Serological Assessment of 18 Pathogens and Risk of AIDS-Associated Non-Hodgkin Lymphoma
Gordana HalecTim WaterboerNicole BrennerJulia ButtWilliam D. HardyGypsyamber D’SouzaSteven M. WolinskyBernard MacatangayMichael PawlitaRoger DetelsOtoniel Martı́nez-MazaShehnaz K. Hussain
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Abstract:
Background: HIV infection is associated with increased susceptibility to common pathogens, which may trigger chronic antigenic stimulation and hyperactivation of B cells, events known to precede the development of AIDS-associated non-Hodgkin lymphoma (AIDS-NHL). Methods: To explore whether cumulative exposure to infectious agents contributes to AIDS-NHL risk, we tested sera from 199 AIDS-NHL patients (pre-NHL, average lead time 3.9 years) and 199 matched HIV-infected controls from the Multicenter AIDS Cohort Study, for anti-IgG responses to 18 pathogens using multiplex serology. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using conditional logistic regression models. Results: We found no association between cumulative exposure to infectious agents and AIDS-NHL risk (OR 1.01, 95% CI: 0.91 to 1.12). However, seropositivity for trichodysplasia spinulosa polyomavirus (TSPyV), defined as presence of antibodies to TSPyV capsid protein VP1, was significantly associated with a 1.6-fold increase in AIDS-NHL risk (OR 1.62, 95% CI: 1.02 to 2.57). High Epstein–Barr virus (EBV) anti-VCA p18 antibody levels closer to the time of AIDS-NHL diagnosis (<4 years) were associated with a 2.6-fold increase in AIDS-NHL risk (OR 2.59, 95% CI: 1.17 to 5.74). In addition, high EBV anti-EBNA-1 and anti-ZEBRA antibody levels were associated with 2.1-fold (OR 0.47, 95% CI: 0.26 to 0.85) and 1.6-fold (OR 0.57, 95% CI: 0.35 to 0.93) decreased risk of AIDS-NHL, respectively. Conclusions: Our results do not support the hypothesis that cumulative exposure to infectious agents contributes to AIDS-NHL development. However, the observed associations with respect to TSPyV seropositivity and EBV antigen antibody levels offer additional insights into the pathogenesis of AIDS-NHL.Cite
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Lymphomas are malignant neoplasms arising from lymphocytes B cell or T cell that affects mainly lymph nodes, spleen and other non hematopoietic tissues. They are classified as Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL). Diffuse large B-cell lymphoma (DLBL) is the most common variant of non-Hodgkin's lymphomas and frequently involves extranodal sites. In the oral soft tissues lesions can occur as hard and diffuse tumors involving oral vestibule, gums and posterior region of the hard palate. Most lymphomas, including DLBL arise from B cells are characterized by diffuse population of large cells with cleaved or non cleaved oval nuclei. Both histopathlogical and immunohistochemical (IHC) analysis were strongly advisable for proper management and prognosis. We hereby report a rare case of Diffuse large B-cell variant of non-Hodgkin's lymphoma in a male patient of age 50yrs in left upper buccal vestibule.
Vestibule
Buccal mucosa
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Epstein-Barr virus (EBV) infection is highly associated with specific subtypes of malignant lymphoma. In our previous report on nodal malignant lymphoma in Thailand, we found that 64% of classical Hodgkin's lymphoma (cHL), 51% of non-Hodgkin's lymphoma, T-cell (NHL-T), and 13% of non-Hodgkin's lymphoma, B-cell (NHL-B) were EBV-related. In the present research, we conducted a retrospective study of primary extranodal non-Hodgkin's lymphoma of the sinonasal tract (e-NHL-ST) and primary extranodal non-Hodgkin's lymphoma of the nasopharynx (e-NHL-NP) in Southern Thailand, between 1997 and 2004. EBV-encoded RNA (EBER) expression by in situ hybridization was performed in all cases and a T-cell receptor (TCR)-g gene rearrangement study was performed in NHL-T cases. There were 18 cases of e-NHL-ST and 42 cases of e-NHL-NP detected by histologic and immunohistochemistry examinations. The percentages of e-NHL-ST and e-NHL-NP as compared to nodal malignant lymphoma were 3.7% and 6.8%, respectively. Sixteen cases (88.9%) of e-NHL-ST and 7 cases (16.7%) of e-NHL-NP were NHL-T, and the remainder were NHL-B. All of the NHL-T cases in both sites were EBER-positive. Two (5.4%) of the NHL-B cases in the nasopharynx showed EBER positive. Monoclonal bands of the TCR-gamma gene were detected in 71.4% of the extranodal NK/T-cell lymphomas, nasal type, patients; 50.0% of peripheral T-cell lymphoma, unspecified, patients; and one case of angioimmunoblastic T-cell lymphoma. This study indicates a very strong association of NHL-T in the sinonasal tract or nasopharynx with EBV infection, the link apparently being weaker in NHL-B patients. The study also indicates that most cases of extranodal NK/T-cell lymphoma, nasal type, are not the germline configuration of the TCR genes.
