Part I: Hodgkin's lymphoma—molecular biology of Hodgkin and Reed-Sternberg cells

Thomas, Roman K.; Ré, Daniel; Wolf, Jürgen; Diehl, Volker

doi:10.1016/s1470-2045(03)01319-6

Cited by 130 publications

(95 citation statements)

References 66 publications

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“…For details consult main text. BAFF, B-cell activating factor; CD40L, CD40 ligand, IkB, inhibitor of NF-kB; IKK, IkB kinase; IL, interleukin; IRAK, IL-1R-associated kinase; FADD, Fas-associated death domain protein; LPS, lipopolysaccharides; LTb, lymphotoxinb; NEMO, NF-kB essential modulator; NF-kB, nuclear factor kappa B; NIK, NF-kB-inducing kinase; RIP, receptor interacting protein; TLR, toll-like receptor; TNF, tumor necrosis factor; TRADD, TNF receptor-associated protein with a death domain; TRAF, TNF receptor-associated factor; Ub, ubiquitin 11 The constitutive activity of NF-kB has first been shown for HRS cell lines 12 and then in primary HRS cells. 13 Specifically, the transcriptionally active homodimer p50 accounts for constitutive NF-kB activation in HRS cells.…”

Section: Constitutive Activity Of Nf-jb In Hematologic Malignanciesmentioning

confidence: 99%

“…Autonomously active surface receptors, including CD30, CD40, receptor activator of NF-kB (RANK), and Notch 1, have been implicated in NF-kB activation in HRS. 11 Alternatively, or in addition, EBV might mediate NF-kB activation through virally encoded genes such as latent membrane protein (LMP)1, LMP2a, and EBV nuclear antigen (EBNA), whose transcription has been detected in HRS cells. 15 In particular, LMP1 can mimic CD40 signaling, and this could explain how latent EBV infection causes the upregulation of antiapoptotic target genes via NF-kB.…”

Section: Constitutive Activity Of Nf-jb In Hematologic Malignanciesmentioning

confidence: 99%

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Targeting NF-κB in hematologic malignancies

et al. 2006

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The transcription factor nuclear factor kappa B (NF-jB) can intervene in oncogenesis by virtue of its capacity to regulate the expression of a plethora of genes that modulate apoptosis, and cell survival as well as proliferation, inflammation, tumor metastasis and angiogenesis. Different reports demonstrate the intrinsic activation of NF-jB in lymphoid and myeloid malignancies, including preneoplastic conditions such as myelodysplastic syndromes, underscoring its implication in malignant transformation. Targeting intrinsic NF-jB activation, as well as its upstream and downstream regulators, may hence constitute an additional approach to the oncologist's armamentarium. Several small inhibitors of the NF-jB-activatory kinase IjB kinase, of the proteaseome, or of the DNA binding of NF-jB subunits are under intensive investigation. Currently used cytotoxic agents can induce NF-jB activation as an unwarranted side effect, which confers apoptosis suppression and hence resistance to these drugs. Thus, NF-jB inhibitory molecules may be clinically useful, either as single therapeutic agents or in combination with classical chemotherapeutic agents, for the treatment of hematological malignancies.

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Section: Constitutive Activity Of Nf-jb In Hematologic Malignanciesmentioning

confidence: 99%

Section: Constitutive Activity Of Nf-jb In Hematologic Malignanciesmentioning

confidence: 99%

Targeting NF-κB in hematologic malignancies

et al. 2006

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“…(Horie et al, 2003;Thomas et al, 2004). The peculiar activated phenotype of H-RS cells and their pattern of cytokine secretion, which contribute to the pathological appearance and clinical manifestations of the disease, are believed to be consequences of constitutive NF-kB activation (Skinnider and Mak, 2002).…”

