Background: Diffuse large B-cell lymphoma (DLBCL) is considered the most common aggressive subtype of lymphoma. A number of DLBCL patients fail to achieve a response to currently available therapies or develop resistance. β-Elemene is derived from herb Curcuma wenyujin, and exhibits anti-tumor activity in both solid and non-solid tumors through modulating several molecular signaling pathways. We aimed to explore the role of β-elemene in DLBCL treatment and elucidate the involved mechanism. Materials and methods: Cell viability, apoptosis and expressions of related proteins were assessed and in vivo study were performed to determine the tumor suppressive effect of β-elemene and explore the molecular mechanisms. Results: β-Elemene significantly suppressed the viability of DLBCL cells, and β-elemene down-regulated the lncRNA HULC expression and regulated key pro-apoptotic and anti-apoptotic proteins to induce significant apoptosis of DLBCL cells. HULC overexpression could decrease the β-elemene induced apoptosis, while HULC knockdown increased the apoptosis in DLBCL cells. In vivo study further confirmed that β-elemene could suppress the growth of DLBCL xenograft and regulate the HULC expression and the critical proteins of the apoptotic pathway. Conclusion: β-Elemene performs as a tumor suppressor and modulator of HULC-mediated apoptotic pathway in DLBCL and will be an alternative candidate for clinical application.
Aplastic anemia (AA) is an autoimmune disease characterized by peripheral blood pancytopenia and bone marrow failure. Recently, a research study verified bone marrow failure of AA patients resulting from hematopoietic stem and progenitor cell (HSPC) attack by active T cells. Nonetheless, whether B cells, as one of the important immune cells, destruct the hematopoiesis is still unclear. Here, a large-scale single-cell transcriptomic sequencing of 20,000 bone marrow cells from AA patients and healthy donors was performed. A total of 17 clusters and differentially expressed genes were identified in each cluster relative to other clusters, which were considered potential marker genes in each cluster. The top differentially expressed genes in HSPCs (S100A8, RETN, and TNFAIP3), monocytes (CXCL8, JUN, and IL1B), and neutrophils and granulocytes (CXCL8, NFKBIA, and MT-CYB) were related to immune and inflammatory injury. Then, the B-cell receptor (BCR) diversities and pairing frequencies of V and J genes were analyzed. The highest pairing frequencies in AA patients were IGHV3-20-IGKJ2, IGHV3-20-IGKJ4, and IGHV3-20-IGHLJ2. Meanwhile, there were 3 V genes, including IGHV3-7, IGHV3-33, and IGLV2-11, with elevated expression in B cells from AA patients. Cell type–specific ligand–receptor was further identified in B-cell interaction with hematopoietic cells in the bone marrow. The changed ligand–receptor pairs involved antigen presentation, inflammation, apoptosis, and proliferation of B cells. These data showed the transcriptomic landscape of hematopoiesis in AA at single-cell resolution, providing new insights into hematopoiesis failure related with aberrance of B cells, and provide available targets of treatment for AA.
