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Objective:To investigate the impact of malnutrition diagnosed with Global Leadership Initiative on Malnutrition (GLIM) criteria on the outcomes of patients with primary gastrointestinal lymphoma (PGIL).Methods:Patients with PGIL admitted into Gansu Provincial People's Hospital from January 2014 to July 2022 were retrospectively enrolled. Nutritional risk screening was conducted using Nutritional Risk Screening 2002 (NRS 2002) scale, and malnutrition was diagnosed as per GLIM criteria. Kaplan-Meier survival analysis and multivariate Cox regression analysis were performed to investigate the effect of malnutrition as per GLIM criteria on the outcomes of PGIL patients.Results:A total of 82 patients were included. The phenotypic parameters, including body mass index (BMI), arm circumference, leg circumference and grip strength, were at significantly lower levels in the 28 malnourished patients, compared with the other non-malnourished patients. The median overall survival of patients with malnutrition as per GLIM criteria was 10 months, while that of patients without malnutrition was 41 months, showing significant differences between groups. The univariate analysis revealed that age, loss of muscle mass, tumor stage based on Lugano classification and malnutrition as per GLIM criteria were the impacting factors for survival in patients with PGIL. The multivariate analysis further demonstrated that tumor stage based on Lugano classification and malnutrition as per GLIM criteria were the independent impacting factors for survival in patients with PGIL.Conclusion:Malnutrition based on GLIM criteria is an independent risk factor for unfavorable outcomes in patients with PGIL and could be utilized as a prognostic indicator.
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Objective:To investigate the efficacy and safety of BeEAM (bendamustine+cytarabine+etoposide+melphalan) regimen in pretreatment of autologous hematopoietic stem cell transplantation for patients with lymphoma.Methods:The clinical data of 15 patients with lymphoma who underwent autologous hematopoietic stem cell transplantation after pretreatment with BeEAM regimen from January 2020 to February 2021 in Gansu Provincial Hospital were retrospectively analyzed. The transplant-related adverse reactions and hematopoietic reconstitution were evaluated.Results:During the pretreatment process of 15 patients, 13 patients had gastrointestinal adverse reactions such as nausea, vomiting and diarrhea, 2 patients had hypokalemia, and 1 patient had abnormal liver function, but all of them were grade 1-2, and no grade 3-4 adverse reactions occurred. One patient had poor platelet implantation, and the remaining 14 patients all achieved hematopoietic reconstruction. After transplantation, the median time of peripheral blood neutrophils and platelets good implantation in patients was 10 d (9-14 d) and 11 d (9-17 d), respectively. Until March 2021, all patients were alive during follow-up.Conclusions:The efficacy of BeEAM regimen in pretreatment of autologous hematopoietic stem cell transplantation for patients with lymphoma is good, and the adverse reactions are tolerable.
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Objective:To investigate the early efficacy and safety of pomalidomide-based regimen in relapsed/refractory multiple myeloma (MM) in the real world.Methods:The clinical data of 15 patients with relapsed/refractory MM treated with pomalidomide-based regimen who were admitted to Gansu Provincial Hospital from January 2021 to July 2021 were retrospectively analyzed, and the early efficacy and safety were also evaluated.Results:There were 8 males and 7 females, and the median age of onset of 15 patients was 60 years (43-83 years); the median time for the diagnosis of relapse and refractory was 15 months (4-84 months). All 15 patients previously received bortezomib-based treatment regimens, 9 patients previously received lenalidomide treatment, and 7 cases received autologous hematopoietic stem cell transplantation. All patients received pomalidomide-based regimen combined with two-drug or three-drug regimen (pomalidomide combined with bortezomib,daratumumab,bendamustine, dexamethasone, cyclophosphamide or lenalidomide). The median treatment cycle was 2 cycles (2-4 cycles). After 2 cycles of treatment, the therapeutic efficacy was evaluated; the overall response rate was 73% (11/15), including 3 cases of complete remission, 3 cases of very good partial remission, and 5 cases of partial remission. Hematological toxicity occurred in 9 patients, of which 5 cases had grade 3-4 hematological toxicity, 4 cases had grade 1-2 hematological toxicity, and other adverse reactions were mild and tolerable.Conclusion:Pomalidomide-based regimen is effective and safe for relapsed/refractory MM patients.
