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Melanoma

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Articles 1 - 30 of 32

Full-Text Articles in Cancer Biology

Mechanisms And Immunogenicity Of Nspef-Induced Cell Death In B16f10 Melanoma Tumors, Alessandra Rossi, Olga N. Pakhomova, Andrei G. Pakhomov, Samantha Weygandt, Anna A. Bulysheva, Len E. Murray, Peter A. Mollica, Claudia Muratori Jan 2019

Mechanisms And Immunogenicity Of Nspef-Induced Cell Death In B16f10 Melanoma Tumors, Alessandra Rossi, Olga N. Pakhomova, Andrei G. Pakhomov, Samantha Weygandt, Anna A. Bulysheva, Len E. Murray, Peter A. Mollica, Claudia Muratori

Bioelectrics Publications

Accumulating data indicates that some cancer treatments can restore anticancer immunosurveillance through the induction of tumor immunogenic cell death (ICD). Nanosecond pulsed electric fields (nsPEF) have been shown to efficiently ablate melanoma tumors. In this study we investigated the mechanisms and immunogenicity of nsPEF-induced cell death in B16F10 melanoma tumors. Our data show that in vitro nsPEF (20-200, 200-ns pulses, 7 kV/cm, 2 Hz) caused a rapid dose-dependent cell death which was not accompanied by caspase activation or PARP cleavage. The lack of nsPEF-induced apoptosis was confirmed in vivo in B16F10 tumors. NsPEF also failed to trigger ICD-linked responses ...


Genome-Wide Screening Identifies Genes And Biological Processes Implicated In Chemoresistance And Oncogene-Induced Apoptosis, Tengyu Ko Oct 2018

Genome-Wide Screening Identifies Genes And Biological Processes Implicated In Chemoresistance And Oncogene-Induced Apoptosis, Tengyu Ko

LSU Doctoral Dissertations

Anti-proliferative responses such as senescence and apoptosis are often used by normal cells to combat oncogenic insults and to prevent tumorigenesis. However, oncogenic mutations are frequently found in cancers, suggesting that additional mutations may occur to facilitate the bypass of these anti-proliferative responses. It is believed that some of these additional mutations may also contribute to the chemoresistance of cancers. This dissertation focused on identifying novel genes and biological processes implicated in chemoresistance and tumorigenesis.

Cisplatin-based chemotherapeutic regimens are frequently used for treatments of solid tumors. However, tumor cells may have inherent or acquired resistance to cisplatin, and the underlying ...


Periostin Antisense Oligonucleotide Suppresses Bleomycin-Induced Formation Of A Lung Premetastatic Niche For Melanoma, Takashi Semba, Eiji Sugihara, Nagisa Kamoshita, Sayaka Ueno, Keitaro Fukuda, Masafumi Yoshino, Kazumasa Takao, Kazunori Yoshikawa, Kenji Izuhara, Yoshimi Arima, Makoto Suzuki, Hideyuki Saya May 2018

Periostin Antisense Oligonucleotide Suppresses Bleomycin-Induced Formation Of A Lung Premetastatic Niche For Melanoma, Takashi Semba, Eiji Sugihara, Nagisa Kamoshita, Sayaka Ueno, Keitaro Fukuda, Masafumi Yoshino, Kazumasa Takao, Kazunori Yoshikawa, Kenji Izuhara, Yoshimi Arima, Makoto Suzuki, Hideyuki Saya

Open Access Articles

Metastasis is the leading cause of cancer death. A tumor-supportive microenvironment, or premetastatic niche, at potential secondary tumor sites plays an important role in metastasis, especially in tumor cell colonization. Although a fibrotic milieu is known to promote tumorigenesis and metastasis, the underlying molecular contributors to this effect have remained unclear. Here we show that periostin, a component of the extracellular matrix that functions in tissue remodeling, has a key role in formation of a fibrotic environment that promotes tumor metastatic colonization. We found that periostin was widely expressed in fibrotic lesions of mice with bleomycin-induced lung fibrosis, and that ...


