Relevant bibliographies by topics / Melanoma cell proliferation

Academic literature on the topic 'Melanoma cell proliferation'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Melanoma cell proliferation"

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Schadendorf, D., A. Möller, B. Algermissen, M. Worm, M. Sticherling, and B. M. Czarnetzki. "IL-8 produced by human malignant melanoma cells in vitro is an essential autocrine growth factor." Journal of Immunology 151, no. 5 (September 1, 1993): 2667–75. http://dx.doi.org/10.4049/jimmunol.151.5.2667.

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Abstract Normal melanocytes require a number of exogenous growth factors in contrast to most metastatic malignant melanomas. This investigation demonstrates that endogenously produced human IL-8 can act as an important growth factor for human melanoma cells. In the present study, six out of eight human melanoma cell lines tested secrete IL-8 protein into the culture supernatant. In two of these IL-8-secreting melanoma cell lines, SK-MEL 13 and SK-MEL 23, we have determined the IL-8 requirement for their proliferative capacity. These melanoma cell lines produced significant amounts of bioactive IL-8 as measured by the ELISA technique. Secretion of human IL-8 was inducible by IL-1 and by PMA. Human IL-8-specific mRNA was already detected in unstimulated melanoma cells. In addition, human IL-8-R mRNA could be detected for the first time in human melanoma cells. Exposure of the two melanoma cell lines in vitro to antisense oligonucleotides targeted against two different sites of human IL-8 mRNA-inhibited cell proliferation, colony formation in soft agar, and secretion of IL-8 protein into culture supernatant in a dose dependent fashion. Effects were reversible either by removal of the oligomers or by addition of exogenous IL-8 protein. In contrast, exposure to IL-8 sense probes or oligonucleotides in sense or antisense orientation specific for IL-7, TGF-alpha, TGF-beta, and MGSA had no such effect. A monospecific immune serum and two IL-8-specific mAb were also capable of inhibiting melanoma cell proliferation in the same manner. These results provide strong evidence for an autocrine IL-8 synthesis and for an IL-8-dependent proliferation in a subgroup of human melanomas. Furthermore, they suggest that IL-8 may play a role not only in immunomodulation but also in melanoma progression and metastatic spread.
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Chen, Xianjin, Lili Chang, Yan Qu, Jinning Liang, Waishu Jin, and Xiujuan Xia. "Tea polyphenols inhibit the proliferation, migration, and invasion of melanoma cells through the down-regulation of TLR4." International Journal of Immunopathology and Pharmacology 31 (January 1, 2018): 039463201773953. http://dx.doi.org/10.1177/0394632017739531.

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Melanoma is the most common skin cancer and malignant melanoma which can cause skin cancer-related deaths. Toll-like receptor 4 (TLR4) had been reported to play an important role in melanoma, and tea polyphenol (TP) is regarded as an anticancer substance. However, the relationship between TP and TLR4 in melanoma is not well explored. Therefore, our aim is to figure out how TP has an influence on melanoma. Melanoma cell lines (B16F10 and A375) were treated with TP and lipopolysaccharides (LPS). Western blot assay was used to examine TLR4 expression, and MTT assay was conducted to assess proliferation. Wound healing assay was conducted to evaluate the migration of melanoma cells, and transwell assay was used to examine the melanoma cells’ invasiveness. Besides, in vivo experiments were practiced for TP function in mice with melanoma cells. TP inhibited the proliferation, migration and invasion ability of melanoma cells, which displayed a dosage and time dependence. TLR4 was highly expressed in melanoma cells compared with normal skin cells. TP could suppress TLR4 expression both in normal melanomas and in stimulated melanomas by TLR4 agonist LPS. Suppressing TLR4 in melanomas could inhibit cell function (proliferation, migration, and invasion), and blocking the expression of 67LR could abolish TP function on TLR4. TP can inhibit melanoma (B16F10) growth in vivo.
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La, Ting, Lei Jin, Xiao Ying Liu, Ze Hua Song, Margaret Farrelly, Yu Chen Feng, Xu Guang Yan, et al. "Cylindromatosis Is Required for Survival of a Subset of Melanoma Cells." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 28, no. 4 (September 1, 2020): 385–98. http://dx.doi.org/10.3727/096504020x15861709922491.

