Generation of a new therapeutic D-peptide that induces the differentiation of acute myeloid leukemia cells through A TLR-2 signaling pathway.

Acute myeloid leukemia (AML) is caused by clonal disorders of hematopoietic stem cells. Differentiation therapy is emerging as an important treatment modality for leukemia, given its less toxicity and wider applicable population, but the arsenal of differentiation-inducing agents is still very limited. In this study, we adapted a competitive peptide phage display platform to search for candidate peptides that could functionally induce human leukemia cell differentiation.

Bone Marrow Mesenchymal Stem Cells-Derived Exosomal miR-425-5p Inhibits Acute Myeloid Leukemia Cell Proliferation, Apoptosis, Invasion and Migration by Targeting WTAP.

Introduction: Acute myeloid leukemia (AML) is a predominant blood malignancy with high mortality and severe morbidity. AML is affected by microRNAs (miRNAs) loaded in exosomes derived from bone marrow mesenchymal stem cells (BM-MSCs). MiR-425-5p has been reported to participate in different cancer models.

MicroRNA‑93 knockdown inhibits acute myeloid leukemia cell growth via inactivating the PI3K/AKT pathway by upregulating DAB2.

Acute myeloid leukemia (AML) is associated with a poor prognosis in elderly adults and currently lacks optimal treatment strategies. MicroRNAs (miRNAs or miRs) have increasingly been reported to be associated with AML progression; however, the mechanisms of action of miR‑93 in AML with the involvement of disabled 2 (DAB2) are currently unknown. In the present study, miR‑93 expression was assessed in patients with AML and in AML cell lines.

MiR-335-3p inhibits cell proliferation and induces cell cycle arrest and apoptosis in acute myeloid leukemia by targeting EIF3E.

Here, we aimed to investigate the biological roles and the regulatory mechanisms of miR-335-3p in acute myeloid leukemia (AML). We first found miR-335-3p was significantly downregulated in blood samples from leukemia patients and cell lines using reverse transcription quantitative polymerase chain reaction. Through CCK-8 assay and flow cytometry, we observed that miR-335-3p overexpression significantly inhibited cell proliferation and induced cell cycle G0/G1 arrest and apoptosis in AML cell lines (THP-1 and U937).

A Regulatory Loop Involving Notch and Wnt Signaling Maintains Leukemia Stem Cells in T-Cell Acute Lymphoblastic Leukemia.

Leukemia-initiating cells play critical role in relapse, resistance to therapies and metastases but the mechanism remains largely elusive. We report that β-catenin is over-expressed in almost all T-ALL patients and flow sorted β-catenin fractions are highly resistant to therapy, leading to liver metastases in nude mice as well as dysregulated lncRNAs. Pharmacological inhibition through XAV-939 as well as si-RNA mediated inhibition of β-catenin is initially effective in re-sensitization to therapy, however, prolonged inhibition shifts dependency from β-catenin to Notch signaling, with particularly high levels of receptors Notch 1 and Notch 2.

An Immune Risk Score Predicts Survival of Patients with Acute Myeloid Leukemia Receiving Chemotherapy.

Purpose: Prediction models for acute myeloid leukemia (AML) are useful, but have considerable inaccuracy and imprecision. No current model includes covariates related to immune cells in the AML microenvironment. Here, an immune risk score was explored to predict the survival of patients with AML.

Esophageal squamous cell cancer coincides with myelodysplastic syndrome/acute myelogenous leukemia: A case report and review of the literature.

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors, and has high incidence and mortality rates, worldwide. Myelodysplastic syndrome (MDS), a disorder of hematopoietic stem or progenitor cells, results in marrow failure, which increases the risk of acute myeloid leukemia (AML). Few studies had reported patients who have suffered from both ESCC and MDS/AML simultaneously.

High serum extracellular vesicle miR-10b expression predicts poor prognosis in patients with acute myeloid leukemia.

Background: Increasing evidence have demonstrated that serum extracellular vesicle microRNAs (EV-miRNAs) are promising noninvasive biomarkers for various cancer types.

Objective: In this study, we aimed to investigate and evaluate the potential clinical significance of serum EV-miR-10b for acute myeloid leukemia (AML).

Methods: Blood samples were collected from a cohort of 95 de novo AML patients and 80 healthy individuals.

PRDX6 promotes proliferation and induces chemo-resistance via peroxidase activity in Toledo diffuse large B-cell lymphoma cells.

Background: Diffuse large B cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphomas. Despite the application of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen being effective on 70-80% of DLBCL patients, the remaining 20-30% develop an even more aggressive relapsed tumor. PRDX6 has been shown to play important roles in multiple cancers.

CircRNA circ_0000190 inhibits the progression of multiple myeloma through modulating miR-767-5p/MAPK4 pathway.

Background: Multiple myeloma (MM) accounts for 10% of all hematological malignancies. Dysregulation of microRNAs (miRNAs) or long non-coding RNAs (lncRNAs) has important impacts on progression of MM. Circular RNAs (circRNAs) are correlated with malignancy in the modulation of tumor progression.

A Case of Unicentric Castleman Disease and Langerhans Cell Histiocytosis: Two Entities in One Lymph Node.

Castleman disease (CD) is a lymphoproliferative disorder and Langerhans cell histiocytosis (LCH) is a clonal disease of the monocyte-macrophage system. The authors describe a rare case of CD coexistent with LCH at diagnosis in one lymph node. Hematologic investigation and intrapulmonary mass biopsy were performed.

Knockdown of Long Noncoding RNA HOXA-AS2 Suppresses Chemoresistance of Acute Myeloid Leukemia via the miR-520c-3p/S100A4 Axis.

