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Title: Alternate applications of anticancer drugs on COS-7 normal cells.
Creator: Morris, Deborah., Harriet L. Wilkes Honors College
Abstract/Description: Anticancer drugs, including nocodazole and vinblastine, work by disrupting the dynamics of microtubules. Unfortunately, these drugs often produce numerous side effects, including nausea, vomiting, loss of appetite, loss of hair, increased chance of infection, and fatigue. My thesis research evaluated the efficacy of using repeated low doses of microtubule drugs instead of a single high dose, in an attempt to minimize side effects. Using nocodazole and vinblastine, I first established the...
Show moreAnticancer drugs, including nocodazole and vinblastine, work by disrupting the dynamics of microtubules. Unfortunately, these drugs often produce numerous side effects, including nausea, vomiting, loss of appetite, loss of hair, increased chance of infection, and fatigue. My thesis research evaluated the efficacy of using repeated low doses of microtubule drugs instead of a single high dose, in an attempt to minimize side effects. Using nocodazole and vinblastine, I first established the minimum effective concentration that disrupts the microtubules in normal human cells grown in vitro and treated cells with those concentrations over a period of several days. I found that microtubules were increasingly depolymerized as the days progressed. Next, I tested a combination of nocodazole and vinblastine at low concentrations.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/209996
Subject Headings: Cancer cells, Growth, Regulation, Antineoplastic agents, Physiological effect, Cell cycle, Effect of drugs on, Cancer, Chemotherapy
Format: Document (PDF)

Title: An investigation of the role of PAK6 tumorigenesis.
Creator: Roberts, JoAnn, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: The function and role of PAK6, serine/threonone kinase, in cancer progressionhas not yet been clearly identified. Several studies reveal that PAK6 may participate in key changes contributing to cancer progression such as cell survival, cell motility, and invasiveness. Basedon the membrane localization of PAK6 in prostate and breast cancer cells,we speculated that PAK6 plays a rolein cancer progression cells by localizing on the membrane and modifying proteins linked to motility and...
Show moreThe function and role of PAK6, serine/threonone kinase, in cancer progressionhas not yet been clearly identified. Several studies reveal that PAK6 may participate in key changes contributing to cancer progression such as cell survival, cell motility, and invasiveness. Basedon the membrane localization of PAK6 in prostate and breast cancer cells,we speculated that PAK6 plays a rolein cancer progression cells by localizing on the membrane and modifying proteins linked to motility and proliferation. We isolated the raft domain of breast cancer cells expressing either wild type (WT), constitutively active (SN), or kinase dead PAK6 (KM) and found that PAK6 is a membrane associated kinase which translocates from the plasma membrane to the cytosol when activated. The downstream effects of PAK6 are unknown ; however, results from cell proliferation assays suggest a growth regulatory mechanism.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3356888
Subject Headings: Apoptosis, Cancer, Etiology, Cancer cells, Proliferation, Cellular signal transduction, Cellular control mechanisms, Cell cycle, Regulation
Format: Document (PDF)

Title: Investigation of cell stiffness and cytoskeletal remodeling in response to inflammatory mediators using atomic force microscopy (AFM).
Creator: Magny, Sherlyne, Wojcikiewicz, Ewa P.
Date Issued: 2013-04-05
PURL: http://purl.flvc.org/fcla/dt/3361120
Subject Headings: Atomic force microscopy, Inflammation--Mediators, Cancer cells, Cytoskeleton
Format: Document (PDF)