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The deubiquitinase cylindromatosis (CYLD) functions as a tumor suppressor inhibiting cell proliferation in many cancer types including melanoma. Here we present evidence that a proportion of melanoma cells are nonetheless addicted to CYLD for survival. The expression levels of CYLD varied widely in melanoma cell lines and melanomas in vivo, with a subset of melanoma cell lines and melanomas displaying even higher levels of CYLD than melanocyte lines and nevi, respectively. Strikingly, although short hairpin RNA (shRNA) knockdown of CYLD promoted, as anticipated, cell proliferation in some melanoma cell lines, it reduced cell viability in a fraction of melanoma cell lines with relatively high levels of CYLD expression and did not impinge on survival and proliferation in a third type of melanoma cell lines. The decrease in cell viability caused by CYLD knockdown was due to induction of apoptosis, as it was associated with activation of the caspase cascade and was abolished by treatment with a general caspase inhibitor. Mechanistic investigations demonstrated that induction of apoptosis by CYLD knockdown was caused by upregulation of receptor-interacting protein kinase 1 (RIPK1) that was associated with elevated K63-linked polyubiquitination of the protein, indicating that CYLD is critical for controlling RIPK1 expression in these cells. Of note, microRNA (miR) profiling showed that miR-99b-3p that was predicted to target the 3-untranslated region (3-UTR) of the CYLD mRNA was reduced in melanoma cell lines with high levels of CYLD compared with melanocyte lines. Further functional studies confirmed that the reduction in miR-99b-3p expression was responsible for the increased expression of CYLD in a highly cell line-specific manner. Taken together, these results reveal an unexpected role of CYLD in promoting survival of a subset of melanoma cells and uncover the heterogeneity of CYLD expression and its biological significance in melanoma.
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Kang, Wesuk, Dabin Choi, Soyoon Park, and Taesun Park. "Carvone Decreases Melanin Content by Inhibiting Melanoma Cell Proliferation via the Cyclic Adenosine Monophosphate (cAMP) Pathway." Molecules 25, no. 21 (November 7, 2020): 5191. http://dx.doi.org/10.3390/molecules25215191.

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Melanin, which determines the color of the skin and hair, is initially synthesized to protect the skin from ultraviolet light; however, excessive melanin pigmentation caused by abnormal cell proliferation can result in various melanocytic lesions. Cyclic adenosine monophosphate (cAMP) is known to regulate cell cycle progression and consequently to inhibit the division of abnormally proliferating cells. In this work, we aimed to test whether carvone, a scent compound from plants, inhibits proliferation and subsequently reduces melanin content of melanoma cells and to determine whether its beneficial effects are mediated by the cAMP pathway. We found that carvone decreases melanin content and inhibits melanoma cell proliferation in a concentration-dependent manner. Meanwhile, it inhibited the activation of cell cycle-associated proteins such as cyclin-dependent kinase 1 (CDK1). Of note, the beneficial effects of carvone were abrogated by cAMP inhibition. Our findings indicate potential benefits of carvone for the treatment of melanomas and presumably other hyperpigmentation-related dermatological disorders such as melasmas, lentigines, and excessive freckles.
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Wellbrock, Claudia, and Richard Marais. "Elevated expression of MITF counteracts B-RAF–stimulated melanocyte and melanoma cell proliferation." Journal of Cell Biology 170, no. 5 (August 29, 2005): 703–8. http://dx.doi.org/10.1083/jcb.200505059.

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The protein kinase B-RAF is a human oncogene that is mutated in ∼70% of human melanomas and transforms mouse melanocytes. Microphthalmia-associated transcription factor (MITF) is an important melanocyte differentiation and survival factor, but its role in melanoma is unclear. In this study, we show that MITF expression is suppressed by oncogenic B-RAF in immortalized mouse and primary human melanocytes. However, low levels of MITF persist in human melanoma cells harboring oncogenic B-RAF, suggesting that additional mechanisms regulate its expression. MITF reexpression in B-RAF–transformed melanocytes inhibits their proliferation. Furthermore, differentiation-inducing factors that elevate MITF expression in melanoma cells inhibit their proliferation, but when MITF up-regulation is prevented by RNA interference, proliferation is not inhibited. These data suggest that MITF is an antiproliferation factor that is down-regulated by B-RAF signaling and that this is a crucial event for the progression of melanomas that harbor oncogenic B-RAF.
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Tsai, Alexander, and Eduardo Davila. "A multikinase inhibitor and DNA-PK inhibitor combination reduces tumor growth and alters the tumor microenvironment of B16 melanoma." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 213.2. http://dx.doi.org/10.4049/jimmunol.196.supp.213.2.

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Abstract Recent breakthroughs in targeted therapies and immunotherapies for melanoma have prolonged survival in certain patients. Yet, many patients are not candidates for targeted therapies and response rates to immunotherapies remain low. Thus, there is an unmet need to develop novel melanoma therapies that generate: the high response rates that are characteristic of targeted therapies, the durable responses often observed with immunotherapies, and can be used in a majority of melanoma patients. Therefore, a high-throughput approach evaluating nearly 2,000 compounds was taken to identify FDA-approved therapies that alter the expression of immunologically relevant molecules commonly found on human melanomas. Eight compounds were identified based on their ability to reduce melanoma proliferation without negatively impacting T cell proliferation and function. Studies examining the expression of immunosuppressive molecules on melanoma, melanoma proliferation, and T cell-melanoma co-cultures were used to select a multikinase inhibitor and DNA-PK inhibitor for further investigation. The compounds sensitized melanoma to T cell cytotoxicity which was associated with increased MHC class I and antigen expression. In mice with established B16 tumors, the therapeutic combination significantly reduced tumor growth while prolonging survival. Preliminary data suggests that the drug combination impacts the tumor microenvironment and alters various immune cells present in the tumor. Studies using alternative models of melanomas and additional therapeutic combinations are ongoing. These studies represent a proof of concept demonstrating the ability to repurpose drugs to immunosensitize tumors to T cell-based therapies.
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Lucas, Lauren M., Vipasha Dwivedi, Rania H. Mohamedelhassan, Erin L. Harrell, Connor M. Kelley, Elizabeth L. Knerr, Jessica A. Markham, and David J. Riese. "Abstract 4000: ERBB4 is sufficient and necessary for proliferation of BRAF WT melanoma cell lines." Cancer Research 82, no. 12_Supplement (June 15, 2022): 4000. http://dx.doi.org/10.1158/1538-7445.am2022-4000.

