SCLCs all lung cancers represent approximately 15%. Characterized Finely granular chromatin and absent or small epithelial tumor cells from Inconspicuous nucleoli. Necrosis is a frequent and widespread, mitotic Count is high. Less than 10% of SCLCs also show a mixture of non-small cell lung cancer histological type, usually adenocarcinoma, squamous cell carcinoma, large Carcinoma and those of "combined SCLCs» is called. Molecular abnormalities The pathogenesis of small cell lung cancer is closely linked with smoking, now is an important more information about the molecules involved in the pathogenesis. Autocrine growth factors in neuroendocrine regulation of these peptides (Eg: bompesinis / gastrin - releasing peptide) SCL is evident. Dominant The MYC family oncogenes frequently overexpressed (and can be enhanced) Small cell lung cancer and non small cell lung cancer, all KRAS oncogene is not mutated in a moment of SCLC. The TP53 is mutated in over 90% of SCLCs, RB gene is inactivated in further More than 90% of SCLCs. Non-small cell lung cancer, p16INK4A, unlike other components retinoblastoma/p16 path is more rare in SCLC. Genome-wide 400 polymorphic markers distributed around the study allelotyping Size 10 cm in the human genome showed that on average 17 loci showed NSCLC SCLCs individual and a loss of about 22 heterozygosity (AU) The loss of about 50-60 cm and the average size of the average frequency of microsatellite Every five tumors the deviation. Loss of 22 kinds of "hot spots" were heterozygosity, the preference for non-small cell lung SCLC, 7 settings 13; 2 all. This provides clear evidence for genome-wide scale SCLC And inactivation of tumor suppressor genes is NSCLC differ significantly Pathogenesis them. Moreover, differences in DNA methylation profiles SCLC and NSCLC tumors was found between.
Minggu, 13 November 2011
SMALL CELL LUNG CANCER PATHOLOGY
SCLCs all lung cancers represent approximately 15%. Characterized Finely granular chromatin and absent or small epithelial tumor cells from Inconspicuous nucleoli. Necrosis is a frequent and widespread, mitotic Count is high. Less than 10% of SCLCs also show a mixture of non-small cell lung cancer histological type, usually adenocarcinoma, squamous cell carcinoma, large Carcinoma and those of "combined SCLCs» is called. Molecular abnormalities The pathogenesis of small cell lung cancer is closely linked with smoking, now is an important more information about the molecules involved in the pathogenesis. Autocrine growth factors in neuroendocrine regulation of these peptides (Eg: bompesinis / gastrin - releasing peptide) SCL is evident. Dominant The MYC family oncogenes frequently overexpressed (and can be enhanced) Small cell lung cancer and non small cell lung cancer, all KRAS oncogene is not mutated in a moment of SCLC. The TP53 is mutated in over 90% of SCLCs, RB gene is inactivated in further More than 90% of SCLCs. Non-small cell lung cancer, p16INK4A, unlike other components retinoblastoma/p16 path is more rare in SCLC. Genome-wide 400 polymorphic markers distributed around the study allelotyping Size 10 cm in the human genome showed that on average 17 loci showed NSCLC SCLCs individual and a loss of about 22 heterozygosity (AU) The loss of about 50-60 cm and the average size of the average frequency of microsatellite Every five tumors the deviation. Loss of 22 kinds of "hot spots" were heterozygosity, the preference for non-small cell lung SCLC, 7 settings 13; 2 all. This provides clear evidence for genome-wide scale SCLC And inactivation of tumor suppressor genes is NSCLC differ significantly Pathogenesis them. Moreover, differences in DNA methylation profiles SCLC and NSCLC tumors was found between.
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