Looking back on 20 Years of, or an Experimental Protocol on �Mouse Skin-Painting Studies�

2015 ◽  
pp. 18-42 ◽  
Author(s):  
Peter Bernfeld
Keyword(s):  
Mouse Skin ◽  
Experimental Protocol ◽  
Skin Painting ◽  
Looking Back

SKH-1 mouse skin painting: A short-term assay to evaluate the tumorigenic activity of cigarette smoke condensate

2010 ◽  
Vol 192 (2) ◽  
pp. 155-161 ◽  
Author(s):  
E. Roemer ◽  
T.H. Ottmueller ◽  
H.-J. Urban ◽  
C. Baillet-Mignard
Keyword(s):  
Cigarette Smoke ◽  
Mouse Skin ◽  
Cigarette Smoke Condensate ◽  
Short Term ◽  
Tumorigenic Activity ◽  
Skin Painting

Carcinoma formation in NMRI mouse skin painting studies is a process suggesting greater than two stages

1995 ◽  
Vol 16 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Annette Kopp-Schneider ◽  
Christopher J. Portier
Keyword(s):  
Mouse Skin ◽  
Nmri Mouse ◽  
Two Stages ◽  
Skin Painting

scholarly journals The Role of Skin Painting in Predicting Lung Cancer

2007 ◽  
Vol 26 (4) ◽  
pp. 345-351 ◽  
Author(s):  
Z. Walaszek ◽  
M. Hanausek ◽  
T. J. Slaga
Keyword(s):  
Lung Cancer ◽  
Squamous Cell ◽  
Tobacco Smoke ◽  
Precancerous Lesions ◽  
Mouse Skin ◽  
Practical Method ◽  
Tumor Formation ◽  
Test Method ◽  
Epithelial Cancers ◽  
Skin Painting

The mouse skin cancer model provides an important system for studying mechanisms involved in the various stages of carcinogenesis and for bioassaying tobacco smoke constituents and additives for carcinogenic/cocarcinogenic and tumor-promoting properties as well as for identifying compounds that may inhibit tumor formation and malignant conversion. In addition, it is an excellent model for studying the formation of precancerous lesions as well as squamous cell carcinomas. It relates very well to other squamous cell carcinoma models and contributes to better understanding of the human epithelial cancers including lung cancer. The SENCAR mouse is an established model system demonstrated to be more sensitive than the B6C3F1 or Swiss CD-1 strains in the initiation/promotion skin-painting test method. Although the relationship between mouse skin tumors and any manifestation of the toxicity of tobacco smoke and other complex environmental mixtures in humans is unknown, the skin-painting model is the only assay that provides a practical method of obtaining a tumorigenic end point with cigarette smoke condensates and other complex mixtures. This assay provides a rapid response with relative ease of quantification of various parameters of tumorigenic response including tumor incidence, latency, multiplicity, and malignancy.

Computerization of data capture for mouse skin painting studies

1981 ◽  
Vol 12 (5) ◽  
pp. 419-431 ◽  
Author(s):  
C. Musy ◽  
K.T. Morgan ◽  
C.R.E. Coggins
Keyword(s):  
Mouse Skin ◽  
Data Capture ◽  
Skin Painting

scholarly journals The Composition of Cigarette Smoke: A Chronology of the Studies of Four Polycyclic Aromatic Hydrocarbons

2006 ◽  
Vol 22 (3) ◽  
pp. 208-254
Author(s):  
A Rodgman ◽  
TA Perfetti
Keyword(s):  
Polycyclic Aromatic Hydrocarbons ◽  
Cigarette Smoke ◽  
Aromatic Hydrocarbons ◽  
Tobacco Smoke ◽  
Mouse Skin ◽  
Laboratory Animals ◽  
Current Evidence ◽  
United States Department ◽  
Polycyclic Aromatic ◽  
Skin Painting

