[Toxicity Management and Efficacy Evaluation of BCMA-CART in the Treatment of Relapsed and Refractory Multiple Myeloma].

Objective: To investigate the toxicity management and efficacy evaluation of BCMA-chimeric antigen receptor T cells(CART) in the treatment of relapsed and refractory multiple myeloma (MM).

Methods: The efficacy and adverse reactions of 21 patients with MM who received BCMA-CART treatment at the First Affiliated Hospital of Wenzhou Medical University from December 2017 to September 2020 were evaluated, and the efficacy assessment and survival analysis for high-risk patients and non-high-risk patients were evaluated.

Results: After infusion of BCMA-CART cells in 21 MM patients, the number of effective cases was 17, of which the complete remission (sCR/CR) was 10, and the partial remission (VGPR/PR) was 7.

Interaction between CD9 and PI3K‑p85 activates the PI3K/AKT signaling pathway in B‑lineage acute lymphoblastic leukemia.

Our previous study has shown that knockdown could suppress cell proliferation, adhesion, migration and invasion, and promote apoptosis and the cytotoxicity of chemotherapeutic drugs in the B‑lineage acute lymphoblastic leukemia (B‑ALL) cell line SUP‑B15. In this study, we further investigated the molecular mechanism underlying the effects of CD9 on leukemic cell progression and the efficacy of chemotherapeutic agents in B‑ALL cells. Using the CD9‑knockdown SUP‑B15 cells, we demonstrated that the silencing of the gene significantly reduced the expression of phosphorylated‑phosphatidylinositol‑3 kinase (p‑PI3K), phosphorylated‑protein kinase B (p‑AKT), P‑glycoprotein (P‑gp), multidrug resistance‑associated protein 1 (MRP1), breast cancer resistance protein (BCRP), matrix metalloproteinase 2 (MMP2) and phosphorylated‑focal adhesion kinase (p‑FAK).

Normal Absolute Monocyte Count at the Time of Relapse is Associated with Improved Survival After First Salvage Therapy in Adult Patients with Early Relapsed B-Lineage Acute Lymphoblastic Leukemia.

Background: Peripheral monocytes, a key cell type for innate immunity, have been shown to be associated with survival in various types of hematological malignancies. However, no previous studies regarding the prognostic impact of peripheral absolute monocyte count (AMC) in early relapsed B-lineage acute lymphoblastic leukemia (B-ALL) have been reported.

Methods: Forty-nine cases of early relapsed adult B-ALL were reviewed.

Effect of initial absolute monocyte count on survival outcome of patients with de novo non-M3 acute myeloid leukemia.

Increased absolute monocyte count (AMC) at presentation has recently been associated with clinical outcome in different types of hematological malignancies. This study aimed to assess the prognostic value of AMC on survival in 193 adult patients with de novo non-M3 acute myeloid leukemia (AML). The median AMC for all patients at diagnosis was 0.

Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.

HOTAIR is significantly overexpressed in various cancers and facilitates tumor invasion and metastasis. However, whether HOTAIR plays oncogenic roles in acute myeloid leukemia (AML) is still unknown. Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts.

Pure curcumin increases the expression of SOCS1 and SOCS3 in myeloproliferative neoplasms through suppressing class I histone deacetylases.

Suppressors of cytokine signaling, SOCS1 and SOCS3, are important negative regulators of Janus kinase 2/signal transducers and activators of transcription signaling, which is constitutively activated in myeloproliferative neoplasms (MPNs) and leukemia. Curcumin has been shown to possess anticancer activity through different mechanisms. However, whether curcumin can regulate the expression of SOCS1 and SOCS3 is still unknown.

[Clinical study of correlation between the expression of ICBP90 and hematopoietic suppression in patients with chronic benzene poisoning].

Objective: To observe the change of ICBP90 expression in patients with chronic benzene poisoning and explore the correlation between the expression of ICBP90 and benzene-induced hematotoxicity.

Methods: The bone marrow samples were from 13 chronic benzene poisoning cases with hematopoietic suppression, 11 chronic benzene poisoning cases with hematopoietic regeneration and 10 controls. Western-blot was applied to detect the ICBP90 expression in bone marrow mononuclear cells (BMNCs).

Pure curcumin decreases the expression of WT1 by upregulation of miR-15a and miR-16-1 in leukemic cells.

Background: Pure curcumin has been reported to down-regulate the expression of WT1 in leukemic cells. However, the molecular mechanism underlying the down-regulation of WT1 by curcumin is not completely delineated. The purpose of this present study is to identify a new miRNA-mediated mechanism which plays an important role in the anti-proliferation effects of curcumin in leukemic cells.

miR-15a and miR-16-1 inhibit the proliferation of leukemic cells by down-regulating WT1 protein level.

Background: miR-15a and miR-16-1(miR-15a/16-1) have been implicated as tumor suppressors in chronic lymphocytic leukemia, multiple myeloma, and acute myeloid leukemic cells. However the mechanism of inhibiting the proliferation of leukemic cells is poorly understood.

Methods: K562 and HL-60 cells were transfected with pRS-15/16 or pRS-E, cell growth were measured by CCK-8 assay and direct cell count.

miR-15a/16-1 enhances retinoic acid-mediated differentiation of leukemic cells and is up-regulated by retinoic acid.

miR-15a and miR-16-1 (miR-15a/16-1) have been implicated in apoptosis, cell cycle regulation and chemosensitivity of tumor cells, but little is known about the role of miR-15a/16-1 in the differentiation of leukemic cells. In this study, we found that the expression level of miR-15a/16-1 was up-regulated by all-trans retinoic acid (ATRA) treatment in NB4, HL-60 and U937 cell lines and primary leukemic cells. Overexpression of miR-15a/16-1 could not directly drive cells to undergo differentiation but enhanced ATRA-induced differentiation in NB4 and U937 cells.

[Anti-cD20scFv/CD80/CD28/zeta specific T lymphocytes eradicate primary chronic lymphocytic leukemia cells in vitro].

Objective: To construct anti-CD20scFv/CD80/CD28/zeta recombinant gene modified T cells, test its effectiveness of eradicating CD20 positive primary chronic lymphocytic leukemia (CLL) cells and provide a promising tool for tumor adoptive immunotherapy.

Methods: The recombinant vectors were transduced into PA 317 cells and high titer retroviruses were obtained to infect human peripheral blood T lymphocytes. Resistant T cells were obtained by G418 selection for one week.

Synergistic apoptosis induction in leukemic cells by miR-15a/16-1 and arsenic trioxide.

MicroRNAs (miRNAs) are small noncoding RNAs that regulate target gene expression through translation repression or messenger RNA degradation. MiR-15a and 16-1 form a cluster at the chromosomal region 13q14, which is frequently deleted or down-regulated in chronic lymphocytic leukemia. Arsenic trioxide (As(2)O(3), ATO) has been successfully applied to treat acute promyelocytic leukemia (APL).