Suberoylanilide hydroxamic acid (SAHA; vorinostat), the second generation of histone deacetylase (HDAC) inhibitor, has been approved for the treatment of cutaneous manifestations of cutaneous T cell lymphoma (CTCL). It has also shown its anticancer activity over a large range of other hematological and solid malignancies, but few studies have been reported in B cell lymphoma. In this study, we aimed to investigate the antitumor activity of SAHA on murine B cell lymphoma cell line A20 cells. We treated A20 cells with different concentrations of SAHA. The effect of SAHA on the proliferation of A20 cells was studied by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium (MTT) assay in vitro; the anti-proliferation activity in vivo was evaluated by proliferating cell nuclear antigen (PCNA) of xenograft tumor tissues through immunocytochemical staining. Apoptosis were detected by Hoechst 33258 staining and Annexin V/propidium iodide (PI) double-labeled cytometry in vitro. The effect of SAHA on cell cycle of A20 cells was studied by a propidium iodide method. Autophagic cell death induced by SAHA was confirmed by transmission electron microscopy (TEM). Angiogenesis marker (CD31) was measured by immunocytochemical staining to investigate the anti-angiogenic effect of SAHA. Western blot was used to detect the expression of signaling pathway factors (phospho-AKT, phospho-ERK, AKT, ERK, Nur77, HIF-1α, and VEGF). Our results showed that SAHA inhibited the proliferation of A20 cells in a time- and dose-dependent manner, induced cell apoptosis and G0/G1 phase arrest of cell cycle, promoted autophagic cell death, and suppressed tumor progress in NCI-A20 cells nude mice xenograft model in vivo. SAHA decreased the activation of AKT (phospho-AKT: p-AKT) and ERK1/2 (phospho-ERK: p-ERK) proteins and inhibited the expression of pro-angiogenic factors (VEGF and HIF-1α), downregulated its downstream signaling factor (Nur77), which might be contributed to the antitumor mechanisms of SAHA.

Peripheral T-cell lymphomas (PTCLs) account for 12% of non-Hodgkin’s lymphomas (NHLs). Immunoglobulin (Ig) A pemphigus is an autoimmune blistering disease characterized by tissue-bound and circulating IgA antibodies that target epidermal cell surface components. Malignant lymphomas are often linked with autoimmune disease and the autoimmune blistering disease, paraneoplastic pemphigus, has been associated with NHL. However, cases of PTCLs that are complicated by IgA pemphigus are particularly rare. The current study presents the first known case of PTCL complicated by IgA pemphigus. A 43-year-old male was admitted to the Union Hospital (Wuhan, China) in March 2012 with multiple swollen lymph nodes. Pathology examinations revealed PTCL. Immunohistochemical staining was positive for cluster of differentiation (CD)2, CD3, CD5, CD7 and CD47, and negative for CD20. Ki-67 was ~40% positive. The patient was treated with four cycles of cyclophosphamide, Adriamycin, vincristine and prednisone, and two cycles of gemcitabine, cisplatin and dexamethasone; in addition, the patient received radiation of the retroperitoneal region (total dose, 36 Gy). The patient underwent thalidomide maintenance therapy for 20 days before flaccid blisters appeared on the trunk and limbs. Histopathology and immunofluorescence indicated IgA pemphigus, and intravenous methylprednisolone was administered, followed by treatment with prednisone. Subsequently, no evidence of recurrent lymphoma or pemphigus has been observed.

Endothelial progenitor cells (EPCs) play an important role in non-Hodgkin's lymphoma (NHL) development. Endostar is an anti-angiogenic drug designed to stop cancer by nullifying a tumor's ability to obtain oxygen and nutrients. In this study, we examined the anti-angiogenic activities of Endostar on NHL cell lines and murine xenograft model of NHL in vitro and in vivo, respectively, and explored the underlying antiangiogenic mechanism of Endostar. Results showed that Endostar may inhibit the EPC proliferation by reducing the expression of p-protein kinase B, but not p-ERK expression. Our finding could lead to a better understanding of the effects of Endostar on NHL.

Background The hyaluronan-mediated motility receptor (HMMR) is excessive expression in a great deal of malignancies and has been implicated in cancer invasion and metastasis. Nevertheless, the prognostic values of HMMR in lung adenocarcinoma and its connection to immunological infiltrates are still unknown. As a result, we investigated the importance of HMMR in lung tumor prognosis and its relationship with immune infiltrates. Methods The Cancer Genome Atlas (TCGA) provided transcriptional profiling of HMMR in normal samples and pulmonary adenocarcinoma samples. The expression of the HMMR protein was analyzed by the Human Protein Atlas (HPA) and the Clinical Proteomic Tumor Analysis Consortium (CPTAC). To distinguish lung adenocarcinoma from normal tissues in the vicinity, we used the receiver operating characteristic (ROC) curve. Kaplan-Meier method was conducted to assess the effect of HMMR on survival. The STRING program created protein-protein interaction (PPI) networks. Functional enrichment analysis was carried out using the "ClusterProfiler" program. The association between HMMR mRNA immune infiltrates and expression was identified using tumor-immune system interaction database (TISIDB) and tumor immune estimate resource (TIMER). Results In lung adenocarcinoma tissues, the HMMR expression was substantially higher than in surrounding normal tissues. Lymphoma node metastases and high TNM stage were linked to increase HMMR mRNA expression. HMMR's specificity, sensitivity, and accuracy for distinguishing pulmonary cancer from neighboring controls were 86.2, 98.3, and 87.4 percent, respectively, at a cutoff level of 2.103, according to the ROC curve analysis. The prognosis for patients with high-HMMR lung adenocarcinoma was worse than for those with low-HMMR (41.9 vs. 59.9 months, P < 0.001), according to a Kaplan-Meier survival analysis. Correlation study revealed that the expression of HMMR mRNA was linked to immunological infiltrates and tumor purity. Conclusion In lung adenocarcinoma, immune infiltrates and poor survival are associated with upregulated HMMR. Our findings imply that HMMR may be utilized in lung adenocarcinoma as a predictor of poor prognosis and a possible biomarker for immune treatment.