Title: Devising a noncancerous model system to study multipolar spindle formation.
Creator: Nagarsheth, Nisha., Harriet L. Wilkes Honors College
Abstract/Description: Aneuploid tumor cells have characteristically unstable genomes which can be caused by mitotic defects such as multipolar spindles. Multipolarity relies upon the presence of extra centrosomes to form. However, some cells, both cancerous and noncancerous are able to avoid the formation of multipolar spindles through centrosomal clustering. Previous research has shown that there are a large number of genes whose activity contributes to the clustering activity, making analysis of individual...
Show moreAneuploid tumor cells have characteristically unstable genomes which can be caused by mitotic defects such as multipolar spindles. Multipolarity relies upon the presence of extra centrosomes to form. However, some cells, both cancerous and noncancerous are able to avoid the formation of multipolar spindles through centrosomal clustering. Previous research has shown that there are a large number of genes whose activity contributes to the clustering activity, making analysis of individual components of the process difficult. In order to better understand centrosomal clustering in cancer cells, we induced supernumerary centrosomes in a genomically normal cell line, RPE, to observe how the normal cells cope with extra centrosomes. Using colcemid to induce extra centrosomes in the RPE cell line, we observed an intact clustering mechanism in fixed cells. Further manipulation of the cells has allowed us to induce multipolarity in this cell line using various disrupters of cell-cycle checkpoint and dynein function.
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Date Issued: 2010
PURL: http://purl.flvc.org/FAU/3335107
Subject Headings: Centrosomes, Research, Cancer, Genetic aspects, Cellular signal transduction, Cell division
Format: Document (PDF)

Title: Deamplification of supernumerary centrosomes by centrosomal clustering.
Creator: Thomas, Ezekiel., Harriet L. Wilkes Honors College
Abstract/Description: Supernumerary centrosomes can arise in a cell through a variety of methods. The presence of supernumerary centrosomes has been observed in nearly all types of cancer and promotes chromosomal instability, with rates of incident increasing as the cancer progresses. An oral squamous cell carcinoma line was treated with hydroxyurea to induce supernumerary centrosomes in the cells. NuMA was then knocked down using shRNA to promote centrosomal clustering and bipolar mitotic division in cells with...
Show moreSupernumerary centrosomes can arise in a cell through a variety of methods. The presence of supernumerary centrosomes has been observed in nearly all types of cancer and promotes chromosomal instability, with rates of incident increasing as the cancer progresses. An oral squamous cell carcinoma line was treated with hydroxyurea to induce supernumerary centrosomes in the cells. NuMA was then knocked down using shRNA to promote centrosomal clustering and bipolar mitotic division in cells with supernumerary centrosomes. Immunofluorescence with an antibody against SAS 6 accuately stained the centrioles for observation. The cells exhibiting supernumerary centrosomes undergoing bipolar mitotic division were studied to look for a possible pattern in centrosomal clustering where the majority of centrosomes are at one pole with a single centrosome at the other pole. Initial results suggest the presence of such a mechanism, which would describe a previously unknown mechanism for cells to deamplify supernumerary centrosomes by centrosomal clustering.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3359328
Subject Headings: Centrosomes, Cell division, Cellular signal transduction, Cancer, Genetic aspects
Format: Document (PDF)

Title: Development of MnO2 Hollow Nanoparticles for Drug Delivery.
Creator: Greene, Allison, Kang, Yunqing, Florida Atlantic University, Department of Ocean and Mechanical Engineering, College of Engineering and Computer Science
Abstract/Description: This thesis reports the development of a novel drug delivery system consisting of hollow nanoparticles, formed from manganese dioxide (δ-MnO2) sheets, that are coated with polydopamine and folic acid to selectively target cancer cells. The biodegradability and colloidal stability of the uncoated hollow nanoparticles were investigated in comparison to solid MnO2 nanoparticles and graphene oxide sheets. The MnO2 hollow nanoparticles degraded at a faster rate and seem to have a higher surface...
Show moreThis thesis reports the development of a novel drug delivery system consisting of hollow nanoparticles, formed from manganese dioxide (δ-MnO2) sheets, that are coated with polydopamine and folic acid to selectively target cancer cells. The biodegradability and colloidal stability of the uncoated hollow nanoparticles were investigated in comparison to solid MnO2 nanoparticles and graphene oxide sheets. The MnO2 hollow nanoparticles degraded at a faster rate and seem to have a higher surface area and better colloidal dispersion than solid MnO2 nanoparticles. Xanthan gum was proven to improve colloidal dispersion of these hollow nanoparticles and were used for further cell studies. In this study, cancer and healthy cells were treated with coated hollow nanoparticles, and results indicate that this novel hollow nanoparticle may preferentially target and kill cancer cells. Particle aggregation has shown to be toxic to cells. Further studies with this novel drug delivery system may lead to a groundbreaking solution to targeted cancer therapy.
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Date Issued: 2020
PURL: http://purl.flvc.org/fau/fd/FA00013513
Subject Headings: Drug Delivery Systems, Nanoparticles, Manganese dioxide, Xanthan gum, Cancer cells
Format: Document (PDF)

