scholarly journals Role of B-Cell Translocation Gene 1 in the Pathogenesis of Endometriosis

2019 ◽  
Vol 20 (13) ◽  
pp. 3372
Author(s):  
Jeong Sook Kim ◽  
Young Sik Choi ◽  
Ji Hyun Park ◽  
Jisun Yun ◽  
Soohyun Kim ◽  
...  
Keyword(s):  
B Cell ◽  
Cellular Proliferation ◽  
Suppressor Gene ◽  
Cellular Migration ◽  
Matrix Metalloproteinase 2 ◽  
Control Group ◽  
Endometrial Stromal Cells ◽  
Eutopic Endometrium ◽  
Ectopic Endometrium

Estrogen affects endometrial cellular proliferation by regulating the expression of the c-myc gene. B-cell translocation gene 1 (BTG1), a translocation partner of the c-myc, is a tumor suppressor gene that promotes apoptosis and negatively regulates cellular proliferation and cell-to-cell adhesion. The aim of this study was to determine the role of BTG1 in the pathogenesis of endometriosis. BTG1 mRNA and protein expression was evaluated in eutopic and ectopic endometrium of 30 patients with endometriosis (endometriosis group), and in eutopic endometrium of 22 patients without endometriosis (control group). The effect of BTG1 downregulation on cellular migration, proliferation, and apoptosis was evaluated using transfection of primarily cultured human endometrial stromal cells (HESCs) with BTG1 siRNA. BTG1 mRNA expression level of eutopic and ectopic endometrium of endometriosis group were significantly lower than that of the eutopic endometrium of the control group. Migration and wound healing assays revealed that BTG1 downregulation resulted in a significant increase in migration potential of HESCs, characterized by increased expression of matrix metalloproteinase 2 (MMP2) and MMP9. Downregulation of BTG1 in HESCs significantly reduced Caspase 3 expression, indicating a decrease in apoptotic potential. In conclusion, our data suggest that downregulation of BTG1 plays an important role in the pathogenesis of endometriosis.

Inhibition of METTL3/m6A/miR126 promotes the migration and invasion of endometrial stromal cells in endometriosis

2021 ◽  
Author(s):  
Xiaoou Li ◽  
Wenqian Xiong ◽  
Xuefeng Long ◽  
Xin Dai ◽  
Yuan Peng ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Diagnostic Biomarker ◽  
Rna Modifications ◽  
Normal Endometrium ◽  
Endometrial Stromal Cells ◽  
Ectopic Endometrium

Abstract N6-methyladenosine (m6A), one of the most abundant RNA modifications, is involved in the progression of many diseases, but its role and related molecular mechanisms in endometriosis remain unknown. To address these issues, we detected m6A levels in normal, eutopic and ectopic endometrium and found the m6A levels decreased in eutopic and ectopic endometrium compared with normal endometrium. In addition, we proved that methyltransferase-like 3 (METTL3) downregulation accounted for m6A reduction in endometriosis. Furthermore, we observed that METTL3 knockdown facilitated the migration and invasion of human endometrial stromal cells (HESCs), while METTL3 overexpression exerted opposite effects, suggesting that METTL3 downregulation might contribute to endometriosis development by enhancing cellular migration and invasion. Mechanistically, METTL3-dependent m6A was involved in the DGCR8-mediated maturation of primary microRNA126 (miR126, pri-miR126). Moreover, miR126 inhibitor significantly enhanced the migration and invasion of METTL3-overexpressing HESCs, whereas miR126 mimics attenuated the migration and invasion of METTL3-silenced HESCs. Our study revealed the METTL3/m6A/miR126 pathway, whose inhibition might contribute to endometriosis development by enhancing cellular migration and invasion. It also showed that METTL3 might be a novel diagnostic biomarker and therapeutic target for endometriosis.

scholarly journals Estradiol promotes cells invasion by activating β-catenin signaling pathway in endometriosis

Reproduction ◽  
2015 ◽  
Vol 150 (6) ◽  
pp. 507-516 ◽  
Author(s):  
Wenqian Xiong ◽  
Ling Zhang ◽  
Lan Yu ◽  
Wei Xie ◽  
Yicun Man ◽  
...  
Keyword(s):  
Severe Combined Immunodeficiency ◽  
Uterine Cavity ◽  
Beta Catenin ◽  
Dependent Manner ◽  
Endometrial Stromal Cells ◽  
Eutopic Endometrium ◽  
T Cell Factor ◽  
17Β Estradiol ◽  
Enhancer Factor

