CCL17, CCL22 and their receptor CCR4 in hematologic malignancies.

Hematological malignancies (HM) are common malignant tumors with high morbidity and mortality rates, and are malignant diseases that seriously affect human health, with chemotherapy prone to recurrence and toxic side effects. Therefore, the development of precise, effective, and safe targeted therapeutic agents has become a hotspot in the current research of antitumor technology. More and more studies have shown that the interaction of C-C chemokine ligand 17 (CCL17) and C-C chemokine ligand 22 (CCL22) with the receptor C-C chemokine receptor type 4 (CCR4) promotes the immune escape of tumors and is closely related to the occurrence, development, and prognosis of hematological tumors.

Recent advances in the treatment and prevention of peripheral neuropathy after multiple myeloma treatment.

The incidence of multiple myeloma (MM) is increasing year by year, requiring chemotherapy drugs to control the condition. With the advent of new proteasome inhibitors, immunomodulators, and monoclonal antibodies, the prognosis of patients has improved significantly. However, peripheral neuropathy caused by drugs limits the dose and duration of treatment, which seriously affects patients' quality of life and treatment outcome.

Animal models of chemotherapy-induced peripheral neuropathy for hematological malignancies: A review.

Chemotherapy is one of the main treatments for hematologic malignancies. However, chemotherapy-induced peripheral neuropathy (CIPN) is one of the most common long-term toxic reactions in chemotherapy, and the occurrence of CIPN affects patients' quality of life and can cause interruption of chemotherapy in severe cases, thus reducing the efficacy of chemotherapy. We currently summarize the existing CIPN animal models, including the characteristics of several common animal models such as bortezomib-induced peripheral neuropathy, vincristine-induced peripheral neuropathy, and oxaliplatin-induced peripheral neuropathy.

[Expression and Clinical Significance of CTGF in Patients with Multiple Myeloma].

Objective: To detect the relationship between CTGF in the bone marrow of MM patients and osteolytic lesion of myeloma, moreover, to investigate the clinical significance of CTGF in MM.

Methods: Fifity-four MM patients treated in our hospital from March 2019 to April 2020 were enrolled, and 28 healthy volunteers were selected as the control group. The plasma in bone marrow of the patients was collected, and the ELISA was used to detect the level of CTGF in bone marrow plasma and the relationship between its and clinical characteristics were statistically analyzed.

DPEP1 expression promotes proliferation and survival of leukaemia cells and correlates with relapse in adults with common B cell acute lymphoblastic leukaemia.

Dehydropeptidase-1 (DPEP1) is a zinc-dependent metalloproteinase abnormally expressed in many cancers. However, its potential role in adults with B cell acute lymphoblastic leukaemia (ALL) is unknown. We found that in adults with common B cell ALL high DPEP1, transcript levels at diagnosis were independently associated with an increased cumulative incidence of relapse (CIR) and worse relapse-free survival (RFS) compared with subjects with low transcript levels.

Knockdown of eukaryotic translation initiation factor 3 subunit B inhibits cell proliferation and migration and promotes apoptosis by downregulating WNT signaling pathway in acute myeloid leukemia.

The study aimed to investigate the effect of eukaryotic translation initiation factor 3 subunit B (EIF3B) on cell proliferation, migration, and apoptosis as well as the underlying mechanism in acute myeloid leukemia (AML). EIF3B expression was detected in AML-193, HL-60, OCI-AML2, and KG-1 cell lines and human primary bone marrow mononuclear cells (BMMC). EIF3B knockdown was realized by transfecting EIF3B ShRNA plasmids, and EIF3B knockdown and WNT2 overexpression were established by transfecting EIF3B ShRNA plasmids and WNT2 overexpression plasmids into KG-1 cells.

polysaccharides regulate the innate immunity of colorectal cancer cells by modulating the TLR4 signaling pathway.

Background: It has been well-recognized that the polysaccharides from (PAM) are immune system enhancers, which can facilitate the proliferation of lymphocytes and stimulate immune cells. Nevertheless, the antitumor effects of PAM and their molecular mechanisms remain unclear.

Aim: Our research aimed to evaluate the anti-cancer effects of PAM on colorectal cancer (CRC).

Human Bone Marrow Mesenchymal Stem Cells Rescue Endothelial Cells Experiencing Chemotherapy Stress by Mitochondrial Transfer Via Tunneling Nanotubes.

Tunneling nanotubes (TNTs) are newly discovered tubular structures between two distant cells that facilitate the intercellular exchange of signals and components. Recent reports show that mesenchymal stem cells (MSCs) can rescue injured target cells and promote recovery from a variety of stresses via TNT-mediated mitochondrial transfer. In this study, we explored how TNTs form between bone marrow MSCs and endothelial cells (ECs) by using a human umbilical cord vein endothelial cell (HUVEC) model.

mTOR up-regulation of PFKFB3 is essential for acute myeloid leukemia cell survival.

Although mTOR (mammalian target of rapamycin) activation is frequently observed in acute myeloid leukemia (AML) patients, the precise function and the downstream targets of mTOR are poorly understood. Here we revealed that PFKFB3, but not PFKFB1, PFKFB2 nor PFKFB4 was a novel downstream substrate of mTOR signaling pathway as PFKFB3 level was augmented after knocking down TSC2 in THP1 and OCI-AML3 cells. Importantly, PFKFB3 silencing suppressed glycolysis and cell proliferation of TSC2 silencing OCI-AML3 cells and activated apoptosis pathway.

Rosiglitazone Promotes Bone Marrow Adipogenesis to Impair Myelopoiesis under Stress.

Objective: The therapeutic use of thiazolidinediones (TZDs) causes unwanted hematological side effects, although the underlying mechanisms of these effects are poorly understood. This study tests the hypothesis that rosiglitazone impairs the maintenance and differentiation of hematopoietic stem/progenitor cells, which ultimately leads to hematological abnormalities.

Methods: Mice were fed a rosiglitazone-supplemented diet or a normal diet for 6 weeks.

[Expression and significance of MMP-26, TIMP-4 and MMP-9 in diffuse large B-cell lymphoma cells].

The aim of this study was to investigate the expression of matrix metalloproteinase 26 (MMP-26), tissue inhibitor of metalloproteinase-4 (TIMP-4) and matrix metalloproteinase 9 (MMP-9) in patients with diffuse large B cell lymphoma (DLBCL) and their correlations with pathogenesis and development of DLBCL. A total of 95 specimens excised from DLBCL patients were prepared. Expression of MMP-26, TIMP-4 and MMP-9 were tested by SABC immunohistochemistry method and its correlation to clinicopathology indexes were analyzed.