The expression of MUM1 in cutaneous T-cell lymphoproliferative disorders

Wasco, Matthew J.; Fullen, Douglas R.; Su, Lyndon D.; Ma, Linglei

doi:10.1016/j.humpath.2007.08.013

Cited by 33 publications

(25 citation statements)

References 24 publications

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“…have described IRF4/MUM1 expression in only 2 of 10 cases of C-ALCL. Consistent with our results, more recent immunohistochemical studies have shown IRF4/ MUM1 and TRAF1 expression in 80-100% of C-ALCL cases(Wasco et al, 2008;Benner et al, 2009;Feldman et al, 2009).…”

supporting

confidence: 93%

Cutaneous Anaplastic Large Cell Lymphoma and Peripheral T-Cell Lymphoma NOS Show Distinct Chromosomal Alterations and Differential Expression of Chemokine Receptors and Apoptosis Regulators

Kester

Tensen

Vermeer

et al. 2010

Journal of Investigative Dermatology

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Primary cutaneous anaplastic large cell lymphoma (C-ALCL) has an indolent clinical course and favorable prognosis. On the contrary, primary cutaneous peripheral T-cell lymphoma not otherwise specified (PTL-NOS) shows aggressive clinical behavior. To identify genomic events relevant in the pathogenesis of these cutaneous T-cell lymphomas (CTCLs), we carried out array-based comparative genomic hybridization (CGH) analysis. Simultaneously, gene expression profiling was conducted to gain insight into gene expression programs associated with the different clinical behavior of these CTCLs. C-ALCL was characterized by gains on chromosome 7q and 17q and losses on 6q and 13q. PTL-NOS similarly showed gains on 7q and 17q, but was distinguished by gains on chromosome 8 and loss of a focal overlapping region on 9p21. We identified minimal common regions harboring candidate oncogenes and tumor suppressor genes in C-ALCL and PTL-NOS. Genes with a role in lymphocyte chemotaxis, apoptosis, and proliferation were overrepresented among genes differentially expressed between these lymphomas. C-ALCL showed higher expression of the skin-homing chemokine receptor genes CCR10 and CCR8, which may explain the lower tendency to disseminate to extracutaneous sites. Furthermore, C-ALCL and PTL-NOS showed aberrant expression of distinct genes implicated in apoptosis and proliferation, such as IRF4/MUM1 and PRKCQ, which may account for differences in clinical aggressiveness.

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confidence: 93%

Cutaneous Anaplastic Large Cell Lymphoma and Peripheral T-Cell Lymphoma NOS Show Distinct Chromosomal Alterations and Differential Expression of Chemokine Receptors and Apoptosis Regulators

Kester

Tensen

Vermeer

et al. 2010

Journal of Investigative Dermatology

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“…Such data have also to be confirmed in view of the poor reproducibility of microarray profiling techniques (Marshall, 2004;Sherlock, 2005). Interestingly, CALCL did not bear gains at 6p25.3, a region containing the IRF4/MUM1 gene, which is highly expressed at the protein level in CALCL and CD30 þ CTCL (Wasco et al, 2008;Benner et al, 2009). Balanced rearrangements of the IRF4/MUM1 gene have been recently reported in CALCL and T-MF cases (Feldman et al, 2009;Pham-Ledard et al, 2009).…”

Section: Discussionmentioning

confidence: 85%

Genome-Wide Analysis of Cutaneous T-Cell Lymphomas Identifies Three Clinically Relevant Classes