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To evaluate the specific inhibition of antisense u-PAR on the u-PAR expressions in highly invasive cell subclones and to determine its blocking function in the invasion by those cells, a cDNA fragment of u-PAR obtained by RT-PCR was inserted into a plasmid vector named pcDNA3 in antisense orientation. Then the antisense u-PAR recombinant was transfected into highly invasive cell subclones. The u-PAR expression in neo-resistant cells was examined by RT-PCR and immunohistochemical assay. Compared to the control cells, the content of mRNA and protein of u-PAR in transfected cells decreased sharply, and the rate of inhibition was 53% and 73%, respectively, indicating that an antisense u-PAR might have played a specific inhibitory role in its expression in the cells, which may provide a good cell model for making further investigation of the inhibitory effects of the antisense u-PAR on invasion in highly invasive cell subclones of human prostate carcinoma.
Subject(s)
Humans , Male , Cell Line, Tumor , Cloning, Molecular , Neoplasm Invasiveness , Plasmids , Prostatic Neoplasms , Metabolism , Pathology , RNA, Antisense , Genetics , Receptors, Cell Surface , Genetics , Receptors, Urokinase Plasminogen Activator , Reverse Transcriptase Polymerase Chain Reaction , Transfection , Urokinase-Type Plasminogen Activator , Genetics , MetabolismABSTRACT
To observe the inhibitory effects of an antisense u-PAR vector on invasion of highly invasive PC-3M cell subclones, the effects of the antisense u-PAR on activity of MMP-9 in those highly invasive cell subclones were detected by a quantitative RT-PCR and zymography. The monolayer invasion assay and colony formation assay in soft agar were used. And tumorigenesis rate and invasions by the cell subclones with or without the antisense u-PAR were observed in nude mice. It was found that in vitro growth of highly invasive PC-3M cell subclones transfected with the antisense u-PAR was declined, and the ability of anchorage-independent growth of those cell subclones was found decreased sharply, with the inhibiting rate becoming 79% and 60%, respectively. Although the antisense u-PAR didn't change MMP-9 gene transcription, they could inhibit the activation of MMP-9 of highly invasive PC-3M cell subclones. Moreover, the tumorigenesis rate of the cell subclones with the antisense u-PAR decreased and the growth of a neoplasm also slowed down. The t tests showed the difference between experimental and control groups was statistically significant (P < 0.01). The antisense u-PAR vector could not only inhibit the invasion ability of highly invasive PC-3M cell subclones in vitro but also restrain the growth of those cell subclones in vivo.
Subject(s)
Animals , Humans , Male , Mice , Antisense Elements (Genetics) , Genetics , Pharmacology , Cell Division , Cloning, Molecular , Matrix Metalloproteinase 9 , Genetics , Metabolism , Mice, Inbred BALB C , Mice, Nude , Neoplasm Invasiveness , Prostatic Neoplasms , Metabolism , Pathology , RNA, Antisense , Receptors, Cell Surface , Genetics , Metabolism , Receptors, Urokinase Plasminogen Activator , Reverse Transcriptase Polymerase Chain Reaction , Transfection , Tumor Cells, CulturedABSTRACT
To compare the anti-tumor effects of transmembrane TNF-alpha (TM-TNF) and secreted TNF-alpha (S-TNF) in vivo, mouse fibroblasts NIH3T3 were transfected separately with three types of retrovirus containing wild type TNF-alpha (Wt-TNF), TM-TNF mutant (TM-TNFm), S-TNF mutant (S-TNFm). Southern blot, RT-PCR, FACS and bioassay were used to investigate TNF-alpha gene integration, expression and its biological activity. It was found that both fixed cells and supernatant of NIH3T3/Wt-TNF, the fixed cells of NIH3T3/TM-TNFm and the supernatant of NIH3T3/S-TNFm could express high level of TNF-alpha or its mutants and effectively kill H22 in vitro. The transfected NIH3T3 were separately injected into the mice at the sites of H22 tumor cell inoculation according to a ratio of 5:1 or 1:1 (effector/target cells, E/T) after the third day of H22 challenge, respectively. At the E/T = 5:1, the NIH3T3/TM-TNFm induced the highest tumor regression, while NIH3T3/S-TNFm exerted the strongest tumor depressing effect at the E/T = 1:1 in vivo. No obvious side effects were noted throughout the course of treatment. The results suggest that both TM-TNF and S-TNF could cause tumor regression. The anti-tumor effect of TM-TNF would be more powerful and safe than that of S-TNF at the proper E/T ratio.
