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Distinct gene expression profiles in ovarian cancer linked to Lynch syndrome.

Jönsson, Jenny-Maria LU ; Bartuma, Katarina LU ; Dominguez, Mev LU ; Harbst, Katja LU orcid ; Ketabi, Zohreh ; Malander, Susanne LU orcid ; Jönsson, Mats LU ; Carneiro, Ana LU orcid ; Måsbäck, Anna LU and Jönsson, Göran B LU , et al. (2014) In Familial Cancer 13(4). p.537-545
Abstract
Ovarian cancer linked to Lynch syndrome represents a rare subset that typically presents at young age as early-stage tumors with an overrepresentation of endometrioid and clear cell histologies. We investigated the molecular profiles of Lynch syndrome-associated and sporadic ovarian cancer with the aim to identify key discriminators and central tumorigenic mechanisms in hereditary ovarian cancer. Global gene expression profiling using whole-genome c-DNA-mediated Annealing, Selection, extension, and Ligation was applied to 48 histopathologically matched Lynch syndrome-associated and sporadic ovarian cancers. Lynch syndrome-associated and sporadic ovarian cancers differed by 349 significantly deregulated genes, including PTPRH, BIRC3, SHH... (More)
Ovarian cancer linked to Lynch syndrome represents a rare subset that typically presents at young age as early-stage tumors with an overrepresentation of endometrioid and clear cell histologies. We investigated the molecular profiles of Lynch syndrome-associated and sporadic ovarian cancer with the aim to identify key discriminators and central tumorigenic mechanisms in hereditary ovarian cancer. Global gene expression profiling using whole-genome c-DNA-mediated Annealing, Selection, extension, and Ligation was applied to 48 histopathologically matched Lynch syndrome-associated and sporadic ovarian cancers. Lynch syndrome-associated and sporadic ovarian cancers differed by 349 significantly deregulated genes, including PTPRH, BIRC3, SHH and TNFRSF6B. The genes involved were predominantly linked to cell growth, proliferation, and cell-to-cell signaling and interaction. When stratified for histologic subtype, hierarchical clustering confirmed distinct differences related to heredity in the endometrioid and serous subtypes. Furthermore, separate clustering was achieved in an independent, publically available data set. The distinct genetic signatures in Lynch syndrome-associated and sporadic ovarian cancers point to alternative preferred tumorigenic routes and suggest that genetic discriminators may be relevant for molecular diagnostics and targeted therapeutics. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Familial Cancer
volume
13
issue
4
pages
9 pages
publisher
Springer Science and Business Media B.V.
external identifiers
  • pmid:24848881
  • wos:000345093500003
  • scopus:84937512186
  • pmid:24848881
ISSN
1389-9600
DOI
10.1007/s10689-014-9728-1
project
Precision Medicine in Hereditary Cancer and Sarcoma; targeted surveillance, immunotherapy and individualized follow-up
language
English
LU publication?
yes
id
fd5287ec-7e51-40a2-bcf1-762510921388 (old id 4453962)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24848881?dopt=Abstract
date added to LUP
2016-04-01 10:43:45
date last changed
2025-01-14 21:52:44
@article{fd5287ec-7e51-40a2-bcf1-762510921388,
  abstract     = {{Ovarian cancer linked to Lynch syndrome represents a rare subset that typically presents at young age as early-stage tumors with an overrepresentation of endometrioid and clear cell histologies. We investigated the molecular profiles of Lynch syndrome-associated and sporadic ovarian cancer with the aim to identify key discriminators and central tumorigenic mechanisms in hereditary ovarian cancer. Global gene expression profiling using whole-genome c-DNA-mediated Annealing, Selection, extension, and Ligation was applied to 48 histopathologically matched Lynch syndrome-associated and sporadic ovarian cancers. Lynch syndrome-associated and sporadic ovarian cancers differed by 349 significantly deregulated genes, including PTPRH, BIRC3, SHH and TNFRSF6B. The genes involved were predominantly linked to cell growth, proliferation, and cell-to-cell signaling and interaction. When stratified for histologic subtype, hierarchical clustering confirmed distinct differences related to heredity in the endometrioid and serous subtypes. Furthermore, separate clustering was achieved in an independent, publically available data set. The distinct genetic signatures in Lynch syndrome-associated and sporadic ovarian cancers point to alternative preferred tumorigenic routes and suggest that genetic discriminators may be relevant for molecular diagnostics and targeted therapeutics.}},
  author       = {{Jönsson, Jenny-Maria and Bartuma, Katarina and Dominguez, Mev and Harbst, Katja and Ketabi, Zohreh and Malander, Susanne and Jönsson, Mats and Carneiro, Ana and Måsbäck, Anna and Jönsson, Göran B and Nilbert, Mef}},
  issn         = {{1389-9600}},
  language     = {{eng}},
  number       = {{4}},
  pages        = {{537--545}},
  publisher    = {{Springer Science and Business Media B.V.}},
  series       = {{Familial Cancer}},
  title        = {{Distinct gene expression profiles in ovarian cancer linked to Lynch syndrome.}},
  url          = {{https://lup.lub.lu.se/search/files/2085989/5043369.pdf}},
  doi          = {{10.1007/s10689-014-9728-1}},
  volume       = {{13}},
  year         = {{2014}},
}