Literature DB >> 816464

Regression kinetics of mouse skin papillomas.

F J Burns, M Vanderlaan, A Sivak, R E Albert.   

Abstract

The persistence and proliferation rate of mouse skin papillomas were studied in HA/ICR mice initiated with 7,12-dimethylbenz(a)anthracene and promoted three times weekly with phorbol myristate acetate. When the promoter treatments were stopped, rapid (half-time, 24 days) and slow (half-time, greater than 140 days) components of papilloma regression were observed. When the promoter dose was increased, the major effect was an increase among the rapidly regressing papillomas. Increases in the epidermal pulse-labeling index and the number of dermal inflammatory cells produced by phorbol myristate acetate in normal skin were reversible when the phorbol myristate acetate was stopped, but high pulse-labeling index values in papillomas were not reversible. Antithymocyte serum had no effect on regression, although ethylphenylpropriolate, a nonpromoting irritant, slowed the regression sufficiently to increase the half-time from 24 to 57 days. The action of the promoter in overcoming the regression tendency of the papillomas may explain certain features of the role of nonspecific irritation and the importance of promotion frequency in determining tumor yield.

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Year:  1976        PMID: 816464

Source DB:  PubMed          Journal:  Cancer Res        ISSN: 0008-5472            Impact factor:   12.701


  11 in total

1.  Carcinogen-induced mutations in the mouse c-Ha-ras gene provide evidence of multiple pathways for tumor progression.

Authors:  K Brown; A Buchmann; A Balmain
Journal:  Proc Natl Acad Sci U S A       Date:  1990-01       Impact factor: 11.205

2.  Proliferation, apoptosis, and survivin expression in a spectrum of melanocytic nevi.

Authors:  Scott R Florell; Anneli R Bowen; Adrianne N Hanks; Kelley J Murphy; Douglas Grossman
Journal:  J Cutan Pathol       Date:  2005-01       Impact factor: 1.587

3.  UVB-induced apoptosis drives clonal expansion during skin tumor development.

Authors:  Wengeng Zhang; Adrianne N Hanks; Kenneth Boucher; Scott R Florell; Sarah M Allen; April Alexander; Douglas E Brash; Douglas Grossman
Journal:  Carcinogenesis       Date:  2004-10-21       Impact factor: 4.944

4.  Tumor persistence and regression in skin carcinogenesis. An experimental study.

Authors:  F Stenbäck
Journal:  Z Krebsforsch Klin Onkol Cancer Res Clin Oncol       Date:  1978

5.  Cell-cell contact interactions conditionally determine suppression and selection of the neoplastic phenotype.

Authors:  Harry Rubin
Journal:  Proc Natl Acad Sci U S A       Date:  2008-04-23       Impact factor: 11.205

6.  Transfection of the EJ rasHa gene into keratinocytes derived from carcinogen-induced mouse papillomas causes malignant progression.

Authors:  J R Harper; D R Roop; S H Yuspa
Journal:  Mol Cell Biol       Date:  1986-09       Impact factor: 4.272

7.  A new method for the analysis of cohort studies: implications of the multistage theory of carcinogenesis applied to occupational arsenic exposure.

Authors:  C C Brown; K C Chu
Journal:  Environ Health Perspect       Date:  1983-04       Impact factor: 9.031

8.  Malignant conversion and metastasis of mouse skin tumors: a comparison of SENCAR and CD-1 mice.

Authors:  H Hennings; E F Spangler; R Shores; P Mitchell; D Devor; A K Shamsuddin; K M Elgjo; S H Yuspa
Journal:  Environ Health Perspect       Date:  1986-09       Impact factor: 9.031

9.  Approach to risk assessment for genotoxic carcinogens based on data from the mouse skin initiation-promotion model.

Authors:  F Burns; R Albert; B Altshuler; E Morris
Journal:  Environ Health Perspect       Date:  1983-04       Impact factor: 9.031

Review 10.  Alterations in epidermal biochemistry as a consequence of stage-specific genetic changes in skin carcinogenesis.

Authors:  S H Yuspa; A Kilkenny; C Cheng; D Roop; H Hennings; F Kruszewski; E Lee; J Strickland; D A Greenhalgh
Journal:  Environ Health Perspect       Date:  1991-06       Impact factor: 9.031

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