Evidence map›Paper›PMID 15024645›Full record

ArticleJournal of cancer research and clinical oncology2004

Allelotype of ampulla of Vater cancer: highly frequent involvement of chromosome 11.

Patrick S Moore, Edoardo Missiaglia, Stefania Beghelli, Emma Bragantini, Maria M Mina, Giuseppe Zamboni, Massimo Falconi, Aldo Scarpa

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Article in Journal of cancer research and clinical oncology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed, 6 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Patrick S MooreDipartimento di Patologia-Sezione di Anatomia Patologica, Università di Verona, Strada Le Grazie, 37134 Verona, Italy.
Edoardo Missiaglia
Stefania Beghelli
Emma Bragantini
Maria M Mina
Giuseppe Zamboni
Massimo Falconi
Aldo Scarpa
University of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo determine the genetic differences/similarities in ampulla of Vater cancers (AVC) with respect to other pancreatic tumor types.

methodsWe analyzed eight cases of primary AVC by genome-wide allelotyping on DNA obtained from frozen tissue. A total of 372 microsatellite loci were used for each case, for a total of 2,976 microsatellites analyzed.

resultsOf the 2,159 informative markers, 400 were allelic losses and 1,759 markers were retained for an average fractional allelic loss of 0.19. Seven cases showed LOH on at least two markers on chromosomal arm 11p, while six cases showed allelic losses on 11q. The high frequency of LOH on chromosome 11 was also confirmed by analysis of an additional 17 paraffin-embedded AVC. Frequent LOH (50% or greater) was also found on chromosome arms 5q, 6q, 9p, 13, 16p, 17p, and 18p.

conclusionsIt can be inferred that the targets of inactivation on chromosomes 5q, 9p, and 17p appear to be APC, p16, and p53, respectively, while the critical target(s) of inactivation at the other frequently lost loci remain to be characterized. The resulting allelotype reveals that distinctive chromosomal alterations are present in these neoplasms, indicating that it is a tumor entity distinct from pancreatic adenocarcinoma.

Indexed as

AllelesAmpulla of VaterChromosomes, Human, Pair 11AdultAgedCommon Bile Duct NeoplasmsFemaleHumansLoss of HeterozygosityMaleMicrosatellite RepeatsMiddle AgedPancreatic Neoplasms

Identifiers

PMID15024645
PMCPMC12161850
OpenAlexW2037630952

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.