describe the cancer stem cell hypothesis

Tumour Biol 2016; 37: 14463–14477. Google Scholar. 13–11). volume 97, pages1142–1151(2017)Cite this article. Goss AM, Tian Y, Tsukiyama T et al, Wnt2/2b and beta-catenin signaling are necessary and sufficient to specify lung progenitors in the foregut. EMT is a process that is described in a variety of biological scenarios to account for the ability of cells to transdifferentiate from one morphology and function to another, specifically to transform from a polarized epithelial phenotype to a motile, mesenchymal cell phenotype (Kalluri and Weinberg, 2009) (Fig.

For example, parthenolide, a natural product derived from the traditional medicinal herb feverfew that inhibits the nuclear factor kappa B (NF-κB) pathway, has been shown to induce apoptosis in LSCs while sparing normal hematopoiesis in xenograft models of AML (Guzman et al, 2007). Nature 2005; 438: 820–827. • CSCs have been best demonstrated in AML, but have also been demonstrated in solid tumors, such as breast carcinoma, colorectal carcinoma, and head and neck squamous carcinoma. 19, Sec.

FIGURE 13–11 Technical criticisms of the CSC hypothesis. The second criterion is that the injected CSC must differentiate and recapitulate the phenotype of the tumor from which they were derived, although multilineage differentiation as seen in normal somatic stem cells is not a requirement for transplanted cells to be labeled as CSC. Greening DW, Gopal SK, Mathias RA et al, Emerging roles of exosomes during epithelial-mesenchymal transition and cancer progression. News-Medical.Net provides this medical information service in accordance Scheel C, Weinberg RA . The CSC subpopulation within these tumors was not resistant to this treatment, and an improvement in survival was seen in a mouse xenograft model. Gregory PA, Bracken CP, Bert AG et al, MicroRNAs as regulators of epithelial-mesenchymal transition. Las pruebas de esto vienen del trabajo de Thomas Brabletz (2005) y de Mani, que fue publicado en célula en 2008. El objetivo directo de CSCs, con interferencia con los caminos de la transmisión de señales y los factores de la transcripción implicados en EMT, y la producción de CSC - ablación llamada - evitarían así que las células madres de cáncer ofrecieran las células distinguidas para poblar el Massachusetts del tumor. Finally, techniques to study the epigenetic regulation of CSCs are improving rapidly and should provide further mechanistic data on the validity of the CSC hypothesis (and EMT). CSCs have been identified in many solid cancers, including squamous cell carcinoma of the head and neck (Prince et al, 2007), colorectal cancer (Dalerba et al, 2007; O’Brien et al, 2007; Ricci-Vitiani et al, 2007), pancreatic carcinoma (Hermann et al, 2007; Li et al, 2007), hepatocellular carcinoma (Ma et al, 2007; Yang et al, 2008), ovarian carcinoma (Zhang et al, 2008; Stewart et al, 2011), and prostate carcinoma (Collins et al, 2005; Patrawala et al, 2006), as well as cancers of the breast, brain, and melanoma that are discussed in detail below (Fig. Nat Genet 2010; 42: 1113–1117. In vitro self-renewal was measured by assessing the rate of secondary sphere formation in a limiting dilution assay; clonogenicity, the ability to form a new colony, again matched tumor grade. 13–2). Injections into NOD/SCID or NSG mice are often performed in conjunction with Matrigel, a heterogeneous mixture of basement membrane proteins secreted by mouse sarcoma cells, which enhances tumor transplantability.

More dormant, slow-cycling, infrequently dividing cells can be identified by staining a cell population with lipophilic fluorescent dyes, such as PKH26, then selecting fluorescent cells after a period of time in culture; CSC are thought to be less likely to divide and are therefore brighter. 2). Int J Cancer 2011; 129: 2310–2314.

The CSC phenotype correlates with markers of patient outcome such as progression, survival, and distant metastasis. Dev Cell 2009; 17: 290–298. Other microRNAs are also important in the regulation of thyroid cancer. Dhamija S, Diederichs S . For example, just over half of cells in this sample (bottom left panel) are white blood cells, and of the remaining 48% of cells, ~10% are endothelial cells. Other scientists demonstrated that only a fraction of mouse lymphoma cells were capable of forming colonies in an irradiated mouse (Bruce and Van Der Gaag, 1963).

