2011
DOI: 10.1371/journal.pone.0028250
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Chromosome 3 Anomalies Investigated by Genome Wide SNP Analysis of Benign, Low Malignant Potential and Low Grade Ovarian Serous Tumours

Abstract: Ovarian carcinomas exhibit extensive heterogeneity, and their etiology remains unknown. Histological and genetic evidence has led to the proposal that low grade ovarian serous carcinomas (LGOSC) have a different etiology than high grade carcinomas (HGOSC), arising from serous tumours of low malignant potential (LMP). Common regions of chromosome (chr) 3 loss have been observed in all types of serous ovarian tumours, including benign, suggesting that these regions contain genes important in the development of a… Show more

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Cited by 89 publications
(76 citation statements)
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“…ALK rearrangements are identified in a minority of NSCLC cases, occurring in 2% to 7% of all NSCLC patients [7,8]. Additionally, ROS1 rearrangement was found in different types of malignant tumors, including NSCLC [9][10][11]. ROS1 gene rearrangements have recently been identified and are observed in 1% to 2% of all lung cancer patients [11,12].…”
Section: Introductionmentioning
confidence: 99%
“…ALK rearrangements are identified in a minority of NSCLC cases, occurring in 2% to 7% of all NSCLC patients [7,8]. Additionally, ROS1 rearrangement was found in different types of malignant tumors, including NSCLC [9][10][11]. ROS1 gene rearrangements have recently been identified and are observed in 1% to 2% of all lung cancer patients [11,12].…”
Section: Introductionmentioning
confidence: 99%
“…However, its function, both in normal physiology and disease, remains poorly defined mainly because of its still unidentified ligand. Chromosomal rearrangements resulting in oncogenic activation of ROS1 have been observed in a subset of patients with glioblastoma (6-9), NSCLC (10)(11)(12)(13)(14), cholangiocarcinoma (15), ovarian cancer (16), angiosarcoma (17), inflammatory myofibroblastic tumors (18), and Spitzoid melanoma (19). To date, interchromosomal translocations or intrachromosomal deletions have resulted in the production of 20 different N-terminal ROS1 fusion genes in a variety of cancers (Table S1).…”
mentioning
confidence: 99%
“…In most cases, ROS1 signaling is activated by interchromosomal translocation or intrachromosomal deletion that results in N-terminal ROS1 fusion genes. Several ROS1 kinase fusion proteins have been identified, including the Fused in Glioblastoma-ROS1 (FIG-ROS) that was first discovered in a human glioblastoma cell line (2) and more recently in patients with NSCLC (4), cholangiocarcinoma (3), and serous ovarian carcinoma (6). The SLC34A2-ROS1 (SLC-ROS) fusion is present in a subset of patients with NSCLC (1, 7) and gastric cancer (8).…”
mentioning
confidence: 99%