Endometriosis is an estrogen-dependent disease that involves the adhesion, invasion, and angiogenesis of endometrial tissues outside of the uterine cavity. We hypothesized that a link exists between estrogen and beta-catenin (β-catenin) signaling in the pathogenesis of endometriosis. Human endometrial stromal cells (HESCs) were separated from eutopic endometrial tissues that were obtained from patients with endometriosis. β-catenin expression and cells invasiveness ability were up-regulated by 17β-estradiol (E2) in an estrogen receptor (ESR)-dependent manner, whereas β-catenin siRNA abrogated this phenomenon. Moreover, co-immunoprecipitation and dual immunofluorescence studies confirmed ESR1, β-catenin, and lymphoid enhancer factor 1/T cell factor 3 co-localization in the nucleus in HESCs after E2 treatment. To determine the role of β-catenin signaling in the implantation of ectopic endometrium, we xenotransplanted eutopic endometrium from endometriosis patients into ovariectomized severe combined immunodeficiency mice. The implantation of the endometrium was suppressed by β-catenin siRNA. Collectively, studies regarding β-catenin signaling are critical for improving our understanding of the pathogenesis of estrogen-induced endometriosis, which can translate into the development of treatments and therapeutic strategies for endometriosis.

Hepatitis C Virus Infection and B-Cell Non-Hodgkin’s Lymphoma.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4668-4668
Author(s):  
Janet G. Grudeva
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cell ◽  
Hcv Infection ◽  
Control Group ◽  
Cell Infection ◽  
Serum Samples ◽  
Pathogenetic Role ◽  
Significant Difference

Backgroud: An increasing number of bacterial and viral infections have been linked with specific subtypes of lymphoma. Preliminary evidence suggests that hepatitis C virus (HCV) might play a pathogenetic role in autoimmune-related, non-malignant B-cell lymphoproliferation, as well as a subset of B-cell non-Hodgkin, s lymphomas (B-NHL), often with extranodal localization. Design and methods: The study was conducted in the Department of Hematology and consisted 149 (86 male, 63 female) untreated patients with a new diagnosis of B-NHL for 5-years period (2000–2004). HCV infection was investigated by testing for HCV antibodies in serum samples. The controls were 587 patients (without intravenous drug users) in other departments of the same hospital. Results: HCV infection was documented in 13 cases (8,4%) with NHL. The infected patients were not clinically relevant cryoglobulinemic activity, increased rate of autoimmune disorders and extranodal localizations prevalence. There was statistically significant difference between the NHL and control group (p<0,01) and no statistically significant difference between man/women carriers (p>0,05) into the NHL group. Overall, the clinical outcome of HCV-positive NHL does not seem to be different from that of NHL patients without HCV infection. However, the evidence of a significant liver injury may predict a worse prognosis in these cases. Conclusions: Our date suggest that HCV infection may be associated with B-NHL. With regard to the mechanism(s) by which HCV might favor B-cell expansion and malignant transformation, most date support an indirect pathogenetic role of the virus as an exogenous trigger. A direct oncogenetic role of HCV by direct cell infection and deregulation has only been hypothesized on the basis of the lymphotropism of the virus.

Evaluation of Parvovirus B19 and Herpesvirus-6 Serology in Brazilian Children with Common B Cell Precursor Acute Lymphoblastic Leukemia

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3944-3944
Author(s):  
Fernanda A Silva ◽  
Gisele M Vasconcelos ◽  
Synara NS Cordeiro ◽  
Mariana Sant’Ana ◽  
Silvia Maia Farias de Carvalho ◽  
...  
Keyword(s):  
B Cell ◽  
Parvovirus B19 ◽  
Lymphoblastic Leukemia ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Diagnostic Purpose ◽  
Cell Precursor ◽  
Blood Samples ◽  
Brazilian Children