Rho Inhibition Promotes Vemurafenib Resistance In Braf Mutant Melanoma, Jeremy Bobera, Christopher Stipp Jan 2018

Rho Inhibition Promotes Vemurafenib Resistance In Braf Mutant Melanoma, Jeremy Bobera, Christopher Stipp

Honors Theses at the University of Iowa

Current treatments for patients with BRAF mutated melanoma show limited success utilizing the drug vemurafenib by only temporarily stopping cancer cell growth. Eventually BRAF mutated cells come back completely resistant to vemurafenib. The mechanisms behind emerging resistance are not well understood, yet studies suggest that actin polymerization through Rho small family GTPase signaling have an important role. In an attempt to address this working hypothesis we created an in vitro model using the A375 cell line and treated the cells with vemurafenib combined with RNAi knockdowns of Rho or using a drug named fasudil, which inhibits ROCK kinase a downstream ...


Melk Promotes Melanoma Growth By Stimulating The Nf-Kappab Pathway, Radoslav Janostiak, Navin Rauniyar, Tukiet T. Lam, Jianhong Ou, Lihua Julie Zhu, Michael R. Green, Narendra Wajapeyee Dec 2017

Melk Promotes Melanoma Growth By Stimulating The Nf-Kappab Pathway, Radoslav Janostiak, Navin Rauniyar, Tukiet T. Lam, Jianhong Ou, Lihua Julie Zhu, Michael R. Green, Narendra Wajapeyee

Open Access Articles

Melanoma accounts for more than 80% of skin cancer-related deaths, and current therapies provide only short-term benefit to patients. Here, we show in melanoma cells that maternal embryonic leucine zipper kinase (MELK) is transcriptionally upregulated by the MAPK pathway via transcription factor E2F1. MELK knockdown or pharmacological inhibition blocked melanoma growth and enhanced the effectiveness of BRAFV600E inhibitor against melanoma cells. To identify mediators of MELK function, we performed stable isotope labeling with amino acids in cell culture (SILAC) and identified 469 proteins that had downregulated phosphorylation after MELK inhibition. Of these proteins, 139 were previously reported as substrates of ...


Comparative Oncogenomics Identifies Novel Regulators And Clinical Relevance Of Neural Crest Identities In Melanoma, Arvind M. Venkatesan Dec 2017

Comparative Oncogenomics Identifies Novel Regulators And Clinical Relevance Of Neural Crest Identities In Melanoma, Arvind M. Venkatesan

GSBS Dissertations and Theses

Cancers often resurrect embryonic molecular programs to promote disease progression. In melanomas, which are tumors of the neural crest (NC) lineage, a molecular signature of the embryonic NC is often reactivated. These NC factors have been implicated in promoting pro-tumorigenic features like proliferation, migration and therapy resistance. However, the molecular mechanisms that establish and maintain NC identities in melanomas are largely unknown. Additionally, whether the presence of a NC identity has any clinical relevance for patient melanomas is also unclear. Here, using comparative genomic approaches, I have a) identified a novel role for GDF6-activated BMP signaling in reawakening a NC ...


Identification Of Kit As A Suppressor Of Brafv600e-Mutant Melanoma, James V. Neiswender Nov 2017

Identification Of Kit As A Suppressor Of Brafv600e-Mutant Melanoma, James V. Neiswender

GSBS Dissertations and Theses

Genetic changes acquired in the pigment producing cells of the skin, called melanocytes, can lead to formation of the deadly cancer melanoma. Mutations or amplifications leading to the activation of the RAS/MAPK pathway occur in more than 90% of melanomas. Melanocyte development and survival requires the stimulation of this pathway by the receptor tyrosine kinase (RTK) KIT. In ~2% of melanomas, oncogenic KIT mutations drive tumor formation; however, the majority of melanomas lose wild-type KIT expression, suggesting that KIT could suppress melanoma formation. In human melanoma patients of The Cancer Genome Atlas (TCGA), we found an association between BRAF ...