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Abstract Approximately 50% of metastatic melanomas possess wild-type (WT) BRAF alleles. These BRAF-WT tumors are a significant clinical problem, despite the fact that these tumors commonly possess mutations in NF1 or RAS genes, as there are no targeted therapeutics for these tumors. Here we demonstrate that ERBB4 is sufficient and necessary for proliferation of BRAF WT melanoma cell lines, suggesting that disrupting ERBB4 signaling may be effective against BRAF WT melanomas. ERBB4 (HER4) is a member of the ERBB family of receptor tyrosine kinases, which includes the epidermal growth factor receptor (EGFR/ERBB1/HER1), ERBB2 (Neu/HER2), and ERBB3 (HER3). EGFR and ERBB2 are validated targets in a variety of solid tumors, whereas the roles that ERBB4 plays in human malignancies are ambiguous. Our previous in silico analyses of BRAF-WT tumor genomes in The Cancer Genome Atlas skin cutaneous melanoma (TCGA-SKCM) dataset suggest that ERBB4 mutation or overexpression cooperates with NF1 or RAS gene mutations to drive melanomas via activation of the PI3 kinase/AKT signaling pathway. These in silico analyses have also enabled us to prioritize the ERBB4 mutants found in BRAF-WT melanomas. We have tested this hypothesis using a panel of human BRAF-WT melanoma cell lines. We have shown that expression of wild-type ERBB4 causes increased clonogenic proliferation, whereas expression of a dominant-negative ERBB4 mutant (K751M) causes decreased clonogenic proliferation. These data indicate that ERBB4 is sufficient and necessary for clonogenic proliferation of BRAF-WT melanoma cell lines. Analgous studies are testing whether ERBB4 regulates anchorage independence in semi-solid medium and proliferation rates and saturation density in culture dishes. The BRAF-WT melanoma cell lines endogenously express ERBB4 ligands, EGFR, and ERBB2. Moreover, ERBB4 homodimers function as tumor suppressors, whereas ERBB4-EGFR and ERBB4-ERBB2 heterodimers are oncogenic. Thus, we are using gene silencing and pharmacologic tools to determine whether endogenous ERBB4 ligands, endogenous EGFR, or endogenous ERBB2 is required for the oncogenic activity of ERBB4. Furthermore, we are determining whether prioritized ERBB4 mutants found in BRAF-WT melanomas exhibit greater signaling and oncogenic activities than WT ERBB4. Consequently, these experiments will establish a functional role for ERBB4 mutations and expression in BRAF-WT melanomas and will identify potential strategies for disrupting oncogenic ERBB4 signaling in these tumors. Citation Format: Lauren M. Lucas, Vipasha Dwivedi, Rania H. Mohamedelhassan, Erin L. Harrell, Connor M. Kelley, Elizabeth L. Knerr, Jessica A. Markham, David J. Riese. ERBB4 is sufficient and necessary for proliferation of BRAF WT melanoma cell lines [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 4000.
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Wang, Shu Jing, Jia Liu, Fei Wang, Ning Chen, Shan Jiang, Lin Liu, Ying Zhao, and Xiao Dan Zhang. "Tumstatin 7 Peptide Affect Biological Activity of B16 Melanoma Cell." Advanced Materials Research 641-642 (January 2013): 915–18. http://dx.doi.org/10.4028/www.scientific.net/amr.641-642.915.

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To study the effect of biological activity of Tumstatin 7 peptide on the cell proliferation and apoptosis of B16 melanoma. Tumstatin 7 peptide was synthesized and its purity is 98.4532% by high-performance liquid chromatography. The effect of 7 peptide on B16 melanoma was observed by MTT, cell growth curve, the observation of the transmission electron microscope (TEM). 7 peptide can significantly inhibit B16 melanoma cell proliferation, showing dose- and time-dependent .Its IC50 was 72.53 μg/ml.The morphology of B16 melanoma cell was obviously changed by TEM, such as karyopyknosis and apoptotic bodies. So7 peptides can inhibit the proliferation of melanoma cells and promote melanoma cells apoptosis. It will be of great potential value to melanoma treatment.
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Henderson, Evita, and Curtis E. Margo. "Iris Melanoma." Archives of Pathology & Laboratory Medicine 132, no. 2 (February 1, 2008): 268–72. http://dx.doi.org/10.5858/2008-132-268-im.

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AbstractThe iris is the least common site of primary uveal melanoma. The prognosis of iris melanoma is better than that of melanoma of the ciliary body and choroid, but the reason for this difference is unclear. One possible explanation is that iris melanoma is smaller than its posterior segment counterparts at the time of diagnosis. Most iris melanomas are spindle cell types, according to a modified Callender classification system. There is evidence that the proliferation of melanocytes of the anterior iris surface (iris plaque) and diffuse stromal invasion may be risk factors for local recurrence and metastasis, respectively.
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Vital, Patrik da Silva, Murilo Bonatelli, Marina Pereira Dias, Larissa Vedovato Vilela de Salis, Mariana Tomazini Pinto, Fátima Baltazar, Silvya Stuchi Maria-Engler, and Céline Pinheiro. "3-Bromopyruvate Suppresses the Malignant Phenotype of Vemurafenib-Resistant Melanoma Cells." International Journal of Molecular Sciences 23, no. 24 (December 9, 2022): 15650. http://dx.doi.org/10.3390/ijms232415650.

