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Relevant bibliographies by topics / Neoplastic Stem Cells

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Academic literature on the topic 'Neoplastic Stem Cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Neoplastic Stem Cells"

1

McCracken, Melissa N., Benson M. George, Kevin S. Kao, Kristopher D. Marjon, Tal Raveh, and Irving L. Weissman. "Normal and Neoplastic Stem Cells." Cold Spring Harbor Symposia on Quantitative Biology 81 (2016): 1–9. http://dx.doi.org/10.1101/sqb.2016.81.030965.

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Weissman, Irving. "Normal and neoplastic stem cells." Experimental Hematology 43, no. 9 (September 2015): S27. http://dx.doi.org/10.1016/j.exphem.2015.06.015.

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Cherniack, E. Paul, Sahithi Chekuri, and Heather F. Lee. "Potential Non-neoplastic Applications for Polyphenols in Stem Cell Utilization." Current Drug Targets 20, no. 3 (January 25, 2019): 347–53. http://dx.doi.org/10.2174/1389450119666180731092453.

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While polyphenols may have important effects on pluripotential stem cells that make them noteworthy as potential antineoplastic agents, their action on stem cells may portend other health benefits, such as treatments for cardiovascular and neurocognitive disorders. Resveratrol, the beststudied polyphenol, has been found to enable stem cells to differentiate into cardiomyocytes, neurons, osteocytes, and pancreatic beta cells, as well as facilitating augmentation of stem cell populations and protecting them from toxic injury. Curcumin protects mesenchymal stem cells from toxicity, and prevents them from facilitating chondrocytic hypertrophy. Quercetin enabled osteocytic and pancreatic beta cell differentiation, and protected neuronal stem cells from injury. Epigallocatechin gallate prevented damage to osteocyte precursors and averted differentiation into undesirable adipocytes. Genistein facilitated osteogenesis while preventing adipogenesis. Several other polyphenols, daidzein, caffeic and chlorogenic acid, kaempferol, and piceatannol, protect stems cells from reactive oxygen species and foster stem cells differentiation away from adipocytic and toward osteocytic lineages. Further research should better elucidate the pharmacokinetic profiles of each polyphenol, explore novel delivery systems, and expand investigation beyond rodent models to additional species.

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Laurenzana, Ilaria, Daniela Lamorte, Stefania Trino, Luciana De Luca, Concetta Ambrosino, Pietro Zoppoli, Vitalba Ruggieri, et al. "Extracellular Vesicles: A New Prospective in Crosstalk between Microenvironment and Stem Cells in Hematological Malignancies." Stem Cells International 2018 (May 27, 2018): 1–11. http://dx.doi.org/10.1155/2018/9863194.

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The bone marrow (BM) microenvironment in hematological malignancies (HMs) comprises heterogeneous populations of neoplastic and nonneoplastic cells. Cancer stem cells (CSCs), neoplastic cells, hematopoietic stem cells (HSCs), and mesenchymal stromal/stem cells (MSCs) are all components of this microenvironment. CSCs are the HM initiators and are associated with neoplastic growth and drug resistance, while HSCs are able to reconstitute the entire hematopoietic system; finally, MSCs actively support hematopoiesis. In some HMs, CSCs and neoplastic cells compromise the normal development of HSCs and perturb BM-MSCs. In response, “reprogrammed” MSCs generate a favorable environment to support neoplastic cells. Extracellular vesicles (EVs) are an important cell-to-cell communication type in physiological and pathological conditions. In particular, in HMs, EV secretion participates to unidirectional and bidirectional interactions between neoplastic cells and BM cells. The transfer of EV molecular cargo triggers different responses in target cells; in particular, malignant EVs modify the BM environment in favor of neoplastic cells at the expense of normal HSCs, by interfering with antineoplastic immunity and participating in resistance to treatment. Here, we review the role of EVs in BM cell communication in physiological conditions and in HMs, focusing on the effects of BM niche EVs on HSCs and MSCs.

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Jandial, Rahul, Dawn J. Waters, and Mike Y. Chen. "Cancer Stem Cells Can Arise From Differentiated Neoplastic Cells." Neurosurgery 69, no. 2 (August 2011): N22. http://dx.doi.org/10.1227/01.neu.0000400017.39272.62.

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Fan, Xing, and Charles G. Eberhart. "Medulloblastoma Stem Cells." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2821–27. http://dx.doi.org/10.1200/jco.2007.15.2264.

