let-7 was the first miRNA identified as having a role in cancer through validation of RAS
protooncogene mRNA targeting and the association of low levels of let-7 with a poor prognosis in lung cancer [36].
[4] Human genes: BCR, BCR, RhoGEF and GTPase activating protein; ABU, ABL
protooncogene 1, non-receptor tyrosine kinase; IGH, immunoglobulin heavy; BCL2, BCL2, apoptosis regulator; MYC, MYC proto-oncogene, bHLH transcription factor.
Effect of peroxisome proliferators on the methylation and protein level of the c-myc
protooncogene in B6C3F1 mice liver.
This syndrome is characterized by autosomal-dominant inheritance and is associated with various mutations of the RET
protooncogene.
Src (sarcoma) is a
protooncogene encoding a tyrosine kinase; it is highly expressed on OCs, where it is activated, during the bone resorption, in the process of RANK signalling and after the integrin binding.
Neonatal exposure to high doses of the phytoestrogens equol and coumestrol is correlated with hypermethylation of a
protooncogene in the rat pancreas (Lyn-Cook et al.
Their identification heightened interest in the field, leading to the discovery of other less common (up to 1%--2%) but also actionable fusion genes such as those involving ROS
protooncogene 1, receptor tyrosine kinase (ROS1), and ret
protooncogene (RET) (5--8).
Cadmium also induced the transcript of bcl-2, with the amount of bcl-2 reaching a maximum at 1-2 hr of exposure; this increase occurred earlier than cadmium-induced increase in the
protooncogene such as c-myc.
[6] Human genes: KRAS, KRAS proto-oncogene, GTPase; EZH2, enhancer of zeste 2 polycomb repressive complex 2 subunit; STAT6, signal transducer and activator of transcription 6; MYD88, myeloid differentiation primary response 88; CD79B, CD79b molecule; CCND3, cyclin D3; ALK, anaplastic lymphoma receptortyrosine kinase; ROS1, ROS
protooncogene 1, receptor tyrosine kinase; RET, ret proto-oncogene; BRAF, B-Raf
protooncogene, serine/threonine kinase; EGFR, epidermal growth factor receptor.
Identification of a point mutation in the catalytic domain of the
protooncogene c-KIT in the peripheral blood mononuclear cells in patients who have mastocytosis with an associated hematological disorder.
Because peroxisome proliferators can affect multiple signaling pathways by transcriptional activation of PPAR-regulated genes, it is likely that alterations in specific regulated pathways (e.g., suppression of apoptosis,
protooncogene expression) are involved in tumor induction by peroxisome proliferators.
Routine blood DNA analyses of the most common genes associated with a familial risk for a pheochromocytoma, SDHB (succinate dehydrogenase complex iron sulfur subunit B), SDHD (succinate dehydrogenase complex subunit D), VHP (von Hippel-Lindau tumor suppressor), and RET (ret
protooncogene), were performed and revealed no mutations.
Classification of variants is pertinent to clinical trials evaluating efficacy of BRAF inhibitors in B-Raf
protooncogene, serine/threonine kinase (BRAF)-mutated cancer patients.
Alterations of the p53 tumor suppressor gene and its association with activation of the c-K-ras-2
protooncogene in pre-malignant and malignant lesions of the human uterine endometrium.