Title: Efficacy of Combining 3-Bromopyruvate with Fenofibrate in Killing the Human Breast Cancer Cell Line MCF-7.
Creator: Graham, Rashean A., Hartmann, James X., Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
Abstract/Description: The goal of our research was to find a cancer treatment that was both effective and cancer specific, sparing immune and normal tissues. We evaluated the efficacy of a combinatorial treatment using the glycolytic inhibitor 3-bromopyruvate and the fatty acid metabolism inhibitor fenofibrate in cancer, immune and normal tissue cells lines. Treatment of the human breast cancer MCF-7 with 3-bromopyruvate and fenofibrate resulted in increased cell death and decreased colony formation. In the immune...
Show moreThe goal of our research was to find a cancer treatment that was both effective and cancer specific, sparing immune and normal tissues. We evaluated the efficacy of a combinatorial treatment using the glycolytic inhibitor 3-bromopyruvate and the fatty acid metabolism inhibitor fenofibrate in cancer, immune and normal tissue cells lines. Treatment of the human breast cancer MCF-7 with 3-bromopyruvate and fenofibrate resulted in increased cell death and decreased colony formation. In the immune cells known as peripheral blood mononuclear cells our combinatorial treatment displayed less toxicity than the traditional chemotherapy doxorubicin. Our combinatorial treatment displayed greater toxicity than doxorubicin towards an established breast cell line MCF- 10A, described in the literature as representing normal breast cells. We have shown for the first time a synergistic relationship between 3-bromopyruvate and fenofibrate.
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Date Issued: 2020
PURL: http://purl.flvc.org/fau/fd/FA00013556
Subject Headings: Breast--Cancer--Treatment, bromopyruvate, Fenofibrate, MCF-7 Cells
Format: Document (PDF)

Title: Cells and cocktails: antioxidants rescue carcinogen induced mitotic defects in both chromosomally stable and unstable cells.
Creator: Griffin, Isabel Sloan., Harriet L. Wilkes Honors College
Abstract/Description: Tumor cells are characterized by an increase in genomic instability, brought about by both chromosomal rearrangement and chromosomal instability. Both of these broad changes can be induced by exposure to carcinogens. During mitosis, cells can exhibit early and late lagging chromosomes, multipolar spindles or anaphase bridges, all of which contribute to genomic rearrantement. We have studied the link between exposure to carcinogen and prevalence of mitotic defect in both chromosomally stable...
Show moreTumor cells are characterized by an increase in genomic instability, brought about by both chromosomal rearrangement and chromosomal instability. Both of these broad changes can be induced by exposure to carcinogens. During mitosis, cells can exhibit early and late lagging chromosomes, multipolar spindles or anaphase bridges, all of which contribute to genomic rearrantement. We have studied the link between exposure to carcinogen and prevalence of mitotic defect in both chromosomally stable and unstable cell lines as well as ecamined the restorative effects of antioxidants in preventing mitotic defects. We have exposed MES-SA uterine cancer cells to vinyl chloride followed by exposure to an antioxidant : ascorbic acid, B-carotene, or lycopene. Treated cells were then scored for the prevalence of mitotic defects within the population and compared to controls. We have also investigated whether pre-treatment with the antioxidants will weaken the effects of carcinogen exposure in these cell lines.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3359304
Subject Headings: Cellular signal transduction, Cell differentiation, Medical genetics, Cancer, Genetic aspects, Antioxidants, Therapeutic use, Cancer, Chemoprevention, Apoptosis, Molecular aspects, Genetic regulation
Format: Document (PDF)

