Factors Influencing Experimental Carcinogenesis in the Hamster Cheek Pouch

Morris, Alvin L.

doi:10.1177/00220345610400012001

Cited by 212 publications

(95 citation statements)

References 11 publications

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“…The amount of carcinogen delivered to each animal was quite uniform using the "wiped brush" method (28). The right buccal pouches of the animals in groups A 1 and C 1 were treated with DMBA for 9 weeks, whereas the right buccal pouches of the animals in groups A 2 , B, and C 2 were treated with DMBA for 14 weeks (Fig.…”

Section: Carcinogenesismentioning

confidence: 99%

“…The hamster cheek pouch oral carcinogenesis model (HOCM) is the best known animal system that closely correlates with sequential common events involved in the development of human oral premalignant and malignant lesions (27,28). In the HOCM, development of epithelial dysplasia occurs at weeks 6 to 9 and development of invasive SCC at weeks 10 to 14 of the carcinogenesis process (27,29).…”

Section: Introductionmentioning

confidence: 99%

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In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

Katoumas

Nikitakis

Perrea

et al. 2015

Cancer Prevention Research

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The antineoplastic properties of the NSAID sulindac have long been studied. The purpose of this study was to explore sulindac's in vivo effects on oral squamous cell carcinoma (SCC) oncogenesis using the hamster cheek pouch oral carcinogenesis model (HOCM). Thirty Syrian golden hamsters were divided into three experimental and two control groups (n ¼ 6 each). The animals' right buccal pouches were treated with carcinogen for 9 weeks in one experimental and one control group and for 14 weeks in all other three groups. The animals of two experimental groups received sulindac from the 1st week and those of the third experimental group from the 10th week. After the end of carcinogenesis, treated buccal pouches were removed and examined. In animals treated with carcinogen for 14 weeks, development of oral SCC and tumor volume were significantly lower in animals that received sulindac from the first week of the experiment. Oral SCC developing in animals that received sulindac were more frequently well differentiated compared with the control group. In animals treated with carcinogen for 9 weeks, the animals that received sulindac developed lower grade of epithelial dysplasia. Proliferation index Ki-67 and positivity for the antiapoptotic molecule survivin were lower in the animals that received sulindac. Treatment with sulindac appears to delays the progression of oral premalignant lesions to oral SCC in the HOCM, also resulting in smaller and better differentiated tumors. These in vivo antineoplastic effects may be related to sulindac's ability to decrease cell proliferation and to prevent survivin expression.

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Section: Carcinogenesismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

Katoumas

Nikitakis

Perrea

et al. 2015

Cancer Prevention Research

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“…pouch produces premalignant and malignant changes that resemble premalignancy and malignancy of human oral mucosa (Morris, 1961). Also DMBA induced oral tumors expressed biochemical and molecular characteristics similar to that of human oral tumors (Shklar et al, 2009).…”

Section: Anti-cellmentioning

confidence: 99%

Anti-cell Proliferative and Anti-angiogenic Potential of Andrographolide During 7,12-Dimethylbenz(a)anthracene Induced Hamster Buccal Pouch Carcinogenesis

Singh

Manoharan²,

Vasudevan³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…4 His technique was later optimized 7 and has been employed extensively over the past half century. 3 SCCs are produced through a reproducible sequence of histopathologic changes, including hyperkeratosis and chronic inflammation at 4-6 weeks, hyperkeratosis and dysplastic hyperplasia at 6-8 weeks, carcinoma in situ at 8-10 weeks with invasive HNSCC occurring between 10 and 16 weeks after application.…”

Section: The Hamster Cheek Pouch Carcinogenesis Modelmentioning

confidence: 99%

Animal models for the study of squamous cell carcinoma of the upper aerodigestive tract: A historical perspective with review of their utility and limitations. Part A. Chemically‐induced de novo cancer, syngeneic animal models of HNSCC, animal models of transplanted xenogeneic human tumors

Smith

Thomas

2005

Intl Journal of Cancer

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Understanding the complex histological, genetic and molecular changes that lead to malignant transformation of squamous epithelia of the head and neck will likely guide the development of methods for improved diagnosis, monitoring and treatment of head and neck squamous cell carcinoma (HNSCC). The development and use of animal models that closely mimic the histopathology and molecular pathogenesis of HNSCC in humans would greatly expand the research possibilities and provide a means of testing potential therapeutic agents. However, many available animal models of HNSCC fall short of this objective. In order for investigators to select the appropriate model to answer scientific questions, it is important to understand the benefits and limitations of available animal models for the study of HNSCC. The purpose of this work is to give an overview of the most pertinent animal models of HNSCC, and to discuss future directions of research in this field. ' 2005 Wiley-Liss, Inc.Head and neck squamous cell carcinoma (HNSCC) involves the upper aerodigestive tract and can destroy the structure and function of organs involved in voice, speech, taste, smell and hearing, as well as vital structures necessary for survival. Approximately half of all patients with HNSCC have advanced stage disease at the time of diagnosis, with an expected 5-year survival rate between 10 and 40%.1 Despite treatments that may consist of mutilating surgery, radiotherapy and/or chemotherapy, overall long-term survival remains low due to uncontrollable persistent or recurrent disease. The survival rate of patients with locoregional and distant recurrences has highlighted the need for new approaches for diagnosis and treatment. To this end, a better understanding of the genetic, molecular and immunoregulatory processes leading to neoplastic transformation and progression of HNSCC is needed, so that novel and more effective diagnostic and therapeutic approaches can be designed.Although in vitro study systems are useful for studying the interactions between different cell populations in culture and are convenient and simple to use, they do not reproduce the complexity of HNSCC. For this reason, the development of new therapies will require clinically relevant animal models of HNSCC. Adequate animal models are necessary to test the translational potential of preventive and therapeutic agents, as well as to understand the biological mechanisms of epithelial carcinogenesis and progression. The ideal experimental animal tumor model for HNSCC must reproduce the characteristic features of the disease, including the complicated patterns of tumor-host interactions such as immune response, angiogenesis, invasion and metastasis. In the ideal model, clinical symptoms and laboratory abnormalities should be similar to the human disease and therapeutic agents should be as effective in both systems. The ideal model must also be easy to use, accessible to genetic and immunologic manipulations, reproducible and progress rapidly to allow timely investigations.Animal mod...

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Factors Influencing Experimental Carcinogenesis in the Hamster Cheek Pouch

Cited by 212 publications

References 11 publications

In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

In VivoAntineoplastic Effects of the NSAID Sulindac in an Oral Carcinogenesis Model

Anti-cell Proliferative and Anti-angiogenic Potential of Andrographolide During 7,12-Dimethylbenz(a)anthracene Induced Hamster Buccal Pouch Carcinogenesis

Animal models for the study of squamous cell carcinoma of the upper aerodigestive tract: A historical perspective with review of their utility and limitations. Part A. Chemically‐induced de novo cancer, syngeneic animal models of HNSCC, animal models of transplanted xenogeneic human tumors

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