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Example sentences for: nsgcts
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The overall higher frequency of promoter methylation seen in NSGCTs is noticeably evident in DNA repair genes RASSF1A, BRCA1 , and MGMT , and the hypermethylated in cancer 1 ( HIC1 ) gene, which encodes a transcription factor.
NSGCTs display complex differentiation patterns that include embryonal, extra-embryonal, and somatic tissue types [ 6 ] . Teratomas with somatic differentiation can undergo additional malignant transformation with characteristics of epithelial, mesenchymal, neurogenic, or hematologic tumors [ 7 ] . While the majority of GCTs exhibit exquisite sensitivity to cisplatin-based chemotherapy, a small proportion of metastatic tumors remain resistant.
3 region to which RASSF1A maps undergoes deletions in many solid tumor types, including GCTs [ 9 ] . RASSF1A encodes a splice variant of human RAS effector homologue, which interacts with the XPA protein and functions as a negative regulator of cell growth [ 16 17 ] . RASSF1A has been shown to be inactivated by promoter methylation in a variety of tumor types [ 16 17 18 19 ] . The 17q21 and 17p13 regions, to which BRCA1 and HIC1 map, respectively, also have been characterized by high frequency of LOH in GCT [ 9 ] . The BRCA 1 gene plays critical roles in DNA repair and recombination, cell cycle checkpoint control, and transcription and has been shown to be hypermethylated in breast-ovarian cancer [ 4 ] . The HIC1 gene is also often hypermethylated in many human cancers [ 20 21 22 ] . The DNA repair gene MGMT encodes O(6)-methylguanine-DNA methyltransferase and this enzyme effectively removes DNA adducts formed by alkylating agents [ 23 ] . Epigenetic inactivation of the MGMT gene was reported in a wide variety of cancers [ 24 25 ] . Also, a low frequency of methylation of the APC , RARB , and FHIT genes was detected in NSGCTs.
Several studies have shown that both NSGCTs and SGCTs exhibit similar genetic alterations, including isochromosome for the short arm of chromosome 12, i(12p) [ 6 ] . Thus epigenetic alterations such as those detected in the current study is one distinct molecular change that distinguishes these two histologic subsets.
A unique feature of GCTs is their origin from germ cells at a stage in development where they undergo epigenetic reprogramming [ 6 13 ] . The absence of this epigenetic modification in SGCTs is consistent with their GC-like nature as previously noted [ 6 14 ] . On the other hand, the extensive promoter hypermethylation seen in NSGCTs suggests a mechanistic role in their potential for embryonal and extra-embryonal lineage differentiation [ 6 14 ] . Establishment of DNA methylation in the mammalian genome is controlled by at least three DNA methyltransferases (DNMTs), DNMT1 , DNMT3a and DNMT3b [ 15 ] . The role of these DNMTs in differential de novo methylation in SGCT vs.
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