Recurrent fusion oncogenes in carcinomas.

@article{Teixeira2006RecurrentFO,
  title={Recurrent fusion oncogenes in carcinomas.},
  author={Manuel R. Teixeira},
  journal={Critical reviews in oncogenesis},
  year={2006},
  volume={12 3-4},
  pages={
          257-71
        }
}
  • M. Teixeira
  • Published 1 December 2006
  • Medicine, Biology
  • Critical reviews in oncogenesis
Chromosome structural aberrations giving rise to fusion oncogenes is one of the most common mechanisms in oncogenesis. Although this type of gene rearrangement has long been recognized as a fundamental pathogenetic mechanism in hematologi-cal malignancies and soft-tissue tumors, it has until recently only rarely been described in the common carcinomas. In this review, the existing information on recurrent fusion oncogenes characterizing carcinomas is summarized, namely, the RET and NTRK1 fusion… 

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References

SHOWING 1-10 OF 71 REFERENCES

Cytogenetics and molecular genetics of carcinomas arising from thyroid epithelial follicular cells

TLDR
Cytogenetic and molecular analyses of thyroid tumors have indicated that these neoplasms represent a good model for analyzing human epithelial cell multistep carcinogenesis and could provide significant molecular tools for a better differential diagnosis and for the development of novel therapeutic avenues for thyroid cancer.

PAX8-PPARgamma1 fusion oncogene in human thyroid carcinoma [corrected].

TLDR
T(2;3)(q13;p25), a translocation identified in a subset of human thyroid follicular carcinomas, results in fusion of the DNA binding domains of the thyroid transcription factor PAX8 to domains A to F of the peroxisome proliferator-activated receptor (PPAR) gamma1.

Fusion oncogenes in tumor development.

  • P. Åman
  • Biology
    Seminars in cancer biology
  • 2005

The RET proto-oncogene in human cancers

TLDR
The identification of RET mutations in most MEN 2 families (95%) has translated into improved care for MEN 2 patients, and further investigation of the signaling pathways contributing to tumorigenesis in relevant tissues will eventually help to develop novel strategies to prevent or to treat human papillary thyroid carcinomas, MEN 2 disease, as well as the sporadic cancers relevant to MEN2 disease.

Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer.

RET Oncogene Activation in Papillary Thyroid Carcinoma

TLDR
The RET proto-oncogene encodes a cell membrane tyrosine-kinase receptor protein whose ligands belong to the glial cell line–derived neurotrophic factor and the close association between their presence and the papillary carcinoma phenotype indicates that they play a causative role in tumor development.

BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinoma.

TLDR
It is demonstrated that BRD4 is fused with nearly the entire transcript of the novel 15q13 gene, NUT (nuclear protein in testis), forming a 6.4-kb fusion oncogene,BRD4-NUT, which is the first fusiononcogene mechanism identified in a highly lethal form of carcinoma.

TMPRSS2:ETV4 gene fusions define a third molecular subtype of prostate cancer.

TLDR
This work interrogated the expression of all ETS family members in prostate cancer profiling studies and identified marked overexpression of ETV4 in 2 of 98 cases, which defines a third molecular subtype of prostate cancer and supports the hypothesis that dysregulation of E TS family members through fusions with TMRPSS2 may be an initiating event in prostate cancers development.

TMPRSS2-ERG gene fusion causing ERG overexpression precedes chromosome copy number changes in prostate carcinomas and paired HGPIN lesions.

TLDR
It is demonstrated for the first time that the TMPRSS2-ERG fusion gene can be detected in a proportion of HGPIN lesions and that this molecular rearrangement is an early event that may precede chromosome-level alterations in prostate carcinogenesis.

Chromosome translocations in sarcomas and the emergence of oncogenic transcription factors.

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