Microphthalmia transcription factor immunohistochemistry for FNA biopsy of ocular malignant melanoma

Abstract Context.—Osteoclast-like giant cells (GCs) in giant cell tumors (GCTs) are thought to derive from a monocyte-macrophage lineage. Microphthalmia transcription factor (MITF) is necessary for osteoclast gene expression and tartrate-resistant acid phosphatase (TRAP) activation; c-Kit plays a role in regulation of MITF. Objective.—To gain insight into the differentiation of GCTs of bone (GCTBs) and GCTs tendon sheath (GCTTSs) by investigating immunohistochemical staining for c-Kit, MITF, TRAP, and HAM-56 in the GCs and stroma. Design.—Immunoreactivity for CD117 (c-Kit), MITF, TRAP, and HAM-56 was studied in 35 GCTBs, 15 GCTTSs, and 5 foreign-body GC controls. Results.—Across tumors, MITF and TRAP but not c-Kit were generally expressed in GCs; TRAP was variably expressed in stromal cells. The MITF was expressed more consistently in stromal cells of GCTTSs than GCTBs (P < .001). The GCTBs showed more intense MITF stromal (P < .001) and TRAP GC staining (P = .04) than GCTTSs. HAM-56 staining by stromal cells was associated with MITF stromal staining (r2 = 0.6, P < .001). Conclusions.—Results suggest that MITF and TRAP are expressed during osteoclast differentiation and that a proportion of mononuclear cells in GCTs express the macrophage marker HAM-56. Both GCTBs and GCTTSs show similar patterns of immunohistochemical expression.

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Reliability of immunostaining using pan-melanoma cocktail, SOX10, and microphthalmia transcription factor in confirming a diagnosis of melanoma on fine-needle aspiration smears

Cancer Cytopathology ◽

10.1002/cncy.21458 ◽

2014 ◽

Vol 122 (10) ◽

pp. 779-785 ◽

Cited By ~ 16

Author(s):

Jessica Clevenger ◽

Cicily Joseph ◽

Marilyn Dawlett ◽

Ming Guo ◽

Yun Gong

Keyword(s):

Transcription Factor ◽

Fine Needle Aspiration ◽

Needle Aspiration ◽

Fine Needle ◽

Microphthalmia Transcription Factor

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Upregulation of HMG1 Leads to Melanoma Inhibitory Activity Expression in Malignant Melanoma Cells and Contributes to Their Malignancy Phenotype

Molecular and Cellular Biology ◽

10.1128/mcb.23.8.2991-2998.2003 ◽

2003 ◽

Vol 23 (8) ◽

pp. 2991-2998 ◽

Cited By ~ 74

Author(s):

Ina Poser ◽

Michaela Golob ◽

Reinhard Buettner ◽

Anja K. Bosserhoff

Keyword(s):

Transcription Factor ◽

Malignant Melanoma ◽

Inhibitory Activity ◽

Melanoma Cells ◽

Peptide Sequence ◽

Transcriptional Level ◽

Promoter Element ◽

Promoter Activation ◽

Mobility Shift ◽

Melanoma Inhibitory Activity

ABSTRACT Malignant transformation of melanocytes to melanoma cells closely parallels activation of melanoma inhibitory activity (MIA) expression. We have previously shown that upregulation of MIA occurs on a transcriptional level and involves the highly conserved region (HCR) promoter element. We further observed that the HCR element interacts with the melanoma-associated transcription factor (MATF) and thereby confers strong promoter activation. In this study we identify the peptide sequence of MATF and show that it is identical with the transcription factor HMG1. HMG1 was upregulated in malignant melanoma cells and further activated by hypophosphorylation. Stable antisense-HMG1 expression in melanoma cells led to the reduction of MIA promoter activity and protein expression, indicating that HMG1 is a potent regulator of MIA expression. Interestingly, chromatin immunoprecipitation and electrophoretic mobility shift experiments indicated that HMG1 and the NF-κB family member p65 both interact and bind to the HCR promoter element. In summary, our study proves HMG1 and p65 to be important factors in MIA regulation and melanoma progression.

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