Background/aim: Significant transcription factors - including c-Fos (gene locus: 14q24.3) and c-Jun (gene locus: 1p32-p31) - regulate cell homeostasis preventing abnormal signal transduction to nucleus. Their over-activation seems to be associated with an aggressive phenotype in non-small cell lung carcinomas (NSCLCs).
View Article and Find Full Text PDFDuring lung carcinoma development, progression and metastasis, a variety of gross (chromosome) and specific (gene) genomic alterations are detected in dysplastic, neoplastic, and progressively malignant transformed epithelia as early or late genetic events. Oncogenes' overactivation combined with suppressor genes silence are crucial genetic events in malignant and pre-malignant epithelia. Especially, deregulation of crucial signalling transduction pathways that interact with strong transcription factors - such as c-Fos and c-Jun - leads to an aberrant expression of other critical genes responsible for cell homeostasis.
View Article and Find Full Text PDFLaryngeal squamous cell carcinoma (LSCC) demonstrates increased rates due to pathogenetic factors including tobacco, chronic alcohol consumption and also viral-mediated deregulation. During carcinogenetic process, laryngeal epithelia accumulate gross chromosome and specific gene aberrations. Oncogenes’ overactivation is a crucial genetic event in malignant and pre-malignant neoplastic epithelia.
View Article and Find Full Text PDFDNA mismatch repair system (DNA MMR) is a crucial genetic mechanism for DNA homeostasis in prokaryotic and eukaryotic cells. During DNA replication and also recombination, point intra-nucleotide errors including base deletion, insertion, and mis-incorporation happen. These raised abnormalities in the newly synthesized DNA strand could affect negatively the stability of the molecule and the function of the corresponding genes.
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