Abstract Background. Indirect epidemiologic evidences have suggested that viral infections may represent an important risk factor in the etiological mechanisms of B cell precursor lymphoblastic leukemia (BpALL), specially common-ALL. Parvovirus B19 (PvB19) is associated with aplastic crisis, thrombocytopenia, and congenital anemia. Five studies have reported the concurrent PvB19 infection in pediatric ALL. In a view of the increasing contest about the direct or indirect role of viral infection in ALL, we evaluated the possible associations of PvB19 and herpes virus 6 (HHV-6) in samples from children suffering from hematological disorders in order to estimate the magnitude of risk of association with common-BpALL. Material and Methods. A total of 659 blood samples were randomly selected to perform the serological tests. They were part of diagnostic samples referred to CPq-INCA-Rio de Janeiro, Brazil, from 2002–2006, for diagnostic purpose. Blood samples were exclusively selected from patients in whom samples were taken at the time of the onset of sickness. The diagnosis of BpALL was based on immunophenotyping methods according to EGIL criteria. The presence of serum antibodies for PvB19 and HHV-6 were determinate by enzyme-linked immunosorbent assay. Statistical analyses were conducted using SPSS for Windows 11.0. All p values were two sided; p&lt;0.05 was considered statistically significant. Results. Common-ALL (n=176) and non-leukemic samples (n=107) considered as control group were stratified according to age-groups at diagnosis. Age distribution was: less than 2 years (15.5%); 2–6 years-old (46.0%), and 7–12 years-old (17.7%). The estimation of associated risk PvB19 IgG+ antibodies with common-BpALL was OR 0.53 95% CI (0.52–0.54); whereas HHV-6 IgG was OR 2.36, 95% CI (1.08–5.17). Conclusions. We find out a higher prevalence of HHV-6 antibodies in patients with common-BpALL, suggesting an association between HHV-6 infection e common-BpALL in Brazilian children. There is a long history in developed countries regarding the role of infections in leukemogenesis process. Further tests are necessary to confirm these results.

Grifolin Inhibits Proliferation, Migration, and Invasion of Lung Cancer A549 Cells by Regulating miRNA-1251-5p

2020 ◽  
Vol 12 (3) ◽  
pp. 376-382
Author(s):  
Xiao Liu ◽  
Yuanlan Chen ◽  
Zhijiao Jiang
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinase ◽  
Cellular Proliferation ◽  
A549 Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Control Group ◽  
Inhibitory Influence ◽  
Proliferation Inhibition ◽  
Inhibition Rate

To investigate the effect and molecular mechanism of grifolin on the proliferation, transfer, and infiltration of lung cancer (LC) cells. A control group, low grifolin group, midium grifolin group and high grifolin group, anti-miRNA-NC group, anti-miRNA-1251-5p group, grifolin + miRNA-NC group, and grifolin + miRNA-1251-5p group were established based on LC A549 cells. MTT was employed to detect cellular proliferation inhibition rate; Transwell assay was used to detect cellular transfer and infiltration; Western blot was used to test Cyclin D1, cyclin-dependent kinase inhibitor 1A (p21), matrix metalloproteinase 2 (MMP-2), and matrix metalloproteinase 9 (MMP-9) protein expression; and finally RT-qPCR was employed to test miRNA-1251-5p expression. After treatment with different concentrations of grifolin, an increase in proliferation inhibition rate of A549 cells, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, an increase in p21 expression, and a decrease in miRNA-1251-5p expression in a manner of concentration dependence was observed (P < 0.05). Inhibiting miRNA-1251-5p expression led to an increase in cellular proliferation inhibition rate, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, and an increase in p21 expression (P < 0.05). Overexpression of miRNA-1251-5p reversed the inhibitory influence of grifolin on the proliferation, transfer, and infiltration of A549 cells. Grifolin likely inhibits the proliferation, transfer, and infiltration of LC A549 cells by down-regulating miRNA-1251-5p.

scholarly journals Expression of BDNF and TrKB in Patients With Endometriosis and Their Correlation With Dysmenorrhea

2021 ◽  
Author(s):  
Sha wang ◽  
Hua Duan ◽  
Bohan Li ◽  
Wei Hong ◽  
Xiao Li ◽  
...  
Keyword(s):  
Laparoscopic Surgery ◽  
Mrna Level ◽  
Stage Iv ◽  
Stage Iii ◽  
Benign Tumors ◽  
Control Group ◽  
Normal Endometrium ◽  
Eutopic Endometrium ◽  
Mammalian Female ◽  
Ectopic Endometrium