AbstractAmong the polycyclic aromatic hydrocarbons (PAHs), a major class of identified cigarette mainstream smoke (MSS) components, are several shown to be tumorigenic in laboratory animals and suspect as possible tumorigens to humans. To date, nearly 540 PAHs have been completely or partially identified in tobacco smoke [Rodgman and Perfetti (1)]. A detailed chronology is presented of studies on four much discussed PAHs identified in tobacco smoke, namely, benz[a]anthracene (B[a]A), its 7,12-dimethyl derivative (DMB[a]A), dibenz[a, h]anthracene (DB[a, h]A), and benzo[a]pyrene (B[a]P). Of the four, DMB[a]A, DB[a, h]A, and B[a]P are considered to be potently tumorigenic on mouse skin painting and subcutaneous injection. Opinions on the tumorigenicity of B[a]A to mouse skin vary. DMB[a]A is frequently used in tumorigenicity studies as an initiator. Examination of the number of tobacco smoke-related citations listed for these four PAHs reveals the enormous effort devoted since the early 1950s to B[a]P vs. the other three. An annotated chronology from 1886 to date describes the tobacco smoke-related research pertinent to these four PAHs, their discovery, isolation and/or identification, quantitation, and contribution to the observed biological activity of MSS or cigarette smoke condensate (CSC). Much of the major literature on these four PAHs in tobacco smoke is presented in order to permit the reader to decide whether the current evidence is sufficient to classify them as a health risk to smokers. There has certainly been a tremendous effort by researchers to learn about these PAHs over the past several decades. Each of these PAHs when tested individually has been shown to possess the following biological properties: 1) Mutagenicity in certain bacterial situations, 2) tumorigenicity in certain animal species, to varying degrees under various administration modes, and 3) a threshold limit below which no tumorigenesis occurs. For more than five decades, it has been known that some of the PAHs, when co-administered in pairs of a potent tumorigen plus a non-tumorigen or weak tumorigen, show inhibitory effects on the tumorigenicity of the most potent, e.g., B[a]A plus DB[a, h]A; B[a]A plus B[a]P; anthracene plus DB[a, h]A. Over the period studied, some regulatory agencies considered these tobacco smoke PAHs to be serious health concerns, others did not.With respect to cigarette MSS, certainly the ‘danger is in the dose’ for any MSS component tested singularly to be tumorigenic. But is the level of any of these MSS PAHs high enough to be of concern to smokers? The information herein presented indicates that over the last five decades the following has occurred: 1) The per cigarette yields of these four PAHs have decreased substantially, 2) compared to CSC or Federal Trade Commission (FTC) ‘tar’, their per cigarette yields have also decreased to a point that they may be below any significance biologically, and 3) the specific tumorigenicity in mouse skin-painting studies of the CSC has decreased. These are the three criteria originally proposed to define the ‘less hazardous’ cigarette. Actually, criterion 1) was first directed only at B[a]P. Previous studies highlighted the concern that some regulatory bodies had in attempting to understand why lung cancer and other forms of cancer seemed more prevalent in smokers. But cigarette smoking alone could not reconcile the evidence. Social, ethnic, environmental, and economic factors are also very important in understanding the entire biological effect. In fact, the level of B[a]P in CSC could only explain about 2% of its specific tumorigenicity observed in skin-painted mice and the combination of the levels of all the known tumorigenic PAHs in CSC could only explain about 3% of its tumorigenicity. Despite an 18-month study in the late 1950s, the search for a ‘supercarcinogen’ in MSS and CSC to explain the observed biological effects was unsuccessful. In addition, the exceptional study on MSS PAHs by United States Department of Agriculture (USDA) personnel in the 1970s indicated no ‘supercarcinogen’ was present. Only recently has the concept of complex mixtures in relation to the understanding of the complexity of carcinogenesis taken hold. Perhaps the reason why MSS is less tumorigenic than expected in humans is because of the presence of other MSS components that inhibit or prevent tumorigenesis. For example, it is well known that MSS contains numerous anticarcinogens present in quantities significantly greater than those of the PAHs of concern. When one reviews the history of these four PAHs in MSS or CSC it is clear that many unanswered questions remain.

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