Section: Introductionmentioning

confidence: 99%

Aberrant NF-κB2/p52 expression in Hodgkin/Reed–Sternberg cells and CD30-transformed rat fibroblasts

et al. 2005

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“…The two types of HL have their own unique malignant cells, designated as mononuclear Hodgkin's cells and multinucleated Reed-Sternberg (HRS) cells in cHL whereas they are called LP (lymphocyte predominant) cells in NLPHL, respectively (Poppema et al, 2008). Unlike the LP cells of NLPHL, EBV DNA genomes are frequently detected in HRS cells of cHL patients, in which the viruses display the type II form of latency expressing all of the type II-related 6 viral genes (Weiss et al, 1989;Weiss et al, 1999;Thomas et al, 2004;Kuppers, 2009). Since EBV is an oncogenic virus, this high association rate with EBV in HRS cells strongly suggests a possible role of EBV latent gene expression in the generation of the malignancies.…”

Section: Ebv Latency and Hlmentioning

confidence: 99%

Epstein-Barr Virus-Associated Classical Hodgkin Lymphoma and Its Therapeutic Strategies

Lee¹

2011

Biomolecules and Therapeutics

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Lymphoma is a type of cancer involving cells of the immune system, and has two major categories: Hodgkin lymphoma (HL) and all other lymphomas (non-HL). Although the two types may display the same symptoms, they are readily distinguishable via microscopic examination, and differ in the way they develop, spread and are treated. HL is a unique clinicopathological disorder characterized by the rare presence of malignant cells (usually accounting for 0.1% to 10% of the cells in the total tumor mass) in a background of a nonneoplastic cellular microenvironment comprising T-and Blymphocytes and other cell types (Weiss et al., 1999). In the United States, about 8,500 new cases of HL were expected to be diagnosed in 2010, and the overall incidence is increasing each year (Maggioncalda et al., 2011).Although the pathogenesis of HL is still largely unknown, the association of HL with Epstein-Barr virus (EBV) infection has been demonstrated in many reports. For examples, HL patients show elevated antibody titers to EBV antigens (Levine et al., 1971), and the risk of developing HL is increased up to three-fold in population that have experienced infectious mononucleosis caused by primary EBV infection (Gutensohn Over the past few decades, our understanding of the epidemiology and immunopathogenesis of Hodgkin lymphoma (HL) has made enormous advances. Consequently, the treatment of HL has changed signifi cantly, rendering this disease of the most curable human cancers. To date, about 80% of patients achieve long-term disease-free survival. However, therapeutic challenges still remain, particularly regarding the salvage strategies for relapsed and refractory disease, which need further identifi cation of better prognostic markers and novel therapeutic schemes. Although the precise molecular mechanism by which Epstein-Barr virus (EBV) contributes to the generation of malignant cells present in HL still remains unknown, current increasing data on the role of EBV in the pathobiology of HL have encouraged people to start developing novel and specifi c therapeutic strategies for EBVassociated HL. This review will provide an overview of therapeutic approaches for acute EBV infection and the classical form of HL (cHL), especially focusing on EBV-associated HL cases. and Cole, 1980), and EBV DNA/RNA can be detected in HL tissues (Brink et al., 1997), suggesting that as a primary event in the development of this disease, EBV infection may play a very crucial role in the pathogenesis of HL. AbstractAccording to a population-based cohort study, the frequency of EBV associated HL among total HL cases varies from 30 to 50% (in certain cases even higher; >90% in developing and underdeveloped countries, and >95% in HIV associated cases), and most of them appear in classical Hodgkin lymphoma (cHL), the major type of HL (Herbst et al., 1991;Pallesen et al., 1991;Ambinder et al., 1993;Leoncini et al., 1996). Since EBV is an oncogenic virus that is able to subvert cellular processes supporting growth and survival, the approach to unravel the f...

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Part I: Hodgkin's lymphoma—molecular biology of Hodgkin and Reed-Sternberg cells

Cited by 130 publications

References 66 publications

Targeting NF-κB in hematologic malignancies

Targeting NF-κB in hematologic malignancies

Aberrant NF-κB2/p52 expression in Hodgkin/Reed–Sternberg cells and CD30-transformed rat fibroblasts

Epstein-Barr Virus-Associated Classical Hodgkin Lymphoma and Its Therapeutic Strategies

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