scholarly journals INFECTIONS AND FOLLICULAR LYMPHOMA: IS THERE A LINK?

2017 ◽  
Vol 9 (1) ◽  
pp. e2017035
Author(s):  
Francesco Zallio ◽  
Giulia Limberti ◽  
Marco Ladetto
Keyword(s):  
Follicular Lymphoma ◽  
B Cell ◽  
Bacterial Infections ◽  
Classical Model ◽  
Infectious Agent ◽  
Epidemiological Studies ◽  
Gastric Malt Lymphoma ◽  
Infectious Agents ◽  
Non Hodgkin Lymphoma ◽  
Treatment And Prevention

Several infectious agents appear to provide a proliferative signal -- “antigen-drive” – that  could be implicated in the pathogenesis of various type of Non-Hodgkin Lymphoma (NHL). A classical model of infection-driven lymphoprolipherative disorder is Helicobacter pylori-induced gastric MALT lymphoma, where antibiotic therapy allows eradication of both the infectious agent and the clonal B-cell expansion;  following the footsteps of these example, several retrospective studies have found a correlation with other pathogens and B-cell Lymphomas, adding new important informations about pathogenesis and laying the groundwork for chemotherapy-free treatments.Although no clear association with infectious agents has yet been identified for Follicular Lymphoma (FL), a growing number of biological and clinical observations suggests that interaction with physiological and pathological microbial populations might play a role also in this subtype of lymphoma: in the last years epidemiological studies investigating the association of known risk factors and FL found a potential correlation with viral or bacterial infections; moreover recent findings about the stimulation of FL clones support the importance of microbial exposure to lymphomagenesis and disease progression.In the following review we make an attempt to find tangible evidences in favor of a role of either physiological and pathological exogenous microbial species in the pathogenesis of FL, and try to integrate the findings coming from epidemiological, biological and interventional studies to define future  novel treatment and prevention strategies for FL.

Lymphomas

2017 ◽  
Author(s):  
Kieron Dunleavy ◽  
Wyndham H Wilson
Keyword(s):  
Gene Expression ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Group Performance ◽  
Cell Lymphoma ◽  
International Prognostic Index ◽  
Prognostic Index ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Lymphoma is the fifth most common type of cancer in the United States, with 74,490 new cases estimated in 2009. Approximately 15% of patients with lymphoma have Hodgkin lymphoma; the remainder have one of the non-Hodgkin lymphomas. The incidence of non-Hodgkin lymphoma has increased steadily over recent decades. This chapter reviews the epidemiology, classification, clinical features, pathology, diagnostic evaluation, staging and prognosis, and treatment of Hodgkin and non-Hodgkin lymphoma. Other topics discussed include the acute and chronic effects of therapy for Hodgkin disease, as well as the subtypes of non-Hodgkin lymphomas, including indolent B cell lymphoma, follicular lymphoma, small lymphocytic lymphoma, mantle cell lymphoma, marginal-zone lymphoma, diffuse large B cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNSL), Burkitt lymphoma, and HIV-related non-Hodgkin lymphoma. Figures illustrate the cellular appearance of Hodgkin lymphoma subtypes and DLBCL, diagnosis of DLBCL subtypes by gene expression, computed tomography and plain chest film in primary mediastinal cell lymphoma, MRI of the brain in PCNSL, and gene expression and gene expression predictors of survival among patients with DLBCL treated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], and prednisone (R-CHOP). Tables describe the Ann Arbor classification and the Cotswold modification for staging of lymphoma; the International Prognostic Score for advanced Hodgkin lymphoma; the World Health Organization classification of hematopoietic neoplasms; chromosomal translocations in non-Hodgkin lymphoma; the Eastern Cooperative Oncology Group performance scale; the International Prognostic Index for aggressive non-Hodgkin lymphoma; and the Follicular Lymphoma International Prognostic Index. This chapter has 185 references. This review contains 9 tables, 7 figures and 185 references