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Medulloblastoma and other embronal brain tumors are similar in appearance and differentiation potential to neural stem and progenitor cells. Expression studies performed using human tumor samples, as well as the analysis of murine transgenic models, suggest that both multipotent cerebellar stem cells and lineage-restricted progenitors of the external germinal layer can be transformed into medulloblastoma by genetic alterations. These molecular changes frequently involve constitutive activation of signaling pathways such as Wnt, Hedgehog, and Notch, which play a key role in non-neoplastic neural stem cells. Pharmacologic blockade of the Hedgehog and Notch pathways suppresses the growth of medulloblastoma in culture and in vivo and may prove effective in targeting the small cancer stem-cell subpopulation required for tumor initiation and long-term propagation.

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Schulenburg, Axel, Kira Brämswig, Harald Herrmann, Heidrun Karlic, Irina Mirkina, Rainer Hubmann, Sylvia Laffer, et al. "Neoplastic stem cells: Current concepts and clinical perspectives." Critical Reviews in Oncology/Hematology 76, no. 2 (November 2010): 79–98. http://dx.doi.org/10.1016/j.critrevonc.2010.01.001.

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Ruch, Randall. "Connexin43 Suppresses Lung Cancer Stem Cells." Cancers 11, no. 2 (February 2, 2019): 175. http://dx.doi.org/10.3390/cancers11020175.

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Alterations in gap junctions and their protein components, connexins, have been associated with neoplastic transformation and drug resistance, and more recently have been shown to play important roles in cancer stem cells (CSCs). However, there is less knowledge of connexins and gap junctions in lung CSCs. To address this, Connexin43 (Cx43), the major human lung epithelial gap junction protein, was expressed ectopically in poorly expressing National Cancer Institute-125 (NCI-H125) metastatic human lung adenocarcinoma cells, and phenotypic characteristics of malignant cells and abundance of CSCs were evaluated. The ectopic expression of Cx43 resulted in the formation of functional gap junctions; a more epithelial morphology; reduced proliferation, invasion, colony formation, tumorsphere formation, pluripotency marker expression, and percentage of aldehyde dehydrogenase (ALDH)-positive cells; and increased cisplatin sensitivity. Similarly, in NCI-H522 (human lung adenocarcinoma) and NCI-H661 (human lung large cell carcinoma) cell lines, which express Cx43 and functional gap junctions endogenously, the Cx43 content was lower in tumorspheres and ALDH-positive cells than in bulk cells. These results demonstrate that Cx43 can reverse several neoplastic characteristics and reduce the abundance of human lung CSCs.

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Xiao, Ying, Daniel T. Thoresen, Jonathan S. Williams, Chaochen Wang, James Perna, Ralitsa Petrova, and Isaac Brownell. "Neural Hedgehog signaling maintains stem cell renewal in the sensory touch dome epithelium." Proceedings of the National Academy of Sciences 112, no. 23 (May 26, 2015): 7195–200. http://dx.doi.org/10.1073/pnas.1504177112.

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The touch dome is a highly patterned mechanosensory structure in the epidermis composed of specialized keratinocytes in juxtaposition with innervated Merkel cells. The touch dome epithelium is maintained by tissue-specific stem cells, but the signals that regulate the touch dome are not known. We identify touch dome stem cells that are unique among epidermal cells in their activated Hedgehog signaling and ability to maintain the touch dome as a distinct lineage compartment. Skin denervation reveals that renewal of touch dome stem cells requires a perineural microenvironment, and deleting Sonic hedgehog (Shh) in neurons or Smoothened in the epidermis demonstrates that Shh is an essential niche factor that maintains touch dome stem cells. Up-regulation of Hedgehog signaling results in neoplastic expansion of touch dome keratinocytes but no Merkel cell neoplasia. These findings demonstrate that nerve-derived Shh is a critical regulator of lineage-specific stem cells that maintain specialized sensory compartments in the epidermis.

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Bryukhovetskiy, I. S., A. S. Bryukhovetskiy, P. V. Mischenko, I. A. Merkulov, and Y. S. Khotimchenko. "STEM CELL THERAPY OF MALIGNANT BRAIN TUMORS: REALITY AND PROSPECTS." Journal of Clinical Practice 4, no. 4 (December 15, 2013): 45–54. http://dx.doi.org/10.17816/clinpract4445-54.