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(1) BRAF mutations are associated with high mortality and are a substantial factor in therapeutic decisions. Therapies targeting BRAF-mutated tumors, such as vemurafenib (PLX), have significantly improved the overall survival of melanoma patients. However, patient relapse and low response rates remain challenging, even with contemporary therapeutic alternatives. Highly proliferative tumors often rely on glycolysis to sustain their aggressive phenotype. 3-bromopyruvate (3BP) is a promising glycolysis inhibitor reported to mitigate resistance in tumors. This study aimed to evaluate the potential of 3BP as an antineoplastic agent for PLX-resistant melanoma treatment. (2) The effect of 3BP alone or in combination with PLX on viability, proliferation, colony formation, cell death, migration, invasion, epithelial-mesenchymal marker and metabolic protein expression, extracellular glucose and lactate, and reactive species were evaluated in two PLX-resistant melanoma cell lines. (3) 3BP treatment, which was more effective as monotherapy than combined with PLX, disturbed the metabolic and epithelial-mesenchymal profile of PLX-resistant cells, impairing their proliferation, migration, and invasion and triggering cell death. (4) 3BP monotherapy is a potent metabolic-disrupting agent against PLX-resistant melanomas, supporting the suppression of the malignant phenotype in this type of neoplasia.
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Dissertations / Theses on the topic "Melanoma cell proliferation"

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Ortega, Rose Mara 1974. "Análise dos mecanismos antiproliferativos decorrentes da inibição farmacológica da enzima ácido graxo sintase em células de melanoma murino B16-F10 : resultados in vitro e in vivo." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289497.

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Orientadores: Karina Gottardello Zecchin, Edgard Graner
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
Made available in DSpace on 2018-08-24T17:35:39Z (GMT). No. of bitstreams: 1 Ortega_RoseMara_D.pdf: 2691297 bytes, checksum: ea4bceee611c0e68c84223cc02b8fd52 (MD5) Previous issue date: 2014
Resumo: Ácido graxo sintase (FASN - fatty acid synthase, EC 2.3.1.85) é a enzima metabólica responsável pela síntese endógena do ácido graxo saturado palmitato, a partir dos precursores acetil-CoA e malonil-CoA. Diversos estudos mostram que, em contraste com a maioria das células normais, FASN é altamente expressa em vários tipos de neoplasias malignas humanas, tais como as de próstata, mama e melanoma sendo que, em alguns destes tumores, a alta expressão de FASN está associada a um pior prognóstico. A inibição da enzima FASN resulta em inibição da proliferação e induz morte celular em diversas neoplasias malignas. Recentemente demonstramos que, in vitro, a inibição específica da atividade de FASN em linhagem celular de melanoma murino, B16-F10, induz a via intrínseca da apoptose, com liberação de citocromo c e ativação de caspase-3, assim como altera a composição dos ácidos graxos livres presentes nas mitocôndrias das células B16-F10. O objetivo deste trabalho foi investigar de que maneira a inibição farmacológica de FASN reduz a proliferação de células B16-F10, in vitro e in vivo, utilizando C75 como inibidor de FASN. O tratamento de células e animais com C75 reduziu significativamente a proliferação celular e induziu apoptose. Houve significativa redução de células na fase S do ciclo celular, com acúmulo de células de G0/G1, em comparação com os controles. Western blottings feitos a partir de extratos de células em cultura e de tumores intraperitoneais mostraram aumento de p21WAF1/Cip1, p27Kip1, redução de Skp2 e cdk2, sem mudanças nos níveis de cdk4, 6 e ciclina E após tratamento com C75. A especifidade destes resultados foi confirmada pela redução da atividade enzimática de FASN após tratamento com C75 e pelo silenciamento de FASN com RNAi. Efeito anti-tumoral de C75 foi sugerido pela formação de tumores subcutâneos de menor volume quando comparados aos tumores de animais controle. Nossos achados mostram que a proliferação de células de melanoma é dependente de FASN, e que sua inibição primeiramente altera os níveis de proteínas envolvidas na transição de G1 para S, para posteriormente induzir apoptose em células de melanoma B16-F10
Abstract: Fatty acid synthase (FASN) is the metabolic enzyme responsible for the endogenous synthesis of the saturated long-chain fatty acid palmitate, from the precursors acetyl-CoA and malonyl-CoA. In contrast to most normal cells, the overexpression of FASN in several human malignancies, such as those of prostate, breast, ovary, melanoma, and soft tissue sarcomas has been associated with poor prognosis. FASN inhibition reduces cell proliferation by blocking DNA replication during S-phase, and induces apoptosis in several malignant neoplasias. We have previously shown that the specific inhibition of FASN activity significantly reduce proliferation and promote apoptosis, as demonstrated by the cytochrome c release and caspase-9 and -3 activation, as well as induces signi?cant changes in the free fatty acids composition of B16-F10 cells mitochondria. Here we investigated the events involved in cell cycle arrest subsequent to FASN inhibition with C75. C75 treatment significantly reduced melanoma cells proliferation and induced apoptosis in vitro and in mice. Cell cycle arrest after C75 treatment was evidenced by a significant increase in G0/G1 phase, as well as decline of the S phase, in comparison with untreated cells. Western blotting analysis showed significant accumulations of the tumor suppressor proteins p21WAF1/Cip1 and p27Kip1, together with decreased amounts of Skp2, essential for the proteasomal degradation of p27Kip1, and cdk2, a Ser/Thr protein kinase necessary for the G1/S transition, in C75-treated cells or mice tumors. The levels of other proteins involved in G1/S cell cycle progression, such as cyclin E, cdk4, and cdk6 were not affected by FASN inhibition. These results were confirmed by inhibition of FASN activity after C75 treatment and by RNAi for FASN. Antitumoral effect of C75 was suggested by reduced subcutaneous tumors volume when compared to controls mice. Our results suggest that melanoma murine B16-F10 cells proliferation is dependent on FASN activity, and its inhibition first modify the levels of some proteins involved in the transition G1?S of cell cycle, to finally induce apoptosis in neoplasic cells
Doutorado
Estomatologia
Doutora em Estomatopatologia
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Haridas, Parvathi. "In vitro characterisation of melanoma progression in a melanoma skin equivalent model." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/118574/1/Parvathi_Haridas_Thesis.pdf.

