Zusammenfassung
To investigate the potential role of the PTEN tumor-suppressor gene
in the carcinogenesis of ovarian endometrioid carcinoma and its related
subtype, clear cell carcinoma, we examined 20 ovarian endometrioid
carcinomas, 24 clear cell carcinomas and 34 solitary endometrial
cysts of the ovary for LOH at 10q23.3 and point mutations of the
PTEN gene, using a laser-assisted microdissection method. LOH was
found in 8 of 19 ovarian endometrioid carcinomas (42.1%), 6 of 22
clear cell carcinomas (27.3%) and 13 of 23 solitary endometrial cysts
(56.5%). Somatic mutations in the PTEN gene were identified in 4
of 20 ovarian endometrioid carcinomas (20.0%), 2 of 24 clear cell
carcinomas (8.3%) and 7 of 34 solitary endometrial cysts (20.6%).
In 5 endometrioid carcinomas with endometriosis, 3 displayed LOH
events common to both the carcinoma and the endometriosis. In 7 clear
cell carcinomas with endometriosis, 3 displayed LOH events common
to both the carcinoma and the endometriosis. In no cases there were
LOH events in the endometriosis only. These results indicate that
inactivation of the PTEN gene is an early event in the development
of both endometrioid and clear cell carcinoma of the ovary. A laser-assisted
microdissection method enables us to collect target cells without
contamination by non-tumor cells. We expect that this technique will
be very useful for investigating genetic alterations in cancerous
or precancerous lesions. Early genetic alterations in various precancerous
cells detected by light microscopy can be readily identified by the
tissue-microdissection method.
- adenocarcinoma,_clear_cell,_genetics
- carcinoma,_endometrioid,_genetics
- dissection,_methods
- female
- genes,_tumor_suppressor,_genetics
- genetic_techniques
- gene_silencing
- humans
- lasers
- loss_of_heterozygosity
- ovarian_neoplasms,_genetics
- phosphoric_monoester_hydrolases,_genetics
- point_mutation
- precancerous_conditions,_genetics
- pten_phosphohydrolase
- tumor_suppressor_proteins
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