Abl Kinase Regulation By Braf/Erk And Cooperation With Akt In Melanoma, Aditi Jain, Rakshamani Tripathi, Courtney P. Turpin, Chi Wang, Rina Plattner Aug 2017

Abl Kinase Regulation By Braf/Erk And Cooperation With Akt In Melanoma, Aditi Jain, Rakshamani Tripathi, Courtney P. Turpin, Chi Wang, Rina Plattner

Pharmacology and Nutritional Sciences Faculty Publications

The melanoma incidence continues to increase, and the disease remains incurable for many due to its metastatic nature and high rate of therapeutic resistance. In particular, melanomas harboring BRAFV600E and PTEN mutations often are resistant to current therapies, including BRAF inhibitors (BRAFi) and immune checkpoint inhibitors. Abl kinases (Abl/Arg) are activated in melanomas and drive progression; however, their mechanism of activation has not been established. Here we elucidate a novel link between BRAFV600E/ERK signaling and Abl kinases. We demonstrate that BRAFV600E/ERK play a critical role in binding, phosphorylating and regulating Abl localization and Abl ...


Tumor Formation In Response To Loss Of Chromatin Remodeler Chd5 In Zebrafish, Taylor R. Sabato, Erin L. Sorlien, Dr. Joseph P. Ogas Aug 2017

Tumor Formation In Response To Loss Of Chromatin Remodeler Chd5 In Zebrafish, Taylor R. Sabato, Erin L. Sorlien, Dr. Joseph P. Ogas

The Summer Undergraduate Research Fellowship (SURF) Symposium

Chromodomain helicase DNA binding protein 5 (CHD5) has been identified as a tumor suppressor in humans. Deletion or mutation of CHD5 has been observed in numerous cancers, including neuroblastoma and melanoma. We hypothesize that chd5 is also a tumor suppressor in zebrafish, a powerful model system to study tumorigenesis. Many genes involved in tumorigenesis are conserved in zebrafish, and they develop fully penetrant tumor phenotypes. We have created chd5 knock-out zebrafish using CRISPR/Cas9 and are monitoring them for tumor development. In addition to the chd5 knock-outs, we are undertaking a double-mutant approach by coupling loss of ...


Inhibition Of Pannexin 1 Reduces Tumorigenic Properties Of Human Melanoma, Taylor J. Freeman Jul 2017

Inhibition Of Pannexin 1 Reduces Tumorigenic Properties Of Human Melanoma, Taylor J. Freeman

Electronic Thesis and Dissertation Repository

Pannexin 1 (PANX1) is a channel-forming glycoprotein that allows the passage of important signaling molecules, including ATP. We examined PANX1 levels in a panel of human melanomas and evaluated its potential as an effective target for melanoma therapy. We are the first to report endogenous PANX1 levels in multiple human melanoma cell lines, patient-derived melanoma biopsies, and primary melanoma cells. Treatment with two PANX1 channel blockers, Carbenoxolone (CBX) and Probenecid (PBN), on A375 and A375-MA2 melanoma cells significantly reduced cell growth and migration, and increased the production of melanin, a marker for a melanocytic-like phenotype. Daily treatment with CBX or ...


Paracrine Regulation Of Melanocyte Genomic Stability: A Focus On Nucleotide Excision Repair, Stuart Gordon Jarrett, Katharine Marie Carter, John August D'Orazio May 2017

Paracrine Regulation Of Melanocyte Genomic Stability: A Focus On Nucleotide Excision Repair, Stuart Gordon Jarrett, Katharine Marie Carter, John August D'Orazio

Markey Cancer Center Faculty Publications

UV radiation is a major environmental risk factor for the development of melanoma by causing DNA damage and mutations. Resistance to UV damage is largely determined by the capacity of melanocytes to respond to UV injury by repairing mutagenic photolesions. The nucleotide excision repair (NER) pathway is the major mechanism by which cells correct UV photodamage. This multistep process involves the basic steps of damage recognition, isolation, localized strand unwinding, assembly of a repair complex, excision of the damage‐containing strand 3′ and 5′ to the photolesion, synthesis of a sequence‐appropriate replacement strand, and finally ligation to restore continuity ...


