These results suggest that TDGF-1 growth factor may represent an autocrine growth factor that may be involved in the process of development of testicular neoplasms.
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16.
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16.
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16.
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16.
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16.
Our results suggest that the KLK-L4 gene is expressed in normal and cancerous testicular tissue; however, its five variants are all expressed in normal tissue but not in testicular tumors.
Immunohistochemical analysis of the MGMT protein in a subgroup (n=20) of the testicular tumours supported the hypothesis of gene silencing being the functional consequence of the promoter methylation.
However, 'knock-in' mice homozygous for the CDK4(R24C) mutation were noted to develop multiple neoplasia, most commonly including endocrine tumours: pituitary adenomas, insulinomas and Leydig cell testicular tumours.
In contrast, absence of AMH or p27 causes earlier onset and more aggressive development of testicular tumor, with an earlier death of double mutant mice.
TDE2, a gene with sequence similarity to the mouse testicular tumor-differentially-expressed (Tde1/MUSTETU) gene, was identified by serial analysis of gene expression (SAGE) in nonsmall cell lung cancers (NSCLC).
In contrast, absence of AMH or p27 causes earlier onset and more aggressive development of testicular tumor, with an earlier death of double mutant mice.
In contrast, absence of AMH or p27 causes earlier onset and more aggressive development of testicular tumor, with an earlier death of double mutant mice.
In contrast, absence of AMH or p27 causes earlier onset and more aggressive development of testicular tumor, with an earlier death of double mutant mice.
TDE2, a gene with sequence similarity to the mouse testicular tumor-differentially-expressed (Tde1/MUSTETU) gene, was identified by serial analysis of gene expression (SAGE) in nonsmall cell lung cancers (NSCLC).
TDE2, a gene with sequence similarity to the mouse testicular tumor-differentially-expressed (Tde1/MUSTETU) gene, was identified by serial analysis of gene expression (SAGE) in nonsmall cell lung cancers (NSCLC).