scholarly journals Microphthalmia transcription factor immunohistochemistry for FNA biopsy of ocular malignant melanoma

2015 ◽  
Vol 123 (7) ◽  
pp. 394-400 ◽  
Author(s):  
Carmen M. Perrino ◽  
Jeff F. Wang ◽  
Brian T. Collins
Keyword(s):  
Transcription Factor ◽  
Malignant Melanoma ◽  
Microphthalmia Transcription Factor

scholarly journals Expression of microphthalmia transcription factor, S100 protein, and HMB-45 in malignant melanoma and pigmented nevi

2016 ◽  
Vol 5 (3) ◽  
pp. 327-331 ◽  
Author(s):  
Jianxin Xia ◽  
Yanlong Wang ◽  
Fuqiu Li ◽  
Jinfeng Wang ◽  
Yan Mu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Malignant Melanoma ◽  
S100 Protein ◽  
Microphthalmia Transcription Factor ◽  
Hmb 45 ◽  
Pigmented Nevi

Microphthalmia Transcription Factor in the Immunohistochemical Diagnosis of Metastatic Melanoma

2001 ◽  
Vol 25 (2) ◽  
pp. 205-211 ◽  
Author(s):  
Markku Miettinen ◽  
Martin Fernandez ◽  
Kaarle Franssila ◽  
Zoran Gatalica ◽  
Jerzy Lasota ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Metastatic Melanoma ◽  
Microphthalmia Transcription Factor ◽  
Immunohistochemical Diagnosis

scholarly journals Role of microRNA508-3p in melanogenesis by targeting microphthalmia transcription factor in melanocytes of alpaca

animal ◽  
2017 ◽  
Vol 11 (2) ◽  
pp. 236-243 ◽  
Author(s):  
J. Zhang ◽  
Y. Liu ◽  
Z. Zhu ◽  
S. Yang ◽  
K. Ji ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Microphthalmia Transcription Factor

Giant Cell Tumors: Inquiry Into Immunohistochemical Expression of CD117 (c-Kit), Microphthalmia Transcription Factor, Tartrate-Resistant Acid Phosphatase, and HAM-56

2005 ◽  
Vol 129 (3) ◽  
pp. 360-365
Author(s):  
Rolando Y. Ramos ◽  
Helen M. Haupt ◽  
Peter A. Kanetsky ◽  
Rakesh Donthineni-Rao ◽  
Carmen Arenas-Elliott ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Acid Phosphatase ◽  
Giant Cell ◽  
Stromal Cells ◽  
Mononuclear Cells ◽  
Osteoclast Differentiation ◽  
Tartrate Resistant Acid Phosphatase ◽  
Immunohistochemical Expression ◽  
Giant Cell Tumors ◽  
Microphthalmia Transcription Factor

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.

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

2003 ◽  
Vol 23 (8) ◽  
pp. 2991-2998 ◽  
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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