Lymphomas

2018 ◽  
Author(s):  
Kieron Dunleavy ◽  
Wyndham H Wilson
Keyword(s):  
Gene Expression ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Group Performance ◽  
Cell Lymphoma ◽  
International Prognostic Index ◽  
Prognostic Index ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Lymphoma is the fifth most common type of cancer in the United States, with 74,490 new cases estimated in 2009. Approximately 15% of patients with lymphoma have Hodgkin lymphoma; the remainder have one of the non-Hodgkin lymphomas. The incidence of non-Hodgkin lymphoma has increased steadily over recent decades. This chapter reviews the epidemiology, classification, clinical features, pathology, diagnostic evaluation, staging and prognosis, and treatment of Hodgkin and non-Hodgkin lymphoma. Other topics discussed include the acute and chronic effects of therapy for Hodgkin disease, as well as the subtypes of non-Hodgkin lymphomas, including indolent B cell lymphoma, follicular lymphoma, small lymphocytic lymphoma, mantle cell lymphoma, marginal-zone lymphoma, diffuse large B cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNSL), Burkitt lymphoma, and HIV-related non-Hodgkin lymphoma. Figures illustrate the cellular appearance of Hodgkin lymphoma subtypes and DLBCL, diagnosis of DLBCL subtypes by gene expression, computed tomography and plain chest film in primary mediastinal cell lymphoma, MRI of the brain in PCNSL, and gene expression and gene expression predictors of survival among patients with DLBCL treated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], and prednisone (R-CHOP). Tables describe the Ann Arbor classification and the Cotswold modification for staging of lymphoma; the International Prognostic Score for advanced Hodgkin lymphoma; the World Health Organization classification of hematopoietic neoplasms; chromosomal translocations in non-Hodgkin lymphoma; the Eastern Cooperative Oncology Group performance scale; the International Prognostic Index for aggressive non-Hodgkin lymphoma; and the Follicular Lymphoma International Prognostic Index. This chapter has 185 references.

Expression of complement inhibitors CD46, CD55, and CD59 on tumor cells does not predict clinical outcome after rituximab treatment in follicular non-Hodgkin lymphoma

Blood ◽  
2001 ◽  
Vol 98 (5) ◽  
pp. 1352-1357 ◽  
Author(s):  
Wen-Kai Weng ◽  
Ronald Levy
Keyword(s):  
Clinical Outcome ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Tumor Cells ◽  
Antitumor Effect ◽  
Non Hodgkin Lymphoma ◽  
Complement Inhibitors ◽  
Response Groups

Rituximab is a chimeric monoclonal antibody that targets B-cell–specific antigen CD20 and an effective treatment for B-cell non-Hodgkin lymphoma. Although it is readily used in clinical practice, the exact mechanism of its antitumor effect is unclear. One potential mechanism involves complement-mediated cytotoxicity. It has been shown that rituximab induces complement-mediated cytotoxicity in follicular lymphoma cells in vitro, and complement inhibitors CD55 and CD59 may regulate this process. To determine whether complement inhibitors play a role in regulating the antitumor effect of rituximab, the expression of complement inhibitors CD46, CD55, and CD59 was analyzed in pretreatment tumor cells from 29 rituximab-treated follicular lymphoma patients. Among them, 8 patients achieved complete responses, 11 patients achieved partial responses, and 10 patients showed no or minimal responses to rituximab treatment. Expression of surface CD20, CD46, CD55, and CD59 was determined by 2-color flow cytometry. Although the CD59 level was slightly lower in the complete response group, there was no statistically significant difference in the expression of individual complement inhibitor CD46 (mean channel fluorescence [MCF]: NR, 26.4; PR, 21.9; CR, 29.9), CD55 (MCF: NR, 16.4; PR, 14.9; CR, 23.2), or CD59 (MCF: NR, 41.6; PR, 40.6; CR, 30.6), the combination of any 2 inhibitors, or all 3 on tumor cells from 3 response groups. In addition, there was no difference in the rituximab-induced complement-mediated cytotoxicity in an in vitro assay using tumor cells from 3 response groups. Thus, CD46, CD55, and CD59 expression on pretreatment tumor cells, or their susceptibility to in vitro complement-mediated killing, does not predict clinical outcome after rituximab treatment.

scholarly journals Bacterial Infection and Non-Hodgkin B-Cell Lymphoma: Interactions between Pathogen, Host and the Tumor Environment

2021 ◽  
Vol 22 (14) ◽  
pp. 7372
Author(s):  
Monika Maria Biernat ◽  
Tomasz Wróbel
Keyword(s):  
B Cell ◽  
Malt Lymphoma ◽  
B Lymphocyte ◽  
Lymphocyte Transformation ◽  
Infectious Agent ◽  
B Cell Lymphoma ◽  
Achromobacter Xylosoxidans ◽  
Infectious Agents ◽  
Tumor Environment ◽  
H Pylori