Abstract Background: Brain-derived neurotrophic factor (BDNF) has been recognized as a regulator in the formation and maintenance of chronic pain in various chronic disorders. BDNF together with its high-affinity tyrosine kinase type B (TrkB) receptor were found to be extensively expressed in mammalian female reproductive system. However, BDNF and TrkB expression in different stages of endometriosis, and the correlation between their expression in ectopic lesions and endometriosis pain remains unclear.Methods: This study enrolled sixty-two women underwent laparoscopic surgery. Forty-six women diagnosed as ovarian endometrioma, were recruited in the study group. Sixteen women diagnosed as ovarian benign tumors were recruited in the control group. Samples from eutopic endometrium and ovarian endometriotic lesions were obtained at laparoscopic surgery. The message RNA (mRNA) level of BDNF and TrKB was detected by real-time PCR, while the protein level was detected by immunohistochemical staining for eutopic and ectopic endometrium in both groups. Dysmenorrhea was assessed by the visual analogue scale (VAS) before the surgery.Results: The expression of BDNF and TrKB were higher in ovarian endometriotic lesions than those in eutopic endometrium and normal endometrium (P<0.05), and there was no cyclical change. While their expression in eutopic endometrium were higher than those in the normal endometrium (P<0.05). The expression of BDNF and TrKB in ovarian endometriotic lesions stage IV were higher than those in stage III and II (P<0.05). Their expression in stage III were higher than those in stage II but there were no significance (P>0.05). Furthermore, the correlation between the mRNA expression of BDNF, TrKB in eutopic endometrium, and dysmenorrhea VAS score revealed that r=0.52 and 0.56, respectively (P<0.05). The correlation between BDNF and TrKB in both eutopic and ectopic endometrium were revealed that r=0.82 and 0.66, respectively (P<0.05).Conclusions: BDNF and TrKB may play essential roles in promoting disease progression during the development of endometriosis, and are closely related to dysmenorrhea caused by endometriosis.

scholarly journals Genital endometriosis and melatonin: a role in the pathogenesis and its possible use in the treatment of the disease

2019 ◽  
Vol 68 (3) ◽  
pp. 51-60 ◽  
Author(s):  
Maria I. Yarmolinskaya ◽  
Saimat Sh. Tkhazaplizheva ◽  
Arseniy S. Molotkov ◽  
Natalia N. Tkachenko ◽  
Valentina L. Borodina ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Melatonin Receptors ◽  
Reproductive Age ◽  
Control Group ◽  
Eutopic Endometrium ◽  
Relative Expression ◽  
Treatment Regimens ◽  
Daily Urine ◽  
New Treatment

Hypothesis/aims of study. Melatonin is found in almost all living organisms, the range of its effects being quite diverse. Effects of this hormone in the human body are realized via two ways, through specific receptors and non-receptor pathways. Melatonin may act through both membrane and nuclear receptors. In the present work, the expression of MTR1 and MTR2 melatonin receptors was studied in the eutopic endometrium and endometrioid heterotopies, and the level of melatonin metabolite, 6-sulfatoxymelatonin, in daily urine in patients with genital endometriosis (GE) was analyzed. Study design, materials and methods. The experimental group included 67 patients of reproductive age with a verified diagnosis of GE, and the control group consisted of 18 individuals with an ovulatory menstrual cycle without gynecological pathology. The 6-sulfatoxymelatonin level in daily urine was determined by enzyme immunoassay. The study of MTR1 and MTR2 melatonin receptor expression in the endometrium and endometrioid heterotopies was performed in 24 patients with GE and in 10 women of reproductive age who were examined for infertility who did not have gynecological pathology based on diagnostic laparoscopy. To study the expression of melatonin receptors, the endometrium and endometrial heterotopy sampling was carried out from day 18 to day 22 of the menstrual cycle. Morphological assessment included histological and immunofluorescence studies using confocal laser scanning microscopy. Results. In patients with GE, there was found a tendency to a decrease in 6-sulfatoxymelatonin excretion in daily urine compared to the control group. It was also found that the total relative expression area of melatonin receptors in the endometrium of women with GE was significantly lower compared to the endometrium of patients from the control group. Significant differences between the average brightness and optical density were not found. In addition, it was revealed that the relative expression areas of MTR1 and MTR2 melatonin receptors in the eutopic endometrium and in endometrioid heterotopies did not differ significantly. A negative correlation was stated between the relative expression area of melatonin receptors and GE prevalence. Particular attention is paid to the role of melatonin in the development of GE and to the possibilities of working out new treatment regimens with its use. Conclusion. The data obtained confirm the undoubted role of melatonin in the pathogenesis of GE, however, the development of new treatment regimens with its use requires further study.

scholarly journals Klotho/IGF-1R Regulates Tumor Growth and Predicts Prognosis in Diffuse Large B-Cell Lymphoma

