Abnormal activator protein 1 transcription factor expression in CD30-positive cutaneous large-cell lymphomas

Mao, Xin; Orchard, Guy; Russell‐Jones, Robin; Whittaker, Sean

doi:10.1111/j.1365-2133.2007.08150.x

Cited by 16 publications

(9 citation statements)

References 43 publications

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“…Many human cancers exhibit overexpression of Jun family members ( Neyns et al, 1996 ; Langer et al, 2006 ; Kharman-Biz et al, 2013 ). Consistent with the idea that c-Jun can promote tumorigenicity, overexpression of this transcription factor is observed in some of the more aggressive CD30-positive lymphomas ( Drakos et al, 2007 ; Mao et al, 2007 ). In breast cancer, alteration of RB, VEGF, and EGFR pathways has been shown to induce c-Jun overexpression ( Kharman-Biz et al, 2013 ).…”

Section: The Ap-1 Pathway a Key Regulator Of Cellular Transformationsupporting

confidence: 75%

Hijacking of the AP-1 Signaling Pathway during Development of ATL

et al. 2018

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Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T-cell leukemia (ATL). One way to address the pathology of the disease lies on conducting research with a molecular approach. In addition to the analysis of ATL-relevant signaling pathways, understanding the regulation of important and relevant transcription factors allows researchers to reach this fundamental objective. HTLV-1 encodes for two oncoproteins, Tax and HTLV-1 basic leucine-zipper factor, which play significant roles in the cellular transformation and the activation of the host’s immune responses. Activating protein-1 (AP-1) transcription factor has been linked to cancer and neoplastic transformation ever since the first representative members of the Jun and Fos gene family were cloned and shown to be cellular homologs of viral oncogenes. AP-1 is a dimeric transcription factor composed of proteins belonging to the Jun (c-Jun, JunB, and JunD), Fos (c-Fos, FosB, Fra1, and Fra2), and activating transcription factor protein families. Activation of AP-1 transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. AP-1 is also involved in various cellular events including differentiation, proliferation, survival, and apoptosis. Deregulated expression of AP-1 transcription factors is implicated in various lymphomas such as classical Hodgkin lymphomas, anaplastic large cell lymphomas, diffuse large B-cell lymphomas, and adult T-cell leukemia. Here, we review the current thinking behind deregulation of the AP-1 pathway and its contribution to HTLV-induced cellular transformation.

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Section: The Ap-1 Pathway a Key Regulator Of Cellular Transformationsupporting

confidence: 75%

Hijacking of the AP-1 Signaling Pathway during Development of ATL

et al. 2018

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“…Similar to MUM1, TRAF‐1 is expressed in most LyP cases (84%) and in only 7% of primary cutaneous ALCL and secondary cutaneous ALCL, allowing reliable distinction of LyP from primary and secondary cutaneous ALCL. Whereas TRAF‐1 and MUM1 are upregulated in LyP, activator protein 1 transcription factor (AP‐1) is expressed in only a few cases of LyP (11%) 25 . Further studies on larger series of LyP and primary cutaneous ALCL are needed to clarify if a combination of these two or more markers will allow an even better discrimination of LyP and ALCL than MUM1 and TRAF‐1 alone.…”

Section: Discussionmentioning

confidence: 99%

“…Whereas TRAF-1 and MUM1 are upregulated in LyP, activator protein 1 transcription factor (AP-1) is expressed in only a few cases of LyP (11%). 25 Further studies on larger series of LyP and primary cutaneous ALCL are needed to clarify if a combination of these two or more markers will allow an even better discrimination of LyP and ALCL than MUM1 and TRAF-1 alone.…”

Section: Discussionmentioning

confidence: 99%

MUM1 expression in cutaneous CD30+ lymphoproliferative disorders: a valuable tool for the distinction between lymphomatoid papulosis and primary cutaneous anaplastic large-cell lymphoma

et al. 2008

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“…They described that the two transcription factors are expressed in only a small percentage of cutaneous ALCL and lymphomatoid papulosis. 35 NF-κB transcription factors are thought to play important roles in T-cell activation and development and variable expression of NF-κB target genes has been reported in PTCL. While published data on the potential role of NF-κB in the various subgroups of PTCL remain -for the most part -inconclusive, there is some evidence that NF-κB expression may be lower in ALCL than in PTCL-NOS.…”

