Добірка наукової літератури з теми "Metastasis"

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Пов'язані теми наукових робіт:

Статті в журналах з теми "Metastasis":

1
Lambert, W. Clark, and Robert A. Schwartz. "Metastasis." Journal of the American Academy of Dermatology 27, no. 1 (July 1992): 131–33. http://dx.doi.org/10.1016/s0190-9622(08)80829-8.
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2
Bosman, Fred, Linda Meade-Tollin, and Cornelis Van Noorden. "Metastasis." American Scientist 86, no. 2 (1998): 130. http://dx.doi.org/10.1511/1998.2.130.
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3
Noorden, Cornelis J. Van, Linda Meade-Tollin, and Fred Bosman. "Metastasis." American Scientist 86, no. 2 (1998): 130. http://dx.doi.org/10.1511/1998.21.860.
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4
BRODLAND, DAVID G. "Metastasis." Dermatologic Surgery 22, no. 3 (March 1996): 228–33. http://dx.doi.org/10.1111/j.1524-4725.1996.tb00313.x.
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5
Fisher, C. "Metastasis." Journal of Clinical Pathology 42, no. 11 (November 1989): 1231. http://dx.doi.org/10.1136/jcp.42.11.1231-c.
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6
Maureen Seaton. "Metastasis." Missouri Review 33, no. 3 (2010): 121. http://dx.doi.org/10.1353/mis.2010.0068.
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7
Abba, Mohammed, Nitin Patil, Jörg Hendrik Leupold, and Heike Allgayer. "MicroRNAs—from metastasis prediction to metastasis prevention?" Molecular & Cellular Oncology 3, no. 2 (December 2015): e1074336. http://dx.doi.org/10.1080/23723556.2015.1074336.
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8
Bankaitis, Katherine, Lucia Borriello, Thomas Cox, Conor Lynch, Andries Zijlstra, Barbara Fingleton, Miodrag Gužvić, Robin Anderson, and Josh Neman. "Meeting report: Metastasis Research Society–Chinese Tumor Metastasis Society joint conference on metastasis." Clinical & Experimental Metastasis 34, no. 3-4 (March 2017): 203–13. http://dx.doi.org/10.1007/s10585-017-9842-1.
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9
Zhu, Mingyu, Xin Liu, Yuan Qu, Silong Hu, Yingjian Zhang, Wentao Li, Xiaoyan Zhou, et al. "Bone metastasis pattern of cancer patients with bone metastasis but no visceral metastasis." Journal of Bone Oncology 15 (April 2019): 100219. http://dx.doi.org/10.1016/j.jbo.2019.100219.
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10
Rades, D., L. Gerdan, B. Segedin, V. Nagy, M. T. Khoa, N. T. Trang, and S. E. Schild. "Brain metastasis." Strahlentherapie und Onkologie 189, no. 12 (October 2013): 996–1000. http://dx.doi.org/10.1007/s00066-013-0442-y.
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Дисертації з теми "Metastasis":

1
Björndahl, Meit A. "Lymphangiogenesis and lymphatic metastasis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-562-3/.
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2
Clark, S. R. "The investigation of tumour metastasis." Electronic Thesis or Dissertation, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370241.
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3
Liu, Hui Ph D. Massachusetts Institute of Technology. "Identification of a novel metastasis enhancer, CDCP1, and analysis of its functions during melanoma metastasis." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/47881.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2009.
Includes bibliographical references.
Nearly 90% of cancer mortality from solid tumors is due to metastasis of malignant cells to the distant vital organs. It is now well established that a plethora of stromal cells are present within the tumor, and contribute in various ways to tumor initiation and progression, and plasma membrane proteins are the mediators for tumor-stromal communications. In this thesis, I focused on plasma membrane proteins that may contribute to tumor metastasis. I applied quantitative mass spectrometry technology to first identify plasma proteins that are expressed at different levels in melanoma cells with high versus low metastatic abilities. Using SILAC (stable isotope labeling with amino acids in culture) coupled with nano-spray tandem mass spectrometry, this work led to the discovery of C̲ub Ḏomain C̲ontaining Protein 1 (CDCP1) as one of those differentially expressed transmembrane proteins. We found that CDCP1 is not only a surface marker for cells with higher metastatic potential, it is also functionally engaged in enhancing tumor metastasis. When searching for the underlying mechanisms, we found that CDCP1 is important for soft agar colony-forming abilities, suggesting that CDCP1 might regulate the balance between cell proliferation and anoikis. Making use of 3D Matrigel culture system, we found that CDCP1 also regulates scattered growth of melanoma cells. We speculate these two factors may contribute to enhanced-metastatic ability observed in mice.