Background:Allogeneic stem-cell transplantation (SCT) is a well-established immunotherapeutic strategy for multiple myeloma (MM) with a potent and often sustained graft-vs.-myeloma effect. This multicenter investigation aimed to analyze the complications and survival of haploidentical SCT in patients with MM, and compare the main outcomes with matched-related donors (MRDs).Methods:Haploidentical and MRD SCT was identified from a cohort of 97 patients with MM who received a myeloablative transplantation in 13 hospitals from May 2001 to December 2017. A matched-pair analysis was designed. For each haplo recipient, the recipients were randomly selected from the MRD group and were matched according to the following criteria: year of the hematopoietic SCT (±2 years), disease status at transplantation, and the length of follow-up.Results:Seventy cases received MRD and 27 received haploidentical transplantation. The two groups showed no significant differences regarding age, gender, cytogenetic risk, and diagnostic stage. The cumulative incidences of non-relapse mortality (NRM) at 1 and 3 years based on donor type were 20.5% (95% confidence interval [CI], 10.90–30.10%) and 24.2% (95% CI, 13.81–34.59%) for the MRD group and 16.80% (95% CI, 1.71–31.89%) and 28.70% (95% CI, 8.71–48.69%) for the haplo group, respectively. Cumulative incidence of NRM did not differ significantly between the two groups (χ2 = 0.031, P = 0.861). The cumulative incidences of progression-free survival (PFS) and 1 year and 3 years by type of donors were 59.8% (95% CI, 48.24–71.36%) and 45.4% (95% CI, 33.44–57.36%), and 65.6% (95% CI, 47.18–84.02%) and 26.8% (95% CI, 7.59–46. 01%) for MRD and haploidentical donor, respectively. Cumulative incidence of PFS did not differ significantly between the two groups (χ2 = 0.182, P = 0.670). In multivariate analyses, no statistically significant differences were observed between haploidentical and MRD for relapse, NRM, PFS, and overall survival. There were no statistically differences on main outcomes after haploidentical and MRD.Conclusion:Haploidentical SCT could be performed safely and feasibly for patients with MM in need.
Rationale:Acute lymphoblastic leukemia (ALL) secondary to multiple myeloma (MM) is rare. Here we report a rare case of secondary ALL transformed from MM.Patient concerns:A 64-year-old woman was diagnosed as MM IgG light chain type in 2001. She achieved complete remission after 2 cycles of therapy, and received maintenance therapy with thalidomide. The patient suffered from MM relapse in September 2011. Bone marrow examination showed that the percentage of primary lymphocytes was 59%, indicating ALL-L2 (Pre-B-ALL). The patient reached complete remission after 1 cycle of chemotherapy, and has been maintained for more than 6 years.Diagnoses:Immunophenotyping analysis revealed that the abnormal cell population accounted for approximately 66% which expressed HLA-DR, CD4, CD22, CD33, CD34, and cCD79a. These results indicated acute B lymphoblastic leukemia. Chromosome presented 47, XX, +5, −7, +19. Leukemia fusion gene analysis demonstrated positive EVI1 and negative IgH and TCR gene rearrangement.Interventions:The patient accepted 1 cycle of VDCLP chemotherapy and reached complete remission, followed with consolidation therapies with VDCLP, MA, CAG and other chemotherapy regimens.Outcomes:This patient has maintained CR1 of ALL for more than 6 years.Lessons:Even secondary lymphoblastic leukemia has been rarely reported in patients with MM, we still need perform bone marrow examination, flow cytology, and gene tests, especially during maintenance therapy.
Rationale: Peripheral T cell lymphoma, coexisting with Castleman's disease (CD), is rarely seen in clinical practice and is not frequently reported in the literature. Patient concerns: A 68-year-old female was admitted to our hospital for the first time due to “multiple lumps in the neck that progressively enlarged over 7 months”. 1.5 years later, the patient returned to our hospital complaining of “ difficulty breathing and purulent blood in the mouth for more than 20 days”. Diagnosis: The postoperative pathology from the (right) cervical lymph node biopsy confirmed the diagnosis of Castleman Disease (Vascular follicular type). 1.5 years after the diagnosis of CD, the patient developed secondary peripheral T cell lymphoma of unspecified type (PTCL-U). Interventions: The patient received 5 courses of chemotherapy: 2 courses of CHOP, Chidamide combined with GemOx, GDP and Hyper CVAD Bregimen. Outcomes: After 3 courses of treatment, the curative effect was partly remitted (PR). The patient was discharged in a good condition and the follow-up was uneventful. Lessons: The mechanism responsible for CD concurrent or secondary lymphoma is not clear. Epstein-Barr virus (EBV) infection may be the most common reason of CD and PTCL-U. Further understanding the mechanisms of the condition is needed.
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