Laharanne

Oumouhou

Bonnet

et al. 2010

Journal of Investigative Dermatology

105

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This study was undertaken to identify recurrent genetic alterations of the three main types of cutaneous T-cell lymphomas (CTCLs): mycosis fungoides (MF), Sézary syndrome (SS), and cutaneous anaplastic large-cell lymphoma (CALCL). Using array-based comparative genomic hybridization, the molecular cytogenetic profiles of 72 samples obtained from 58 patients with CTCL corresponding to 24 transformed MF (T-MF), 16 SS, and 18 CALCLs were determined. T-MF was characterized by gains of 1q25-31, 7p22-11.2, 7q21, 7q31, and 17q12, and losses of 9p21, 10p11.2, and 10q26. SS exhibited gains of 8q23-24.3 and 17q23-24, as well as losses of 9p21, 10p12-11.2, 10q22-24, 10q25-26, and 17p13-q11.1. Finally, CALCL exhibited 6q27 and 13q34 losses. Such imbalances were statistically associated with one CTCL subtype. Unsupervised hierarchical clustering defined three categories of clinical relevance: (1) CALCL apart from epidermotropic-CTCL, (2) an SS-only category, and (3) a mixed category with T-MF and SS cases, with both primary and secondary SS cases. In rare cases, the genetic classification did not correspond to the inclusion diagnosis, possibly reflecting the association of two diseases in the same patient or initial misdiagnosis according to follow-up. Finally, different samples in the same patient clustered together, showing reproducibility of such a classifier.

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“…It has been described in CD30 + T-cell lymphoproliferative disorders, including systemic anaplastic large cell lymphoma (ALCL) and LyP. 29 Although some report utility in this stain for differentiating between LyP and primary cutaneous ALCL, 30 other studies have reported that it does not distinguish between the two. 31,32 The presence of CD8 + CD30 + LyP and ALCL in 7 of 7 cases suggest that it may represent an adjunctive marker for CD8 + lymphoproliferative disease.…”

Section: Immunohistochemical and Molecular Featuresmentioning

confidence: 99%

Characterization of Primary Cutaneous CD8+/CD30+ Lymphoproliferative Disorders

Martires

Abdulla

et al. 2015

The American Journal of Dermatopathology

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CD30 primary cutaneous lymphoproliferative diseases include both lymphomatoid papulosis (LyP) and primary cutaneous anaplastic large cell lymphoma (PCALCL). The neoplastic cell of most primary CD30 lymphoproliferative disorders is CD4 positive. The terminology LyP "type D" has been used to describe a growing number of cases of LyP with a predominantly CD8 infiltrate. PCALCL with a CD8 phenotype has also been described, which presents a particularly difficult diagnostic and management challenge, given the difficulty in distinguishing it histologically from other cytotoxic lymphomas such as primary cutaneous aggressive epidermotropic CD8 cytotoxic T-cell lymphoma and CD8 gamma/delta and natural killer/T-cell lymphoma. We report 7 additional cases of these rare cutaneous CD8/CD30 lymphoproliferative disorders. We also present a unique case of CD8/CD30 LyP with histologic similarities to LyP type B. In all 7 of our cases of CD8 LyP and CD8 anaplastic large cell lymphoma, we found focal to diffuse MUM-1 positivity. We propose that MUM-1 may represent an adjunctive marker for CD8 lymphoproliferative disease. Finally, we review the current literature on cases of CD8 LyP and PCALCL. For the 106 cases examined, we found similar clinical and histologic features to those reported for traditional CD4CD30 LyP and PCALCL.

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The expression of MUM1 in cutaneous T-cell lymphoproliferative disorders

Cited by 33 publications

References 24 publications

Cutaneous Anaplastic Large Cell Lymphoma and Peripheral T-Cell Lymphoma NOS Show Distinct Chromosomal Alterations and Differential Expression of Chemokine Receptors and Apoptosis Regulators

Cutaneous Anaplastic Large Cell Lymphoma and Peripheral T-Cell Lymphoma NOS Show Distinct Chromosomal Alterations and Differential Expression of Chemokine Receptors and Apoptosis Regulators

Genome-Wide Analysis of Cutaneous T-Cell Lymphomas Identifies Three Clinically Relevant Classes

Characterization of Primary Cutaneous CD8+/CD30+ Lymphoproliferative Disorders

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