromosome-positive leukemia.

Methods: The defection of morphology, cytogenetics, immunology and molecular biology was performed in 4 cares of variant Ph chromosome-positive leukemia, and the therepeuitics outcome of 4 patients was evaluated.

Results: Among 4 cases of variant Ph+ leukemia, 3 cases were patients with CML, including 1 case in chronic phase and 2 cases in accelerated phase; and 1 cases was patient with adult B acute lymphoblasric leukemia(B-ALL).

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Objective: To investigate the curative effect and safety of decitabine combined with IAG regimen for treating senile MDS-transformed AML patients.

Methods: Two cases of senile MDS-transformed AML were treated with decitabine combined with IAG regimen (decitabine 25 mg/d,qd,ivgtt,d1-5,Idarubicin 10 mg/d,qd,ivgtt,d6,Ara-C 10 mg/m,q12h, sc,d 6-19,G-CSF 300 µg,qd,ih,d6-19). The efficacy and adverse reactions were observed in these cases.

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Objective: To explore the action mechanism of chlorambucil against mantle cell lymphoma cell line Jeko-1.

Methods: The effect of chlorambucil on Jeko-1 cell proliferation was measured by MTT method. The effect of chlorambucil on the apoptosis of Jeko-1 cell was detected by Hoechst staining and Annexin V-FITC dual staining.

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Objective: To study the impact of high concentration insulin on the proliferation and apoptosis of K562 cell strain.

Methods: K562 cells were treated with different concentrations of insulin. The proliferation activity was tested by CCK-8 assay, cytometry, and trypan blue exclusion.

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Objective: To investigate the inhibitory effect of high concentration insulin on K562 cell proliferation and its underlying mechanism.

Methods: K562 cells were treated by different concentration of insulin and/or anti-IGF-1R antibody (IGF-1R-Ab), MTT assay and flow cytometry were used to detect the K562 cells proliferation and apoptosis, respectivety; Western blot was used to measure the expression and phosphorylation level of IGE-IR, Akt, Erk1/2 in K562 cells under the different concentration of insulin.

Results: MTT assay showed that less than 40 mU/ml insulin could promote K562 cell proliferation, while high concentration (> 40 mU/ml) insulin has been shown to inhibit K562 cell proliferation; Flow cytometry showed that 40 mU/ml insulin suppressed K562 cell apoptosis (P < 0.

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Objective: To explore the expression and promoter CpG island methylation status of miR-34b in leukemia cell lines and their clinical significance.

Methods: A total of 10 cases of non-hematologic diseases were selected as control group, and the bone marrow cells of control group and HL-60, K562 cells were selected; the relative expression of miR-34b was detected in bone marrow cells, HL-60 and K562 cell lines by fluorescence quantitative PCR, and the MiR-34b methylation status was detected by methylation-specific PCR, the HL-60 and K562 cell lines were treated with decitabine, and the expression levels and methylation status of miR-34b in the 2 cell lines were detected by the same method. Has-miR-34b was transfected into K562 cells, which were divided into non-transfection group, negative control group and Has-miR-34b transfection group; if the transfection was successful, the cell proliferation should be recorded at different time points of culture, and the proliferation inhibition rate should be calculated.

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Objective: To explore the effect of 2-methoxyestradiol (2-ME2) on apoptosis of human acute T lymphoblastic leukemia cells, and its underlying mechanism.

Methods: The growth inhibition of CEM cells was detected by MTT assay; apoptotic cells were detected by DNA laddering analysis; the expressions of P53 mRNA and protein were detected by RT-PCR and Western blot respectively.

Results: 2-ME2 remarkably inhibited the CEM cell growth and the 50% growth inhibitory concentration (IC50) at 48 h was 2 µmol/L.

