Epstein–Barr virus‐positive aggressive lymphoma as a consequence of immunosuppression after multiple salvage treatments for follicular lymphoma

Orlandi, Ester; Paulli, Marco; Viglio, Alessandra; Pagnucco, G.; Riboni, Roberta; Baldanti, Fausto; Lazzarino, Mario

doi:10.1046/j.1365-2141.2001.02579.x

Cited by 17 publications

(13 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[59][60][61] In a proportion of cases, IDA-LPDs are related to one or more underlying viral infections, such as those sustained by EBV or, less frequently, HHV8. [62][63][64][65][66][67][68][69][70][71] Finally, the concept of defective immune regulation, which is the common denominator of all these disorders, is itself broad, encompassing wellknown conditions such as primary immunodeficiency, HIV infection and post-transplant or methotrexateinduced immunosuppression and newly recognized factors, related, for instance, to old age and malnutrition. [72][73][74][75] Cases were analysed using a wide range of techniques, as the information provided by cell Aggressive B-cell lymphomas 251 morphology alone is often inadequate to make a firm diagnosis or to predict the outcome of the process and to identify risk factors, which can assist in clinical decision making.…”

Section: Lymphoproliferative Disorders In Immunocompromised Patients mentioning

confidence: 99%

Aggressive B‐cell lymphomas: a review based on the workshop of the XI Meeting of the European Association for Haematopathology

et al. 2005

View full text Add to dashboard Cite

The generic term aggressive B-cell lymphoma includes a variety of entities, each with particular diagnostic and therapeutic issues. To define these entities better and to help confront such issues, a workshop was organized by the European Association of Haematopathology (EAHP) and the Society of Haematology during the XI Meeting of the EAHP, held in Italy in May 2002. Participants were asked to submit cases under various categories and all cases submitted were examined and reviewed by the panel members. The panel's diagnoses formed the basis for discussion at the workshop and a limited number of cases were selected to be presented in more detail and discussed during the workshop. After the workshop the panel met again to discuss the outcome, summarized in this report, which describes the panel's proposals regarding diagnostic criteria, terminology, the definition of new entities and evaluation of biological differential and new prognostic parameters.

show abstract

Section: Lymphoproliferative Disorders In Immunocompromised Patients mentioning

confidence: 99%

Aggressive B‐cell lymphomas: a review based on the workshop of the XI Meeting of the European Association for Haematopathology

et al. 2005

View full text Add to dashboard Cite

show abstract

“…These viruses can execute two distinct life cycles: latency and lytic replication. The switch from latent to lytic life cycle in the context of chronic infection increases the risk of virus-driven cancer (Campbell, Borok et al, 2000; Meerbach, Wutzler et al, 2008; Feng, Cohen et al, 2004; Orlandi, Paulli et al, 2001). Thus, host factors that regulate viral lytic cycle, including during chronic infection, are likely to also play a role in either restricting or promoting viral lymphomagenesis.…”

Section: Introductionmentioning

confidence: 99%

ATM supports gammaherpesvirus replication by attenuating type I interferon pathway

et al. 2017

View full text Add to dashboard Cite

Ataxia-Telangiectasia mutated (ATM) kinase participates in multiple networks, including DNA damage response, oxidative stress, and mitophagy. ATM also supports replication of diverse DNA and RNA viruses. Gammaherpesviruses are prevalent cancer-associated viruses that benefit from ATM expression during replication. This proviral role of ATM had been ascribed to its signaling within the DNA damage response network; other functions of ATM have not been considered. In this study increased type I interferon (IFN) responses were observed in ATM deficient gammaherpesvirus-infected macrophages. Using a mouse model that combines ATM and type I IFN receptor deficiencies we show that increased type I IFN response in the absence of ATM fully accounts for the proviral role of ATM during gammaherpesvirus replication. Further, increased type I IFN response rendered ATM deficient macrophages more susceptible to antiviral effects of type II IFN. This study identifies attenuation of type I IFN responses as the primary mechanism underlying proviral function of ATM during gammaherpesvirus infection.

show abstract

“…Increased viral reactivation from latency is associated with increased risk of developing KSHV- or EBV-driven cancers (Campbell, Borok et al, 2000;Meerbach, Wutzler et al, 2008;Feng, Cohen et al, 2004;Orlandi, Paulli et al, 2001). Therefore, identification of host factors that suppress or promote viral reactivation in vivo is likely to offer an important insight into the mechanism of gammaherpesvirus-driven lymphomagenesis.…”

Section: Introductionmentioning

confidence: 99%

ATM facilitates mouse gammaherpesvirus reactivation from myeloid cells during chronic infection

Kulinski¹,

Darrah²,

Broniowska³

et al. 2015

Virology

View full text Add to dashboard Cite

Gammaherpesviruses are cancer-associated pathogens that establish life-long infection in most adults. Insufficiency of Ataxia-Telangiectasia mutated (ATM) kinase leads to a poor control of chronic gammaherpesvirus infection via an unknown mechanism that likely involves a suboptimal antiviral response. In contrast to the phenotype in the intact host, ATM facilitates gammaherpesvirus reactivation and replication in vitro. We hypothesized that ATM mediates both pro- and antiviral activities to regulate chronic gammaherpesvirus infection in an immunocompetent host. To test the proposed proviral activity of ATM in vivo, we generated mice with ATM deficiency limited to myeloid cells. Myeloid-specific ATM deficiency attenuated gammaherpesvirus infection during the establishment of viral latency. The results of our study uncover a proviral role of ATM in the context of gammaherpesvirus infection in vivo and support a model where ATM combines pro- and antiviral functions to facilitate both gammaherpesvirus-specific T cell immune response and viral reactivation in vivo.

show abstract

Epstein–Barr virus‐positive aggressive lymphoma as a consequence of immunosuppression after multiple salvage treatments for follicular lymphoma

Cited by 17 publications

References 13 publications

Aggressive B‐cell lymphomas: a review based on the workshop of the XI Meeting of the European Association for Haematopathology

Aggressive B‐cell lymphomas: a review based on the workshop of the XI Meeting of the European Association for Haematopathology

ATM supports gammaherpesvirus replication by attenuating type I interferon pathway

ATM facilitates mouse gammaherpesvirus reactivation from myeloid cells during chronic infection

Contact Info

Product

Resources

About