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2924-2924
Author(s):  
Xiangxiang Zhou ◽  
Ying Li ◽  
Xinyu Li ◽  
Lingyun Geng ◽  
Ya Zhang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
B Cell ◽  
Cell Lines ◽  
Xenograft Model ◽  
B Cell Lymphoma ◽  
Control Group ◽  
Klotho Protein ◽  
Xenograft Models

Abstract Introduction: Klotho is an anti-aging gene with an extracellular domain. Mice with Klotho knockout exhibited obvious impairment in B-cell development. Evolving evidence indicates that Klotho modulates the proliferation and survival via targeting insulin-like growth factor-1 receptor (IGF-1R) in several cancers. However, the expression and biological role of Klotho in B-cell non-Hodgkin lymphoma (B-NHL) has not been elucidated to date. We hypothesized that Klotho could modulate the tumor growth and predicts prognosis in diffuse large B-cell lymphoma (DLBCL) through inhibiting IGF-1R activation. The aim of this study is to characterize the functional significance of Klotho and the therapeutic potential of its secreted form in DLBCL. Methods: Lymph nodes samples from 50 de novo DLBCL and 20 reactive hyperplasia cases were collected with informed consents. Klotho expression were assessed by Immunohistochemistry. CD19+ B-cells and peripheral blood mononuclear cells were isolated with informed consents from healthy donors. Expression levels of Klotho mRNA and protein in DLBCL cells were determined by quantitative RT-PCR and western blotting. Lentivirus vectors either encoding Klotho (LV-KL) or empty lentiviral vector (LV-Con) were stably transfected into DLBCL cells. Cell viability and apoptosis were analyzed by cell counting kit-8 and Annexin V-PE/7AAD staining. Animal experiments were performed in accordance with the principles of the Institutional Animal Care. SCID-Beige mice were subcutaneously injected with DLBCL cells to establish xenograft model. Results: We observed markedly decreased level of Klotho protein in DLBCL lymph nodes (Fig. 1A). Expression of Klotho protein exhibited significantly negative correlation with Ann Arbor stage of DLBCL patients (p=0.002). Level of Klotho protein was negatively correlates with the media overall survival (OS), suggesting lower Klotho expression is associated with poor OS in DLBCL ((Fig. 1B, p=0.045). Reduction of Klotho was also confirmed in DLBCL cell lines at mRNA and protein level (Fig. 1C). We next functionally interrogated the role of Klotho in DLBCL cell lines and xenograft models. Stably expression of LV-KL in DLBCL cell lines resulted in dramatically decreased cell proliferation and incremental apoptotic rates when compared to LV-Con (Fig. 2A and B). We validated the changed expression of critical targets known to govern apoptosis in DLBCL cells transfected with LV-KL. Xenograft models with Klotho overexpression revealed significantly abrogated tumor growth compared to control group (Fig. 2C). Interestingly, lower levels of Ki67 were observed in mice treated with LV-KL (Fig. 2D). These results highlighted the proliferation-inhibitory and apoptosis-inductive activities of Klotho in DLBCL cells. The underlying mechanism driving the tumor suppressive potential of Klotho was investigated. Surprisingly, we observed that the Klotho-induced inhibition of cell viability was only fewer restored by IGF-1 in DLBCL cells transfected with LV-KL (Fig. 3A). Reductive phosphorylation of IGF-1R and its downstream targets (AKT and ERK1/2) were observed in DLBCL cells with Klotho overexpression (Fig. 3B). In addition, we evaluated the regulation of Klotho on IGF-1R signaling in vivo. Decreased phosphrolation of IGF-1R as well as its downstream targets were observed in mice treated with LV-KL compared to the control group (Fig. 3C). Lastly, we explored the activity of secreted Klotho protein (rhKL). The rhKL was found to be active in vitro and significantly reduced the viabilities of DLBCL cells (Fig. 3D). Moreover, combination with rhKL increased the sensitivity of DLBCL cells to adriamycin. The in vivo activity of rhKL in DLBCL xenograft model was also detected. Significantly decreased tumor volumes were noted in mice treated with rhKL compared with those treated with vehicle control (Fig. 3E). Moreover, reductive expression level of Ki67 was observed in rhKL-treated group (Fig. 3F). Conclusions: Our observations identified for the first time that loss of Klotho expression contributed to the development and poor prognosis via activating IGF-1R in DLBCL. Given the in vivo tumor suppressive activity of secreted Klotho protein, it may serve as a potential strategy for the development of novel therapeutic interventions for DLBCL. Figure 1 Figure 1. Figure 2 Figure 2. Figure 3 Figure 3. Disclosures No relevant conflicts of interest to declare.