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Article Synopsis
  • * A novel mutation c.946G>T/p.G316C was discovered in the COL1A2 gene, inherited from the father, while neither the mother nor other healthy relatives carried this mutation.
  • * The identified mutation is believed to be pathogenic and harmful, suggesting that future pregnancies should involve genetic screening for this COL1A2 mutation to assess the risk of OI type I in offspring.
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Objective: To reveal the molecular genetic pathogenesis of the glycogen storage disease type III (GSDIII) and to provide a prerequisite for prenatal gene diagnosis in future.

Method: All the coding regions as well as the border areas between exons and introns of the AGL gene and the parental relevant mutation sites were directly sequenced, so that to affirm the origin of the mutation. Then, detected novel heterozygous mutation was confirmed by cloning sequencing.

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Many reports have documented a role of insulin and insulin-like growth factor 1 (IGF-1) as growth factors in many cancers. The sequence and structure of insulin receptor (IR) and IGF receptor (IGF-1R) are highly similar. Both receptors are overexpressed in leukemia cells.

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As a hormone with a number of biological effects, insulin not only displays the function of classic metabolic regulation, but also can regulate cell proliferation and differentiation, and ensure growth and development of embryos and young individuals. In vitro insulin can stimulate cell proliferation and differentiation. Insulin is also an important growth regulator in vivo, which has been proved in more and more studies.

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Here in a co-cultivation system of natural killer (NK) cells and K562 cells, monocytes (MO) and/or interleukin (IL)-2/phytohemagglutinin (PHA) were administered. After MO were administered, reactive oxygen metabolites (ROM)/reactive nitrogen metabolites (RNM) productions increased, while tumor necrosis factor (TNF)-β/interferon (IFN)-γ levels and NK cell cytotoxicity (NCC) decreased, the changes of which after administering tiopronin (TIP) or glutamylcysteinylglycine (GSH) were opposite. In conclusions, the activated MO could inhibit the NK cell activity to kill K562 cell by secreting ROM and RNM.

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Objective: To explore the effects of the exogenous and endogenous reactive nitrogen metabolites (RNM) as NK cell inhibitors on NK cell-mediated killing of K562 cells and the influence of Tiopronin (TIP), glutamylcysteinylglycine (GSH) and histamine dihydrochloride (DHT) as RNM scavengers on reversing the suppressing effect of RNM.

Methods: The exogenous ONOO(-) was administered in the NK+K562 culture system, then the RNM scavengers were added in the NK+K562+ONOO(-) culture system, respectively. The concentrations of RNM, TNF-beta and IFN-gamma, K562 cell inhibition rate (KIR) and the percentage of living NK cells were examined.

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Objective: To identify the mutations of iduronate-2-sulfatase (IDS) gene, to reveal its mutation features, and to establish a basis for genetic counseling and prenatal gene diagnosis of Hunter syndrome.

Methods: Urine glycosaminoglycans (GAGs) assay, PCR and DNA sequencing were performed to detect mutation of IDS gene of the patient and his parents.

Results: The result showed that the patient was: DS(++), HS(++), KS(-), CS(-), and that both of his parents were negative.

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To investigate the reversal effect of reduced glutathione (GSH) on suppression of NK cells by reactive oxygen metabolites (ROM) in K562 cells, interleukin-2 (IL-2) or mononuclear cell (Mo) was added in cultured cell line of K562 cells and NK cells, the yield of ROM and K562 cell suppression rate were observed. Then the histamine dihydrochloride (DHT) or GSH was added in the mixed cultured cell lines, the ROM production and K562 cell suppression rate were observed. The results showed that the ROM yield increased from 33.

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To investigate the effect of a new reactive oxygen metabolites (ROM) scavenger as immune adjuvant in NK cell-mediated killing effect on K562 cell, IL-2 and PHA were used to activate monocyte to produce ROM, and different concentrations of tiopronin as ROM scavenger was used in the cultivated systems with different ratio of monocytes plus NK cells and K562 cells, while histamine dihydrochloride (DHT) with different concentrations was used as positive control. The reuslts indicated that after IL-2 and PHA were supplemented in the cultivated systems mixing with NK cells and K562 cells as the E/T ratio was 10/1, the ROM production increased from 33.17 +/- 25.

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