ABSTRACT
Objective: To assess the clinical significance of changes in levels of serum β2 microglobulin (β2-MG), vascular endothelial growth factor (VEGF), and lactate dehydrogenase (LDH) in patients with diffuse large B-cell lymphoma (DLBCL) after treatment. Methods: A total of 89 patients with DLBCL who were admitted to the hospital between February 2015 an July 2017 were included in the DLBCL group and 40 normal, healthy persons admitted during the same period were selected as the control group. All DLBCL patients underwent standard chemotherapy after admission. Peripheral venous blood was collected before and after chemotherapy to determine any changes in serum β2-MG, VEGF, and LDH levels. Biomarker levels were also compared with those from normal, healthy subjects. The clinical and pathological data of all DLBCL patients were collected and the relationships between changes in biomarker levels, clinical and pathological parameters of DLBCL, and curative effects were analyzed. Results: The levels of serum β2-MG, VEGF, and LDH in the DLBCL group were higher than those in the control group (P<0.05) and all levels in DLBCL group decreased after chemotherapy (P<0.05). The effective rate of the R-CHOP group was higher than that of the CHOP group (P<0.05). Serum LDH levels were higher in patients with typical B symptoms than in those without such symptoms (P<0.05). Serum levels of β2-MG, VEGF, and LDH were higher in patients with Ann Arbor stageⅢ-Ⅳlymphoma, with bone marrow involvement, whose international prognostic index (IPI) was high-risk, and with treatment failure than in those with stageⅠ-Ⅱlymphoma, without bone marrow involvement, with low-risk IPI, and with treatment response (P<0.05). The levels of serum VEGF, β2-MG, and LDH were positively correlated with each other, and all three biomarkers were negatively correlated with treatment response (P<0.05). Conclusions: Levels of serum β2-MG, VEGF, and LDH are elevated in patients with DLBCL but are significantly decreased after treatment. Changes in expression levels of these three biomarkers are related to clinical stage, bone marrow involvement, IPI, and treatment response. These biomarkers can be used as a basis for monitoring DLBCL and evaluating curative effect and prognosis.
ABSTRACT
In order to investigate the expression of endothelin receptor B (ETR-B) in human malignant melanoma (MM) cells A375 and SK-mel-1 and the proliferative effects of endothelin 3 (ET3) on A375 cells, RT-PCR was applied to detect the expression of ETR-B gene in human MM cells A375 and SK-mel-1. MTT method was used to evaluate the growth enhancing effects of ET3 on A375 cell line in vitro. The results showed that ETR-B gene was expressed in both MM A375 and SK-mel-1 cells. ET3 had stronger ability to enhance the proliferation of A375 cells in vitro in a concentration-dependent manner. It was suggested that ET3/ETR-B might play an important proliferative role in MM.
Subject(s)
Cell Line, Tumor , Cell Proliferation/drug effects , Endothelin-3/pharmacology , Melanoma/metabolism , Melanoma/pathology , Receptor, Endothelin B/metabolism , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
In order to compare the clinical characteristics of familial and non-familial bullous lichen planus (BLP), the archival data of 36 BLP patients with positive family history and 21 BLP patients with negative family history diagnosed according to the clinical features and histopathology were collected in our department from 1956 to 2003. The clinical features were analyzed and compared. There were significant differences between familial and non-familial BLP in age of onset, duration of disease and extension of eruption (P<0.01). It was concluded that familial BLP appeared to differ from the non-familial form in its earlier age of onset, longer duration of the disease, more extensive eruption and more tendency to involve nails. Hereditary factors may play a role in the pathogenesis of familial BLP.
ABSTRACT
In order to compare the clinical characteristics of familial and non-familial bullous lichen planus (BLP), the archival data of 36 BLP patients with positive family history and 21 BLP patients with negative family history diagnosed according to the clinical features and histopathology were collected in our department from 1956 to 2003. The clinical features were analyzed and compared. There were significant differences between familial and non-familial BLP in age of onset, duration of disease and extension of eruption (P＜0.01). It was concluded that familial BLP appeared to differ from the non-familial form in its earlier age of onset, longer duration of the disease, more extensive eruption and more tendency to involve nails. Hereditary factors may play a role in the pathogenesis of familial BLP.
ABSTRACT
In order to investigate the expression of endothelin receptor B (ETR-B) in human ma-lignant melanoma (MM) cells A375 and SK-mel-1 and the proliferative effects of endothelin 3 (ET3) on A375 cells, RT-PCR was applied to detect the expression of ETR-B gene in human MM cells A375 and SK-mel-1. MTT method was used to evaluate the growth enhancing effects of ET3 on A375 cell line in vitro. The results showed that ETR-B gene was expressed in both MM A375 and SK-mel-1 cells. ET3 had stronger ability to enhance the proliferation of A375 cells in vitro in a con- centration-dependent manner. It was suggested that ET3/ETR-B might play an important proliferative role in MM.
ABSTRACT
The ras oncogene product ras p21, which is structurally homologous to G protein, participates in the regulation of cellular proliferation and differentiation. The histopathology of psoriasis is characterized by hyperkeratosis and parakeratosis. The purpose of this study was to investigate, by dot blot and Dig DNA labeling in situ hybridization techniques, the expression of c Ha ras proto oncogene in normal skin and active plaque psoriatic lesions. The results showed: (1) dot blot revealed one fold elevation of c Ha ras gene transcript levels in psoriatic lesions compared with normal controls. (2) In normal epidermis, only a few basal cells expressed ras gene, however, the ras gene was expressed throughout all layers of epidermis of active psoriatic lesions except horny layer and predominantly in prickle cells. Our results suggest that overexpression of c Ha ras oncogene and changes of expression pattern might be central to the pathogenesis of psoriatic epidermal hyperplasia and abnormal pattern of cellular differentiation.