(cont.) When investigating signaling pathways that may mediate the functions of CDCP1, we found that overexpression of CDCP1 correlates with hyper-activation of Src family kinases. While wild-type CDCP1 enhances SFK activation, point mutation that abolished CDCP1 functions (in scattered growth and in metastasis) also abolished SFK hyper-activation, suggesting that CDCP1 might function through the activation of SFKs. Such notion was further supported since pharmacological reagents PP2 and Dasatinib, which are two SFK inhibitors, blocked in vitro functions of CDCP1 in scattered growth. Thus the work in this thesis has identified a novel metastasis enhancer, CDCP1, and has gained insight into the mechanisms by which CDCP1 functions.
by Hui Liu.
Ph.D.
4
Onder, Tamer T. "Role of e-cadherin in tumor metastasis and discovery of compounds targeting metastasis cancer cells." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/43226.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2008.
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The epithelial cell adhesion molecule E-cadherin is often downregulated during carcinoma progression and metastatic spread of tumors. However, the precise mechanism and molecular basis of metastasis promotion by E-cadherin loss is not completely understood. To investigate its role in metastasis, I utilized two distinct methods of E-cadherin inhibition that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. While the disruption of cell-cell contacts alone does not enable metastasis in vivo, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition (EMT), invasiveness and anoikis-resistance. E-cadherin binding partner f3-catenin is necessary but not sufficient for these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes. In addition to promoting metastasis, loss of E-cadherin and the accompanying EMT renders cells resistant to conventional chemotherapeutic drugs. As the cells that have undergone an EMT represent the pool of cancer cells most competent to metastasize and lead to tumor recurrence, it is of vital importance to find therapies that effectively target such cells. Paired cell lines that differ in their differentiation state were utilized to discover compounds with selective toxicity against cells that have undergone an EMT. High-throughput screening of small molecule libraries resulted in a number of compounds that specifically affect the viability of cells that have undergone an EMT while having minimal cytotoxic effects on control epithelial cells. These studies establish a proof-of-principle for discovering compounds that target highly metastatic and otherwise chemotherapy resistant cancer cells.
by Tamer T. Onder.
Ph.D.
5
Garcia, López Marta. "Experimental Models of Prostate Cancer Bone Metastasis - Establishment, characterization and imaging of xenograft bone metastasis models -." DoctoralThesis, Universitat Autònoma de Barcelona, 2003. http://hdl.handle.net/10803/120182.
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En païssos industrialitzats, el càncer de pròstata (CP) és la neoplasia més comunment diagnosticada en homes i la segona causa de mort relacionada amb càncer, donat que els nivells de mortalitat en aquesta població són molt més baixos que els que es troben en els païssos en desenvolupament, es veu un clar benefici en els avenços tant en el diagnòstic precoç com el desenvolupament de teràpies eficients. No obstant, la disseminació metastàtica més que el tumor primari en sí és la responsable dels problemes de mortalitat i morbiditat associats al CP. Les metàstasis esquelètiques estan presents en més d’un 70% dels casos de CP avançat i confereixen alts nivells de morbiditat, un 25% de supervivència als 5 anys i una mitjana de supervivència de 40 mesos després de ser diagnosticats. Tot i que les fractures patològiques i la compressió de la columna vertebral són les complicacions més probables pel pacient metastàtic, el major símptoma és el dolor. Les metàstasis òssies del CP comporten un estat d’acceleració de la remodelació òssia que es caracteritza per una activació patològica tant dels osteoblasts com dels osteoclasts. Aquesta elevada activació dels osteoclasts està directament correlacionada amb un increment en la incidència de les complicacions òssies, de la progressió tumoral i la mort. A més, una vegada el tumor metastatitza a os, la malaltia esdevé incurable i les teràpies actuals són solament pal·liatives i principalment es dirigeixen a les cèl·lules tumorals o als osteoclasts. Per tant, per entendre millor la biologia de les metàstasis òssies del PC i poder investigar noves teràpies és important desenvolupar nous models animals. En aquesta tesi, s’han establert nous models experimentals de metàstasis del CP mitjançant la inoculació de cèl·lules humanes en ratolins immunodeficients per diferents vies, intraòssia, intracardíaca o intratibial. Finalment, diferents estratègies s’han dut a terme per descriure noves dianes moleculars involucrades en el mecanisme de les metàstasis i poder desenvolupar un model adequat per la evaluació de possibles compostos candidats a ser futures aproximacions terapèutiques. Per concloure, aquests models proporcionen una fiable reproducció de la situació clínica i permeten tant la caracterització com el diseny de tractaments efectibles per compendre millor els mecanismes moleculars de les metàstasis òssies del CP.
