human : 43
|Human||MAML2||84441||mastermind-like 2 (Drosophila)|
MAM-3 (MoAbs 115G3, 67D11) antigen was distributed in intercalated and striated duct cells of the normal salivary glands, and in luminal tumour cells and squamous metaplastic cells of pleomorphic adenomas.
|Human||FSD1||79187||fibronectin type III and SPRY domain containing 1|
This study showed different patterns of expression of tenascin and fibronectin along the process of tumorigenesis and tumor progression in pleomorphic adenoma, a fact that might play a role in invasion properties of these tumors
|Human||WIF1||11197||WNT inhibitory factor 1|
WIF1 is a recurrent target in human salivary gland oncogenesis and that downregulation of WIF1 plays a role in the development and/or progression of pleomorphic adenomas
|Human||LECT1||11061||leukocyte cell derived chemotaxin 1|
These findings indicate that lacuna cells and neoplastic myoepithelial cells express ChM-I mRNA and that mature ChM-I, which lacuna cells and neoplastic myoepithelial cells translate, is deposited in the chondroid matrix of pleomorphic adenomas.
ChM-I was immunolocalized to the lacunae in the chondroid elements of pleomorphic adenomas (100%).
To elucidate which cells express ChM-I mRNA in pleomorphic adenomas, we examined the expression and localization of ChM-I mRNA in this type of tumor using an in situ hybridization technique.
To elucidate the relationship between chondroid formation and hypovascularity in salivary pleomorphic adenomas, we immunohistochemically examined the expression and localization of ChM-I in 35 cases of this tumor.
Recently, using immunohistochemical techniques, we reported that cartilage-specific matrix protein, chondromodulin-I (ChM-I), was deposited on the inter-territorial matrix of the chondroid area in salivary pleomorphic adenomas and that ChM-I, which is also a strong angio-inhibitory factor, plays an important role in the avascular nature of the chondroid area and the chondroid formation in this type of tumor.
These findings suggested that lacuna cells and neoplastic myoepithelial cells expressed ChM-I, and that this molecule may play an important role in hypovascularity and chondroid differentiation in pleomorphic adenoma.
In conclusion, pleomorphic adenoma expressed ChM-I, which is involved in hypovascularity and chondroid formation in this type of tumor.
In conclusion, lacuna cells and neoplastic myoepithelial cells express ChM-I mRNA ectopically in pleomorphic adenoma, and this plays an important role in chondroid formation and hypovascularity in this type of tumor.
Immunoreactivity for ChM-I was observed in the inter-territorial matrix of the chondroid area, especially around the lacunae, and in the cytoplasm of neoplastic myoepithelial cells of the myxoid element of pleomorphic adenomas.
|Human||TP63||8626||tumor protein p63|
In all tumor types differentiated towards luminal and myoepithelial lineages (pleomorphic adenomas, basal cell adenomas, adenoid cystic carcinomas, and epithelial-myoepithelial carcinomas), p63 was expressed in myoepithelial cells, whereas luminal cells were always negative.
Using isoform-specific PCR, we found that all isoforms of p63 were expressed in normal parotid tissue whereas the pleomorphic adenomas, myoepitehliomas, and basal cell adenomas dominantly expressed the transactivation-incompetent truncated isoforms.
Expression and mutation of p53, p73, and p63 were examined by direct DNA sequencing, reverse transcription PCR using isoform-specific primers, and by immunohistochemistry in normal parotid tissue ( n=10), and various tumors of the salivary gland (42 pleomorphic adenomas, 12 myoepitheliomas, 8 basal cell adenomas, 5 oncocytomas, 5 canalicular adenomas, and 20 adenolymphomas).
|Human||GDF5||8200||growth differentiation factor 5|
CDMP-1 was immunolocalized in the cuboidal neoplastic myoepithelial cells around the chondroid areas of the pleomorphic adenomas, whereas these molecules were not localized in the spindle-shaped neoplastic myoepithelial cells of the myxoid element or the lacuna cells of the chondroid element in these tumors.
