Hepatitis C virus-related B cell subtypes in non Hodgkin's lymphoma

Pellicelli, A.; Marignani, Massimo; Zoli, Valerio; Romano, Mario R.; Morrone, Andrea; Nosotti, L.; Bárbaro, Giuseppe; Picardi, Antonio; Gentilucci, Umberto Vespasiani; Remotti, Daniele; D’Ambrosio, C.; Furlan, Caterina; Mecenate, F.; Mazzoni, Ettore; Majolino, Ignazio; Villani, R.; Andreoli, A.; Barbarini, Giorgio

doi:10.4254/wjh.v3.i11.278

Cited by 44 publications

(33 citation statements)

References 26 publications

(37 reference statements)

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“…Indeed, hepatic flare after rituximab seems to be rare 49,50 and associated with a good outcome and low mortality. 28,48,51 Nevertheless, it may lead to discontinuation of potentially life-saving immunochemotherapy. 51 Although prophylactic antihepatitis B therapy during chemotherapy is the standard of care, concurrent administration of immunochemotherapy with IFN-based HCV treatments is usually not feasible because of the increased hematological and liver toxicity.…”

Section: Aggressive Hcv-associated Nhlmentioning

confidence: 99%

“…47,48 In these patients, unlike patients with hepatitis B, the immunosuppression induced by rituximab does not usually cause HCV reactivation. Indeed, hepatic flare after rituximab seems to be rare 49,50 and associated with a good outcome and low mortality.…”

Section: Aggressive Hcv-associated Nhlmentioning

confidence: 99%

“…21 There is limited evidence of a direct role of intracellular viral proteins. HCV may be able to 55 8 SLVL (n ϭ 57 18 SLVL (n ϭ 44 13 LPL (n ϭ 56 18 LPL (n ϭ 16) 13 0 8 10 9 13 SLVL (n ϭ 1) FL (n ϭ 1) Pellicelli et al, 2011 48 11 SMZL (n ϭ 45 134 SMZL (n ϭ 23) 44 11* 36 82 63 106 NMZL (n ϭ 12) EMZL (n ϭ 25) LPL (n ϭ 7) FL (n ϭ 5) SLL/CLL (n ϭ 1) Others (n ϭ 27) RBV indicates ribavirin; CR, complete response; ORR, overall response rate (complete ϩ partial); SLVL, splenic marginal zone lymphoma with circulating villous lymphocytes; SMZL, splenic marginal zone lymphoma; EMZL, extranodal marginal zone lymphoma of the mucosa-associated lymphoid tissue; and NMZL, nodal marginal zone lymphoma. *Five additional patients were treated with PegIFN␣ alone.…”

Section: Direct Oncogenic Effect On B-lymphocytesmentioning

confidence: 99%

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Hepatitis C virus-associated B-cell non-Hodgkin lymphomas

Vannata

Zucca

2014

Hematology

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Epidemiological studies have demonstrated an increased risk of developing B-cell lymphomas in patients with chronic hepatitis C virus (HCV) infection. However, the strength of the association shows great geographic discrepancies, with higher relative risk in countries with high HCV prevalence. It remains unclear whether additional environmental and genetic factors are involved or if the international variability is simply a consequence of the variable infection prevalence. Therefore, a causal relationship remains controversial. Other confounding factors may affect the comparability of the different studies, including the method of HCV assessment, the selection of normal controls, the lymphoma classification used, and the year of publication. The most convincing proof is the observation, mainly limited to some indolent subtypes, of B-cell lymphoma regressions after HCV eradication with IFN and ribavirin. However, the molecular mechanisms of the HCV-induced lymphomagenesis are mainly hypothetical. According to the model considered to be most plausible, lymphoma growth is a consequence of the continuous antigenic stimulation of the B-cell immunologic response induced by the chronic viral infection. This review summarizes the current epidemiological and biological evidence of a role of HCV in lymphomagenesis, describing the putative mechanisms for a causative relationship. The clinical characteristics and management difficulties of the HCV-associated lymphomas are also discussed. HCV treatment with IFN cannot be given safely in concomitance with cytotoxic lymphoma treatment because of hematological and liver toxicity. However, novel and better tolerated antiviral regimens are under development and will hopefully make the treatment of both lymphoma and hepatitis easier in the future. Learning Objectives• To understand the current lines of evidence linking HCV infection and lymphomagenesis • To review the specific problems of the clinical management of patients with chronic HCV infection

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Section: Aggressive Hcv-associated Nhlmentioning

confidence: 99%

Section: Aggressive Hcv-associated Nhlmentioning

confidence: 99%

Section: Direct Oncogenic Effect On B-lymphocytesmentioning

confidence: 99%

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Hepatitis C virus-associated B-cell non-Hodgkin lymphomas

Vannata

Zucca

2014

Hematology

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“…The management of HCV-associated DLBCLs remains based on immunochemoterapy with antracycline containing regimens in combination with rituximab as in their HCV-negative counterpart, and there are no specific recommendations for this subset of patients [Pellicelli et al 2011;Borchardt and Torres, 2014]. It is unclear whether patients with HCV-positive DLBCL still have a significantly worse outcome than those with HCV-negative disease [Ennishi et al 2010;Visco and Finotto, 2014].…”

Section: Hcv-associated Diffuse Large B-cell Lymphomasmentioning

confidence: 99%

Hepatitis C virus-associated B-cell non-Hodgkin’s lymphomas: what do we know?

Vannata

Arcaini

Zucca

2015

Therapeutic Advances in Hematology

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Abstract:Epidemiological studies have shown an increased risk of developing B-cell lymphomas in patients with chronic hepatitis C virus (HCV) infection. There is, however, a great geographic variability and it remains unclear whether additional environmental and genetic factors are involved or whether the international discrepancies represent simply a consequence of the variable prevalence of HCV infection in different countries. Other confounding factors may affect the comparability of the different studies, including the method of HCV assessment, the selection of normal controls, the lymphoma classification used and the year of publication. The most convincing evidence for a causal relationship comes from the observation, mainly limited to some indolent subtypes, of B-cell lymphoma regressions after successful HCV eradication with antiviral treatment. Yet, the molecular mechanism of HCV-induced lymphomagenesis are mainly hypothetical. According to most plausible models, lymphoma growth is a consequence of continuous antigenic stimulation induced by the chronic viral infection. This review will summarize the current knowledge on HCV-associated lymphomas and their management.

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“…Because HCV genotype 2 is associated with a longer duration of viral infection, it has been speculated that over time it may induce a persistent chronic immune stimulation of B cells (Pellicelli et al, 2011).…”

Section: Hcv Genotypes and Lymphoproliferative Disordersmentioning

confidence: 99%