MicroRNA-145-5p modulates KLF5 and inhibits the migration and invasion in nasopharyngeal carcinoma

2021 ◽  
Author(s):  
Chien-Han Yuan ◽  
Wei-Chi Hsu ◽  
A-Mei Huang ◽  
Ben-Chih Yuan ◽  
I-Hung Chen ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Invasion ◽  
Cellular Proliferation ◽  
Colorimetric Assay ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Potential Therapeutic Target ◽  
Zinc Finger Transcription Factor ◽  
Precise Role

Abstract Human krüppel like factor 5 (KLF5) is a zinc finger transcription factor, which contributes to tumor suppression in nasopharyngeal carcinoma (NPC). However, the precise role of KLF5 in NPC remains poorly understood. In the present study, the association between KLF5 and miR-145-5p in NPC cells was elucidated. Cellular proliferation was detected using the WST-1 colorimetric assay. Cellular migration and invasion were studied using wound healing assays and the ECMatrix cell invasion assay, respectively. The protein expression was examined by western blot. Transfection was subsequently performed for generating NPC cells overexpressing KLF5 and miR-145-5p. The upregulation of KLF5 or miR-145-5p inhibited the migration and invasion of NPC cells. It was observed that miR-145-5p could induce the expression of the KLF5 protein in the NPC cell lines. Additionally, the activity of the migration marker, focal adhesion kinase (FAK), was suppressed following the overexpression of miR-145-5p and KLF5 in NPC cells. The results of this study indicated that miR-145-5p may repress the migration and invasion of NPC cells via KLF5, and could be a potential therapeutic target for NPC.

A Prospective Study of Thyomosin α1 and Intravenous Immunoglobulin Role to Prevent the Infectious Pneumonia Related to Rituximab Based Immuno-Chemotherapy for B Cell Lymphoma

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5394-5394
Author(s):  
Tongyu Lin ◽  
Raj Shrestha Prem ◽  
He Huang ◽  
Xueying Li ◽  
Huangming Hong ◽  
...  
Keyword(s):  
High Risk ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Control Group ◽  
Study Group ◽  
Chop Regimen ◽  
Exact Test ◽  
A Prospective Study

Abstract Background: Rituximab (Rtx) with Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone (R-CHOP) regimen could improve the survivalship in treatment of B cell lymphoma, however, also increases the possibilities of infectious disease including pulmonary pneumonia. Methods and materials: A prospective study was conducted in Sun Yat-sen University Cancer Center from Feb 2008 to Oct 2015 to analyze the addition of thyomosin (Th α1) and intravenous immunoglobulin (IVIG) supportive therapy impact in preventive role of pulmonary adverse effect (PAE) incidence rate related to Rtx based immuno-chemotherapy. Results: Out of 379 cases, 215 in Th α1 and IVIG (study) group and 164 in non Th α1 and IVIG (control) group compared; 80 (21.1%) of them developed PAE: 39 Rtx immuno-chemotherapy induced interstitial pulmonary disease (IPD) and 41 infectious pneumonia (IP) cases were developed after the 4rth median cycles (2.8 months) of R-CHOP regimen from the first exposure until prior to induced PAE and 11 cases of IP were isolated with etiology. In comparing the role of Th α1 and IVIG vs. control group; out of 41 R-CHOP induced pneumonia cases: 9 (2.4%) vs. 32 (8.4%) with p <0.001, respectively found. In multivariate analysis, Th α1 and IVIG (p <0.001) was the independent highly significant factors related to decrease infectious pneumonia prevalence rate. Furthermore chemotherapy disruption rate due to pneumonia was 4.2% vs. 38.5%, in study and control group (p = 0.005), respectively. Incidence of pneumonia was found significantly lower in study group than control group in account of high risk advanced stages (Fisher's Exact Test, p <0.001) and age≥60 (Fisher's Exact Test, p = 0.002) group. 6 years of event free survival (EFS) was found higher in study group 73.2% in compare to control group 52.6% with p<0.001. Conclusions: The B cell lymphoma patients with high risk factors along with the risk of developing infectious pneumonia may be substantially decreased by the regular implication of Th α1 and IVIG along the Rtx based chemotherapy that may result effective in improving EFS too. Disclosures No relevant conflicts of interest to declare.

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