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Modern methods for the treatment of malignant brain tumors are insufficiently effective. One reason for this is that the existing technologies and methods are focused on removing all neoplastic cellsfrom the body. Understanding the mechanisms of systemic migration of stem cells provides a new view on the role of this phenomenon in the development of malignant tumors. Migration and homing of normal stem cells, being originally the regulatory process, ensuring revascularization and remodeling of ischemic or traumatic injury of brain, play a role of the axial conductor of neoplastic process in carcinogenesis. The use of the phenomenon of migration and homing of stem cells in the tumor center for therapeutic purposes opens the possibility of overcoming the blood-brain barrier, reducing the toxicity of chemotherapy and increasing the radiation therapy efficiency, makes possible the directed influence on the hypoxic zone of the tumor, can directly affect to the key life processes of tumor stem cells. These arguments allow to consider the mechanisms of systemic migration and homing of stem cells to neoplastic foci as a fundamental theoretical platform for the creation of a fundamentally new class of anti-cancer, cell personalized medicines.

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Dissertations / Theses on the topic "Neoplastic Stem Cells"

1

O'Shaughnessy, Ryan Francis Lucas. "Analysis of gene expression in normal and neoplastic keratinocytes." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325883.

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Turhan, Ali G. "Clonality of normal and malignant hemopoiesis." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/31369.

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In the normal adult human, hemopoiesis appears to be maintained by the simultaneous activity of many stem cell-derived clones. Conversely, most examples of human myeloid malignancies have been shown to represent clonal populations arising as a result of the unregulated expansion of a single transformed hemopoietic stem cell. The limits of the proliferative capacity of normal hemopoietic stem cells in humans and their persistence in hemopoietic malignancies have, however, not been extensively Investigated. One of the most likely reasons for this is the lack, until very recently, of a widely applicable method to analyze the clonality status of human cell populations. Methylation analysis of two polymorphic genes. HPRT and PGK, now allows such studies to be performed in approximately 50 % of females. The possibility that normal human hemopoietic stem cells might have the capacity to mimic the behaviour of some transformed stem cells by generating clones of progeny that could dominate the entire hemopoietic system was then examined. Such a phenomenon has been well documented in animal models of marrow cell transplantation. I therefore undertook an analysis of all allogeneic marrow transplants performed over a 1 to 1-1/2 year period where the genotype of the donor made clonality analysis using the HPRT or PGK systems possible. Using this approach, I obtained evidence in two patients suggesting that a single or, at most, a very small number of normal primitive hemopoietic stem cells were able to reconstitute the hemopoietic system. In one case the data suggested that such reconstitution was likely to have derived from a stem cell with both lymphopoietic and myelopoietic potential. However, in all other cases hemopoiesis in the transplant recipient was found to be polyclonal. Such findings indicate that clonal dominance in the hemopoietic system is not sufficient to infer that a genetically determined neoplastic change has occurred. In addition, these findings have implications for the design of future gene therapy protocols. The same methodology was also applied to investigate the clonality of different hemopoietic cell populations in patients with chronic myelogenous leukemia (CML) and essential thrombocytosis (ET). In both of these myeloproliferative disorders, the neoplastic clone produces terminally differentiated progeny that appear minimally different from normal. Data from the CML studies confirmed the non-clonal nature of the cells emerging in long-term CML marrow cultures. Similarly, patients transplanted with cultured autologous marrow were shown to undergo polyclonal and bcr-negative reconstitution of their hemopoietic system. Analysis of a series of patients with a clinical diagnosis of ET showed that polyclonal hemopoiesis in the presence of an amplified neoplastic clone is not a rare event in this disorder, and that clonality results do not always correlate with other neoplastic markers associated with myeloproliferative diseases in general. Another example of polyclonal hemopoiesis in the presence of an amplified neoplastic clone was demonstrated in a patient with Ph¹-positive ALL whose disease appeared to have originated in a lymphoid-restricted stem cell. The studies described in this thesis reveal a level of complexity of normal and neoplastic stem cell dynamics not previously documented. They highlight the need for more precise information about the molecular basis of regulatory mechanisms that govern hemopoietic cell proliferation and survival at every level of differentiation. Finally they support the accumulating evidence that acquisition of full malignant potential requires several additive genetic changes first postulated many years ago as the somatic mutation theory of carcinogenesis.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate

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Jergil, Måns. "Pluripotent Stem Cells of Embryonic Origin Applications in Developmental Toxicology /." Uppsala : Acta Universitatis Upsaliensis, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-109946.

