From the Oncogenes to the Oncologists: Exploring the Ali Baba's Cave (original) (raw)

Oncogenes and Tumor Suppressor Genes

Acta Oncologica, 1988

The artificial selection of the directly acting or acute RNA tumor viruses for high transforming ability has led to the isolation of defective retroviral genomes that have picked up, by accidental recombination, some of the important genes that influence, trigger or regulate cell division. These genes belong to at least four functionally different groups. Each of them can contribute to tumor development and/or progression after activation by structural or regulatory changes. Growth factor genes may act as oncogenes following constitutive activation in a cell that normally responds to, but does not produce, the corresponding growth factor (the autocrine model, exemplified by sis). Growth factor receptors may be fixed in a state of continuous, faulty signalling by the truncation of their external, ligand binding portion (examples: erb-B, fms). Genes coding for proteins involved in signal transduction may be activated by point mutations in certain, important domains (example: the ras-family). DNA binding proteins, presumably involved in DNA replication may drive cell division after constitutive activation by retroviral insertion, chromosomal translocation or gene amplification (example: the mycfamily).

Mechanisms of Oncogene Activation

New Aspects in Molecular and Cellular Mechanisms of Human Carcinogenesis, 2016

The main modifications that characterize cancer are represented by alterations in oncogenes, tumor-suppressor genes, and non-coding RNA genes. Most of these alterations are somatic and the process is a multistep one. Tumors often arise from an initial transformed cell, and after subsequent genetic alterations different cytogenetically clones lead to tumor heterogeneity. Oncogenes encode proteins that control cell processes such as proliferation and apoptosis. Among these proteins are transcription factors, chromatin remodelers, growth factors, growth factor receptors, signal transducers, and apoptosis regulators. Oncogenes activation by structural alteration (chromosomal rearrangement, gene fusion, mutation, and gene amplification) or epigenetic modification (gene promoter hypomethylation, mi-croRNA expression pattern) confers an increased or a deregulated expression. Therefore, cells with such alterations possess a growth advantage or an increased survival rate. Given the fact that expression profiling of these alterations determines specific signatures associated with tumor classification, diagnosis, staging, prognosis, and response to treatment, it highlights the importance of studying oncogenes activation mechanisms and the great potential that they hold as therapeutic tools in the near future.

Cell transformation: the role of oncogenes and growth factors

An attempt is made to draw together diverse areas of biological research which have recently converged and opened up new experimental approaches to understanding the nature of cancer. In particular, the powerful techniques of molecular biology have been brought to bear on tissue culture systems. The case is made for the continued use of cell transformation in vitro as a real and useful model for cancer development. The hallmark of all cancer cells is loss of control over the cell cycle and the cellular elements involved, growth factors, growth factor receptors and signal transducers have been identified and in some instances shown to be encoded in cellular oncogenes. Moreover, as the molecular mechanisms underlying cell growth control are unravelled, those aspects involved in neoplastic change will be identified and this will lead to the development of definitive short-term tests for the detection of chemical carcinogens.

Reviewing Oncogenes and Proto-Oncogenes

International Journal of Scientific Research in Science and Technology, 2021

This article is an examination of the Reviewing oncogenes and Proto-oncogenes The scientific development and subsequent “oncogenes and Proto-oncogenes” continues to influence the researchers all over the globe today. This article examines the research done and published by researchers and scientists. Consideration of current trends and data in scientific queries and demonstrates further aspects of this relationship. Additionally, this article explores options for oncogenes and Proto-oncogenes relationships.

Oncogenes as Novel Targets for Cancer Therapy (Part I)

American Journal of PharmacoGenomics, 2005

introduced the new technologies responsible for the advancement of oncogene identification, target validation, and drug design. Because of such advances, new specific and more efficient therapeutic agents can be developed for cancer. This part of the review continues the exploration of various oncogenes, which we have grouped within seven categories: growth factors, tyrosine kinases, intermediate signaling molecules, transcription factors, cell cycle regulators, DNA damage repair genes, and genes involved in apoptosis. Part I included a discussion of growth factors and tyrosine kinases. This portion of the review covers intermediate signaling molecules and the various strategies used to inhibit their expression or decrease their activities.

Cancer genes, proto-oncogenes, and development

Experimental Cell Research, 1987

The retroviral cancer genes have in a number of observations been shown to interfere with the developmental program of target cells. Here we are concerned with the interface between cancer genes/proto-oncogenes and developmental processes. Research in this field serves two purposes; to delineate key developmental controls and to identify these as kt@etS for OnCOgenk agentS.

Growth regulation by oncogenes — new insights from model organisms

Current Opinion in Genetics & Development, 2001

A great deal of work has focused on how oncogenes regulate the cell cycle during normal development and in cancer, yet their roles in regulating cell growth have been largely unexplored. Recent work in several model organisms has demonstrated that homologs of several oncogenes regulate cell growth and has suggested that some of the effects of oncogenes on the cell cycle may be a result of growth promotion. These studies have also suggested how growth and cell-cycle progression may be coupled.