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Melanoma is a fatal form of skin cancer which progresses in an orchestrated pattern in human skin. Characterising these phases of melanoma in vitro can provide key insights into mechanisms of the disease progression. In this thesis, we investigate how in vitro three-dimensional (3D) model assays that recapitulate human skin can be used to identify key features underlying melanoma progression. In particular, we construct a 3D melanoma skin equivalent model using melanoma cells from the early and late phase of the disease. We further quantify melanoma cell migration, proliferation, invasion, as well as melanoma nest formation.
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SIPES, NANCY JO. "GROWTH REGULATION OF HUMAN MELANOMA: FACTORS INVOLVED IN THE EXPRESSION OF THE TRANSFORMED PHENOTYPE (SOFT AGAR, GROWTH FACTORS, PLATELETS, ENDOTHELIAL CELLS, PARACRINE)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183788.

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Cellular transformation is accomplished in vitro through the concerted action of growth factors and oncogenes. This association has demonstrated that malignant growth results from aberrations in pathways that normally operate to control proliferation. Activation of genes that code for growth factors, their receptors, and/or molecules essential in the transduction of signals from the cell surface to the nucleus are all potential mechanisms by which tumor cells could establish a selective growth advantage over normal cells. This dissertation addresses the question of what oncogenic mechanisms are important in the development and progression of human melanoma. These studies show that melanoma growth is regulated by endogenous substances produced by the melanoma cells themselves (autocrine stimulation), as well as by exogenous substances supplied by neighboring cells and platelets (paracrine stimulation). These factors work to drive the expression of the transformed phenotype for melanoma as evidenced by induction of serum-free soft agar growth. Human platelets were found to the the richest source of paracrine growth promoters. The factor from human platelets was characterized and partially purified. Melanoma cells respond to this 60,000 molecular weight, disulfide-bond-containing protein in colony formation assays. In addition, the protein has endothelial cell growth factor activity. Purified fractions which promoted optimal colony formation for human melanoma cells also maximally stimulated monolayer growth of bovine aortic endothelial cells, while melanocytes were nonresponsive. This implies that melanoma cells are expressing receptors for a protein which plays no known or apparent role in the normal growth of melanocytes. Melanoma cells are sensitive to growth regulatory molecules of autocrine and paracrine nature. This dissertation provides clues to the genetic lesions which have occurred in these melanoma cells to influence their proliferation. The aberrations appear to reside in those genes important in growth factor pathways at the level of endogenous production and misguided response to exogenous factors through receptor expression. We can not hope to fully inhibit the proliferation of tumor cells until we identify and understand those forces which drive their growth. These studies have increased our knowledge of those signals which stimulate melanoma cellular proliferation, and thus provide insight into important therapeutic targets.
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Petti, Carlotta. "Identification of molecular targets of oncogenic NRAs and BRAF involved in regulation of melanoma cell proliferation." Thesis, Open University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437808.

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Stacy, Andrew Jared. "Regulation of ΔNp63α by TIP60 promotes cellular proliferation." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1596151919161674.

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Thieme, Sebastian, Sabine Stopp, Martin Bornhäuser, Fernando Ugarte, Manja Wobus, Matthias Kuhn, and Sebastian Brenner. "Expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells regulates proliferation, differentiation, and maintenance of hematopoietic stem and progenitor cells." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-178636.

