Fusion genes and rearranged genes as a linear function of chromosome aberrations in cancer

Mitelman, Felix; Johansson, Bertil; Mertens, Fredrik

doi:10.1038/ng1335

Cited by 295 publications

(234 citation statements)

References 23 publications

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“…The array CGH meta-analysis divides the cancer samples in separate clusters based on tissue origin as well as on embryonic origin. Based on balanced translocations, the distinction between hematological and mesenchymal tumors on the one hand and solid tumors on the other was questionable (Mitelman et al, 2004). In contrast, a distinction between tumors of hematological and mesenchymal origin versus solid tumors has recently also been observed using micro-RNA profiling (Lu et al, 2005), consistent with the data presented here using array CGH meta-analysis.…”

Section: Discussionsupporting

confidence: 84%

“…Such meta-analysis is important because: it gives the possibility to achieve more robust and reliable results by considering data sets from different studies, it offers the ability to perform analysis of samples from different types of cancers from different geographical locations and, finally, it allows the identification of subgroups of samples not only within a cancer type but also across different types of cancers. Such cross-cancer-type patterns may show specific biological and/or clinical features (Weiss et al, 2003;Mitelman et al, 2004;Lu et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors

et al. 2006

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A series of studies have been published that evaluate the chromosomal copy number changes of different tumor classes using array comparative genomic hybridization (array CGH); however, the chromosomal aberrations that distinguish the different tumor classes have not been fully characterized. Therefore, we performed a meta-analysis of different array CGH data sets in an attempt to classify samples tested across different platforms. As opposed to RNA expression, a common reference is used in dual channel CGH arrays: normal human DNA, theoretically facilitating cross-platform analysis. To this aim, cell line and primary cancer data sets from three different dual channel array CGH platforms obtained by four different institutes were integrated. The cell line data were used to develop preprocessing methods, which performed noise reduction and transformed samples into a common format. The transformed array CGH profiles allowed perfect clustering by cell line, but importantly not by platform or institute. The same preprocessing procedures used for the cell line data were applied to data from 373 primary tumors profiled by array CGH, including controls. Results indicated that there is no apparent feature related to the institute or platform and that array CGH allows for unambiguous cross-platform meta-analysis. Major clusters with common tissue origin were identified. Interestingly, tumors of hematopoietic and mesenchymal origins cluster separately from tumors of epithelial origin. Therefore, it can be concluded that chromosomal aberrations of tumors from hematopoietic and mesenchymal origin versus tumors of epithelial origin are distinct, and these differences can be picked up by meta-analysis of array CGH data. This suggests the possibility of prospectively using combined analysis of diverse copy number data sets for cancer subtype classification.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors

et al. 2006

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“…• Gene Fusions in Carcinoma-The missing Link: While leukemias/ lymphomas and bone/soft tissue sarcomas, which together represent only 10% of all human cancers account for more than 80% of all known gene fusions, common epithelial, cancers which account for 80% of cancer related deaths, account for only about 10% of recurrent gene fusions 15,19 . This paradox has been challenged by the recent discoveries of gene fusions in prostate and lung cancers.…”

Section: Bcr-abl1 Is a Specific Therapeutic Targetmentioning

confidence: 99%

“…Gene fusions described among epithelial cancers so far have included RET-NTRK1 fusions in papillary thyroid carcinoma, PAX8-PPARG in follicular thyroid carcinoma, MECT1-MAML2 in mucoepidermoid carcinoma, the TFE3-TFEB in kidney carcinomas, and BRD4-NUT in midline carcinomas etc (reviewed16). Remarkably, recurrent gene fusions have not previously been detected in the most prevalent carcinomas including prostate, breast (with the exception of rare, secretory breast cancers), lung, gastrointestinal and gynecologic tumors 17 , despite compelling arguments that predict their occurence 15,18,19 . The absence of gene fusions in common solid tumors has been attributed to the technical difficulties associated with their cytogenetic analysis.…”

Section: Introductionmentioning

confidence: 99%

Recurrent gene fusions in prostate cancer

2008

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The discovery of recurrent gene fusions in a majority of prostate cancers has important clinical and biological implications in the study of common epithelial tumors. Gene fusion and chromosomal rearrangements were previously thought to be the primary oncogenic mechanism of hematological malignancies and sarcomas. The prostate cancer gene fusions that have been identified thus far are characterized by 5' genomic regulatory elements, most commonly controlled by androgen, fused to members of the ETS family of transcription factors, leading to the over-expression of oncogenic transcription factors. ETS gene fusions likely define a distinct class of prostate cancer which may have a bearing on diagnosis, prognosis and rational therapeutic targeting.

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“…Epitheliale Tumoren (Karzinome), die die häufigsten Tumoren beim Menschen darstellen und bei Mor bidität und Mortalität von Krebserkran kungen führend sind, waren bisher in we niger als 1% der Fälle durch krankheits spezifische rekurrente Genfusionen cha rakterisiert [1,2,3]. Unsere Entdeckung der TMPRSS2-ETS Genfusionen im Jahr 2005 veränderte das Verständnis über Genrearrangements in soliden Tumoren daher dramatisch [4].…”

Section: Genfusion Beim Prostatakarzinom -Ein Paradigmenwechselunclassified

„Dangerous liaisons“ im Prostatakarzinom

Perner

2010

Pathologe

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Fusion genes and rearranged genes as a linear function of chromosome aberrations in cancer

Cited by 295 publications

References 23 publications

Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors

Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors

Recurrent gene fusions in prostate cancer

„Dangerous liaisons“ im Prostatakarzinom

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