In industrialized countries, prostate cancer (PCa) is the most common malignancy in men, but mortality rates are much lower than those recorded in developing countries, reflecting benefits from advances in early diagnosis and effective treatment. However, the metastatic disease rather than the primary tumor is responsible for much of the resulting morbidity and mortality. Skeletal metastases occur in more than 70% of cases of late-stage of PCa and they confer a high level of morbidity, a 5 year survival rate of 25% and median survival of approximately 40 months. Though fractures and spinal cord compression are potential complications, the most common symptom of bone metastases is pain. Bone metastases from PCa lead to an accelerated bone turnover state that features pathological activation of both osteoblasts and osteoclasts. Raised activation of osteoclasts is directly correlated with an increased incidence of skeletal complications, cancer progression and death. Further, once tumor metastasizes to bone, the metastatic disease become incurable and current therapies are palliative and mostly target either tumor cells or osteoclasts. Thus, to better understand the biology of PCa bone metastasis and to investigate new therapy options it is crucial to develop new animal models. In this thesis, we have established new experimental models of PCa bone metastasis by intraosseous (i.o.), intracardiac (i.c.) or intratibial (i.t.) inoculation of human PCa cells in immunodeficient mice. Extensive bone metastasis were monitored by in vivo bioluminescence imaging. Different strategies were performed to describe new molecular targets involved in the mechanisms of PCa bone metastasis and to make a suitable model for evaluating novel compounds as future therapeutic approaches. To conclude, these models provide a reliable reproduction of the clinical situation and allows characterization and design effective treatments by better understanding the molecular mechanisms of PCa bone metastasis.
6
Garcia, López Marta. "Experimental Models of Prostate Cancer Bone Metastasis - Establishment, characterization and imaging of xenograft bone metastasis models -." DoctoralThesis, Universitat Autònoma de Barcelona, 2003. http://hdl.handle.net/10803/120182.
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Анотація:
En païssos industrialitzats, el càncer de pròstata (CP) és la neoplasia més comunment diagnosticada en homes i la segona causa de mort relacionada amb càncer, donat que els nivells de mortalitat en aquesta població són molt més baixos que els que es troben en els païssos en desenvolupament, es veu un clar benefici en els avenços tant en el diagnòstic precoç com el desenvolupament de teràpies eficients. No obstant, la disseminació metastàtica més que el tumor primari en sí és la responsable dels problemes de mortalitat i morbiditat associats al CP. Les metàstasis esquelètiques estan presents en més d’un 70% dels casos de CP avançat i confereixen alts nivells de morbiditat, un 25% de supervivència als 5 anys i una mitjana de supervivència de 40 mesos després de ser diagnosticats. Tot i que les fractures patològiques i la compressió de la columna vertebral són les complicacions més probables pel pacient metastàtic, el major símptoma és el dolor. Les metàstasis òssies del CP comporten un estat d’acceleració de la remodelació òssia que es caracteritza per una activació patològica tant dels osteoblasts com dels osteoclasts. Aquesta elevada activació dels osteoclasts està directament correlacionada amb un increment en la incidència de les complicacions òssies, de la progressió tumoral i la mort. A més, una vegada el tumor metastatitza a os, la malaltia esdevé incurable i les teràpies actuals són solament pal·liatives i principalment es dirigeixen a les cèl·lules tumorals o als osteoclasts. Per tant, per entendre millor la biologia de les metàstasis òssies del PC i poder investigar noves teràpies és important desenvolupar nous models animals. En aquesta tesi, s’han establert nous models experimentals de metàstasis del CP mitjançant la inoculació de cèl·lules humanes en ratolins immunodeficients per diferents vies, intraòssia, intracardíaca o intratibial. Finalment, diferents estratègies s’han dut a terme per descriure noves dianes moleculars involucrades en el mecanisme de les metàstasis i poder desenvolupar un model adequat per la evaluació de possibles compostos candidats a ser futures aproximacions terapèutiques. Per concloure, aquests models proporcionen una fiable reproducció de la situació clínica i permeten tant la caracterització com el diseny de tractaments efectibles per compendre millor els mecanismes moleculars de les metàstasis òssies del CP.