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The melanoma cell adhesion molecule defines mesenchymal stromal cells in the human bone marrow that regenerate bone and establish a hematopoietic microenvironment in vivo. The role of the melanoma cell adhesion molecule in primary human mesenchymal stromal cells and the maintenance of hematopoietic stem and progenitor cells during ex vivo culture has not yet been demonstrated. We applied RNA interference or ectopic overexpression of the melanoma cell adhesion molecule in human mesenchymal stromal cells to evaluate the effect of the melanoma cell adhesion molecule on their proliferation and differentiation as well as its influence on co-cultivated hematopoietic stem and progenitor cells. Knockdown and overexpression of the melanoma cell adhesion molecule affected several characteristics of human mesenchymal stromal cells related to osteogenic differentiation, proliferation, and migration. Furthermore, knockdown of the melanoma cell adhesion molecule in human mesenchymal stromal cells stimulated the proliferation of hematopoietic stem and progenitor cells, and strongly reduced the formation of long-term culture-initiating cells. In contrast, melanoma cell adhesion molecule-overexpressing human mesenchymal stromal cells provided a supportive microenvironment for hematopoietic stem and progenitor cells. Expression of the melanoma cell adhesion molecule increased the adhesion of hematopoietic stem and progenitor cells to human mesenchymal stromal cells and their migration beneath the monolayer of human mesenchymal stromal cells. Our results demonstrate that the expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells determines their fate and regulates the maintenance of hematopoietic stem and progenitor cells through direct cell-cell contact.
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Thieme, Sebastian, Sabine Stopp, Martin Bornhäuser, Fernando Ugarte, Manja Wobus, Matthias Kuhn, and Sebastian Brenner. "Expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells regulates proliferation, differentiation, and maintenance of hematopoietic stem and progenitor cells." Ferrata Storti Foundation, 2013. https://tud.qucosa.de/id/qucosa%3A28908.

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The melanoma cell adhesion molecule defines mesenchymal stromal cells in the human bone marrow that regenerate bone and establish a hematopoietic microenvironment in vivo. The role of the melanoma cell adhesion molecule in primary human mesenchymal stromal cells and the maintenance of hematopoietic stem and progenitor cells during ex vivo culture has not yet been demonstrated. We applied RNA interference or ectopic overexpression of the melanoma cell adhesion molecule in human mesenchymal stromal cells to evaluate the effect of the melanoma cell adhesion molecule on their proliferation and differentiation as well as its influence on co-cultivated hematopoietic stem and progenitor cells. Knockdown and overexpression of the melanoma cell adhesion molecule affected several characteristics of human mesenchymal stromal cells related to osteogenic differentiation, proliferation, and migration. Furthermore, knockdown of the melanoma cell adhesion molecule in human mesenchymal stromal cells stimulated the proliferation of hematopoietic stem and progenitor cells, and strongly reduced the formation of long-term culture-initiating cells. In contrast, melanoma cell adhesion molecule-overexpressing human mesenchymal stromal cells provided a supportive microenvironment for hematopoietic stem and progenitor cells. Expression of the melanoma cell adhesion molecule increased the adhesion of hematopoietic stem and progenitor cells to human mesenchymal stromal cells and their migration beneath the monolayer of human mesenchymal stromal cells. Our results demonstrate that the expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells determines their fate and regulates the maintenance of hematopoietic stem and progenitor cells through direct cell-cell contact.
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Cardim, Sílvia Guedes Braga. "Vesículas extracelulares liberadas pelas células cancerosas modulam a proliferação, morte e migração celular no melanoma humano?" Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-15122017-083004/.

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As células que compõem o tumor podem interagir entre si, através da liberação e incorporação de vesículas extracelulares, muitas vezes contribuindo para a progressão tumoral. Dessa maneira, o presente trabalho teve como objetivo observar se as vesículas extracelulares , como as microvesículas e os exossomas liberados pelas células cancerosas em condições de estresse celular, após quimioterapia e indução de hipóxia conferem alguma vantagem adaptativa às células tumorais. Nossos resultados mostram que vesículas liberadas por células de melanoma humano em hipóxia ou normóxia apresentam tamanho médio característico de exossomos e microvesículas e não modulam os processos de proliferação, morte e migração celular. As vesículas liberadas pelas células após tratamento com o quimioterápico temozolamida também apresentam tamanho característico de exossomos e microvesículas; em adição, o tratamento com a temozolamida induziu um aumento na secreção dessas vesículas pelas células de melanoma. A incubação das células tumorais com vesículas oriundas da terapêutica com a temozolamida aumentou a proliferação celular, conferindo vantagem proliferativa às células de melanoma humano
Tumor cells can interact with each other by releasing and incorporating extracellular vesicles, contributing to tumor progression. Therefore, the aim of this study was to evaluate if extracellular vesicles, such as microvesicles and exossomes, released by cancer cells under cell stress conditions like chemotherapy and hypoxia, induce an adaptive advantage to tumor cells. Our results show that vesicles shed by human melanoma cells under hypoxia, or normoxia exhibit the characteristic size of exossomes and microvesicles and do not modulate cell proliferation, death or migration. The vesicles released by melanoma cells after temozolomide treatment also showed the average size of exossomes and microvesicles; moreover, temozolomide treatment induced an increase in extracellular vesicles shedding by tumor cells. Incubation of tumor cells with vesicles released under temozolamide therapeutics caused an increase in cell proliferation, providing a proliferative advantage to human melanoma cells
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Huang, Jie Min. "An amentoflavone derivative induces apoptosis and interferes with cell proliferation in melanoma by inhibition of the JAK2STAT3 signaling pathway." Thesis, University of Macau, 2017. http://umaclib3.umac.mo/record=b3690910.

