RET Gene Fusions in Malignancies of the Thyroid and Other Tissues

Following the identification of the BCR-ABL1 (Breakpoint Cluster Region-ABelson murine Leukemia) fusion in chronic myelogenous leukemia, gene fusions generating chimeric oncoproteins have been recognized as common genomic structural variations in human malignancies. This is, in particular, a frequen...

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Bibliographic Details
Published in:Genes 2020-04, Vol.11 (4), p.424
Main Authors: Santoro, Massimo, Moccia, Marialuisa, Federico, Giorgia, Carlomagno, Francesca
Format: Article
Language:English
Subjects:
Animals
BCR-ABL protein
Chromosomes
Chronic myeloid leukemia
Deoxyribonucleic acid
DNA
DNA sequencing
Fusion protein
Gene amplification
Gene Fusion
Growth factors
Humans
Kinases
Ligands
Lung cancer
Myeloid leukemia
Neoplasms - genetics
Neoplasms - pathology
Next-generation sequencing
Papillary thyroid carcinoma
Protein-tyrosine kinase receptors
Proteins
Proto-Oncogene Proteins c-ret - genetics
Ret protein
Review
Signal transduction
Thyroid
Thyroid cancer
Thyroid Neoplasms - genetics
Thyroid Neoplasms - pathology
Transfection
Tumors
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Summary:Following the identification of the BCR-ABL1 (Breakpoint Cluster Region-ABelson murine Leukemia) fusion in chronic myelogenous leukemia, gene fusions generating chimeric oncoproteins have been recognized as common genomic structural variations in human malignancies. This is, in particular, a frequent mechanism in the oncogenic conversion of protein kinases. Gene fusion was the first mechanism identified for the oncogenic activation of the receptor tyrosine kinase RET (REarranged during Transfection), initially discovered in papillary thyroid carcinoma (PTC). More recently, the advent of highly sensitive massive parallel (next generation sequencing, NGS) sequencing of tumor DNA or cell-free (cfDNA) circulating tumor DNA, allowed for the detection of RET fusions in many other solid and hematopoietic malignancies. This review summarizes the role of RET fusions in the pathogenesis of human cancer.
ISSN:2073-4425
2073-4425
DOI:10.3390/genes11040424