In Vivo Interaction of Cis‐platinum and Fosfomycin on Squamous Cell Carcinoma

Tandy, James R.; Tandy, Richard D.; Farris, P.; Truelson, John M.

doi:10.1097/00005537-200007000-00029

Cited by 13 publications

(2 citation statements)

References 11 publications

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“…Systemic toxicities such as ototoxicity and nephrotoxicity continues to be the primary dose-limiting factor. 5 Various drug delivery systems have been investigated for local delivery of cisplatin and other anticancer drugs to limit such toxicities. Two such systems that have been studied extensively and tested in clinical trials are Intradose and OPLA-Pt.…”

Section: Discussionmentioning

confidence: 99%

Biodegradable polymer–mediated intratumoral delivery of cisplatin for treatment of human head and neck squamous cell carcinoma in a chimeric mouse model

Chen¹,

Kuriakose²,

Zhou³

et al. 2003

Head & Neck

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Section: Discussionmentioning

confidence: 99%

Biodegradable polymer–mediated intratumoral delivery of cisplatin for treatment of human head and neck squamous cell carcinoma in a chimeric mouse model

Chen¹,

Kuriakose²,

Zhou³

et al. 2003

Head & Neck

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“…They consider that FOS can be used as a potential antidote for the dose-limiting ototoxicity and nephrotoxicity of cisplatin. Tandy et al [42] showed that FOS does not inhibit the tumoricidal activity of this chemotherapeutic agent and that FOS in combination with cisplatin may be useful in treating advanced, and possibly relatively chemoresistant, squamous cell carcinoma of head and neck. They also found that mice treated with FOS had longer survival, which is probably due to lessening of immediate cisplatin systemic toxicity.…”

Section: Discussionmentioning

confidence: 99%

Fosfomycin protects intestinal cells from nuclear changes suggestive of deoxynivalenol-induced apoptosis

et al. 2020

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Background: Fosfomycin (FOS) is a broad-spectrum antibiotic that inhibits cell wall synthesis. It has bactericidal activity against both gram-positive and gram-negative bacteria. FOS also promotes phagocytosis, has immunomodulatory effects, and protects against the toxicity caused by other drugs. On the contrary, deoxynivalenol (DON) causes cytotoxicity on tissues of rapid growth and fast turnover. Objectives: The aim of this study was to determine the percentage of nuclear changes indicative of DONinduced apoptosis on intestinal cell cultures (Caco-2) and to evaluate the protective effect of FOS on mycotoxin-exposed cells. Materials and Methods: Cell cultures were treated as follows: (1) DON: 2.8 µg/mL, (2) calcium FOS: 580 µg/mL, (3) DON 2.8 µg/mL + calcium FOS 580 µg/mL, and (4) negative control. Nuclear morphology was evaluated in fixed cells stained with 4′,6-diamino-2-phenylindol and then visualized under an immunofluorescence microscope. Results: Percentages of cells with nuclear changes were significantly higher in cells treated with DON (31.53% ± 4.17%) compared to those incubated with the antibiotic in conjunction with the mycotoxin (5.63% ± 4.23%). On the contrary, there were no significant differences between cells incubated with DON + FOS and cells incubated only with the antibiotic (1.10% ± 1.55%) when compared to the negative control (3.50% ± 0.09%). Conclusion:The results from this study showed that DON induces nuclear changes suggestive of apoptosis in intestinal cells and that FOS can protect cells from DNA damage. Further studies are needed to determine whether DON induces apoptosis only on cells of epithelial origin and to understand the implications of FOS protective effect under in vivo conditions.

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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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In Vivo Interaction of Cis‐platinum and Fosfomycin on Squamous Cell Carcinoma

Cited by 13 publications

References 11 publications

Biodegradable polymer–mediated intratumoral delivery of cisplatin for treatment of human head and neck squamous cell carcinoma in a chimeric mouse model

Biodegradable polymer–mediated intratumoral delivery of cisplatin for treatment of human head and neck squamous cell carcinoma in a chimeric mouse model

Fosfomycin protects intestinal cells from nuclear changes suggestive of deoxynivalenol-induced apoptosis

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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