The Soy-Derived Peptide Lunasin Inhibits Invasive Potential Of Melanoma Initiating Cells, Chris Shidal, Jun-Ichi Inaba, Kavitha Yaddanapudi, Keith R. Davis Mar 2017

The Soy-Derived Peptide Lunasin Inhibits Invasive Potential Of Melanoma Initiating Cells, Chris Shidal, Jun-Ichi Inaba, Kavitha Yaddanapudi, Keith R. Davis

Plant Pathology Faculty Publications

Lunasin is a 44 amino acid peptide with multiple functional domains including an aspartic acid tail, an RGD domain, and a chromatin-binding helical domain. We recently showed that Lunasin induced a phenotype switch of cancer initiating cells (CIC) out of the stem compartment by inducing melanocyte-associated differentiation markers while simultaneously reducing stem-cell-associated transcription factors. In the present study, we advance the hypothesis that Lunasin can reduce pools of melanoma cells with stem cell-like properties, and demonstrate that Lunasin treatment effectively inhibits the invasive potential of CICs in vitro as well as in vivo in a mouse experimental metastasis model. Mice ...


Melanoma Mystery, Roger J. Davis Jan 2017

Melanoma Mystery, Roger J. Davis

Davis Lab Publications

Biological variability has confounded efforts to confirm the role of PREX2 mutations in melanoma.


Melanocortin 1 Receptor: Structure, Function, And Regulation, Erin M. Wolf Horrell, Mary C. Boulanger, John A. D'Orazio May 2016

Melanocortin 1 Receptor: Structure, Function, And Regulation, Erin M. Wolf Horrell, Mary C. Boulanger, John A. D'Orazio

Physiology Faculty Publications

The melanocortin 1 receptor (MC1R) is a melanocytic Gs protein coupled receptor that regulates skin pigmentation, UV responses, and melanoma risk. It is a highly polymorphic gene, and loss of function correlates with a fair, UV-sensitive, and melanoma-prone phenotype due to defective epidermal melanization and sub-optimal DNA repair. MC1R signaling, achieved through adenylyl cyclase activation and generation of the second messenger cAMP, is hormonally controlled by the positive agonist melanocortin, the negative agonist agouti signaling protein, and the neutral antagonist β-defensin 3. Activation of cAMP signaling up-regulates melanin production and deposition in the epidermis which functions to limit UV ...


Identification Of Gdf-6 Blocking Antibodies As Anti-Melanoma Therapeutics, Ejemel Monir, Danielle Wisheart, Alec Gramann, Arvind Venkatesan, Mark S. Klempner, Craig J. Ceol, Yang Wang May 2016

Identification Of Gdf-6 Blocking Antibodies As Anti-Melanoma Therapeutics, Ejemel Monir, Danielle Wisheart, Alec Gramann, Arvind Venkatesan, Mark S. Klempner, Craig J. Ceol, Yang Wang

UMass Center for Clinical and Translational Science Research Retreat

Through comparative oncogenomic studies and functional analyses, we have identified the bone morphogenetic protein (BMP) factor GDF6 as a new melanoma oncogene. The secreted, carboxy-terminal portion of GDF6 is the active form that binds to cell-surface receptors to initiate BMP signaling. Targeted antibodies directed against secreted proteins are a proven therapeutic modality in several diseases.

To develop therapeutic antibodies against the active form of GDF6, we generated a panel of monoclonal antibodies. Due to the high similarity of human and mouse GDF6 proteins, the C-terminal GDF6 protein was expressed as bacterial recombinant protein with fusion tags to enhance immunogenicity. The ...


Developing Anti-Gdf6 Therapeutics For Treatment Of Advanced Melanoma, Alec Gramann, Arvind Venkatesan, Ejemel Monir, Danielle Wisheart, Yan Wang, Craig J. Ceol May 2016

Developing Anti-Gdf6 Therapeutics For Treatment Of Advanced Melanoma, Alec Gramann, Arvind Venkatesan, Ejemel Monir, Danielle Wisheart, Yan Wang, Craig J. Ceol

UMass Center for Clinical and Translational Science Research Retreat

Melanoma, the leading cause of skin cancer death in the U.S., is increasing in incidence. Targeted therapies have been approved for treatment of advanced melanoma, but few patients experience extended survival benefit. In order to combat poor outcomes, new therapeutic targets are needed. Using cross-species oncogenomic analyses, our lab has identified a novel melanoma driver, Growth differentiation factor 6 (GDF6), a secreted bone morphogenetic protein (BMP) ligand that is amplified and overexpressed in human melanomas. Functional analyses show GDF6 acts via the BMP-SMAD1 pathway as a pro-survival factor in melanomas. Inhibiting GDF6 or the BMP pathway using shRNAs or ...


