These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Growth factors, oncogenes and the autocrine hypothesis.
    Author: Wong RS, Passaro E.
    Journal: Surg Gynecol Obstet; 1989 May; 168(5):468-73. PubMed ID: 2652348.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]