To evaluate this hypothesis, we examined the expression and localization of CDMP-1 and -2 immunohistochemically in 20 normal human salivary glands and 35 pleomorphic adenomas.
These results indicated that the cuboidal neoplastic myoepithelial cells around the chondroid areas expressed CDMP-1 and suggested that this molecule may play a role in the differentiation of neoplastic myoepithelial cells in pleomorphic adenoma.
pleomorphic adenoma expressed cartilage derived morphogenetic protein 1 but not 2
These findings suggested that CDMP-1 and -2 may play essential roles in chondroid formation in salivary pleomorphic adenoma.
In conclusion, pleomorphic adenoma expressed CDMP-1 but not CDMP-2.
|Human||HMGA2||8091||high mobility group AT-hook 2|
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|Human||WNT1||7471||wingless-type MMTV integration site family, member 1|
INT1 and GLI genes are not rearranged or amplified in benign pleomorphic adenomas with chromosome abnormalities of 12q13-15.
Collectively, these findings indicate that neither the INT1 nor the GLI gene appears to be the primary target gene for the translocations and deletions involving the 12q13-15 region in pleomorphic adenomas.
|Human||TP53||7157||tumor protein p53|
TP53 mutations and cyclin-dependent kinase inhibitor 2A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in the malignant progression of pleomorphic adenomas into carcinoma
Both p53 and c-erbB-2 proteins appear to be involved at an early stage of malignization of pleomorphic adenoma
|Human||TGFB3||7043||transforming growth factor, beta 3|
Signals for TGF-beta3 in the normal salivary glands were observed in mucous cells, whereas in pleomorphic adenomas they were observed in the solid nests of neoplastic myoepithelial cells, in the portion showing squamous metaplasia, and in the inner ductal cells of tubulo-glandular structures.
TGF-betas induce ectopic cartilage formation in vivo, but chondroid tissues in pleomorphic adenomas showed only weak TGF-beta3 expression.
|Human||TGFB2||7042||transforming growth factor, beta 2|
In conclusion, pleomorphic adenomas expressed TGF-beta2 and -beta3, which may be associated with differentiation of the inner ductal cells and neoplastic myoepithelial cells.
Signals for TGF-beta2 in the normal salivary glands were observed in the intercalated ducts, while in pleomorphic adenomas they were observed in the inner ductal cells of the tubulo-glandular structures.
|Human||TERT||7015||telomerase reverse transcriptase|
transfection of the hTERT gene in immortalized pleomorphic adenoma does not alter the nature of those cells
Pleomorphic adenomas stained positive for S-100 protein, tenascin, smooth muscle actin, synaptophysin and chromogranin A.
|Human||PLAGL2||5326||pleiomorphic adenoma gene-like 2|
Pleomorphic adenoma gene (PLAG) 1, the main translocation target in pleomorphic adenomas of the salivary glands, is a member of a new subfamily of zinc finger proteins comprising the tumor suppressor candidate PLAG-like1 (also called ZAC1 or lost on transformation 1) and PLAGL2.
|Human||PLAG1||5324||pleiomorphic adenoma gene 1|
Click here to display 31 evidence detail records.
|Human||PDGFB||5155||platelet-derived growth factor beta polypeptide|
Twenty-seven samples of pleomorphic salivary adenoma (PSA) were examined for expression and structure of c-myc, c-Ha-ras, c-erbB-2, c-sis oncogenes by RNA dot blot, DNA dot blot and Southern blot hybridization.