Background/aims: Among different molecular candidates, there is growing data to support that long noncoding RNAs (lncRNAs) play a significant role in acute myeloid leukemia (AML). HOXA-AS2 is significantly overexpressed in a variety of tumors and associated with anti-cancer drug resistance, however, little is known regarding the expression and function of HOXA-AS2 in the chemoresistance of AML. In this study, we aimed to determine the role and molecular mechanism of HOXA-AS2 in adriamycin-based chemotherapy resistance in AML cells.

Rapidly Progressive, Fata Infection Caused by Bacillus Cereus in a Patient with Acute Lymphoblastic Leukemia.

Background: We herein report a fatal case of fulminant septicemia caused by Bacillus cereus in a 49-year-old female with T-cell acute lymphoblastic leukemia receiving chemotherapy.

Methods: Her two blood culture sets were positive for Gram-positive, rod-shaped bacterium. Bacillus cereus was identified by high-throughput MALDI-TOF mass spectrometry and 16S ribosomal RNA gene sequencing.

Multiple Nonleukemic Myeloid Sarcoma Associated Hemophagocytic Lymphohistiocytosis in an Adult.

Background: Nonleukemic myeloid sarcoma (MS) occurs rarely. Hemophagocytic lymphohistiocytosis (HLH) is a rare and potentially fatal condition. We report a rare case of nonleukemic MS associated with HLH.

Acute promyelocytic leukaemia with a PML-RARA insertional translocation and a chromosome 21 abnormality in XYY syndrome: case report.

The concomitant presence of the XYY syndrome with haematological malignancies is rare. This report presents a case of acute promyelocytic leukaemia (APL) with the promyelocytic leukaemia-retinoic acid receptor alpha (PML-RARA) gene insertional translocation and a chromosome 21 abnormality in a 29-year-old XYY male patient. Karyotype analysis revealed an abnormal karyotype of 47,XYY [14]/46,XYY,-21[16].

Inhibition of c-Myc overcomes cytotoxic drug resistance in acute myeloid leukemia cells by promoting differentiation.

Nowadays, drug resistance still represents a major obstacle to successful acute myeloid leukemia (AML) treatment and the underlying mechanism is not fully elucidated. Here, we found that high expression of c-Myc was one of the cytogenetic characteristics in the drug-resistant leukemic cells. c-Myc over-expression in leukemic cells induced resistance to chemotherapeutic drugs, enhanced colony formation capacity and inhibited cell differentiation induced by all-trans retinoic acid (ATRA).

ATO/ATRA/anthracycline-chemotherapy sequential consolidation achieves long-term efficacy in primary acute promyelocytic leukemia.

The combination of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3, ATO) has been effective in obtaining high clinical complete remission (CR) rates in acute promyelocytic leukemia (APL), but the long-term efficacy and safety among newly diagnosed APL patients are unclear. In this retrospective study, total 45 newly diagnosed APL patients received ATRA/chemotherapy combination regimen to induce remission. Among them, 43 patients (95.

Acute pleural and pericardial effusion induced by chemotherapy in treating chronic myelocytic leukemia.

Background: Report of a rare and serious complication of chemotherapy with daunorubicin and cytarabine (DA regimen).

Methods: We report a special case of a patient diagnosed chronic myeloid leukemia (CML) with accelerated phase, who simultaneously suffered from acute pleural and pericardial effusion while receiving chemotherapeutic treatment with DA regimen.

Results: Following treatment with DA regimen, the patient had the symptoms of chest distress and shortness of breath, followed by respiratory failure and pericardial tamponade.

Diagnosis of Felty's syndrome, distinguished from hematological neoplasm: A case report.

Felty's syndrome (FS) is characterized by the three conditions of rheumatoid arthritis (RA), neutropenia and splenomegaly, and occurs in few cases of longstanding erosive RA. Discriminating between rare occurrences of autoimmune diseases and malignancies is crucial. The present study describes the case of a 17-year-old female with a two-year history of RA, presenting with an irregular fever, hepatosplenomegaly and enlarged lymph nodes.

Inhibition of autophagy augments the anticancer activity of α-mangostin in chronic myeloid leukemia cells.

Natural products possessing anticancer activity have been extensively studied because of their low toxicity and potential effect. α-Mangostin, a component of Garcinia mangostana Linn, is a xanthone derivative shown to have antioxidant and antitumor properties. This study was carried out to investigate how to improve the anticancer effects of α-mangostin in chronic myeloid leukemia (CML) cell lines bearing wild-type BCR-ABL or BCR-ABL-T315I mutation.

Diagnosis and treatment of a patient with isolated spinal granulocytic sarcoma: A case report.

A previously healthy 34-year-old female presented with a 5-month history of progressive backache and weakness in the left fingers. Magnetic resonance imaging (MRI) showed soft tissue masses in the spinal canal distributed along the nerve course. The patient's baseline laboratory data were normal.

Inhibition of extracellular signal-regulated kinase activity by sorafenib increases sensitivity to DNR in K562 cells.

The mitogen-activated protein kinase (MAPK) pathway has a protective function on the management of hematologic malignancies. The aim of this study was to assess whether the induction of MAPK-mediated effects contributes to the therapeutic value of combination sorafenib and daunorubicin (DNR) treatment. Herein, we found that DNR increased phosphorylation of extracellular signal-regulated kinases (ERK1/2) in K562 cells.

[Decitabine inhibits cell proliferation and induces apoptosis of all-trans retinoid acid-resistant acute promyelocytic leukemia NB4-R2 cell line].

The aim of this study was to investigate the proliferation-inhibitory and inducing apoptotic effects of decitabine (DAC) on acute promyelocytic leukemia NB4-R2 cells. Cell inhibitory rate was determined by cell proliferation and cytotoxicity assay (WST-1 assay) after NB4-R2 cells were treated with 0.01 - 0.