[Expression of Wilms' Tumor 1 Gene in Bone Marrow of Patients with Myelodysplastic Syndrome and Its Clinical Significance].

Objective: To investigate the expression level and clinical significance of Wilms' tumor 1 (WT1) in bone marrow of patients with myelodysplastic syndromes (MDS).

Methods: The clinical data of 147 MDS patients who accepted real-time quantitative polymerase chain reaction (RT-PCR) to detect the expression level of WT1 in bone marrow before treated in Nanfang Hospital, Southern Medical University from January 2017 to April 2021 were retrospectively analyzed. According to the expression level of WT1, the patients were divided into WT1 group and WT1 group, their clinical characteristics and prognosis were analyzed.

hnRNPK/Beclin1 signaling regulates autophagy to promote imatinib resistance in Philadelphia chromosome-positive acute lymphoblastic leukemia cells.

This study sought to clarify the role of heterogeneous nuclear ribonucleoprotein K (hnRNPK) as a regulator of imatinib resistance in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph ALL). Expression of hnRNPK was assessed in Ph ALL leukemia cells in vitro and in vivo, and imatinib susceptibility was assessed via CCK-8 assay. In cells in which hnRNPK levels had or had not been modulated, LC3Ⅰ/Ⅱ and mTOR/p-ERK/Beclin1 levels were assessed via Western blotting, while electron microscopy was used to evaluate autophagic vacuole formation.

[Establishing the Ion Torrent PGM Sequencing Methods for the Clinical Diagnosis of MPN Patients].

Objective: To investigate the feasibility and relibility of rapidly and accurately acquiring the informations of gene mutations in MPN patients by using self-designed custom MPN mutation-related multipe-PCR primer kit and next generation Ion Torrent PGM sequencing platform.

Methods: The bone marrow samples of 10 MPN patients with JAK2V617F and/or CALR, Ph confirmed by sanger sequencing method were collected and were re-detected by using next generation Ion Torrent PGM sequencing method, then the consistence of results of above-mentioned 2 kinds of detection methods was compared.

Results: In terms of JAK2V617F, MPL and CALR mutations, the results of Ion Torrent PGM sequencing were complete consistent with results of Sanger sequencing, except 52 bp deletion of CALR gene, which conld not be detected by next generation Ion Torrent PGM sequencing method in all bone marrow samples.

Association between the concentration of imatinib in bone marrow mononuclear cells, mutation status of ABCB1 and therapeutic response in patients with chronic myelogenous leukemia.

Low concentrations of imatinib (IM) in bone marrow cells have been linked with poor prognosis in patients with chronic myeloid leukemia (CML), which may be caused by the emergence of ATP-binding cassette transporter B1 (ABCB1) mutations. The aim of present study was to investigate how clinical outcomes vary among patients with different single nucleotide polymorphisms (SNPs) of ABCB1. A total of 48 adult patients with CML and higher than median ABCB1 mRNA levels were selected for testing of ABCB1 SNPs.

Immunophenotypes and immune markers associated with acute promyelocytic leukemia prognosis.

CD2+, CD34+, and CD56+ immunophenotypes are associated with poor prognoses of acute promyelocytic leukemia (APL). The present study aimed to explore the role of APL immunophenotypes and immune markers as prognostic predictors on clinical outcomes. A total of 132 patients with de novo APL were retrospectively analyzed.

[Effects of hOCT1 and ABCB1 gene on the efficacy of imatinib mesylate in chronic myelocytic leukemia].

Objective: To detect the expression of hOCT1 and ABCB1 in marrow cells and examine the efficacy of imatinib mesylate (IM) in patients with chronic myelocytic leukemia (CML).

Methods: hOCT1 and ABCB1 gene in 90 samples with chronic phase CML diagnosed at our hospital from January 2008 and June 2011 were detected by taqman probe real-time reverse transcription-PCR (RT-PCR). The samples were divided into 3 groups: drug-resistant group (n = 17), partial cytological remission (PCyR) group (n = 11) and complete cytogenetic remission (CCR) group (n = 62) according to IM efficacy and 3 - 6, 7 - 12, 13 - 24, 25 - 48, > 48 months five groups (n = 21, 8, 15, 29, 17) according to IM treatment course.

[Detection of the JAK2 gene mutation in familial myeloproliferative neoplasm and its clinical significance].

Objective: To comprehend the abnormalities of JAK2, c-mp, EPOR, MPW515L/K and TET2 genes in patients with familial myeloproliferative neoplasm (MPN) and their relatives, and to explore mechanism of MPN pathogenesis.

Methods: The complete blood counts of 2 brothers diagnosed with MPN in out hospital and their family members (15 persons in together) were performed, and bone marrow (BM) examinations in patients with abnormal blood count were performed PCR, DNA sequencing were used to evaluate the expression of related genes.

Results: The elder brother was diagnosed with essential thrombocythemia (ET), the younger one was polycythemia vera (PV), and others had no clinical manifestation.

[Clinical significance of monitoring BK polyomavirus in patients after hematopoietic stem cell transplantation].

This study was aimed to establish a method for rapid detecting BK polyomavirus (BKV) and to investigate the feasibility and value used in leukemia patients undergoing hematopoietic stem cell transplantation. Primers were designed according to BKV gene sequence; the quantitative standards for BKV and a real-time fluorescent quantitative PCR for BKV were established. The BKV level in urine samples from 36 patients after hematopoietic stem cell transplantation were detected by established method.

Imatinib and bortezomib induce the expression and distribution of anaphase-promoting complex adaptor protein Cdh1 in blast crisis of chronic myeloid leukemia.

Anaphase promoting complex cofactor Cdh1 plays a critical role in tumor suppression and genomic stability in cancer. However, its role in chronic myeloid leukemia (CML) remains unclear. We treated both wild-type and imatinib-resistant K562 cells with imatinib or nilotinib and bortezomib, respectively.