In industrialized countries, prostate cancer (PCa) is the most common malignancy in men, but mortality rates are much lower than those recorded in developing countries, reflecting benefits from advances in early diagnosis and effective treatment. However, the metastatic disease rather than the primary tumor is responsible for much of the resulting morbidity and mortality. Skeletal metastases occur in more than 70% of cases of late-stage of PCa and they confer a high level of morbidity, a 5 year survival rate of 25% and median survival of approximately 40 months. Though fractures and spinal cord compression are potential complications, the most common symptom of bone metastases is pain. Bone metastases from PCa lead to an accelerated bone turnover state that features pathological activation of both osteoblasts and osteoclasts. Raised activation of osteoclasts is directly correlated with an increased incidence of skeletal complications, cancer progression and death. Further, once tumor metastasizes to bone, the metastatic disease become incurable and current therapies are palliative and mostly target either tumor cells or osteoclasts. Thus, to better understand the biology of PCa bone metastasis and to investigate new therapy options it is crucial to develop new animal models. In this thesis, we have established new experimental models of PCa bone metastasis by intraosseous (i.o.), intracardiac (i.c.) or intratibial (i.t.) inoculation of human PCa cells in immunodeficient mice. Extensive bone metastasis were monitored by in vivo bioluminescence imaging. Different strategies were performed to describe new molecular targets involved in the mechanisms of PCa bone metastasis and to make a suitable model for evaluating novel compounds as future therapeutic approaches. To conclude, these models provide a reliable reproduction of the clinical situation and allows characterization and design effective treatments by better understanding the molecular mechanisms of PCa bone metastasis.
7
Bellmunt, i. Tarragó Anna. "Role of MAF in bone metastasis." DoctoralThesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/482079.
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The identification of genes that mediate metastasis is pivotal to better understand the mechanism, to develop novel drugs and to stratify patients with highest risk and consecutively administrate them preventive treatments. Despite significant advances on knowledge, diagnosis and treatment of cancer, metastasis remains the major cause of cancer-associated deaths. Bone is one of the most common organs affected by metastatic lesions for its permeability and favorable conditions for cellular growth. Constant remodeling in bone homeostasis implies an incessant degradation of the bone that release high concentrations of growth factors into the microenvironment. Thereby, growth factors benefit both, formation of new bone and/or tumor cell growth. Although the importance of bone metastatic lesions in cancer patients and the advances on the knowledge of this process, few treatments are currently administrated to patients that suffer this disease, specifically Denosumab and Zoledronic acid (ZOL). Importantly, these treatments can improve the symptoms of bone lesions but cannot cure or reverse metastasis. This fact reflects the need to detect and tackle new targetable elements to reduce bone metastatic lesions. Many molecular mechanisms have been described in bone metastasis, but only one predictor gene has been identified, MAF. MAF is a transcription factor that has been previously involved in carcinogenesis, specially in multiple myeloma (MM) and human angioimmunoblastic T-cell lymphomas (AITLs). Recently, MAF contribution has been associated for the first time with breast cancer bone metastasis. In this thesis, we determined the role of MAF in several contexts. As a first approach we demonstrated that MAF is also a predictive marker of bone metastasis in prostate cancer (PC) patients. However, regarding androgen-independent PC cell lines, an overexpression of MAF was not enough to drive colonization of the mouse bone. Secondly, we report the beneficial effect of MAF downregulation on preventing skeletal metastasis in BoM2, a highly bone metastatic MCF7-derived cell line. MAF impinged bone colonization in a