|Human||NTRK3||4916||neurotrophic tyrosine kinase, receptor, type 3|
To demonstrate the reliability of the probes generated with this protocol, four strategies were employed: (i) probes mapping to cyclin D1 (CCND1) were generated and their performance was compared with that of a commercially available probe for the same gene in a series of 10 FFPETS of breast cancer samples of which five harboured CCND1 amplification; (ii) probes targeting cyclin-dependent kinase 4 were used to validate an amplification identified by microarray-based comparative genomic hybridization (aCGH) in a pleomorphic adenoma; (iii) probes targeting fibroblast growth factor receptor 1 and CCND1 were used to validate amplifications mapping to these regions, as defined by aCGH, in an invasive lobular breast carcinoma with FISH and CISH; and (iv) gene-specific probes for ETV6 and NTRK3 were used to demonstrate the presence of t(12;15)(p12;q25) translocation in a case of breast secretory carcinoma with dual colour FISH.
|Human||NOS3||4846||nitric oxide synthase 3 (endothelial cell)|
In the current study we aimed to find out immunohistochemically whether the expression of both the inducible (iNOS) and endothelial (eNOS) forms of the enzyme nitric oxide synthase (NOS) were changed in pleomorphic adenomas of the parotid compared with normal salivary tissue.
|Human||NME1||4830||NME/NM23 nucleoside diphosphate kinase 1|
To evaluate the role of NM23 in SGN, the expression patterns of NM23 in the following were compared: benign (pleomorphic adenoma) vs malignant (adenoid cystic carcinoma and mucoepidermoid carcinoma) SGN, and primary malignancies with/without evidence of metastasis vs their metastatic implants (MI).
|Human||NFIB||4781||nuclear factor I/B|
Identification of NFIB as recurrent translocation partner gene of HMGIC in pleomorphic adenomas.
In conclusion, our results reveal the recurrent involvement of the NFIB gene as translocation partner gene of HMGIC in pleomorphic adenomas.
Since the chromosome segment 9p12-24 is repeatedly involved as translocation partner of chromosome 12q13-15 in pleomorphic adenomas, we tested whether NFIB might be a recurrent partner of HMGIC.
|Human||MDM2||4193||MDM2 oncogene, E3 ubiquitin protein ligase|
findings suggest that amplification and overexpression of HMGIC and possibly MDM2 might be important genetic events that may contribute to malignant transformation of benign pleomorphic adenoma
To investigate this hypothesis, the present study investigated the expression and localization of lumican in 20 normal human salivary glands and 35 pleomorphic adenomas.
Lumican expression is associated with the formation of mesenchyme-like elements in salivary pleomorphic adenomas.
These findings suggest that lumican expression may be related to the chondroid component in pleomorphic adenomas.
In conclusion, normal salivary glands express lumican, which appears to be related to stromal maintenance, and pleomorphic adenomas express lumican mRNA and protein, which may play important roles in the formation of ;mesenchyme;-like areas in this type of tumour.
These results suggest that lumican is associated with the formation of ;mesenchyme;-like structures in pleomorphic adenomas.
|Human||LIFR||3977||leukemia inhibitory factor receptor alpha|
The recurrent translocation t(5;8)(p13;q12) in pleomorphic adenomas results in upregulation of PLAG1 gene expression under control of the LIFR promoter.
|Human||HMOX2||3163||heme oxygenase (decycling) 2|
In conclusion, this is the first study to examine the expressionof HO-1 and HO-2 within normal salivary glands and pleomorphic adenomas.
Constitutive (HO-2) and inducible (HO-1) haem oxygenase in pleomorphic adenomas of the human parotid: an immunocytochemical study.
Immunocytochemistry using antibodies specific for HO-1 and HO-2were undertaken in 12 pleomorphic adenoma specimens, all sections of which contained adjacent normal salivary tissue.
|Human||HMGA1||3159||high mobility group AT-hook 1|
Pleomorphic adenomas of the salivary glands: absence of HMGIY rearrangements.
Another non-random chromosomal alteration observed in subgroups of several of the tumor entities with 12q14-15 changes are rearrangements of 6p21 resulting in alterations of the HMGIY gene, which have so far not been documented in pleomorphic adenomas of the salivary glands.
The results strongly suggest that pleomorphic adenomas are the only exception to the rule that entities of benign tumors with HMGIC rearrangements also have subtypes with HMGIY rearrangements.