Alternative Methods For The Treatment Of Chemo-Resistant Cancers, Kaitlyn Wong Jan 2016

Alternative Methods For The Treatment Of Chemo-Resistant Cancers, Kaitlyn Wong

Doctoral Dissertations

Great strides have been made in cancer therapy in the past century, yet it remains one of the leading causes of death in the United States today. This work aimed to shed light on novel methods to treat a variety of aggressive and often chemo-resistant cancers both in vitro and in vivo.

The first aim of this work was to evaluate the therapeutic efficacy of poly(methacryloyloxyethyl phosphorylcholine) (polyMPC) prodrugs compared to standard chemotherapeutic agents. Conjugation of polyMPC to drugs such as doxorubicin (Dox) can result in its improved solubility, prolonged half-life and therapeutic efficacy. PolyMPC and polyMPC-Dox (at a ...


The Role Of Endothelin 3 In Melanoma Progression And Metastasis, Nikeisha L. Chin Nov 2015

The Role Of Endothelin 3 In Melanoma Progression And Metastasis, Nikeisha L. Chin

FIU Electronic Theses and Dissertations

Endothelin receptor b (Ednrb) and its ligand Endothelin 3 (Edn3) have been implicated in melanoma. Several studies have shown an upregulation of EDNRB and EDN3 at both the protein and mRNA levels, as melanoma becomes more aggressive. This study investigated the putative role played by Edn3 over-expression in melanoma progression and angiogenesis in vivo. We crossed Tg(Grm1)Epv transgenic mice that aberrantly express metabotropic glutamate receptor1 under the Dopachrome tautomerase promoter, leading to spontaneous melanocytic lesions in the ears and tails that do not metastasize, with transgenics that overexpress Edn3 under the Keratin 5 promoter (K5-Edn3) or overexpress Ednrb ...


Insights Into Melanocyte Regeneration And Melanoma Initiation Using The Zebrafish Model System: A Dissertation, Sharanya Iyengar Oct 2015

Insights Into Melanocyte Regeneration And Melanoma Initiation Using The Zebrafish Model System: A Dissertation, Sharanya Iyengar

GSBS Dissertations and Theses

During regeneration, cells must coordinate proliferation and differentiation to rebuild tissues that are lost. Understanding how source cells execute the regeneration process has been a longstanding goal in regenerative biology with implications in wound healing and cell replacement therapies. Melanocytes are pigment-producing cells in the skin of vertebrates that can be lost during hair graying, injury and disease-related depigmentation. Melanoma is an aggressive skin cancer that develops from melanocytes, and it is hypothesized that melanoma cells have properties that are similar to melanocyte stem cells.

To gain insight into melanocyte regeneration we set out to identify the source of regeneration ...


Uv-Induced Melanoma Mouse Model Dependent On Endothelin 3 Over-Expression, Ana Paula Benaduce Oct 2014

Uv-Induced Melanoma Mouse Model Dependent On Endothelin 3 Over-Expression, Ana Paula Benaduce

FIU Electronic Theses and Dissertations

Melanoma is one of the most aggressive types of cancer. It originates from the transformation of melanocytes present in the epidermal/dermal junction of the human skin. It is commonly accepted that melanomagenesis is influenced by the interaction of environmental factors, genetic factors, as well as tumor-host interactions. DNA photoproducts induced by UV radiation are, in normal cells, repaired by the nucleotide excision repair (NER) pathway. The prominent role of NER in cancer resistance is well exemplified by patients with Xeroderma Pigmentosum (XP). This disease results from mutations in the components of the NER pathway, such as XPA and XPC ...


The Association Between The Il-1 Pathway, Isaac C. Wun May 2014

The Association Between The Il-1 Pathway, Isaac C. Wun

UT GSBS Dissertations and Theses (Open Access)

Cutaneous malignant melanoma (CMM) is a potentially lethal malignancy that warrants attention and further research, as it is known to that there is an increasing rate of incidence in theUnited States, and it is also known that exposure to UV light is its most crucial risk factor, and family history of melanoma is also an important risk factor. Melanoma is an aggressive and lethal cancer in humans. There are an estimated new 132,000 melanoma cases annually worldwide, and the trend has doubled in the past 20 years. However, attempts to treat melanoma have encountered considerable resistance and remained ineffective ...