Section: Discussionmentioning

confidence: 99%

Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30+ T-cell lymphoproliferations

Geissinger¹,

Sadler²,

Roth³

et al. 2010

Haematologica

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ConclusionsSeverely altered expression of the T-cell receptor/CD3 complex, T-cell receptor-associated transcription factors and signal transduction molecules is a common characteristic of systemic and cutaneous CD30 + lymphoproliferations, although the clinical behavior of these entities is very different. Since peripheral T-cell lymphomas, not otherwise specified retain the full expression program required for functioning T-cell receptor signaling, the differential expression of a subset of these markers might be of diagnostic utility in distinguishing peripheral T-cell lymphomas, not otherwise specified from the entire group of CD30 + lymphoproliferations.Key words: systemic and cutaneous CD30 + lymphoproliferations, anaplastic large cell lymphoma, lymphomatoid papulosis, ALCL, LyP, TCR.Citation: Geissinger E, Sadler P, Roth S, Grieb T, Puppe B, Müller N, Reimer P, Vetter-Kauczok CS, Wenzel J, Bonzheim I, Rüdiger T, Müller-Hermelink HK, and Rosenwald A. Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30+ T-cell lymphoproliferations. Haematologica 20010;95(10):1697-1704. doi:10.3324/haematol.2009 This is an open-access paper. Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30 + T-cell lymphoproliferations © F e r r a t a S t o r t i F o u n d a t i o nIntroduction CD30 + T-cell lymphoproliferations comprise a spectrum of clinically heterogeneous entities, including systemic anaplastic large cell lymphomas (ALCL) as well as primary cutaneous CD30 + T-cell lymphoproliferative disorders. Morphologically, these entities are characterized by the proliferation of highly atypical, anaplastic CD30 + T cells. Despite the frequent detection of clonally rearranged Tcell receptor (TCR) genes, the expression of T-cell-specific antigens in the tumor cells is not consistently detectable. 1 Systemic ALCL comprise approximately 15% of all peripheral T-cell lymphomas (PTCL) in Europe 2 and are divided into anaplastic lymphoma kinase (ALK) positive and negative subgroups (ALK + and ALK -systemic ALCL), whereas primary cutaneous CD30 + T-cell lymphoproliferative disorders represent a spectrum of skin lesions with diverging and in part overlapping clinical and morphological features. CD30 + T-cell lymphoproliferative disorders include primary cutaneous ALCL, lymphomatoid papulosis and so-called borderline lesions, [3][4][5] but even with the knowledge of the clinical presentation and a detailed morphological and immunohistochemical picture it is sometimes difficult, if not impossible, to classify a particular cutaneous lesion correctly.While the transforming properties of ALK over-expression have been clearly demonstrated ,6,7 the transformation mechanisms in ALK -systemic ALCL and primary cutaneous CD30 + T-cell lymphoproliferative disorders are poorly understood. CD30 itself, a cytokine receptor belonging to the tumor necrosis factor receptor superfamily, has been a research focus over the past years, but whether CD30 signaling lea...

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Abnormal activator protein 1 transcription factor expression in CD30-positive cutaneous large-cell lymphomas

Abstract: These results suggest the presence of abnormal AP-1 protein expression in CLCL, which may be relevant to CLCL.

Cited by 16 publications

References 43 publications

Hijacking of the AP-1 Signaling Pathway during Development of ATL

Hijacking of the AP-1 Signaling Pathway during Development of ATL

MUM1 expression in cutaneous CD30+ lymphoproliferative disorders: a valuable tool for the distinction between lymphomatoid papulosis and primary cutaneous anaplastic large-cell lymphoma

Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30+ T-cell lymphoproliferations

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