A20 inactivation in ocular adnexal MALT lymphoma

Bi, Yang; Zeng, Naiyan; Chanudet, Estelle; Huang, Yuanxue; Hamoudi, Rifat; H, Liu; Dong, Guangbin; Watkins, A. James; Sc, Ley; Zou, Li; Chen, R; Zhu, Xiaoyan; Du, Miaomiao

doi:10.3324/haematol.2010.036798

Cited by 49 publications

(50 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the prevalence of A20 abnormalities in pSS patients with MALT lymphoma in our study (77%) is higher than what has been generally described in MALT lymphoma (prevalence, 22%-28%). 6,7 This suggests specific involvement of A20 inactivation in lymphoma complicating autoimmune disease.…”

Section: Discussionmentioning

confidence: 97%

“…5 In addition to its role in autoimmunity, A20 inactivation in tumor cells has been found in a number of lymphomas, particularly the mucosa-associated lymphoid tissue (MALT) type of marginal zone lymphoma. 4,[6][7][8][9] In accordance with the well-established role of excessive NF-kB activation in the development of lymphoid malignancies, 10 A20/TNFAIP3 is considered a potent tumor suppressor gene in B-cell lymphoma.…”

Section: 2mentioning

confidence: 94%

See 1 more Smart Citation

Germline and somatic genetic variations of TNFAIP3 in lymphoma complicating primary Sjögren’s syndrome

Nocturne

Boudaoud

Miceli‐Richard

et al. 2013

Blood

107

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 97%

Section: 2mentioning

confidence: 94%

Germline and somatic genetic variations of TNFAIP3 in lymphoma complicating primary Sjögren’s syndrome

Nocturne

Boudaoud

Miceli‐Richard

et al. 2013

Blood

107

View full text Add to dashboard Cite

show abstract

“…These findings appear to be of clinical relevance: complete A20 inactivation is associated with poor lymphoma-free survival, and the patients with A20 mutation/deletion required significantly higher radiation dosages than those without the A20 abnormalities to achieve complete remission. 80 Validation of these findings is presently underway in a large and separate cohort of EMZL collated between several centres belonging to the European Ophthalmological Oncology Group (www.oog.eu.com).…”

Section: Extranodal Marginal Zone B-cell Lymphomamentioning

confidence: 99%

Molecular pathology of lymphoma

Coupland

2012

Eye

View full text Add to dashboard Cite

Ocular lymphomas can be divided into intraocular lymphomas and ocular adnexal lymphomas. The vitreoretinal lymphomausually a diffuse large B-cell lymphoma (DLBCL) of high-grade malignancy-is the most common lymphoid malignancy arising in the eye, while the extranodal marginal zone B-cell lymphoma (EMZL), an indolent often recurrent tumour, occurs most frequently in the ocular adnexal tissue. The two lymphoma subtypes differ significantly in their clinical presentation, subsequent course and outcome as well as in their underlying morphological, immunophenotypical and genetic features. The molecular processes involved in DLBCL and EMZL development are complex, and include chromosomal translocations, mutations caused by aberrant somatic hypermutation, sporadic somatic mutations, and copy number alterations, characterized by deletions and amplifications. These lead to alterations in particular signalling pathways, which in turn activate transcription factors, such as nuclear factor NF-kB. This review provides an overview of the histological features of DLBCL and EMZL, and discusses the current insights into the molecular mechanisms underlying the development of these tumours, when they occur systemically and particularly when they arise in ocular tissues.

show abstract

“…In addition, direct contact of the MTOC with the IS plays a critical role by allowing directed secretion of cytotoxic granules by killer lymphocytes [104]. The formation of microclusters and SMACs depends on the actin cytoskeleton [99,105]. Recently, it was shown that clathrin, a protein involved in endocytic processes, in intracellular compartments and vesicle formation, as well as in the formation of late endosomes termed multivesicular bodies (MVBs), is recruited to and regulates actin accumulation at the IS suggesting that some interactions might occur between MVBs and the IS [106].…”

Section: Molecular Requirements For the Polarization Of The Ismentioning

confidence: 99%

Dysregulation of the antigen-induced NF-κB signaling pathway in the development of human B-cells lymphomas

Messali¹,

Génin

Weil³

2013

J Leuk

View full text Add to dashboard Cite

The adaptive immune response is initiated when microbial or tumor-specific molecules are recognized by antigen receptors present at lymphocyte cell surface. Engagement of these immunoreceptors induces signaling cascades that ultimately activate the transcription factors NF-κB (Nuclear Factor-κB) and NFAT (nuclear factor of activated T-cells) responsible for the establishment of gene expression programs controlling the stimulation, proliferation and survival of activated lymphocytes. Cloning the products of three distinct translocation events found in lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) led to the identification and characterization of a novel NF-κB-activating complex following antigenic stimulation composed by the CARMA1, BCL10, and MALT1 proteins and called the CBM complex. Since the identification of this complex, other regulatory components were discovered which greatly improve our understanding of this signaling pathways.Interestingly, CBM complex activity is not only altered in MALT lymphomas but also in a subtype of activated B cell-like (ABC) of diffuse large B-cell (DLBCL) lymphoma. In this review, we described the key players involved in antigen-induced NF-κB activation and covered the recent advances in the molecular mechanisms that are responsible for the regulation of the components of the CBM complex. Understanding these mechanisms is critical for the elucidation of the role of this NF-κB signaling network in both normal and pathologic conditions and we described how dysregulation of this network leads to the uncontrolled activation of NF-κB and development of two particular subtypes of human B cell lymphomas: the MALT and the DLBCL lymphomas. DAP12) [1]. Engagement of these receptors initiate a signal-activation cascade that includes phosphorylation of two specific tyrosine residues located in the ITAM by the Src family kinases [1]. Tyrosine kinase Syk or ZAP-70 (zeta-chain-associated protein 70 kD) are then recruited to the phosphorylated ITAM through their tandem Src homology 2 (SH2) regions, initiating downstream signaling cascades that lead to the stimulation of mitogen-activated protein kinase (MAPK) activities and ultimately to the activation of the transcription factors NF-κB and NF-AT (nuclear factor of activated T-cells).An outstanding issue of lymphocyte activation was the identification of a complex of proteins comprising CARMA1, BCL10 and MALT1 (also called the CBM complex) as critical regulators of the immunoreceptor signaling pathways. In this review, we will focus on the recent advances concerning the role of the CBM function in antigen-induced NF-κB signaling and detail how this pathway may selectively become dysregulated in lymphoma. The key players of antigen-mediated NF-κB activationAntigen receptor activation initiates a phosphorylation cascade that promotes assembly of the CBM signalosome complex composed of CARMA1, BCL10, and MALT1 that ultimately activates the NEMO/ IKK complex to promote NF-κB transcription (Figure 1). In this

show abstract

A20 inactivation in ocular adnexal MALT lymphoma

Cited by 49 publications

References 31 publications

Germline and somatic genetic variations of TNFAIP3 in lymphoma complicating primary Sjögren’s syndrome

Germline and somatic genetic variations of TNFAIP3 in lymphoma complicating primary Sjögren’s syndrome

Molecular pathology of lymphoma

Dysregulation of the antigen-induced NF-κB signaling pathway in the development of human B-cells lymphomas

Contact Info

Product

Resources

About