higher degree that other treatments against bone metastasis, such as PTHrP antagonist or recombinant OPG. This fact identifies MAF as a new potential target to focus on the generation of new drugs. Finally, MAF showed a tendency to redirect metastases to other organs than bone in the presence of ZOL treatment in vivo. Thus, we validated the association between MAF overexpression and an increase on extraskeletal metastases after ZOL preventive treatment in non-postmenopausal BC patients. Moreover, a mouse model was generated to better understand the biology of MAF- derived bone metastasis within complete stromal interactions. We designed a transgenic mouse model to express MAF in the mammary gland in an inducible manner. To this end, we generated two constructs; the first contains rtTA, renilla and katushka under MMTV promoter, and the second contains MAF, luciferase and tGFP under Tet-On promoter. We demonstrated the incorporation of several copy numbers of both transgenes in two independent colonies and we detected transgene expression under doxycycline activation by means of luminescent signal. Even though both colonies incorporated several copy number of the transgene, their expression was soft and some relevant leakiness was observed in the non-treated MAF mice. No differences were observed in terms of mammary gland development between transgene-expressing MAF mice and wild-type mice, as well as no tumor initiation was detected in any group. Notably, MAF Tg mouse was crossed with MMTV-PyMT to generate double Tg mice (PyMT-MAF). PyMT-MAF tumor growth presented no significant differences compared to PyMT in terms of time to tumor formation and growth rate. Importantly, no bone metastases were observed at 3-month-old mice of any group. Thus, the generation of this animal model provided new insights to generate a novel bone metastatic mouse model.
La identificació de gens implicats en el procés de la metàstasis és bàsica per tal d’entendre el mecanisme d’aquest procés, per reconèixer els pacients amb més risc de patir-lo i tractar-los selectivament i finalment pel desenvolupament de nous fàrmacs. Recentment, s’ha identificat el gen MAF com a predictor d’un alt risc de patir metàstasis òssia en pacients de càncer de mama. En aquesta tesi hem determinat el paper de MAF en diferents contexts. Per una banda, hem demostrat que MAF és un marcador predictiu de les metàstasis òssies també en pacients amb càncer de pròstata. Tot i així, una sobreexpressió de MAF en cèl·lules de càncer de pròstata andrògen-independents no va ser suficient per conduir la colonització a l’òs. Per altra banda, hem demostrat que reduir els nivells de MAF en les cèl·lules BoM2, derivades de les cèl·lules de càncer de mama MCF7, redueix la tendència d’aquestes cèl·lules a metastatitzar a l’òs. Cal destacar que aquest efecte és superior al d’altres tractaments com poden ser OPG recombinant o el pèptid antagonista de PTHrP, indicant MAF com a element potencial per a la generació de nous fàrmacs. Finalment, MAF afecta el patró de metàstasis de les cèl·lules ER- de càncer de mama després del tractament preventiu amb àcid Zoledronic, tal com s’observa en pacients. Per abordar el paper de MAF en el càncer de mama tenint en compte les interaccions amb l’estroma i el sistema immunitari, es va dissenyar un model animal transgènic que sobreexpressava MAF en la glàndula mamària de forma induïble. Es va demostrar la incorporació de vàries còpies del transgen en el ADN genòmic i també es va detectar, per senyal bioluminiscent, la inducció per doxiciclina de l’expressió del transgen. Cal destacar que l’expressió era feble i en molts casos inespecífica i independent al tractament amb doxiciclina. El desenvolupament mamari en aquest model no demostrava cap alteració com tampoc es va detectar cap indici de formació de tumor. Aquest model es va creuar amb MMTV-PyMT, i els tumors de les femelles doble transgèniques (PyMT-MAF) no van presentar cap diferència en el temps necessari per a la formació de tumors ni en la velocitat de creixement comparat amb PyMT. De manera destacable, no es van observar metàstasis òssies en el moment del sacrifici. D’aquesta manera, la generació del ratolí MAF transgènic ens va donar noves perspectives per enfocar la generació d’un nou model animal que generi metàstasis òssies.