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Su, Dan. "Microarray screening and identification of RARgamma regulated genes in F9 teratocarcinoma stem cells /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1428838881&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Abraham, Samuel D. M. "Activation of multiple hemopoietic growth factor genes in Abelson virus transformed myeloid cells." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27786.

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The stringent requirement for hemopoietic growth factors (HGF) in the induction of hemopoiesis in vitro has raised questions as to their possible role(s) in leukemogenesis. Several recent clinical studies have shown aberrant cell growth factor gene activation in patient derived leukemic cells. Assessment of growth factor activity is often based on in vitro bioactivity assays of conditioned media or body fluids. The specificity of this type of endpoint is, however, open to question due to the overlap in biological activities of many HGFs. In assessing the role of growth factor gene expression in a murine myeloid leukemia model I have used a sensitive RNA detection procedure coupled with a vector-probe system that enables the synthesis of uniformly labelled radioactive DNA probes to detect unambiguously the expression of particular growth factor genes. The Abelson murine leukemia virus (A-MuLV) derived myeloid transformants used in this study had previously been shown to produce a multi-lineage colony stimulating activity (CSA). While these A-MuLV transformants were shown to produce GM-CSF, it seemed likely that the multi-lineage CSA was due to another factor. In addition to confirming the expression of GM-CSF mRNA, I was able to show that the cells of all four A-MuLV transformed lines tested also expressed interleukin-3 mRNA. This finding was strongly corroborated by bio-activity data obtained using the CM from the A-MuLV myeloid transformants. Additional preliminary analysis by bioactivity assays have also shown the possible presence of interleukin-6 (IL-6) and a recently described pre-B cell factor suggesting perhaps a common mechanism underlying the activation of these various growth factor genes.
Medicine, Faculty of
Medical Genetics, Department of
Graduate

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Sun, Huayan. "Function of the β4 Integrin in Cancer Stem Cells and Tumor Formation in Breast Cancer: A Masters Thesis." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/814.

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The integrin α6β4 (referred to as β4) is expressed in epithelial cells where it functions as a laminin receptor. Integrin β4 is important for the organization and maintenance of epithelial architecture in normal cells. Particularly, β4 is shown to be essential for mammary gland development during embryogenesis. Integrin β4 also plays important roles in tumor formation, invasion and metastasis in breast cancer. However, the mechanism of how integrin β4 mediates breast tumor formation has not been settled. A few studies suggest that integrin β4 is involved in cancer stem cells (CSCs), but the mechanism is not clear. To address this problem, I examined the expression of β4 in breast tumors and its potential role involved in regulating CSCs. My data shows that β4 is expressed heterogeneously in breast cancer, and it is not directly expressed in CSCs but associated with a basal epithelial population. This work suggests that β4 can regulate CSCs in a non-cell-autonomous manner through the interactions between β4+ non-CSC population and β4- CSC population. My data also shows that β4 expression is associated with CD24+CD44+ population in breast tumor. To further study the role of β4 in breast cancer progression, I generated a β4 reporter mouse by inserting a p2A-mCherry cassette before ITGB4 stop codon. This reporter mouse can be crossed with breast tumor models to track β4+ population during tumor progression.

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Sun, Huayan. "Function of the β4 Integrin in Cancer Stem Cells and Tumor Formation in Breast Cancer: A Masters Thesis." eScholarship@UMMS, 2001. http://escholarship.umassmed.edu/gsbs_diss/814.

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The integrin α6β4 (referred to as β4) is expressed in epithelial cells where it functions as a laminin receptor. Integrin β4 is important for the organization and maintenance of epithelial architecture in normal cells. Particularly, β4 is shown to be essential for mammary gland development during embryogenesis. Integrin β4 also plays important roles in tumor formation, invasion and metastasis in breast cancer. However, the mechanism of how integrin β4 mediates breast tumor formation has not been settled. A few studies suggest that integrin β4 is involved in cancer stem cells (CSCs), but the mechanism is not clear. To address this problem, I examined the expression of β4 in breast tumors and its potential role involved in regulating CSCs. My data shows that β4 is expressed heterogeneously in breast cancer, and it is not directly expressed in CSCs but associated with a basal epithelial population. This work suggests that β4 can regulate CSCs in a non-cell-autonomous manner through the interactions between β4+ non-CSC population and β4- CSC population. My data also shows that β4 expression is associated with CD24+CD44+ population in breast tumor. To further study the role of β4 in breast cancer progression, I generated a β4 reporter mouse by inserting a p2A-mCherry cassette before ITGB4 stop codon. This reporter mouse can be crossed with breast tumor models to track β4+ population during tumor progression.

