Human Disease Model Report: cancer, multiple, RET fusions

General Information

Name

cancer, multiple, RET fusions

FlyBase ID

FBhh0000660

Disease Ontology Term

cancer

Parent Disease

OMIM

Overview

Chromosomal rearrangements involving fusions and subsequent activation of the 'rearranged during transfection' (RET) proto-oncogene have long been associated with nonmedullary thyroid carcinoma. More recently, RET fusions have been implicated in other human cancers, including lung adenocarcinomas and colorectal cancer. A number of RET fusions have been characterized in Drosophila; see 'Related Diseases,' below. In fly models, different RET fusions act through different signaling networks and display different drug sensitivities.

Point mutations of the RET gene have been implicated in familial medullary thyroid carcinoma (FBhh0000025) and multiple endocrine neoplasia (FBhh0000005).

[updated Nov. 2017 by FlyBase; FBrf0222196]

Disease Summary Information

Disease Summary: cancer, multiple, RET fusions

OMIM report

Human gene(s) implicated

Symptoms and phenotype

Genetics

Cellular phenotype and pathology

Molecular information

RET encodes a cellular tyrosine kinase transmembrane receptor. Activation of RET stimulates multiple downstream pathways that promote cell growth, proliferation, survival, and differentiation. These pathways include the mitogen-activated protein kinase (MAPK), the phosphoinositide 3-kinase (PI3K) and protein kinase B, signal transducer and activator of transcription 3, proto-oncogene tyrosine-protein kinase Src1 and focal adhesion kinase pathways (Romei et al., 2016; pubmed:26868437).

(FlyBase Curators, 2013-)

External links