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Reactive species promotion of head a...

Bradburn, Jennifer E.

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Reactive species promotion of head and neck squamous cell carcinoma .

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Reactive species promotion of head and neck squamous cell carcinoma ./
作者:	Bradburn, Jennifer E.
面頁冊數:	204 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6149.
Contained By:	Dissertation Abstracts International67-11B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3241688
ISBN:	9780542965319

Reactive species promotion of head and neck squamous cell carcinoma .
Bradburn, Jennifer E.

Reactive species promotion of head and neck squamous cell carcinoma . - 204 p.

Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6149.

Thesis (Ph.D.)--The Ohio State University, 2007.

Head and neck squamous cell carcinoma (HNSCC), which comprises 3% of all of the cancers in the U.S., is the most common form of oral cancer. The overall 5 year survival rate is 59%, however, this disease is associated with high morbidity. Current standard therapy involves surgical resection of the primary tumor followed by radiotherapy and/or chemotherapy. Many of these tumors involve structures essential for speech, taste, smell, breathing and eating. Surgical resection can compromise these functions as well as leave the patient horribly disfigured. In addition, 3-7% patients per year succumb to a second primary tumor at a related site as a complication of treatment. While in the US this disease is regarded as a preventable cancer with low prevalence it is the 8th most common cancer diagnosed in the world.

ISBN: 9780542965319Subjects--Topical Terms:

1017686
Biology, Cell.

Reactive species promotion of head and neck squamous cell carcinoma .
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245 1 0 $a Reactive species promotion of head and neck squamous cell carcinoma .
300 $a 204 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6149.
500 $a Adviser: Susan R. Mallery.
502 $a Thesis (Ph.D.)--The Ohio State University, 2007.
520 $a Head and neck squamous cell carcinoma (HNSCC), which comprises 3% of all of the cancers in the U.S., is the most common form of oral cancer. The overall 5 year survival rate is 59%, however, this disease is associated with high morbidity. Current standard therapy involves surgical resection of the primary tumor followed by radiotherapy and/or chemotherapy. Many of these tumors involve structures essential for speech, taste, smell, breathing and eating. Surgical resection can compromise these functions as well as leave the patient horribly disfigured. In addition, 3-7% patients per year succumb to a second primary tumor at a related site as a complication of treatment. While in the US this disease is regarded as a preventable cancer with low prevalence it is the 8th most common cancer diagnosed in the world.
520 $a Clinical evidence supports a contribution of sustained inflammation, reactive species (RS) and their sequelae in carcinogenesis. Studies in Chapter 2 focused on elucidating mechanisms by which RS facilitate HNSCC tumorigenesis and included evaluation of RS effects on sustained cell proliferation, induction of a proangiogenic environment and increased growth factor production. Proinflammatory and protumorigenic enzymes upregulated during inflammation include the RS-generating enzymes inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2. While clinical data show upregulation of iNOS and COX-2 in HNSCC development, mechanisms by which these cellular processes occur and downstream consequences have not been characterized. The purpose of this investigation was to assess the effects of reactive oxygen and nitrogen species on selected parameters of the HNSCC tumorigenic phenotype i.e. nuclear factor (NF)kappaB activation, sustained cell proliferation, and production of proinflammatory and proangiogenic proteins. RS donors included TNF, H2O2, NOC18 and SIN1. NFkappaB activation was determined by in situ immunostaining and reporter assay. Protein levels of VEGF, IL-8 and EGFR (determined by ELISA and immunoblot) assessed downstream effects of NFkappaB activation. Results showed that reactive oxygen (H2O2) and for the first time reactive nitrogen (SIN1) activated NFkappaB in HNSCC cells. Notably, TNF, H2O2, NOC18 and SIN1 increased IL-8, VEGF and EGFR protein levels. Our results indicate RS mediate HNSCC development by activation of NFkappaB followed by increased growth factor production.
520 $a Much of cancer research focus is now directed towards the development of a new generation of chemotherapeutics in an effort to prevent cancer. Chemoprevention refers to the use of pharmacologic or natural compounds to either inhibit the invasive phenotype of cancer by blocking progression of initiated cells, or by blocking or reversing immortalization of cancer cells. Goals of chemoprevention therapy must address changes at all levels of disease from clinical presentation to cellular and tissue levels.
520 $a N-acetyl-cysteine (NAC) has previously been identified as a potentially effective chemopreventative agent. As a precursor to L-cysteine, the rate limiting reactant in glutathione (GSH) synthesis, it possesses the innate ability to increase cellular stores of the powerful antioxidant GSH, and inhibit consequences of RS. Matrix metalloproteinases (MMPs) are a family of enzymes noted for their ability to degrade the extracellular matrix, which are activated by RS. Our laboratory recently determined a mechanism by which NAC can inhibit the extracellular activation of MMP-9 by preventing the cysteine switch step of activation. Their overexpression has been linked to the ability of tumors to invade, metastasize and release growth factors bound to proteins in the ECM.
520 $a Chapter 3 studies evaluate the effect of NAC treatment on the induction of MMP-2 and -9 mRNA as well as mRNA levels of the tissue inhibitors of MMPs (TIMP), namely TIMP-1 and -2. TIMP-1 and -2 bind to MMP-2 and -9 thus preventing activation of these enzymes. In addition we evaluate the effect of NAC treatment on RS induced activation of both NFkappaB and activator protein (AP)-1 transcription factors. We hypothesize that NAC pretreatment will block the activation of transcription factors AP-1 and NFkappaB which are upstream of MMP-2 and -9 production in response to RS treatment. Results demonstrated no significant response with respect to the transcription factors NFkappaB or AP-1. In addition, results demonstrated that mRNA levels of MMP-2 and -9 were not affected by NAC pretreatment prior to stimulus with RS. In contrast TIMP-1 and -2 mRNA increased in response to NAC pretreatment and stimulus with SF medium alone, H2O2, or SIN1. ELISA results, however demonstrated no significant changes in either MMP-2, -9, TIMP-1 or -2 proteins in the medium. Conclusions from Chapter 3 studies confirmed NAC pretreatment does not increase MMP-2 or -9 mRNA or protein, but does increase TIMP-1 and -2 mRNA and not extracellular protein. Results, from both Chapters 2 and 3, aid in understanding how RS promote tumorigenesis in HNSCC and how might antioxidants be used to reduce their impact.
590 $a School code: 0168.
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