Non-Hodgkin B-cell lymphomas (NHL) are a heterogeneous group of lymphoid neoplasms with complex etiopathology, rich symptomatology, and a variety of clinical courses, therefore requiring different therapeutic approaches. The hypothesis that an infectious agent may initiate chronic inflammation and facilitate B lymphocyte transformation and lymphogenesis has been raised in recent years. Viruses, like EBV, HTLV-1, HIV, HCV and parasites, like Plasmodium falciparum, have been linked to the development of lymphomas. The association of chronic Helicobacter pylori (H. pylori) infection with mucosa-associated lymphoid tissue (MALT) lymphoma, Borrelia burgdorferi with cutaneous MALT lymphoma and Chlamydophila psittaci with ocular adnexal MALT lymphoma is well documented. Recent studies have indicated that other infectious agents may also be relevant in B-cell lymphogenesis such as Coxiella burnettii, Campylobacter jejuni, Achromobacter xylosoxidans, and Escherichia coli. The aim of the present review is to provide a summary of the current literature on infectious bacterial agents associated with B-cell NHL and to discuss its role in lymphogenesis, taking into account the interaction between infectious agents, host factors, and the tumor environment.

scholarly journals Is Absolute Lymphocyte Count at Time of Diagnosis a Predictor of Overall Survival in Non-Hodgkin Lymphoma Patients?

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 32-32
Author(s):  
Mallak Zatreh ◽  
Anahat Kaur ◽  
Anas Albawaliz ◽  
Sheetal Bulchandani ◽  
Ghazal Khan
Keyword(s):  
Overall Survival ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Lymphocyte Count ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Absolute Lymphocyte Count ◽  
Histopathological Diagnosis ◽  
Non Hodgkin Lymphoma

Introduction:The prognostic significance of absolute lymphocyte count (ALC) has been an area of debate in non-Hodgkin-lymphoma (NHL). Several studies have reported that lymphocyte count during and after chemotherapy independently predict outcome in patients with acute myelocytic lymphoma (AML), follicular lymphoma and diffuse large B-cell lymphoma (DLBCL). Furthermore, lymphocytopenia is a poor prognostic marker in initial staging of NHL and in relapsed DLBCL. Therefore, we aimed to investigate whether ALC at time of diagnosis is an independent predictor of overall survival (OS) in NHL. Methods:We retrospectively reviewed patients with aggressive NHL who were seen at hospitals affiliated with Saint Luke's Health System from January 2000 to December 2017 with at least 2 year longitudinal follow up after diagnosis. We retrieved 447 patients with histopathological diagnosis of DLBCL, Burkitt's Lymphoma, Follicular Lymphoma Grade IIIB, primary Effusion Lymphoma, B-cell Lymphoma unclassifiable, and high-grade B cell lymphoma. Through chart review we determined pathological and clinical characteristics of these patients, calculated the ALC at time of diagnosis, studied the treatment patterns, response to therapy and survival in our center. ALC at time of diagnosis was obtained on 358 patients based on data availability. Results:A multivariate analysis was conducted to see if ALC at time of diagnosis is a predictor of OS by correcting for age at diagnosis, gender, race, stage at diagnosis, international prognostic index (IPI), central nervous system involvement, histopathological diagnosis and type of chemotherapy. ALC at diagnosis after controlling all variables was not a significant predictor of OS (P: 0.7126). Conclusion:We found that ALC at time of diagnosis did not have a statistically significant effect on OS. We believe that prospective large-scale studies are needed to determine whether ALC at time of diagnosis affects OS in NHL patients. Table Disclosures No relevant conflicts of interest to declare.

FCyIIIa Gene Polymorphisms as Response Predictor in Patients with Non-Hodgkin Lymphoma after Treatment with Anti-CD 20 Monoclonal Antibody (Rituximab).

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4487-4487
Author(s):  
Soledad Molnar ◽  
Mariana Nuñez ◽  
Maria L. Rizzi ◽  
Marcelo Lavarda ◽  
Maria I. Balseiro ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Response Rate ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma ◽  
Large B Cell Lymphoma ◽  
End Of Treatment ◽  
Large B Cell