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8

Engel, Høi-Hansen Christina. "Application of stem cell markers in search for neoplastic germ cells in dysgenetic gonads, extragonadal tumors, and in semen of infertile men /." Copenhagen : Univ. Copenhagen, Fac. of Health Sciences, 2008. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016356357&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Chen, Yaoyu. "Critical Molecular Pathways in Cancer Stem Cells of Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/536.

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Chronic myeloid leukemia (CML) is a disease characterized by the expansion of granulocytic cells. The BCR-ABL tyrosine kinase inhibitor imatinib, the frontline treatment for Ph+ leukemias, can induce complete hematologic and cytogenetic response in most chronic phase CML patients. Despite the remarkable initial clinic effects, it is now recognized that imatinib will unlikely cure patients because a small cell population containing leukemic stem cells (LSCs) with self-renewal capacity is insensitive to tyrosine kinase inhibitors. In Chapter I, I briefly review the BCR-ABL kinase and its related signaling pathways. BCR-ABL kinase activates several signaling pathways including MAPK, STAT, and JNK/SAPK. BCR-ABL also mediates kinase-independent pathways through SRC family kinases. I will also discuss pathways involving β-catenin, hedgehog, FoxO and Alox5 are critical to the regulation of self-renewal and differentiation in LSC of CML. As detailed in Chapter II, I describe our work evaluating the effects of omacetaxine, a novel CML drug inducing cell apoptosis by inhibition of protein synthesis, on self-renewal and differentiation of LSCs and BCR-ABL-induced CML and acute lymphoblastic leukemia (B-ALL) in mice. We found that treatment with omacetaxine decreased the number of LSCs and prolonged the survival of mice with CML or B-ALL. In chapter III, I describe that Alox5 is an essential gene in the function of LSCs and CML development. We show evidence that Alox5 affects differentiation, cell division, and survival of long-term LSCs. Treatment of CML mice with a 5-LO inhibitor also impaired the function of LSCs similarly and prolonged survival. In chapter IV, I present evidence of our work showing a further dissection the Alox5 pathway by comparing the gene expression profiles of wild type and Alox5-/- LSCs. We show that Msr1 deletion causes acceleration of CML development. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-catenin. Taken together, these results demonstrate that some pathways including Alox5 and Msr1 play an important role in regulating the self-renewal and differentiation of LSC. More efforts should be put into developing the novel strategies that may effectively target LSCs and thus cure CML.

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Oliveira, Rodrigo Vismari de 1980. "Expressão de antígenos de células-tronco neoplásicas avaliada por imunoistoquímica em neoplasias malignas da mama humana : caracterização e possíveis aplicações clínicas." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312484.