Cx43 Reduces Melanoma Growth Within A Keratinocyte Microenvironment And During Tumorigenesis In Vivo, Mark J. Ableser Aug 2013

Cx43 Reduces Melanoma Growth Within A Keratinocyte Microenvironment And During Tumorigenesis In Vivo, Mark J. Ableser

Electronic Thesis and Dissertation Repository

Connexins have been frequently identified as tumor suppressors in many cancers, however, their role in melanoma tumorigenesis remains controversial. Here, we show that B16-BL6 mouse melanoma cells express low levels of Cx26 and Cx43, rendering them gap junctional intercellular communication (GJIC) deficient. Following ectopic expression of Cx26 and Cx43, gap junction-like plaques were evident at the cell surface and the incidence of dye transfer was significantly increased similar to connexin-rich keratinocytes. The expression of Cx43, but not Cx26, significantly reduced proliferation and anchorage-independent growth relative to controls, whereas migration was unaffected. Additionally, Cx43-expressing melanoma cells displayed significantly reduced growth amongst ...


Galectin-3 Enhances The Malignant Melanoma Phenotype By Regulating Autotaxin, Russell R. Braeuer May 2013

Galectin-3 Enhances The Malignant Melanoma Phenotype By Regulating Autotaxin, Russell R. Braeuer

UT GSBS Dissertations and Theses (Open Access)

In melanoma patient specimens and cell lines, the over expression of galectin-3 is associated with disease progression and metastatic potential. Herein, we have sought out to determine whether galectin-3 affects the malignant melanoma phenotype by regulating downstream target genes. To that end, galectin-3 was stably silenced by utilizing the lentivirus-incorporated small hairpin RNA in two metastatic melanoma cell lines, WM2664 and A375SM, and subjected to gene expression microarray analysis. We identified and validated the lysophospholipase D enzyme, autotaxin, a promoter of migration, invasion, and tumorigenesis, to be down regulated after silencing galectin-3. Silencing galectin-3 significantly reduced the promoter activity of ...


Characterization Of Differentiation And Prognostic Biomarkers On Cd8+ Tumor-Infiltrating Lymphocytes In Metastatic Melanoma, Richard C. Wu May 2013

Characterization Of Differentiation And Prognostic Biomarkers On Cd8+ Tumor-Infiltrating Lymphocytes In Metastatic Melanoma, Richard C. Wu

UT GSBS Dissertations and Theses (Open Access)

CD8+ cytotoxic T lymphocytes (CTL) frequently infiltrate tumors, yet most melanoma patients fail to undergo tumor regression. We studied the differentiation of the CD8+ tumor-infiltrating lymphocytes (TIL) from 44 metastatic melanoma patients using known T-cell differentiation markers. We also compared CD8+ TIL against the T cells from matched melanoma patients’ peripheral blood. We discovered a novel subset of CD8+ TIL co-expressing early-differentiation markers, CD27, CD28, and a late/senescent CTL differentiation marker, CD57. This CD8+CD57+ TIL expressed a cytolytic enzyme, granzyme B (GB), yet did not express another cytolytic pore-forming molecule, perforin (Perf). In contrast, the CD8+CD57+ T ...


Molecular Mechanisms By Which C-Abl And Arg Mediate Melanoma Invasion And Metastasis, Sourik S. Ganguly Jan 2013

Molecular Mechanisms By Which C-Abl And Arg Mediate Melanoma Invasion And Metastasis, Sourik S. Ganguly

Theses and Dissertations--Pharmacology and Nutritional Sciences

Metastasis is one of the main causes of death in cancer patients. Metastatic melanoma is a death sentence, as chemotherapeutic agents have a 5% success rate or do not extend survival beyond 10 months. The lack of effective chemotherapeutic agents for treating metastatic melanoma indicates a dire need to identify new drug targets and develop new therapies. Our lab has previously shown that the kinase activity of Abelson family of non-receptor tyrosine kinases (c-Abl and Arg) is elevated in invasive breast cancer cell lines as compared to non-invasive cell lines. Previous studies from our lab have shown that Abl kinases ...