8
Park, Se Hyung. "Estrogen in ovarian cancer cell metastasis." Electronic Thesis or Dissertation, University of British Columbia, 2008. http://hdl.handle.net/2429/1287.
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Benign ovarian tumors and majority of epithelial ovarian cancers possess steroid receptors including estrogen receptors (ERs). However, the estrogen-ER signaling in ovarian carcinomas is not completely understood. Tumorigenesis is a multiple-step process involving dysregulated cell growth and metastasis. Tumor cells acquire the capacity of migration and invasion by temporal phenotypical and genotypical changes termed epithelial-mesenchymal transition (EMT). Considerable evidence implicates a mitogenic action of estrogen in early ovarian carcinogenesis. In contrast, its influence in the metastatic cascade of ovarian tumor cells remains obscure. In this study, I have focused on the role of 17β-estradiol (E2) in ovarian tumorigenesis. EMT related genes including E-cadherin, Snail, Slug, and Twist were examined. E2 treatment led to clear morphological changes and an enhanced cell migratory propensity. These morphologic and functional alterations were associated with changes in the abundance of EMT-related genes. Upon E2 stimulation, expression and promoter activity of the epithelial marker E-cadherin was strikingly suppressed, whereas EMT-associated transcription factors Snail and Slug were significantly up-regulated. This up-regulation was attributed to the increase in gene transcription activated by E2. Depletion of the endogenous Snail or Slug using small interfering RNA (siRNA) attenuated E2-mediated control in E-cadherin. In addition, the E2-induced cell migration was neutralized by Snail and Slug siRNAs, implying that both transcription factors are indispensable for the pro-metastatic actions of E2. Importantly, by using selective ER agonists as well as over-expression and siRNA approaches, it was identified that E2 triggered the metastatic behaviors exclusively through an ER⍺-dependent pathway. In contrast, overexpression of ERβ opposed the phenotypic changes and down-regulation of E-cadherin induced by ER⍺. In addition, microarray analysis was performed to characterize more putative downstream mediators of E2. Expression levels of 486 genes were found to be altered by at least 50% upon E2 treatment, and included several genes involved in oncogenesis, cell cycle control, apoptosis, signal transduction and the gene expression machinery. These candidate genes may be valuable for better delineating the ER pathways and functions. In summary, this study provides compelling arguments that estrogen can potentiate tumor progression by EMT induction, and highlight the crucial role of ER⍺ in ovarian tumorigenesis.
9
Woolgar, Julia Anne. "Lymph node metastasis in oral cancer." Electronic Thesis or Dissertation, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260368.
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10
Knight, C. Rosamund L. "Transglutaminase activity, tumour growth and metastasis." Electronic Thesis or Dissertation, Nottingham Trent University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278115.
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Книги з теми "Metastasis":

1
Casserez, Raimundo Gómez. Metastasis. Cartagena: Fundación Cultural Héctor Rojas Herazo, 1988.
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2
Wakefield, Lalage, and Kent W. Hunter. Metastasis. Amsterdam: IOS Press, 2007.
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3
Singh, Gurmit, and Shafaat A. Rabbani, eds. Bone Metastasis. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1592598927.
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4
Schirrmacher, Volker, and Reinhard Schwartz-Albiez, eds. Cancer Metastasis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1.
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Prodi, Giorgio, Lance A. Liotta, Pier-Luigi Lollini, Spiridione Garbisa, Sergio Gorini, and Kurt Hellmann, eds. Cancer Metastasis. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-5037-6.
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Lyden, David, Danny R. Welch, and Bethan Psaila, eds. Cancer Metastasis. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511976117.
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Gorelik, Elizier L., ed. Metastasis / Dissemination. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2534-2.
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8
Weiss, Leonard. Principles of metastasis. Orlando: Academic Press, 1985.
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Weiss, Leonard. Principles of metastasis. Orlando: Academic Press, 1985.
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10
Schumacher, Udo, Susan A. Brooks, and M. V. Dwek. Metastasis research protocols. New York: Humana Press, 2014.
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Частини книг з теми "Metastasis":

1
Muschel, Ruth J. "Metastasis." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3671-2.
