Oncogenes

Gene sequences of normal cells with cancer-inducing activity. Oncogenes are created by mutations from so-called proto-oncogenes (e.g. through point mutation, translocation, amplification due to chemical or physical influences, and secondarily also through viral influences).

All physiological cell cycle control genes are potential proto-oncogenes, since their mutation leads to an excessive expression of their gene product. This can lead to dysfunction and loss of control during cell division.

The "gene" in oncogene is not used in the sense of "producing" as in "carcinogenic or mutagenic", but is derived directly from the word gene as part of the genome.

RET oncogene (RET = acronym for "Rearranged during Transfection"): This oncogene codes for a receptor tyrosine kinase that is normally involved in developmental processes. Oncogenic mutations lead to constitutive activation of the tyrosine kinase. This mechanism is of crucial importance for tumor development.

MDM2 and MDMX: MDM2 and MDMX proteins are oncogenic proteins in a finely balanced equilibrium with the p53 protein. Functional single nucleotide polymorphisms (SNP) in the promoter region of the MDM2 gene (SNP309) can lead to an imbalance of oncogenic and tumor-suppressive proteins. This can lead to earlier tumor occurrence in ovarian carcinomas and to higher mortality.

In malignant melanoma, the SNP309 polymorphism also leads to a higher risk of developing malignant melanoma in women < 50 years of age. This risk factor is considered to be greater than the prognostic factor "multiple melanocytic nevi" or UV radiation.

1. Firoz EF et al (2009) Association of MDM2 SNP309, age of onset, and gender in cutaneous melanoma. Clin Cancer Res15: 2573-2580