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Abrantes, Julia Laura Fernandes 1984. "Expressão ectópica de miR-34a em células de melanoma metastático humano = efeitos sobre vias de sinalização relacionadas com sobrevivência, proliferação e morte celular = Ectopic expression of miR-34a in human metastatic melanoma cells: effects on signaling pathways related to survival, proliferation and cell death." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314040.

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Orientador: Carmen Veríssima Ferreira Halder
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-22T16:08:32Z (GMT). No. of bitstreams: 1 Abrantes_JuliaLauraFernandes_D.pdf: 4562084 bytes, checksum: fba9dbca16cd31c006b311ff23a0b41b (MD5) Previous issue date: 2013
Resumo: O melanoma é o tipo mais agressivo de câncer de pele. Seu tratamento permanece como um grande desafio, já que em estágio avançado torna-se extremamente refratário aos tratamentos convencionais. miR-34a é um microRNA supressor de tumor com expressão normalmente reduzida em células cancerosas. A fim de investigar o papel de miR-34a como supressor do melanoma, o principal objetivo deste estudo foi identificar alvos moleculares modulados pela expressão ectópica de miR-34a na linhagem celular de melanoma metastático humano SK-mel-103. miR-34a reduziu significativamente a viabilidade das células de melanoma, o que deve estar relacionado, pelo menos em parte, com o aumento na expressão da proteína pró-apoptótica Bax, ativação da caspase-3 e clivagem da PARP-1. Estes dados sugerem que miR-34a foi capaz de induzir apoptose nas células de melanoma. Além disso, houve redução na expressão de CDK4, CDK6, E2F3 e pRb, proteínas relacionadas com a progressão do ciclo celular. Aumento na expressão de p21, um inibidor de CDKs, também foi observado nessas células. Algumas moléculaschave envolvidas com os processos de proliferação celular e apoptose, como proteínas oncogênicas (Axl, AKT, ERK 1/2, ?-catenina e c-myc) e proteínas supressoras de tumor (p53 e PTEN), foram "down- e upreguladas" por miR-34a, respectivamente. Interessantemente, o fluxo autofágico foi aumentado por miR-34a, efeito que não foi correlacionado com alterações adicionais na viabilidade das células de melanoma. O aumento no fluxo autofágico ocorreu, provavelmente, como uma resposta celular ao estresse de retículo e a agregação de proteínas induzidos por miR-34a, fenômenos que também podem ter contribuído para a indução de apoptose nesse contexto. Os dados obtidos neste estudo trouxeram novos aspectos moleculares da ação de miR-34a como supressor tumoral, e permitem apontar este microRNA como um potencial alvo terapêutico contra o melanoma metastático humano
Abstract: Melanoma is the most aggressive form of skin cancer. Its treatment remains a big challenge, since in advanced stage it is extremely refractory to conventional treatments. miR-34a has emerged as an important tumor suppressor, and its expression is normally reduced in cancer cells. To provide more information about the role of miR-34a as a melanoma suppressor, the main goal of this study was to identify key molecular players modulated by ectopic expression of this microRNA in the metastatic melanoma cell line SK-mel-103. miR-34a caused a reduction of melanoma cells viability, what may be related, at least in part, with the increased expression of pro-apoptotic marker, Bax, activation of caspase 3 and PARP-1 cleavage, which indicates that miR-34a triggered apoptosis in melanoma cells. In addition, the expression of CDK4, CDK6, E2F3 and pRb, proteins related to the cell cycle progression, was reduced. An increase in p21 expression, a CDK inhibitor, was also detected in these cells. Some key molecules involved with proliferation and apoptosis processes, such as oncogenic proteins (Axl, AKT, ERK 1/2 kinases, ?- catenin and c-myc) and tumor suppressor proteins (p53 and PTEN), were down- and upregulated by miR-34a, respectively. Interestingly, the autophagic flux was stimulated by miR-34a, but this effect was not correlated with further alterations in cell viability. The increased autophagy occurred probably as a cellular response against the reticulum stress and the protein aggregation induced by miR-34a in melanoma cells, which can also be contributing to the cell death by apoptosis in this context. Our findings brought up novel molecular aspects about the role of miR-34a as melanoma suppressor. The broad action of this microRNA on key molecular players of melanoma aggressiveness was crucial for reprogramming these cells in favor of apoptosis. Altogether, this study pointed out miR-34a as a potential therapeutic agent against advanced melanoma
Doutorado
Bioquimica
Doutora em Biologia Funcional e Molecular
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Book chapters on the topic "Melanoma cell proliferation"

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Lozhkomoev, Aleksandr S., Georgy Mikhaylov, Vito Turk, Boris Turk, and Olga Vasiljeva. "Application of Crumpled Aluminum Hydroxide Nanostructures for Cancer Treatment." In Springer Tracts in Mechanical Engineering, 211–23. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-60124-9_10.