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Orientador: André Almeida Schenka
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T04:27:58Z (GMT). No. of bitstreams: 1 Oliveira_RodrigoVismaride_M.pdf: 21638955 bytes, checksum: 23e75fa9b7ece343f54fcfd2dcaea03c (MD5) Previous issue date: 2014
Resumo: O câncer de mama é a neoplasia maligna mais frequente no mundo. A hipótese da célula-tronco neoplásica (CTN) é um novo paradigma de carcinogênese. A imunoistoquímica (IHC) é um método de escolha para detecção de CTN em tecidos parafinizados, com as seguintes vantagens: (1) maior adaptação à rotina diagnóstica; (2) menor custo; (3) menor complexidade. Entretanto, há poucos estudos de marcadores imunoistoquímicos CTN na literatura, a maioria com poucos pacientes e resultados controversos. Um painel de marcadores imunoistoquímicos CTN foi usado em 74 casos de câncer mamário, os quais foram diagnosticados, tratados e acompanhados no UNACON- Poços de Caldas, de 2004 a 2006. Objetivos: (1) descrever quali e quantitativamente um amplo painel imunoistoquímico de anticorpos; (2) estabelecer associações entre marcadores CTN e fatores clínicos, patológicos e prognósticos / preditivos de resposta terapêutica; (3) estabelecer o impacto da expressão de marcadores CTN na sobrevida e recidiva tumoral; (4) estabelecer possíveis correlações intermarcadores. Métodos: Foram testados em cortes de TMA, obtidos a partir dos blocos de parafina originais contendo os tumores mamários, os seguintes anticorpos: CD34, c-kit, CD10, SOX-2, Oct 3/4, p63, CD24, CD44, CD133 e ESA/EPCAM. Fotomicrografias foram obtidas das lâminas de imunoistoquímica dos TMAs e as células positivas foram contadas. As variáveis clínicas, patológicas e prognósticas / preditivas de resposta terapêutica foram obtidas dos prontuários médicos. Resultados e conclusões: A média de idade das pacientes foi de 57 anos (28-84), o IMC médio (índice de massa corpórea) foi 27 (13-39), 6,8% eram tabagistas, 58,9% eram menopausadas e 10,8% referiram história familiar de câncer. O acompanhamento clínico médio foi de 52 meses, com recidiva em 28,6% dos casos, tempo médio de recidiva de 37 meses e óbito de 26,7% das pacientes. Os principais anticorpos imunoistoquímicos CTN neste estudo foram CD24, CD44, CD133 e ESA. Os demais anticorpos foram positivos em menos de 15% dos casos. Pelo menos um marcador CTN foi expresso em 85% dos casos. O principal anticorpo CTN individualmente positivo foi o CD44, em 60,8% dos casos. Por motivos didáticos, 2 perfis CTN foram definidos: (1) CD24 - / CD44+ e (2) CD133+ / ESA+. O primeiro perfil CTN foi mais frequente: (1) nas pacientes acima dos 40 anos; (2) em tumores menores de 2,0 cm; (3) em estádios clínicos iniciais (I e II); (4) e sua positividade elevou o risco de óbito em cerca de 4 vezes. A expressão de qualquer marcador CTN foi mais frequente nos graus histológicos elevados (2 e 3). A expressão isolada de CD133 foi mais frequente nas pacientes menopausadas, a expressão isolada de CD24 foi mais frequente nos tumores maiores que 2,0 cm e a expressão isolada de CD44 foi mais frequentes nas pacientes acima de 40 anos de idade. Não foram observadas correlações intermarcadores significativas. Portanto, a imunoistoquímica é um método de baixa sensibilidade para detectar marcadores CTN no câncer mamário humano, limitando a sua análise quantitativa. Por este motivo, não há evidências suficientes que apoiem o valor clínico dos marcadores CTN
Abstract: Breast cancer is the most frequent malignant neoplasm in the world. The neoplastic stem-cell hypothesis (NSC) is a new paradigm of carcinogenesis. Immunohistochemistry (IHC) is a elegible method to detect NSC in paraffinized tissue, with the following advantages: (1) more adaptable to diagnostic routine, (2) lower cost, (3) lower complexity. Though, there are few researches in the literature analysing the NSC antibodies in human breast cancer, the majority with few patients and controversial results. A IHC pannel of NSC markers was used in 74 breast cancer cases, which were diagnosed, treated and followed in Poços de Caldas Cancer Hospital (UNACON), from 2004 to 2006. The present study aims to: (1) describe a large IHC pannel of NSC antibodies, quantitatively and qualitatively; (2) establish associations between NSC markers and clinical, pathological and prognostic / predictive therapeutic response factors; (3) establish the impact of NSC markers expression to the survival and to the tumor relapse; (4) establish possible intermarkers correlations. Methods: The IHC antibodies CD34, c-kit, CD10, SOX-2, Oct 3/4, p63, CD24, CD44, CD133 and ESA/EPCAM were tested in tissue microarrays (TMA) sections, obtained from the original paraffin blocks of breast tumors. Photomicrographies were obtained from the immunohistochemistry TMA slides. The positive cells were counted. Clinical, pathological and prognostic / predictive therapeutic response variables were obtained from the medical records. Results and conclusions: The median patient age was 57 years (range 28-84), the median BMI (body mass index) was 27 (range 13-39), 6,8% were smokers, 58,9% were in menopause and 10,8% related familial cancer history. The median follow-up was 52 months, with tumor relapse in 28,6% of the cases, median relapse time of 37 months and death of 26,7% of the patients. The mainly positive NSC immunohistochemistry antibodies in our study were CD24, CD44, CD133 and ESA. The others antibodies were positive in less of 15% of the cases. At least one NSC marker was expressed in 85% of the cases. The mainly individual positive NSC antibody was CD44, in 60,8% of the cases. For didatic reasons, two NSC profiles were defined: (1) CD24 - / CD44+ cells and (2) CD133+ / ESA+ cells. The first NSC profile was more frequent in: (1) patients older than 40 years; (2) tumors smaller than 2,0 cm; (3) beginning tumor clinical stages (I and II); (4) and this expression rise the death risk in about 4 times. The second NSC profile rise the relapse tumor risk in about 3,75 times. Anyone NSC antibody expression was more frequent in high histologic grades of tumor (2 and 3). Isolated CD133 expression was more frequent in menopaused patients, isolated CD24 expression was more frequent in tumors larger than 2,0 cm and isolated CD44 expression was more frequent in patients upper than 40 years. No significant intermarkers correlations were observed. Thus, immunohistochemistry is a low sensibility method to detect NSC markers in human breast cancer, limiting the quantitative analysis of them. For this reason, there is not sufficient evidences to support the clinical value of NSC markers
Mestrado
Fisiopatologia Médica
Mestre em Ciências