Subject(s)
Animals , Mice , 3T3 Cells , Adenoviruses, Human , Genetics , Cytotoxicity, Immunologic , Allergy and Immunology , Fibroblasts , Cell Biology , Allergy and Immunology , Liver Neoplasms, Experimental , Allergy and Immunology , Pathology , Membrane Proteins , Bodily Secretions , Mutation , Transfection , Tumor Cells, Cultured , Tumor Necrosis Factor-alpha , Genetics , Allergy and Immunology , Bodily SecretionsABSTRACT
Objective:To study the effects of PTK on the respiratory burst and release of NO by neutrophils in response to transmembrane TNF-?( TM-TNF-?) and secreted TNF-? ( S-TNF-?). Methods: The effects of PTK inhibitor on the functions of neutrophils caused by both forms of TNF-? was detected with the chemiluminescence and the nitrate reductase assay.The tyrosine phosphorylation of neutrophils induced by the two forms of TNF-? was compared by Western blotting analysis. Results: The PTK inhibitor genistein (50 ?mol/L) was found not only to depress the respiratory burst of neutrophils induced by S-TNF-?( P
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AIM: To compare the tumorigenecity of H22 cells transfected with TNF-? gene and its mutants (secreted TNF-? mutant, S-TNFm, transmembrane TNF-? mutant, TM-TNFm and wild type of TNF-?, Wt-TNF) in vivo . METHODS: Three kinds of mouse liver cancer cell line H22 expressing TNF-? and its two mutants were mixed with untransfected H22 at different effector/target ratio separately. The growth of tumor was examined after injection of 2.5?10 5 (100 ?L) mixed H22 tumor cells into mice. The lymphocyte infiltration in the site of tumor and the expression of Fas on tumor cells were detected by immunohistochemistry. RESULTS: The tumorigenecity of H22 cells transfected with TNF-? gene and its mutants was significantly weakened ( P
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Objective: To observe the inhibiting effects of an antisense u-PAR vector on invasion by highly invasive PC-3M cell subclones. Methods: The effects of an antisense vector on invasion by highly invasive PC-3M cell subclones were observed and compared in vitro by monolayer invasion assay and soft agar clone. Then, both a quantitative RT-PCR and zymography were used to exam the effects of the antisense u-PAR on activity of MMP-9 in those highly invasive cell subclones. Furthermore, the tumorigenesis rate and invasions by the cell subclones with or without the antisense u-PAR were observed in nude mice. Results: It is found that the speed of growth in vitro was slowing down by highly invasive PC-3M cell subclones transfected with the antisense u-PAR, and the ability of anchorage-independent growth of those cell subclones was also decreasing sharply,and the inhibiting rate was 79% and 60%, respectively. Although the antisense u-PAR didn′t change MMP-9 gene transcription, but they could inhibit the activation of MMP-9 of highly invasive PC-3M cell subclones. Moreover, the tumorigenesis rate of the cell subclones with the antisense u-PAR decreased and the growth of a neoplasm also slowed down. The t tests showed the difference between experimental and control groups reached statistical significance ( P
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Objective: To study the antitumor effects of transmembrane TNF-? and secretory TNF-? in vivo. Methods: Three types of TNF-? cDNA plasmids (wild type TNF-?; transmembrane TNF-? mutant; secretory TNF-? mutant) were directly injected into tumor-tearing mice. Results: The three types of TNF-? could be expressed by tumor cells and all of them could inhibit evidently the rate of tumor growth. The tumor regression after treatment with transmembrane TNF-? mutant at the early stage was more significant than that with the other two types of TNF-?( P