Abstract Background: The main mechanism of action of rituximab is through antibody-dependent cellular cytotoxicity via Fc receptors for immunoglobulin G. Recently a polymorphism of Fc was reported, which consists in the substitution of phenylalanine for valine in position 158. Patients with homozygous 158 valine/valine (V/V) alleles of Fc showed a higher response rate to rituximab treatment in contrast to patients with phenylalanine/valine (F/V) or homozygous phenilalanine (F/F). It would have clinical value to know which patients could have a greater benefit from the treatment with rituximab. Aims: 1-to determine the Fc genotype in patients with Non-Hodgkin lymphoma (NHL) in our population. 2- to analyze the response rate to rituximab of these patients according to the Fc polymorphism. Methods: DNA was isolated from peripheral blood. Genotyping of FCyIIIa polymorphism was performed using a polymerase chain reaction and were confirmed by direct sequencing of the region of interest. To analyse the results the patients were divided into two groups: with valine expression: V/V or V/F, and without valine expression F/F. The response was evaluated after 3 months of treatment and at the end of it. Chi-square and Fisher’s exact tests were used for statistical analysis. Results: 34 patients with NHL: 19 follicular lymphoma, 12 diffuse large B-cell lymphoma, 3 mantle lymphoma. The FcyIIIa polymorphism expression was 11.8% V/V, 52.9% V/F and 35.3% F/F. The complete response (CR) after 3 months of treatment was 50% and 41.7% for V/V-V/F and F/F respectively (not statistically significant (ns)). After end of treatment CR was 86.7% in V/V-V/F and 72.7% in F/F(ns). In patients with follicular lymphoma the CR after end of treatment was 87.5% in V/V-V/F and 79% in F/F (ns). In patients with diffuse large B-cell lymphoma the CR was reached in all patients regardless of polymorphism. Conclusions: FcyIIIa gene polymorphism did not help in predicting response after treatment with rituximab in our group of patients with NHL. A large number of patients would be necessary to draw conclusions, especially in the group with follicular lymphoma.

90Yttrium-Ibritumomab Tiuxetan for Non-Hodgkin Lymphoma: Results after a Median Follow-up of 5 Years in a Single Institution

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4455-4455
Author(s):  
Antonella Anastasia ◽  
Enrico Morello ◽  
Alessandra Tucci ◽  
Alessandro Re ◽  
Marina Motta ◽  
...  
Keyword(s):  
Clinical Practice ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
Single Agent ◽  
Front Line ◽  
Ibritumomab Tiuxetan ◽  
Non Hodgkin Lymphoma

Abstract Introduction: XPO1 (CRM1, Exportin 1) is the sole transporter of many tumor suppressor proteins (including MYC, BCL2, BCL6, BTK, IkB) and is elevated in non-Hodgkin Lymphoma. Selinexor (Sel, KPT-330) is an oral covalent inhibitor of XPO1, the first clinical molecule of the Selective Inhibitors of Nuclear Export drug class. The phase I clinical trial of Sel in hematologic malignancies showed promising early single-agent efficacy with modest toxicity in relapsed Diffuse Large B-cell Lymphoma (DLBCL, Gutierrez et al, ASCO 2014). DLBCL, the most common lymphoid malignancy, is currently cured in only 10% of relapsed patients, and consists of 2 subtypes based on putative cell of origin (COO): activated B-cell (ABC) and germinal center B-cell (GCB). We performed preclinical studies of Sel, modeling its single-agent efficacy in frontline and relapsed DLBCL and its potential synergy with other clinically relevant therapeutics. Long-term follow-up data on patients(pts) treated with Radiolabeled antibody 90-yttrium-Ibritumomab Tiuxetan (RIT) are necessary to define the role of RIT-therapy (RIT-t) in current clinical practice. There are few reports about the use of RIT outside clinical trials. Outcome and toxicity of radioimmunotherapy remain a matter of concern. Incidence of MDS/AML reported after RIT-t as consolidation in front line varies from 3 to 4.3% (Czuczman et al, JCO 2007; Morschhauser et al, JCO 2012). A recent study with RIT and autologous stem cell transplantation (ASCT) as front line therapy in mantle cell lymphoma reported 20% incidence of secondary malignancies, (Arranz et al, Haemat 2013). So the aim of this study was to analyze the outcome of pts treated with RIT-t in clinical practice and to assess the incidence of secondary neoplasia particularly MDS/AML. We included in this retrospective analysis all pts with Diffuse B Large Cell Lymphoma (DBLCL), Follicular Lymphoma (FL) and Marginal Zone lymphoma (MZL), treated with RIT-t over the last decade at our Institution. We adopted the standard RIT therapeutic regimen: infusion of 250 mg/m2 rituximab on day 1, a second 250 mg/m2 dose on day 7, followed by dose of RIT (0.4 mCi/kg), administered 4 h following rituximab infusion. Response assessment was made as recommended by International Workshop criteria. Survival analysis was performed with Kaplan-Meier method and univariate analysis with Log-Rank test with a significance at 0.05. Between March 2006 and January 2014 61 pts underwent RIT-t, of these 57 had complete data and were considered for analysis. There were 16 DBLCL, 29 Follicular Lymphoma and 12 MZL. Twentythree were male, 34 female. Median age at diagnosis was 62 years(yrs) (range 36; 79), 66yrs (range 39;79) at RIT-t. Thirteen pts (all DBLCL) received RIT-t as front line consolidation. Forty-four pts (3 DBLCL, 12 MZL, 29 FL) underwent RIT-t after ≥1 therapy line: one prior line was received by 15pts, 2 by 19, 3 by 8 and 4 by 2. Before RIT-t 24pts were in relapse (2DBLCL, 2MZL, 20FL), 9 were refractory (2 MZL, 7 FL), 7 in partial response (1 DBLCL, 5 MZL, 1FL) while 4 were in complete remission (2 MZL, 2FL). Disclosures No relevant conflicts of interest to declare.