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Books on the topic "Neoplastic Stem Cells"

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Thomas, Dittmar, and Zander Kurt S, eds. Cancer and stem cells. New York: Nova Science Publishers, 2008.

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L, Farrar William, ed. Cancer stem cells. Cambridge: Cambridge University Press, 2009.

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Marcha, Juan Antonio. Therapeutic potential of differentiation in cancer and normal stem cells. New York: Nova Biomedical Books, 2009.

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Antonio, Marcha Juan, ed. Therapeutic potential of differentiation in cancer and normal stem cells. New York: Nova Biomedical Books, 2009.

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Antonio, Marcha Juan, ed. Therapeutic potential of differentiation in cancer and normal stem cells. New York: Nova Biomedical Books, 2009.

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Antonio, Marcha Juan, ed. Therapeutic potential of differentiation in cancer and normal stem cells. New York: Nova Biomedical Books, 2009.

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Allan, Alison Lawrie. Cancer stem cells in solid tumors. New York: Humana Press, 2011.

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Scatena, Roberto, Alvaro Mordente, and B. Giardina. Advances in cancer stem cell biology. New York: Springer, 2012.

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1938-, Hay Robert, Park Jae-Gahb, and Gazdar Adi F, eds. Atlas of human tumor cell lines. San Diego: Academic Press, 1994.

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Okudela, Koji. Cancer stem cells in lung cancer. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Book chapters on the topic "Neoplastic Stem Cells"

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Weissman, Irving L. "Normal and Neoplastic Stem Cells." In Stem Cells: Nuclear Reprogramming and Therapeutic Applications, 35–54. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470091452.ch4.

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Jeter, Collene R. "Investigating the Role of the Embryonic Stem Cell Self-Renewal Gene NANOG in Neoplastic Processes." In Stem Cells and Cancer Stem Cells, Volume 11, 15–27. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7329-5_2.

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Cogle, Christopher R. "Cancer, Stem Cells and the Neoplastic Niche." In Cancer Microenvironment and Therapeutic Implications, 63–78. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9576-4_4.

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Milano, Filippo, Shelly Heimfeld, and H. Joachim Deeg. "Alternative Sources of Hematopoietic Stem Cells and Their Clinical Applications." In Neoplastic Diseases of the Blood, 1179–92. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64263-5_55.

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Gutman, Jonathan A., Shelly Heimfeld, and H. Joachim Deeg. "Alternative Sources of Hematopoietic Stem Cells and Their Clinical Applications." In Neoplastic Diseases of the Blood, 1289–306. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3764-2_57.

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Chabannon, Christian, and Harry Dolstra. "Regulatory Aspects of ATMP Versus Minimally Manipulated Immune Cells." In The EBMT Handbook, 555–62. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_62.

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AbstractIn 2023, three categories of therapeutic products obtained through the collection and subsequent engineering of hematopoietic cells exist and are valuable to patients treated for neoplastic diseases as well as a variety of nonneoplastic disorders: blood cell transfusions, stem and immune cell transplants, and cellular therapy medicinal products. The procurement and nature of various blood products and transfusion practices are described elsewhere in this handbook. In this chapter, we focus on hematopoietic cellular therapies as currently defined and managed in the FACT-JACIE International Standards for Hematopoietic Cellular Therapies (nowadays in version 8). Over the last two decades, major changes have occurred in the EU regulatory framework (as well as in other parts of the world, notably in the USA) that result in the coexistence of two categories of hematopoietic cellular therapies. Innovative and industry-manufactured somatic cell therapy or gene therapy medicinal products have entered the field at an accelerating pace since the last edition of this handbook. Some of them are distributed worldwide on a large scale, and a few of these medicinal products already complete or compete with traditional hematopoietic cell transplantation practices. We here update the description of organizational consequences of this historical transition for academic facilities and the new opportunities as well as challenges these advances are bringing to patients and healthcare practitioners, including strong needs for educational initiatives.

