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At least 19 recordsLinked to original sources
PubMed1989

Growth factors, oncogenes and the autocrine hypothesis.

Many aspects must be studied when considering theories of oncogenesis. Growth factors, the polypeptide hormones that are necessary for cell growth, and oncogenes, the genes that produce cancer, are only two aspects. Proto-oncogenes are found in normal cellular DNA and are believed to play regulatory roles in differentiation and development. Oncoviruses, mutation of DNA and chromosomal damage can activate proto-oncogenes and cause malignant change. Oncogenes can render transformed cells independent of growth factors. A cell can bypass the need for outside growth factors by producing the growth factor and its receptor, thereby using an autostimulatory impetus for growth. This is autocrine growth. An oncogene can also bypass the need for growth factors by activating or modifying growth factor receptors, or by stimulating intracellular events, such as tyrosine phosphorylation, both of which ultimately lead to cell division. The various mechanisms by which oncogenes act provide specific targets for treatment. Specific antigrowth factor or antireceptor antibodies or antagonists could interfere with autocrine regulation. Further research on the activation of oncogenes could provide valuable insight on regulation of the growth of tumors. Ultimately, the understanding of the molecular pathogenesis of cellular transformation will be a key to the prevention and treatment of cancer.

Cell Transformation, Neoplastic↗
PubMed1987

Growth factors, oncogenes, and multistage carcinogenesis.

This paper presents evidence that the full repertoire of cellular genes involved in the carcinogenic process is several times larger than that of the known list of proto-oncogenes. Furthermore, this repertoire includes genes whose normal function is related to growth stimulation, as well as genes whose normal function is to inhibit growth or induce terminal differentiation. Multistage carcinogenesis probably results from a complex series of changes in both categories of genes. Despite this complexity, carcinogenesis can be conceived in terms of disturbances in biochemical functions that normally control the expression or function of growth factors, receptors, and pathways of signal transduction. Several protein kinases play a central role in the process of signal transduction. Our laboratory has recently isolated cDNA clones for the enzyme protein kinase C (PKC). These clones should be useful for clarifying the role of PKC in growth control and tumor promotion. Finally, the existence of genes whose normal function is to inhibit cell growth provides a rationale for new strategies of cancer prevention and treatment.

Animals↗
PubMed1985

Role of growth factors in oncogenesis: growth factor-proto-oncogene pathways of mitogenesis.

Cellular genes which encode proteins involved in the response of cells to stimulation by growth factors may be potential oncogenes. The factors involved in the signal transmission from growth factor-receptor interaction to DNA synthesis constitute a cascade system which we call the 'growth factor-proto-oncogene pathway(s) of mitogenesis'. For each growth factor, all the responsive cells, regardless of cell types and tissue source, have specific growth factor receptors which are similar, if not identical, in molecular weight and biological activity. Thus, we believe that the growth factor-proto-oncogene pathway(s) functions in the same manner in all responsive cells. Platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and brain-derived growth factor (BDGF) are major growth factors for connective tissue cells and do not share a common pathway in mitogenesis in responsive cells. The gene product of c-myc may be involved in the cellular response of cells stimulated by PDGF or FGF, but not directly in the signal transmission which leads to DNA synthesis.

Animals↗
PubMed1990

Growth factors and oncogenes in pancreatic cancer.

There are abnormalities in the structure and/or function of several oncogenes and growth factors in human pancreatic cancer, notably the EGF receptor and its ligand TGF alpha, c-erb B-2 proto-oncogene, Ki-ras oncogene and the tumour suppressor gene p53. The temporal sequence of their activation and the nature of the aetiological agents responsible for their activation are not yet clear. In vitro pancreatic culture systems and transgenic animal experiments are needed to reconstruct and define those molecular events that are necessary and sufficient for the neoplastic phenotype.

Animals↗
PubMed1992

Drugs active against growth factor and oncogene phosphatidylinositol signalling pathways.

Increased knowledge of growth factor and oncogene intracellular signalling presents us with unique opportunities to develop new classes of antiproliferative drugs. The degeneracy of intracellular signalling may allow normal cells to be relatively unaffected by drugs that inhibit just one signalling pathway. Oncoproteins themselves have proved difficult to target and the drugs lack selectivity. More success has come with drugs targeted against other components of signalling pathways. Two examples of such classes of drugs are given. The ether lipid anticancer drugs inhibit intracellular signalling at multiple points; phosphatidylinositol phospholipase C, protein kinase C, intracellular Ca2+ release and phosphatidylinositol-3'-kinase. D-3-deoxy-3-substituted myo-inositols and phosphatidylinositols are a new class of growth inhibitory compounds that appear to act as antagonists of myo-inositol signalling.

Antineoplastic Agents↗
PubMed1989

Growth factors and oncogenes.

Recent findings reporting the structure, the mechanism of action of peptide growth factors and their receptor as well as their presence in human tumors have led to a better knowledge of the events involved in cell growth regulation. The ability of cancer cells to produce and to respond to their own growth factors confers on them a growth autonomy and strengthens the link between growth factors and oncogenes. Oncogenes render the cells growth factor-independent not only by coding for autocrine growth factors of their receptor, but also by amplifying the mitogenic signals generated by the binding of the peptide growth factor to its membrane receptor.

Animals↗
PubMed1992

Crossed signals: oncogenic transcription factors.

Transcription factors operate at key regulatory junctions in the cell's responses to diverse extracellular stimuli. We discuss how the transforming activity of mutated transcription factors encoded by several oncogenes (v-erbA, v-fos, v-jun and v-rel) may result in part from a loss of the integrated response to the signalling network.

Genes, fos↗
PubMed1990

Growth factors and oncogenes in human solid tumors: clinical aspects.

Growth factors, growth factor receptors and oncogenes have been extensively studied in human tumors for some years. The purpose of this paper is to review the clinical results obtained in human cancers and their predisposing conditions or high risk groups as well as their relation with clinical, pathological characteristics and their prognosis.

Brain Neoplasms↗