Loss of heterozygosity in ampulla of Vater neoplasms during adenoma-carcinoma sequence.
BACKGROUND
Ampulla of Vater cancers arise from precancerous lesions and existence of an adenoma-carcinoma sequence is based on morphological observations.


METHODS
We studied the loss of heterozygosity (LOH) in 22 adenomas, 32 carcinomas and 10 metastatic lesions using nine dinucleotide-repeated sequences in 3p, 8p, 8q, 9p, 10q, 13q, 17p, 17q, 18q.


RESULTS
High LOH frequencies (> 50%) of 9p (IFNA) and 17p (TP53) were observed in adenomas and carcinomas. The frequency of LOH is higher in adenoma (55.6%) than in carcinoma (40%) for 8p (D8S261), but it is the same in cases having adenoma (57.1%) and carcinoma (57.1%) in the same lesion. LOH for 13q (D13S118), 17q (D17S520) and for 18q (D18S34) were more common in carcinomas than in adenomas, but statistically a significant difference was observed only on 13q (p < 0.05). Fractional allelic loss (FAL) is not correlated with any of the clinicopathological parameters.


CONCLUSIONS
Tumor suppressor genes located in the 8p, 9p and 17p chromosomes might be associated with the early stage of tumorigenesis and that in 13q is involved during the adenoma-carcinoma progression.
Park
Sunhoo
S
Department of Pathology, Seoul National University College of Medicine, Korea Cancer Center Hospital, Seoul, Korea.
Kim
Sun Whe
SW
Kim
Sun Hee
SH
Lee
Byung Lan
BL
Kim
Woo Ho
WH
D000236:Adenoma / Q000235:genetics* / Q000473:pathology; D014670:Ampulla of Vater; D002277:Carcinoma / Q000235:genetics* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000473:pathology; D002877:Chromosomes, Human; D003138:Common Bile Duct Neoplasms / Q000235:genetics*; D006801:Humans; D019656:Loss of Heterozygosity; D018895:Microsatellite Repeats / Q000235:genetics