Constitutive expression of NF-κB is a characteristic feature of mycosis fungoides: Implications for apoptosis resistance and pathogenesis

Izban, Keith F.; Ergïn, Melek; Qin, Jian‐Zhong; Martinez, Robert L.; Pooley, Rob; Saeed, Shahnaz; Alkan, Serhan

doi:10.1053/hupa.2000.20370

Cited by 118 publications

(93 citation statements)

References 35 publications

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“…40 Both STAT3 and NFkB are known to be constitutively activated in CTCL. 26,27,41 Likewise, we observed expression of the active form of STAT5 (pY-STAT5) in malignant T cells in situ and in cell lysates from malignant T cell lines (Fig. S1A-D and E, respectively), confirming and extending other studies, 35 and suggesting that STAT5 is constitutively activated in CTCL.…”

Section: Resultssupporting

confidence: 90%

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

et al. 2013

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Section: Resultssupporting

confidence: 90%

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

et al. 2013

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“…Multiple mechanisms, well described in B-cell lymphomas, lead to constitutive NF-kB activation, promoting lymphomagenesis [72]. In a similar fashion, NF-kB is constitutively activated in CTCL [73][74][75].…”

Section: Immunopathogenesismentioning

confidence: 92%

“…Immunohistochemical analysis of MF cases demonstrated nuclear localization of p65/RelA in over 90% of the cases examined [73]. Furthermore, pharmacologic NF-kB inhibition in CTCL cell lines decreases NF-kB DNA binding activity, thus promoting cell death [73][74][75][76].…”

Section: Immunopathogenesismentioning

confidence: 98%

“…Furthermore, pharmacologic NF-kB inhibition in CTCL cell lines decreases NF-kB DNA binding activity, thus promoting cell death [73][74][75][76]. While the molecular mechanisms leading to constitutive NF-kB activation in CTCL are poorly understood, the observation that IKK inhibition downregulates NF-kB activity implicates upstream IKK-activating elements [74,75].…”

Section: Immunopathogenesismentioning

confidence: 99%

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Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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Disease overview: Cutaneous T‐cell lymphomas are a heterogenous group of T‐cell lymphoproliferative disorders involving the skin, the majority of which may be classified as Mycosis fungoides (MF) or Sézary syndrome (SS).Diagnosis: The diagnosis of MF or SS requires the integration of clinical and histopathologic data.Risk‐adapted therapy: Tumor, node, metastasis, and blood (TNMB) staging remains the most important prognostic factor in MF/SS and forms the basis for a “risk‐adapted,” multidisciplinary approach to treatment. For patients with disease limited to the skin, expectant management or skin‐directed therapies is preferred, as both disease‐specific and overall survival for these patients is favorable. In contrast, patients with advanced‐stage disease with significant nodal, visceral, or blood involvement are generally approached with biologic‐response modifiers, denileukin diftitox, and histone deacetylase inhibitors before escalating therapy to include systemic, single‐agent chemotherapy. Multiagent chemotherapy may be used for those patients with extensive visceral involvement requiring rapid disease control. In highly‐selected patients with disease refractory to standard treatments, allogeneic stem‐cell transplantation may be considered. Am. J. Hematol., 2011. © 2011 Wiley‐Liss, Inc.

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“…19 In anaplastic large-cell lymphoma, a prior study has shown that BCL-3 expression and both genetic and epigenetic modifications of the bcl-3 gene may be associated with oncogenesis. 13 Izban and colleagues 30 have reported that NF-kB p65 is expressed in cutaneous T-cell lymphoma cell lines and neoplastic T lymphocytes from patient samples of mycosis fungoides, and they also showed that nuclear NF-kB activity is required for cell survival and resistance to apoptosis in the neoplastic cells. Although BCL-3 has a strong preference towards p50 and p52 It is also known that stimuli such as tumor necrosis factor a, interleukin1b not only cause nuclear accumulation of p50-p65 heterodimers, but also induce formation of BCL-3-p50 complexes.…”

Section: Bcl-3 In Lymphomasmentioning

confidence: 99%

Immunohistochemical detection of BCL-3 in lymphoid neoplasms: a survey of 353 cases

et al. 2004

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The bcl-3 gene at chromosome 19q13 encodes a member of the IjB family involved in regulating the NFjB pathway. Originally identified by its involvement in the rare t(14:19)(q32;q13), BCL-3 expression has never been analyzed in a wide variety of lymphomas. We assessed BCL-3 expression in 353 cases of non-Hodgkin lymphoma and Hodgkin lymphoma using formalin-fixed, paraffin-embedded tissue specimens, a monoclonal antibody specific for BCL-3, and immunohistochemical methods. Of 172 B-cell lymphomas, 10 (6%) were positive for BCL-3, including six of 23 (26%) diffuse large B-cell lymphoma, one of 17 (6%) small lymphocytic lymphoma, one of 26 (4%) follicular lymphoma, and two of 49 (4%) mantle cell lymphoma. All other B-cell neoplasms were negative, including marginal zone lymphoma (n ¼ 24, 11 extranodal, nine nodal, four splenic), Burkitt lymphoma (n ¼ 10), lymphoplasmacytic lymphoma (n ¼ 10), lymphoblastic lymphoma (n ¼ 8), and plasmacytoma (n ¼ 5). Of 111 T/NK-cell lymphomas, 25 (23%) were positive for BCL-3, including 13 of 40 (32%) anaplastic large-cell lymphoma, three of 10 (30%) angioimmunoblastic T-cell lymphoma, two of eight (25%) extranodal NK/T-cell lymphoma of nasal type, three of 12 (25%) mycosis fungoides, one of five (20%) enteropathy-type T-cell lymphoma, and two of 21 (10%) peripheral T-cell lymphoma unspecified. All other T-cell neoplasms were negative, including lymphoblastic lymphoma (n ¼ 6), prolymphocytic leukemia (n ¼ 6), and subcutaneous panniculitis-like T-cell lymphoma (n ¼ 3). Of 70 Hodgkin lymphomas, of all types, 29 (41%) were positive for BCL-3. The relatively high frequency of BCL-3 expression in some non-Hodgkin and Hodgkin lymphoma types raises the possibility that BCL-3 is involved in the pathogenesis of these tumors, and may be a target of new therapies.

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Constitutive expression of NF-κB is a characteristic feature of mycosis fungoides: Implications for apoptosis resistance and pathogenesis

Cited by 118 publications

References 35 publications

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Immunohistochemical detection of BCL-3 in lymphoid neoplasms: a survey of 353 cases

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