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Cotta, Claudiu. "Hematopoiesis and Stem Cell Biology." In Neoplastic Hematopathology, 531–44. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_31.

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Shpall, Elizabeth J., and Marcos de Lima. "Clinical Aspects of Hematopoietic Stem Cell Transplantation." In Neoplastic Hematopathology, 505–11. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_28.

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Wright, Nicholas A. "Stem Cells in Intraepithelial Neoplasia." In Pre-Invasive Disease: Pathogenesis and Clinical Management, 3–20. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6694-0_1.

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Marquardt, Jens U., and Snorri S. Thorgeirsson. "Cancer Stem Cells and Liver Cancer." In Molecular Genetics of Liver Neoplasia, 279–99. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6082-5_15.

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Conference papers on the topic "Neoplastic Stem Cells"

1

Weissman, Irving L. "Abstract SY08-02: Normal and neoplastic stem cells." 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-sy08-02.

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Gu, Xiang, Hakim Bouamar, Kyle Pressley, and LuZhe Sun. "Abstract 914: Age-associated neoplastic transformation of mammary stem cells." 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.am2017-914.

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Shay, Jerry W. "Abstract SY33-03: Role of telomerase in normal and neoplastic stem cells." 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-sy33-03.

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Abd Elmageed, Zakaria Y., Yijun Yang, Raju Thomas, Krishnarao Moparty, Manish Ranjan, Debasis Mondal, Krzysztof Moroz, Oliver Sartor, and Asim B. Abdel-Mageed. "Abstract 2612: Tumor associated microvesicles confer neoplastic transformation of patient derived adipose stem cells ." 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.am2013-2612.

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Spike, Benjamin T., Jonathan A. Kelber, Evan Booker, Madhuri Kalathur, Rose Rodewald, Julia Lipianskaya, Justin La, et al. "Abstract 3035: Cripto/GRP78 signaling promotes the stem cell phenotype in normal and neoplastic mammary epithelial cells." 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.am2014-3035.

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Ying, Mingyao, Shuli Xia, and John Laterra. "Abstract 5159: Kruppel-like factor 9 modulates the growth and differentiation of glioblastoma-derived neoplastic stem cells." 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.am10-5159.

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Polacheck, William, and Roger Kamm. "Interstitial Flow and Effects on Tumor Cell Migration." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19446.

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Interstitial flow is the convective transport of fluid through tissue extracellular matrix. This creeping fluid flow has been shown to be important in regulating the development, function, and pathology of tissues. Furthermore, interstitial flow has been shown to affect the morphology and migration of cells such as fibroblasts, cancer cells, endothelial cells, and mesenchymal stem cells (1). Chary and Jain used fluorescence recovery after photobleaching to directly observe fluid flow in the tissue interstitium and determined typical flow velocities are on the order of 0.1–2.0μm/s (2). Interstitial flow is particularly important in driving transport in tumor tissues, as neoplastic tissue is often characterized by increased interstitial pressure (3).

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Spurlock, Brian, and Kasturi Mitra. "Abstract PO-116: High resolution single cell microscopy analyses identifies the cellular redox state that supports conversion to a neoplastic stem cell state." In Abstracts: AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; September 17-18, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.tumhet2020-po-116.

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Raabe, Eric H., Jarek Maciaczyk, Ulf Kahlert, Guido Nikkhah, and Charles Eberhart. "Abstract 4352: Using human neural stem cells to model pediatric high grade gliomas: The role of p53, c-myc, and EGFRvIII in neoplastic transformation." 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.am10-4352.

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Sato, Atsuki, Toshiyuki Ishiwata, Tetsushi Yamamoto, Yoko Matsuda, Hirobumi Asakura, Toshiyuki Takeshita, and Zenya Naito. "Abstract 414: Role of stem cell marker, nestin in human uterine cervical intraepithelial neoplasia and cervical cancer." 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.am2012-414.

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Reports on the topic "Neoplastic Stem Cells"

1

Keckesova, Zuzana. The Role of Epithelial-Mesenchymal Transition in the Formation of Normal and Neoplastic Mammary Epithelial Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada554127.

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