We used high- (ACCM) and low- (ACC2) metastasis cell lines of human adenoid cystic carcinoma (ACC) as an experimental model to study metastatic mechanisms and compare their expression levels for angiogenic-related factor vascular endothelial growth factor (VEGF).
We used high- (ACCM) and low- (ACC2) metastasis cell lines of human adenoid cystic carcinoma (ACC) as an experimental model to study metastatic mechanisms and compare their expression levels for angiogenic-related factor vascular endothelial growth factor (VEGF).
We used high- (ACCM) and low- (ACC2) metastasis cell lines of human adenoid cystic carcinoma (ACC) as an experimental model to study metastatic mechanisms and compare their expression levels for angiogenic-related factor vascular endothelial growth factor (VEGF).
We suggest that ACCS-LN-GFP cells acquire cancer stem cell features involving the up-regulation of NNMT and the loss of gap junction protein alpha-1, leading to epithelial-mesenchymal transition and consequent AdCC metastasis.
We show that the t(6;9)(q22-23;p23-24) translocation in adenoid cystic carcinomas (ACC) of the breast and head and neck consistently results in fusions encoding chimeric transcripts predominantly consisting of MYB exon 14 linked to the last coding exon(s) of NFIB.
We show that the t(6;9)(q22-23;p23-24) translocation in adenoid cystic carcinomas (ACC) of the breast and head and neck consistently results in fusions encoding chimeric transcripts predominantly consisting of MYB exon 14 linked to the last coding exon(s) of NFIB.
We retrieved 27 cases of 1-4-cm-sized adenoid cystic carcinomas (ACCs) arising from the PG (n = 12) and SMG (n = 15). c-KIT, VEGF-R2, and CD31 staining were quantified by image-based analysis to define the positive expression or tumor-associated vessel areas in two representative sections per case.
We retrieved 27 cases of 1-4-cm-sized adenoid cystic carcinomas (ACCs) arising from the PG (n = 12) and SMG (n = 15). c-KIT, VEGF-R2, and CD31 staining were quantified by image-based analysis to define the positive expression or tumor-associated vessel areas in two representative sections per case.
We retrieved 27 cases of 1-4-cm-sized adenoid cystic carcinomas (ACCs) arising from the PG (n = 12) and SMG (n = 15). c-KIT, VEGF-R2, and CD31 staining were quantified by image-based analysis to define the positive expression or tumor-associated vessel areas in two representative sections per case.
We propose from this study that overexpression of Bcl-2 proto-oncogene acts as a strong antiapoptotic in both squamous cells and adenocystic carcinoma may be an important molecular event on oral carcinoma to make these tumors resistant to radiotherapy and chemotherapy.
We previously characterized in salivary adenoid cystic carcinoma (ACC) a novel population of cancer stem cells (CSCs) marked by coexpression of 2 stemness genes, sex-determining region Y (SRY)-related HMG box-containing factor 10 (SOX10) and CD133.
We previously characterized in salivary adenoid cystic carcinoma (ACC) a novel population of cancer stem cells (CSCs) marked by coexpression of 2 stemness genes, sex-determining region Y (SRY)-related HMG box-containing factor 10 (SOX10) and CD133.
We previously characterized in salivary adenoid cystic carcinoma (ACC) a novel population of cancer stem cells (CSCs) marked by coexpression of 2 stemness genes, sex-determining region Y (SRY)-related HMG box-containing factor 10 (SOX10) and CD133.
We performed immunohistochemical assessment of p53 expression and TP53 mutational analysis of 15 malignant neoplasms arising from preexisting benign cylindroma, spiradenoma, and spiradenocylindroma, sporadic or associated with Brooke-Spiegler syndrome.
We now show, for the first time, that ISL triggers the mammalian target of rapamycin (mTOR)-dependent autophagic and apoptotic cell death in adenoid cystic carcinoma (ACC).
We have also demonstrated LOH using markers on chromosome 16q in 8/14 (57%) sporadic cylindromas, indicating that the cyld1 gene is likely to be involved in the genesis of both familial and sporadic cylindromas.