Lymphomas

2017 ◽  
Author(s):  
Kieron Dunleavy ◽  
Wyndham H Wilson
Keyword(s):  
Gene Expression ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Group Performance ◽  
Cell Lymphoma ◽  
International Prognostic Index ◽  
Prognostic Index ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Lymphoma is the fifth most common type of cancer in the United States, with 74,490 new cases estimated in 2009. Approximately 15% of patients with lymphoma have Hodgkin lymphoma; the remainder have one of the non-Hodgkin lymphomas. The incidence of non-Hodgkin lymphoma has increased steadily over recent decades. This chapter reviews the epidemiology, classification, clinical features, pathology, diagnostic evaluation, staging and prognosis, and treatment of Hodgkin and non-Hodgkin lymphoma. Other topics discussed include the acute and chronic effects of therapy for Hodgkin disease, as well as the subtypes of non-Hodgkin lymphomas, including indolent B cell lymphoma, follicular lymphoma, small lymphocytic lymphoma, mantle cell lymphoma, marginal-zone lymphoma, diffuse large B cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNSL), Burkitt lymphoma, and HIV-related non-Hodgkin lymphoma. Figures illustrate the cellular appearance of Hodgkin lymphoma subtypes and DLBCL, diagnosis of DLBCL subtypes by gene expression, computed tomography and plain chest film in primary mediastinal cell lymphoma, MRI of the brain in PCNSL, and gene expression and gene expression predictors of survival among patients with DLBCL treated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], and prednisone (R-CHOP). Tables describe the Ann Arbor classification and the Cotswold modification for staging of lymphoma; the International Prognostic Score for advanced Hodgkin lymphoma; the World Health Organization classification of hematopoietic neoplasms; chromosomal translocations in non-Hodgkin lymphoma; the Eastern Cooperative Oncology Group performance scale; the International Prognostic Index for aggressive non-Hodgkin lymphoma; and the Follicular Lymphoma International Prognostic Index. This chapter has 185 references.

scholarly journals Worse outcome and distinct mutational pattern in follicular lymphoma with anti-HBc positivity

2021 ◽  
Author(s):  
Maria Concpcion Fernandez ◽  
Juan José Rodríguez-Sevilla ◽  
Lierni Fernández-Ibarrondo ◽  
Blanca Sanchez-Gonzalez ◽  
Joan Gibert ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
B Cell ◽  
B Cell Lymphoma ◽  
Epidemiological Studies ◽  
Hbv Infection ◽  
Hbv Reactivation ◽  
Large B Cell Lymphoma ◽  
Mutational Profiling ◽  
Mutational Pattern ◽  
B Virus

Epidemiological studies have demonstrated the association between hepatitis B virus (HBV) infection and B-cell non-Hodgkin lymphomas (NHL), mainly for diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL). We studied a cohort of 121 FL patients for HBV infection status, clinical features and gene mutational profile. Anti-HBc was detectable in sixteen patients (13.2%), although all had undetectable HBV DNA. Anti-HBc+ cases presented with older age at diagnosis than anti-HBc- cases (68.1 vs. 57.2 years, P=0.007) and higher β2-microglobulin (56.3% vs. 28.9%, P=0.04). All patients included in the study fulfilled criteria for treatment and received therapy with rituximab or rituximab-containing chemotherapy. There were no episodes of HBV reactivation or HBV-hepatitis during treatment and/or maintenance. Remarkably, anti-HBc+ patients had significantly lower 10-year PFS (12.9% vs 58.3%; P<0.0001) and OS (22.0% vs. 86.2%, P<0.0001), that remained at multivariate analysis. Gene mutational profiling of all cases showed that anti-HBc+ cases had higher incidence of ARID1A mutations and absence of EP300 mutations, two key epigenetic regulators in FL. Overall, our study shows that FL patients with resolved HBV infection have a worse outcome independently of other well-known clinical risk factors and a distinct gene mutational profile.

Sign in / Sign up

Export Citation Format

Share Document