Cancer Research The Future of Cancer Research: Science and Patient Impact  Cancer Health Disparities Conference 2009
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 23, 1651-1657, November 1, 1963]
© 1963 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fisher, B.
Right arrow Articles by Fisher, E. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fisher, B.
Right arrow Articles by Fisher, E. R.

Local Factors Affecting Tumor Growth

I. Effect of Tissue Homogenates*

Bernard Fisher and Edwin R. Fisher

( Department of Surgery, Laboratory of Surgical Research, and the Department of Pathology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania)

Previous studies demonstrated that liver damage produced by a variety of modalities enhanced the incidence and growth of experimentally induced hepatic metastases. Search for possible mechanisms responsible for this augmentation provided no evidence that a humoral factor related to hepatic damage or regeneration was responsible. It was considered, however, that direct contact of damaged cells with tumor cells could be a factor. Since little information was available relevant to the effect of normal or damaged cells upon adjacent neoplastic elements, studies were carried out, with tissue homogenates, to provide an environment for tumor cells somewhat akin to that in damaged liver.

Homogenates of various organs from adult animals given injections either simultaneously with tumor cells or at separate sites accelerated the onset and subsequent growth of tumor. Freezing or heating of tissues failed to eliminate this response, and species specificity was not a factor.

Injection of homogenate in one member of a parabiotic pair had a similar growth-promoting effect upon tumor growing in the other parabiont. Of particular interest was the occurrence of tumor at the site of homogenate injection in both single and parabiotic animals when this was separate from the location of tumor cell inoculation.

Speculation as to mechanisms responsible for these observations is entertained, and it is suggested that the tumor growth-promoting factor is a product of dead or dying normal cells rather than a humoral factor associated with regeneration.

* Supported by American Cancer Society Grant No. P-142 and U.S.P.H. Grants CA-05716 and CA-05949.

Received 5/15/63.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1963 by the American Association for Cancer Research.