Title: The Impact of Pharmacological Targeting of Abnormal Tumor Metabolism with 3-Bromopyruvate on Dendritic Cell Mediated Tumoral Immunity.
Creator: Lang, Kevin, Hartmann, James X., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Studies have shown that tumor cells are susceptible to pharmacological targeting of their altered glycolytic metabolism with a variety of compounds that result in apoptosis. One such compound, 3-bromopyruvate (3-BP), has been shown to eradicate cancer in an animal model. However, no studies have shown whether the apoptotic fragments resulting from 3-BP treatment have the capacity to elicit an immunogenic cell death that activates dendritic cells, the primary antigen presenting cell in the...
Show moreStudies have shown that tumor cells are susceptible to pharmacological targeting of their altered glycolytic metabolism with a variety of compounds that result in apoptosis. One such compound, 3-bromopyruvate (3-BP), has been shown to eradicate cancer in an animal model. However, no studies have shown whether the apoptotic fragments resulting from 3-BP treatment have the capacity to elicit an immunogenic cell death that activates dendritic cells, the primary antigen presenting cell in the immune system. Immunogenic cell death is critical to eliciting an effective adaptive immune response that selectively kills additional target cells and generates immunological memory. We demonstrated that 3-bromopyruvate induced apoptosis in a number of different murine breast cancer cell lines, including the highly metastatic 4T1 line. The dying tumor cells stimulated immature dendritic cells (DCs) of the immortal JAWS II cell line to produce high levels of the pro-inflammatory cytokine IL-12, and increased their expression of key co-stimulatory molecules CD80 and CD86. The activated dendritic cells showed increased uptake of fragments from dying tumor cells that correlated with the increased levels of calreticulin on the surface and release of high group motility box 1 (HMGB1) of the latter following 3-BP treatment. Additionally, the anti-phagocytic signal CD47 present on breast cancer cells was reduced by treatment with 3-bromopyruvate when compared to the levels on untreated 4T1 cells. 3-BP treated breast cancer cells were able to activate dendritic cells through TLR4 signaling. Signaling was dependent on both the expression of surface calreticulin and on the extracellular release of high mobility group box 1 protein (HMGB1) during the process of immunogenic cell death. Killing by 3-BP was compared to mitoxantrone and doxorubicin, among the few chemotherapeutics that induce immunogenic cell death. 3-BP killing was likewise compared to camptothecin, a compound that fails to induce immunogenic cell death. Importantly, 3-BP did not markedly decrease the levels of the key peptide presenting molecule MHC I on DCs that were co-cultivated with dying tumor cells. Treatment of the highly aggressive triple negative BT-20 human breast cancer cell line with 3-BP also induced an immunogenic cell death, activating human dendritic cells in vitro.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004834
Subject Headings: Apoptosis., Cellular signal transduction., Cell death., Breast--Cancer--Treatment., Carrier proteins., Cancer--Molecular aspects., Biological interfaces.
Format: Document (PDF)

Title: Investigating the Role of CHI3L1 in Promoting Tumor Growth and Metastasis Using Mammary Tumor Models.
Creator: Libreros, Stephania, Iragavarapu-Charyulu, Vijaya, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Metastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with...
Show moreMetastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with inflammation. Using well-established models of breast cancer, we show that CHI3L1 is increased in the serum of tumor bearing mice. We found that CHI3L1 levels are increased at both the “pre-metastatic” and “metastatic stage” and that tumor cells, splenic, alveolar and interstitial macrophages; and myeloid derived population produce CHI3L1. Furthermore, we demonstrated that CHI3L1 has an inhibitory role on the expression of interferon-gamma (IFN γ) by T cells, while enhancing the production of pro-inflammatory mediators by macrophages such as Cchemokine ligand 2 (CCL2/MCP-1), Chemokine CX motif ligand 2 (CXCL2/IL-8) and matrix metalloproteinase-9 (MMP-9), all of which promote tumor growth and metastasis. We demonstrated that in vivo treatment of tumor-bearing mice with chitin microparticles, a TH1 adjuvant and a substrate for CHI3L1, promoted immune effector functions with increased production of IFN-γ but decreased CCL2/MCP-1, CXCL2/IL-8 and MMP-9 expression by splenic and pulmonary macrophages. Significantly, in vivo administration of chitin microparticles decreased tumor growth and pulmonary metastasis in mammary tumor bearing mice. These results suggest that CHI3L1 may play a role in tumor progression. Inflammation plays a pivotal role during tumor progression and metastasis by promoting the production of pro-inflammatory molecules such as CHI3L1. However, little is known about how CHI3L1 expression can affect secondary sites to enhance metastasis. In these studies, we demonstrated that CHI3L1 alters the cellular composition and inflammatory mediators that aid in the establishment of a metastatic niche for the support of infiltrating tumor cells leading to accelerated tumor progression. Since previous studies showed that CHI3L1 modulates inflammation, we determined the role of CHI3L1 in the context of pre-existing inflammation and metastasis. We found that CHI3L1 deficient mice with preexisting inflammation had decreased pro-inflammatory mediators, and significant reduction in tumor volume and metastasis compared to wild type controls. Preexisting inflammation and CHI3L1 may be driving the establishment of a premetastatic milieu in the lungs and aiding in the establishment of metastasis. Understanding the role of CHI3L1 in inflammation during tumor progression could result in the design of targeted therapies for breast cancer patients.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004517, http://purl.flvc.org/fau/fd/FA00004517
Subject Headings: Biopharmaceutics, Breast -- Cancer -- Etiology, Breast -- Cancer -- Molecular aspects, Cell differentiation, Chitinase, Glycoproteins -- Metabolism, Inflammation, Mice as laboratory animals
Format: Document (PDF)