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2
Tu, Shi-Ming. "Metastasis." In Cancer Treatment and Research, 137–46. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5968-3_13.
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3
Popper, Helmut, and Bruno Murer. "Metastasis." In Essentials of Diagnostic Pathology, 275–96. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-22664-0_19.
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4
Muschel, Ruth J. "Metastasis." In Encyclopedia of Cancer, 2785–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_3671.
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5
Armstrong, Carol L. "Metastasis." In Encyclopedia of Clinical Neuropsychology, 1586. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_129.
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Armstrong, Carol L. "Metastasis." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_129-2.
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Popper, Helmut. "Metastasis." In Pathology of Lung Disease, 577–610. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-50491-8_18.
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Muschel, Ruth J. "Metastasis." In Encyclopedia of Cancer, 2260–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3671.
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9
Schiffmann, E., M. L. Stracke, and L. A. Liotta. "Metastasis." In Peptide Growth Factors and Their Receptors II, 587–609. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74781-6_20.
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10
Read, Russell W. "Metastasis." In Intraocular Inflammation, 1511–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-540-75387-2_150.
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Тези доповідей конференцій з теми "Metastasis":

1
"CANCER METASTASIS LEE19-01474." In CANCER METASTASIS LEE19-01474. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-094-3.
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2
Massagué, Joan. "Abstract IA25: Metastasis pathways." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-ia25.
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3
Qian, Bin-Zhi. "Abstract 4620: Signaling cascade of metastasis-associated macrophages determines breast cancer distal metastasis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4620.
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4
Tsou, Ann-Ping, Yu-Lun Liao, Yi-Ming Sun, Jorng-Tzong Horng, and Michael Hsiao. "Abstract 3109: SOX4 and POU2F1 synergistically regulate metastasis-associated NRP1 in HCC metastasis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3109.
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Esmonde-White, Karen A., Joseph Sottnik, Michael Morris, and Evan Keller. "Raman spectroscopy of bone metastasis." In SPIE BiOS. SPIE, 2012. http://dx.doi.org/10.1117/12.909327.
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Massagué, Joan. "Abstract IA-19: Deconstructing metastasis." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-ia-19.
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7
Bowen, Anne, and Abdul N. Malmi-Kakkada. "Physical Signatures of Cancer Metastasis." In PEARC17: Practice and Experience in Advanced Research Computing 2017. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3093338.3104176.
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Quraishi, Nasir. "Spinal Metastasis - Diagnosis and Staging." In eccElearning Postgraduate Diploma in Spine Surgery. eccElearning, 2017. http://dx.doi.org/10.28962/01.3.140.
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Contreras, Lellys M., Boris Sarcevic, Keke M. Pounds, and Danny R. Welch. "Abstract 3258: Breast Metastasis Suppressor 1 (BRMS1) phosphorylation appears necessary for metastasis suppressor activity." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3258.
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Lee, Minnkyong, Amy M. Dworkin, Jens Lichtenberg, Shashank J. Patel, Derek Gildea, David M. Bodine, and Nigel PS Crawford. "Abstract 123: The breast cancer metastasis suppressor RRP1B modulates metastasis through regulation of histone methylation." 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.am2014-123.
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Звіти організацій з теми "Metastasis":

1
Welch, Danny R. Metastasis Genes in Breast Cancer Metastasis to Bone. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427647.
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2
Teng, Yong. Targeting Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada621823.
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3
Wang, Weigang. Hypoxia in Invasion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485743.
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4
Pettaway, Curtis A. Angiogenesis Regulates Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada398034.
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5
Keller, Evan. Novel Aptamers to Target Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada534850.
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6
Massague, Joan. Dissecting and Targeting Latent Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada605186.
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7
Keller, Evan, and Greg Shelley. Novel Aptamers to Target Metastasis. Fort Belvoir, VA: Defense Technical Information Center, November 2012. http://dx.doi.org/10.21236/ada569358.
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8
Zhang, Yan. Antibody Microchips to Study Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418683.
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9
Keller, Evan. Novel Aptamers to Target Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada555311.
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10
Pettaway, Curtis A. Angiogenesis Regulates Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada378066.
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