T-Cell Lymphoma
Peripheral T-cell lymphoma
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The objective of the study was to determine the frequency of bcl-2 gene rearrangement in B-cell Non-Hodgkin's lymphoma (NHL) and identify different breakpoints of bcl-2 gene.Thirty cases of B-cell lymphoma (including 8 cases of follicular lymphoma, 19 cases of diffuse large B-cell lymphoma and 3 cases of T-cell rich B-cell lymphoma) were included in the study. Good quality of DNA was extracted in 4 cases from formalin fixed paraffin embedded tissue and in 26 cases from fine needle aspirate. The polymerase chain reaction was done for major break point region (mbr), minor cluster region (mcr) and intermediate cluster region (icr) of the bcl-2 gene.The bcl-2 gene rearrangement was identified in 23.3% of B-cell lymphoma, 50% of follicular lymphoma, 15% of diffuse large B-cell lymphoma and no bcl-2 rearrangement was identified in any of the T-cell rich B-cell lymphomas. Further analysis showed the icr breakpoint in 16.7% of B-cell lymphoma, 37.5% of follicular lymphoma and 10.5% of diffuse large B-cell lymphoma. Involvement of the mbr breakpoint was found in 6.7% of B-cell lymphoma, 12.5% of follicular lymphoma, and 5.3% of diffuse large B-cell lymphoma. Involvement of the mcr breakpoint was not seen in any of the cases.The bcl-2 gene rearrangement is quite frequent in follicular lymphoma, followed by diffuse large B-cell lymphoma. The commonest breakpoint in present series is icr followed by mbr. This indicates that primers for bcl-2 gene must include icr primer, whenever the bcl-2 gene is being evaluated for B-cell NHL in this part of the world and this might reduce the variability of frequency of bcl-2 gene rearrangement within and between different regions.
Follicular lymphoma
Gene rearrangement
Breakpoint
B-cell lymphoma
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Objective To determine the serum vascular endothelial growth factor(VEGF)level in children with non-Hodgkin’s lymphoma(NHL)and elucidate the relationship between its level and the deve- lopment,the stages,and the relapse of the NHL.Methods Serum VEGF levels were measured in48chil-dren with non-Hodgkin’s lymphoma(group A)before and after treatment by sandwich ELISA,and the33healthy individuals in group B.Results The VEGF levels in the patients with newly diagnosed,or relapsed,and no remitted lymphoma were significantly higher than those in normal controls(P0.01).It was sig-nificantly higher in the patients of stageⅢ,Ⅵthan the patients in stageⅠ,Ⅱ.And also significantly higher in group B in comparison with group A.But significantly lower in the patients with complete remission and partial remission in comparison with the newly diagnosed patients.No marked difference was found between Hodgkin’s lymphoma(HL)and NHL.Conclusions Dynamic changes of VEGF level can be used as the alternate index in diagnosing patients,assessing therapeutic effect and predicting the prognosis of non-Hodgkin’s lymphoma.