Applications For Pulse Power Using Nanosecond Pulsed Electric Fields (Nspefs) In Cell Biology And Cancer Treatment, Stephen J. Beebe Jan 2013

Applications For Pulse Power Using Nanosecond Pulsed Electric Fields (Nspefs) In Cell Biology And Cancer Treatment, Stephen J. Beebe

Bioelectrics Publications

No abstract provided.


Nanosecond Pulsed Electric Field (Nspef) Ablation As An Alternative Or Adjunct To Surgery For Treatment Of Cancer, Ru Chen, Xinhua Chen, Stephen J. Beebe Jan 2013

Nanosecond Pulsed Electric Field (Nspef) Ablation As An Alternative Or Adjunct To Surgery For Treatment Of Cancer, Ru Chen, Xinhua Chen, Stephen J. Beebe

Bioelectrics Publications

Surgery as resection or transplantation remains a fundamental means for cancer treatment and often offers an opportunity for a cure. However, surgery is not always possible because of tumor proximity to blood vessels or ducts or when a patient is not healthy enough to undergo surgery. Application of nanosecond pulsed electric fields (nsPEFs) is a new approach to treat cancer using pulse power technology that was originally designed for military purposes. This novel approach deposits extremely short pulses of high power, low energy electric fields into malignant tissues using electrodes to encompass tumors. Pre-clinical studies show that treatments are effective ...


Screening For Melanoma Modifiers Using A Zebrafish Autochthonous Tumor Model, Sharanya Iyengar, Yariv Houvras, Craig J. Ceol Nov 2012

Screening For Melanoma Modifiers Using A Zebrafish Autochthonous Tumor Model, Sharanya Iyengar, Yariv Houvras, Craig J. Ceol

GSBS Student Publications

Genomic studies of human cancers have yielded a wealth of information about genes that are altered in tumors. A challenge arising from these studies is that many genes are altered, and it can be difficult to distinguish genetic alterations that drove tumorigenesis from that those arose incidentally during transformation. To draw this distinction it is beneficial to have an assay that can quantitatively measure the effect of an altered gene on tumor initiation and other processes that enable tumors to persist and disseminate. Here we present a rapid means to screen large numbers of candidate melanoma modifiers in zebrafish using ...


Metastatic Disease: Interactions Between Tumor Cells And Host Environment During Cancer Cell Spread, Jennifer M. Maclean Jul 2011

Metastatic Disease: Interactions Between Tumor Cells And Host Environment During Cancer Cell Spread, Jennifer M. Maclean

Electronic Thesis and Dissertation Repository

Tumor and metastasis formation are not cell autonomous phenomena, but rather an evolution of disease within and responding to the host environment. Metastatic spread from a primary tumor occurs as a result of a complex interplay between tumor cells and the host, wherein tumor cells must escape the primary tumor, enter the host vasculature, travel to and arrest in a distant tissue and survive and grow in that new organ. It is known that cells that progress through these stages must both escape and exploit host systems, yet the mechanisms used are not fully understood. Therefore, the goal of this ...


Comparative Study Of Long-And Short-Pulsed Electric Fields For Treating Melanoma In An In Vivo Mouse Model, Xinhua Chen, Xinmei Chen, Karl H. Schoenbach, Shusen Zheng, R. James Swanson Jan 2011

Comparative Study Of Long-And Short-Pulsed Electric Fields For Treating Melanoma In An In Vivo Mouse Model, Xinhua Chen, Xinmei Chen, Karl H. Schoenbach, Shusen Zheng, R. James Swanson

Bioelectrics Publications

A mouse melanoma model was set up with green fluorescent protein (GFP) expression in vivo. With the same energy, long- (1 ms) and short- (300 ns) pulsed electric fields were delivered to two melanomas injected into the same mouse. The tumor growth and green fluorescence were followed up to compare the different treatment efficacy of long and short pulses. After two days post treatment, short pulse-treated tumors showed a significantly lower tumor volume compared with long pulse-treated tumors (n=8, p