Title: Manipulation of normal cells to produce a cancer-like mitotic phenotype.
Creator: Luffman, Christina., Harriet L. Wilkes Honors College
Abstract/Description: Most tumors contain multiple karyotypes due to genomic instability gained through chromosomal segregational defects. The variability of genomic changes within a population makes it difficult to study specific processes without the existence of confounding mutations. My project is to create a model system for observation of mitotic defects, specifically multipolar spindles, in a normal cell line, where the genome is intact. Induction of centrosome amplification is required for formation of...
Show moreMost tumors contain multiple karyotypes due to genomic instability gained through chromosomal segregational defects. The variability of genomic changes within a population makes it difficult to study specific processes without the existence of confounding mutations. My project is to create a model system for observation of mitotic defects, specifically multipolar spindles, in a normal cell line, where the genome is intact. Induction of centrosome amplification is required for formation of multipolar spindles. Treatments with colcemid showed a 10% increase in abnormal centrosome numbers over control. However, treatment with hydroxyurea and transfection of hMPSl showed little increase. Extra centrosomes are insufficient to drive multipolarity, therefore, I am using siRNA-mediated knockdown of Nek2 or HSET to decluster the extra centrosomes. Successful declustering will preferably show an increase in multipolar frequency, allowing us to study the formation and resolution of these structres to better understand how they contribute to aneuploidy and tumor progression.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/3325079
Subject Headings: Cell division, Karyokinesis, Cancer, Genetic aspects, Genomics, Cellular signal transduction, Centrosomes
Format: Document (PDF)

Title: Elucidating the role of Semaphorin 7A in breast cancer.
Creator: Garcia-Areas, Ramon A., lragavarapu-Charyulu, Vijaya, Florida Atlantic University, Charles E Schmidt College of Science, Department of Biomedical Science
Abstract/Description: Solid tumors can hijack many of the same programs used in neurogenesis to enhance tumor growth and metastasis, thereby generating a plethora of neurogenesis-related molecules including semaphorins Among them, we have identified Semaphorin7A (SEMA7A) in breast cancer We first used to the DA-3 mammary tumor model to determine the effect of tumor-derived SEMA7A on immune cells We found that tumor-derived SEMA7A can modulate the production of proangiogenic chemokines CXCL2/MIP-2 and CXCL 1, and...
Show moreSolid tumors can hijack many of the same programs used in neurogenesis to enhance tumor growth and metastasis, thereby generating a plethora of neurogenesis-related molecules including semaphorins Among them, we have identified Semaphorin7A (SEMA7A) in breast cancer We first used to the DA-3 mammary tumor model to determine the effect of tumor-derived SEMA7A on immune cells We found that tumor-derived SEMA7A can modulate the production of proangiogenic chemokines CXCL2/MIP-2 and CXCL 1, and prometastatic MMP-9 in macrophages We next aimed to determine the expression and function of SEMA7A in mammary tumor cells We found that SEMA7A is highly expressed in both metastatic human and murine breast cancer cells We show that both TGF-β and hypoxia elicits the production of SEMA 7 A in mammary cells SEMA7 A shRNA silencing in 4T1 cells resulted in decreased mesenchymal markers MMP-3, MMP-13, Vimentin and TGF-β) SEMA7A silenced cells show increased stiffness with reduced migratory and proliferative potential In vivo, SEMA7A silenced 4T1 tumor bearing mice showed decreased tumor growth and metastasis Genetic ablation of host-derived SEMA7A synergized to further decrease the growth and metastasis of 4T1 cells Our findings suggest novel functional roles for SEMA7A in breast cancer and that SEMA7A could be a novel therapeutic target to limit tumor growth and metastasis
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004802
Subject Headings: Breast--Cancer--Diagnosis, Semaphorins, Protein precursors, Cellular signal transduction, Cell receptors
Format: Document (PDF)