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AbstractThe tumormicroenvironment regulates tumor progression and the spread of cancer in the body. Applications of nanomaterials that can dysregulate tumor-microenvironment are emerging as a promising anti-cancer approaches, which can improve the efficacy of existing cancer treatments. We have reported that agglomerates of radially assembled Al hydroxide crumpled nanosheets with the disordered defective surface structure have a large positive charge and therefore can lead to ion imbalance at the cell perimembranous space through the selective adsorption of extracellular anionic species. This effect was demonstrated in vitro by reduced viability and proliferationof tumor cells, and further validated in a murine melanoma cancer model. Furthermore, crumpled Al hydroxide nanostructures showed a much stronger suppressive effect on tumor growth in combination with a minimally effective dose of doxorubicin. Taken together, the described approach of tumor microenvironment dysregulation through selective adsorption properties of folded crumpled nanostructures opened a new avenue for development of innovative anticancer therapy strategies.
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Kim, Yon-Suk, Sun Hee Cheong, Jin-Woo Hwang, Gaurav Lodhi, Kwang-Ho Lee, Dong-Kug Choi, Hyuk Song, et al. "Effect of Taurine on Viability and Proliferation of Murine Melanoma B16F10 Cells." In Taurine 9, 167–77. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15126-7_15.

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Schadendorf, D., M. Worm, K. Jurgovsky, E. Dippel, U. Reichert, and B. M. Czarnetzki. "Effects of Various Synthetic Retinoids on Proliferation and Immunophenotype of Human Melanoma Cells In Vitro." In Recent Results in Cancer Research, 183–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-78771-3_13.

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A., K., E. I., V. Yu., E. V., N. I., A. A., I. N., N. V., and H. M. "T-Cadherin Stimulates Melanoma Cell Proliferation and Mesenchymal Stromal Cell Recruitment, but Inhibits Angiogenesis in a Mouse Melanoma Model." In Research Directions in Tumor Angiogenesis. InTech, 2013. http://dx.doi.org/10.5772/53350.

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Nguyen, Duy, Oanh Nguyen, Honglu Zhang, Glenn D., and Mandi M. "A Bromophosphonate Analogue of Lysophosphatidic Acid Surpasses Dacarbazine in Reducing Cell Proliferation and Viability of MeWo Melanoma Cells." In Research on Melanoma - A Glimpse into Current Directions and Future Trends. InTech, 2011. http://dx.doi.org/10.5772/18702.

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Nordenberg, J., A. Fuchs, L. Wasserman, Z. Malik, and A. Novogrodsky. "Anti-proliferative effects and phenotypic alterations induced by methylurea derivatives in B16 mouse melanoma." In Modern Approaches to Animal Cell Technology, 125–37. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-408-02732-8.50016-x.

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Conference papers on the topic "Melanoma cell proliferation"

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Ollinger, K., and P. Waster. "PO-158 Extracellular vesicles, generated from UVA-exposed melanoma cells, promotes cell proliferation and invasion." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.197.

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Zhan, Yao, Michael S. Dahabieh, Filippa Pettersson, Monica C. Dobocan, Marie Noel M. Boutchou, Leon Van Kempen, Sonia V. del Rincon, and Wilson H. Miller. "Abstract 3710: The role of eIF4E in promoting melanoma cell proliferation and maintaining acquired resistance to Vemurafenib in melanoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3710.

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Zhan, Yao, Michael S. Dahabieh, Sonia V. del Rincon, and Wilson H. Miller. "Abstract B235: The role of eIF4E in promoting melanoma cell proliferation and maintaining acquired resistance to vemurafenib in melanoma." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b235.

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Srivastava, Jaya, Okkyung Rho, and John DiGiovanni. "Abstract 2022: Twist1 regulates UVB-induced epidermal cell proliferation in non-melanoma skin cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2022.

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Shen, Che-Hung, Ping Yuan, Rolando Perez-Lorenzo, Yaqing Zhang, Sze Xian Lee, Yang Ou, Li Cai, John M. Asara, Lewis C. Cantley, and Bin Zheng. "Abstract B09: Phosphorylation of BRAF by AMPK impairs BRAF-KSR1 association and cell proliferation." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-b09.

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Umemura, Masanari, Erdene Baljinnyam, Mariana S. De Lorenzo, Stefan Feske, Lai-Hua Xie, and Kousaku Iwatsubo. "Abstract 1864: Role of store-operated Ca2+ entry in proliferation and cell cycle in melanoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1864.

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ZHANG, YUNA YUAN, Xu Guang Yan, Margaret Farrelly, Hamed Yari, Yuchen Feng, Ting La, Hessam Tabatabaee, Lei Jin, and Xu Dong Zhang. "Abstract 2451: Long noncoding RNA OVAAL promotes melanoma cell proliferation through translational suppression of p27." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2451.

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Shah, Raj, Mengying Zhu, Andrew Boreland, Fabian Filipp, and Suzie Chen. "Abstract 5493: Targeted inhibition of glutaminase in GRM1-expressing melanoma cells inhibits cell proliferation by reducing glutamate bioavailability." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5493.

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Lee, Chih-Shia, Karl J. Dykema, Danielle M. Hawkins, Kyle A. Furge, and Nicholas S. Duesbery. "Abstract LB-232: MEK2 signaling pathway alone is sufficient but not necessary for melanoma cell proliferation." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-232.

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Ganguly, Sourik S., Leann S. Fiore, Jonathan T. Sims, J. Woodrow Friend, DivyaMani Srinivasan, Matthew Thacker, Michael L. Cibull, Wang Chi, and Rina Plattner. "Abstract C51: c-Abl and Arg are activated in human primary melanomas, promote melanoma cell invasion, proliferation, survival, and drive metastatic progression." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c51.

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