Clinical Significance
Therapeutic effect
International Prognostic Index
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Non-Hodgkin lymphoma developing in patients with HIV infection fulfills diagnostic criteria for AIDS. Clinical manifestations of AIDS-NHL are similar to those of malignant lymphoma arising in other acquired and congenital immunodeficiency states. AIDS related NHLs therefore consist primarily of tumours with B cell phenotype, intermediate or high grade histological subtype and rapid clinical progression with a high frequency of unusual extranodal involvement. Treatment of AIDS-NHL has been much less rewarding than treatment of lymphoma in non-HIV infected individuals. Complete response rates are lower than the corresponding rates seen in the non-HIV infected population, and responses that do occur tend to be of short duration. Improvements in treatment for AIDS-NHL will require the use of new therapies, designed to cause less myelosuppression, in conjunction with aggressive efforts to prevent opportunistic infections.
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Aim of the study: To assess the expression of PAX5 in different types and stages of lymphomas and to study its utility in comparison with the classical pan B and T cell markers.
Materials and Methods: Immunohistochemistry was done to detect the expression of PAX5, CD45, CD3, CD20, CD15 and CD30 in all cases of lymphoma reported for a period of two years.
Results: 59 cases were reported as malignant lymphomas giving an overall incidence of 6.3% in our hospital. The age group ranged from 3 years to 75 years with a male preponderance. Nineteen cases were excluded owing to inadequate tissue samples. Of the 40 cases, 28 were nodal and 12 extra-nodal lymphomas. 33 cases were non-Hodgkin’s lymphoma and 7 were Hodgkin’s lymphoma. 23 out of the 40 cases were positive for PAX5 and out of 21 cases of B cell non-Hodgkin’s lymphoma, 18 were positive. Reed-Sternberg cells of Hodgkin’s lymphoma were positive in 5 cases. PAX5 was positive in most of the B cell non-Hodgkin’s lymphoma and Hodgkin’s lymphoma regardless of the stage, age, sex and site. PAX5 was negative in all T cell non-Hodgkin’s lymphoma and the cases of unclassified category.
Conclusions: This study suggests that B cell neoplasms and Reed Stenberg cells strongly expressed PAX5 in comparison to classical lymphoma panel and hence can be a useful marker. However a larger prospective study on PAX 5 expression in Hodgkin’s Lymphoma is vital to look for an increased expression in subset of Indian population.
Keywords: B-cell Lymphoma, Hodgkin’s lymphoma, Immunohistochemistry, PAX5, T-cell Lymphoma
PAX5
CD15
Hodgkin's lymphoma
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4323 Persons with human immunodeficiency virus (HIV) infection are at increased risk of acquired immunodeficiency syndrome-associated non-Hodgkin’s B cell lymphoma (AIDS-NHL). Chronic B cell hyperactivation due to HIV infection and/or disease progression is thought to contribute to this increased risk. Lymphoma can be the initial AIDS-defining condition, but frequently occurs subsequent to some other AIDS-defining condition. In AIDS-NHL cases that follow another AIDS-defining condition, the extent of B cell activation observed prior to the lymphoma diagnosis may be impacted by the prior AIDS diagnosis. In a nested case-control study utilizing samples from participants in the Multicenter AIDS Cohort Study, we assessed serum levels of several B cell stimulatory cytokines and molecules associated with B cell activation. Cases (AIDS+NHL, n=99) were participants who developed AIDS-NHL subsequent to another, non-lymphoma AIDS diagnosis; controls (AIDS, n=99) were participants who developed AIDS, but not lymphoma, matched to cases on time of AIDS diagnosis. Levels of interleukin (IL) 6, IL10, soluble CD23 (sCD23), sCD27, sCD30, C’-reactive protein (CRP), and total IgE were quantified in matched longitudinal serum samples collected at up to three time points prior to lymphoma diagnosis of the case (3-5 years, 1-3 years, and
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AIM: To investigate the possible relationshop between Non Hodgkin's lymphoma and homozygous deletion of P16 gene. METHODS: Fifty one Non Hodgkin's lymphoma specimens were examined for homozygous deletion of P16 gene by multiplex polymerase chain reaction. RESULTS: Of 51 Non Hodgkin's lymphoma specimens, 9 ( 17.65 %) showed homozygous deletion of P16 gene. There was a significant difference between the low malignancy NHL, and the high malignancy NHL (P 0.05 ) in homozygous deletion of P16 gene. CONCLUSIONS: Deletion of P16 gene might contribute to the progression of Non Hodgkin's lymphoma and may be one of the important parameters in estimating the prognosis of patients with NHL.
Multiplex
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