Title: Studies on the mechanism by which sulindac sensitizes cancer cells to oxidative stress.
Creator: Kreymerman, Alexander, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Sulindac is a known NSAID that has also been shown to have anti-cancer activity that is not related to its ability to inhibit COX 1 and 2. During the past 15 years there have been a large number of studies attempting to elucidate its mechanism of action. Our laboratory has shown that sulindac can both protect normal cells and enhance the killing of cancer cells under oxidative stress from H2O2 and TBHP. However, except for mitochondrial dysfunction and ROS production, the mechanism by which...
Show moreSulindac is a known NSAID that has also been shown to have anti-cancer activity that is not related to its ability to inhibit COX 1 and 2. During the past 15 years there have been a large number of studies attempting to elucidate its mechanism of action. Our laboratory has shown that sulindac can both protect normal cells and enhance the killing of cancer cells under oxidative stress from H2O2 and TBHP. However, except for mitochondrial dysfunction and ROS production, the mechanism by which sulindac sensitized the cancer cells to oxidative stress remains unknown. Results of this research project suggest that the effect of sulindac and oxidative stress not only involves mitochondrial ROS production, but also aspects of the preconditioning response. In normal cells this leads to survival by a preconditioning pathway, likely involving PKCε. . However, cancer cells react by initiating a pathway leading to apoptosis involving PKCδ.
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Date Issued: 2011
PURL: http://purl.flvc.org/FAU/3183124
Subject Headings: Proteins, Chemical modification, Cellular signal transduction, Biochemical markers, Diagnostic use, Drug resistance in cancer cells, Oxidation-reduction reaction
Format: Document (PDF)

FAU Theses and Dissertations (7)	+ -
Honors Student Theses (5)	+ -
FAU Undergraduate Student Research (1)	+ -

Cellular signal transduction (7)	+ -
Cancer (6)	+ -
Cancer cells (4)	+ -
Genetic aspects (4)	+ -
Cell division (3)	+ -

Centrosomes (3)	+ -
Apoptosis (2)	+ -
Cell cycle (2)	+ -
Cell differentiation (2)	+ -
Regulation (2)	+ -
Antineoplastic agents (1)	+ -
Antioxidants (1)	+ -
Apoptosis. (1)	+ -
Atomic force microscopy (1)	+ -
Biochemical markers (1)	+ -
Biological interfaces. (1)	+ -
Biopharmaceutics (1)	+ -
Breast -- Cancer -- Etiology (1)	+ -
Breast -- Cancer -- Molecular aspects (1)	+ -
Breast--Cancer--Diagnosis (1)	+ -
Breast--Cancer--Treatment (1)	+ -
Breast--Cancer--Treatment. (1)	+ -
Cancer--Molecular aspects. (1)	+ -
Carrier proteins. (1)	+ -
Cell death. (1)	+ -
Cell receptors (1)	+ -
Cellular control mechanisms (1)	+ -
Cellular signal transduction. (1)	+ -
Chemical modification (1)	+ -
Chemoprevention (1)	+ -

Electronic Thesis or Dissertation (7)	+ -
thesis (5)	+ -
poster (1)	+ -

Florida Atlantic University (5)	+ -
Harriet L. Wilkes Honors College (5)	+ -
Charles E. Schmidt College of Science (3)	+ -
Department of Biological Sciences (3)	+ -
Department of Biomedical Science (3)	+ -

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