Avtor/Urednik     Rajčević, Uroš
Naslov     Ugotavljanje ravni izražanja onkogenov pri raku želodca s fluorescenčnim označevanjem in sočasnim pomnoževanjem genskih prepisov
Tip     monografija
Kraj izdaje     Ljubljana
Založnik     Medicinska fakulteta
Leto izdaje     2002
Obseg     str. 75
Jezik     slo
Abstrakt     Adenocarcinoma of the stomach can be devided into two clinicopathological entities based on histology: "epidemic", intestinal, or well-differentiated carcinoma and diffuse or poorly differentiated carcinoma. While intestinal-type lesions follow a series of well characterized stages progressing from chronic gastritis in a similar pattern as described in colorectal carcinogenesis, poorly differentiated gastric cancer lack well- recognized precursor changes seen in intestinal-type lesions. Factors leading to the development of diffuse type of stomach cancer are less clear. The transformation of normal gastric epithelial cells into a cancer is a multi-step process associated with the progressive accumulation of abnormalties in DNArepair genes, tumor supressor genes and oncogenes such as genes encoding cellular growth factors, surface receptors and celular adhesion molecules. Although there is a lot of confussion concerning the actual sequence of events that gives rise to gastric cancer, there's a consensus that genetic instability, inactivation of tumor supressor genes and overexpression of telomerase appear to be involved in the earfy stages of gastric carcinogenesis, whereas activation of oncogenes, expression of growth factors, cytokines and angiogenic factors promote the later stages of tumor progression and invasion. Cellular oncogenes may be defined as genes which, under certain conditions, are capable of inducing neoplastic transformation of cells. Cellular oncogenes arise by the modification through mutation, or change in the control of expression of a normal gene, referred to as "proto-oncogene". Beside oncogenes deriving from cellular, oncogenes are being carried also by genomes of some oncogenic viruses. (Abstract truncated at 2000 characters).
Deskriptorji     STOMACH NEOPLASMS
ADENOCARCINOMA
ONCOGENE PROTEINS
ALLELES
GENE EXPRESSION REGULATION, NEOPLASTIC
CYCLINS
POLYMERASE CHAIN REACTION
FLUORESCENCE
EPIDERMAL GROWTH FACTOR RECEPTOR PROTEIN-TYROSINE KINASE
FIBROBLAST GROWTH FACTOR
BASE SEQUENCE
ELECTROPHORESIS, CAPILLARY
CHROMATOGRAPHY, HIGH PRESSURE LIQUID
HEPATOCYTE GROWTH FACTOR
PROTO-ONCOGENE PROTEINS