proto-oncogene


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Related to proto-oncogene: tumor suppressor gene

proto-oncogene

[¦prō·dō ′äŋ·kōjēn]
(genetics)
The normal-functioning precursor of an oncogene; mutation of this gene to produce an oncogene causes excessive activity of the gene product, leading to cancer.
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Besides, some molecular and genetic alteration may contribute to malignant transformation, including aberrant somatic hypermutations of proto-oncogenes, DNA methylation of tumor suppressor genes, gains and losses of genetic material, as well as activation of the NF-?B and JAK/STAT signaling pathway.
* The report provides a snapshot of the global therapeutic landscape for Myc Proto-Oncogene Protein (Proto-Oncogene c-Myc or Class E Basic Helix-Loop-Helix Protein 39)
Germline mutations of the RET proto-oncogene are found in 98% of MEN2A, 95% of MEN2B, and in 88% of FMTC patients (13).
Hiai, "Isolation of ret proto-oncogene cDNA with an amino-terminal signal sequence," Oncogene, vol.
In addition to increasing cell proliferation, survival, and migration, [H.sub.2][O.sub.2] activates SRC family proto-oncogenes, which regulate vascular development and vascular permeability [59], the latter of which is an early step in tumor stroma development [60].
Delayed c-fos proto-oncogene expression in the rat hippocampus induced by transient global cerebral ischemia: an in situ hybridization study.
* Qualitative: Conversion from proto-oncogene to transforming gene includes changes in the nucleotide sequence and acquisition of the new properties.
Imatinib binds preferentially to ATP binding sites of c-KIT proto-oncogene product, platelet-derived growth factor receptor (PDGF-R), and Abelson Kinase (c-ABL), impeding the ensuing signal transduction.
In terms of physical interactions, TP53 seemed to be a hub of interactions as it linked itself to the SMAD genes (SMAD2/3/4) and TGFBR1 on one hand and also showed the relation to the MET proto-oncogene and BCL2 tumor promoter.
Germline mutations in the RET proto-oncogene cause hereditary MTC [20-22], and approximately 50% of patients with sporadic MTC have somatic RET mutations [23, 24].
Modulation of c-MET proto-oncogene (HGF receptor) mRNA abundance by cytokines and hormones: Evidence for rapid decay of the 8 kb c-MET transcript.
Genetic evaluation was negative for the RET proto-oncogene and for mutations in the NF1 gene.