Role of Cell Death for Growth and Regression of Hormone-Dependent H-301 Hamster Kidney Tumors

  • Wilfried Bursch
  • Joachim Liehr
  • David Sirbasku
  • Rolf Schulte-Hermann


Cell death by apoptosis is conceived as an important regulatory process for the control of cell number in normal and preneoplastic tissue1–5. In the present study, the potential role of apoptosis for tumor growth was investigated. As a model system we used an estrogen dependent hamster kidney tumor cell line, which was designated H-301 line by Sirbasku and Kirkland6. H-301 cells were previously found to form tumors upon inoculation into hamsters treated with estrogen or diethylstilbestrol (DES7). A typical growth pattern of such tumors is shown in Fig. 1. Within 18 days after inoculation of a H-301 cell suspension tumors of about 1 g had developed. Continuation of DES treatment caused about a doubling of tumor weight within 8 days. However, when DES treatment was stopped tumor weight decreased by about 80% within 4 days after DES withdrawal. In Fig. 1 it is also shown that tumor growth could be reinitiated when DES treatment was resumed after an interruption for 4 days. Within 2 days after resumption of DES administration the tumors reached the weight they had before the interruption of DES treatment.


Necrotic Area Tumor Weight Syrian Hamster Cyproterone Acetate Actual Growth Rate 
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Copyright information

© Springer Science+Business Media New York 1988

Authors and Affiliations

  • Wilfried Bursch
    • 1
  • Joachim Liehr
    • 2
  • David Sirbasku
    • 3
  • Rolf Schulte-Hermann
    • 1
  1. 1.Institut für Tumorbiologie-KrebsforschungUniversitat WienAustria
  2. 2.Department of Pharmacology and ToxicologyUniversity of Texas Medical BranchGalvestonUSA
  3. 3.Department of Biochemistry and Molecular BiologyUniversity of Texas Medical SchoolHoustonUSA

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