LncRNAs are very abundant with estimates of >30 000 lncRNAs transcripts in the human genome.71, 72, 73, 74, 75, 76, 77 One group of investigators estimated that there were close to 60 000 lncRNAs including 8000 oncologic lncRNAs.74 A growing number of these lncRNAs are being isolated and characterized from thyroid and other cancers.75 Some lncRNAs are upregulated, whereas others are downregulated in thyroid cancers, especially in PTCs, which has been the most frequent type of thyroid cancers used to study the role of lncRNAs in thyroid tumors to date. They have a critical role during development and are linked to various diseases including cancers.61, 62, 63, 64, 65 MicroRNAs have been shown to have a role in tumor development and progression, as they may function as oncogenes and/or tumor-suppressor genes in thyroid and other cancers.64 MicroRNAs are increasingly recognized as important regulators of EMT and of CSCs.65, 66, 67, 68, 69, 70 Recent studies have shown that the miR-200 family has a major regulatory role in EMT.65 The miR-200 family has been shown to regulate EMT induced by EGF/EGFR66 and also by targeting TGFβR1.65 Braun et al65 used ATC cell lines to show that overexpression of miR-200 and miR-30 in mesenchymal ATC-derived cells reduced their invasive potential and induced MET. Front Oncol 2014; 66–70. PubMed Central  Mendell JT . This process is thought to occur during normal development and wound healing, and there is increasing evidence that similar processes occur in cancer. Flow cytometry uses fluorescently labeled antibodies to measure semiquantitatively proteins and antigens on intact cells. This property may contribute to the often quite large differences between the phenotypes and genotypes of cell lines derived from human cancers and the ex vivo tumors themselves (van Staveren et al, 2009). J Surg Res 2015; 196: 39–48. Finally, evidence of in vivo self-renewal of SL-IC was obtained, showing that CD34++/CD38– cells could be isolated from primary xenografted animals and transplanted into secondary recipients with similar efficiencies of engraftment and recapitulation of ex vivo phenotype (Lapidot et al, 1994). Loewer S, Cabili MN, Guttman M et al, Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells. Nature 1994; 367: 645–648. PLoS ONE 2014; 9: e103871. Nature 2012; 481: 85–89. Las pruebas más persuasivas de la existencia de células madres dentro de un tumor vienen del análisis de los marcadores de la superficie de la célula. These pathways include, among others, the Notch, Wnt/β-catenin and hedgehog (HH) pathways. Nevertheless, various contradictions related to the mutation theory have been reported previously. Inhibition of chromatin remodeling by inhibition of histone deacetylation (by the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid), or by upstream inhibition of insulin-like growth factor signaling) prevent DTP cells from surviving. They have been analyzed in various types of cancers including those in the thyroid.7, 43, 44, 45, 46, 47, 48, 49, 50, Mammalian cells express four transmembrane Notch receptors including NOTCH-1, NOTCH-2, NOTCH-3 and NOTCH-4.43, 44, 45, 46, 47, 48, 49, 50 Notch signaling has been implicated in self-renewal in CSCs in a variety of cancers. Mod Pathol 2013; 26: 54–61. Cancer Res 2007; 67: 8985–8988. 13–3). © 2003-2020 Chegg Inc. All rights reserved. Vella LJ . CSC markers have been discovered by trial and error, but have frequently been translated from normal stem cell biology to the cancer setting.

Sonic HH (SHH) signaling pathway was activated in benign thyroid tumors such as follicular adenomas.54 Heiden et al53 reported that SHH signaling maintained the CSC self-renewal of ATCs by inducing Snail expression. Tumor maintenance or dissemination is therefore a random or stochastic process, and variation between different behaviors may involve transition to and from epithelial to mesenchymal phenotypes. FIGURE 13–3 Increasingly detailed genomic data from successive generations of DNA sequencing technology reveal the clonal structure of cancer cell populations. 2, Sec. There are, therefore, several competing models to account for epigenetic heterogeneity in normal and malignant tissues. Please note that medical information found Finally, a recent examination of cell phenotypes in genomically normal embryonic stem cell cultures showed the presence of embryonic stem (ES) cells in a so-called super state, where a small (~0.2% to 1.5%) fraction of cells were “totipotent” rather than simply pluripotent (Macfarlan et al, 2012).

Cyclopamine has proven toxic in humans, but a number of synthetic inhibitors of the Hedgehog pathway are in clinical trials in basal cell carcinoma, pancreatic carcinoma, medulloblastoma, head and neck squamous carcinoma, and non–small cell lung cancer (Clayton and Mousa, 2011). CAS  PubMed  From serial transplantation of samples from multiple patients into mice, it became apparent that there were several different populations of LSCs, which the authors termed short-term, long-term, and quiescent long-term SL-ICs. A growing body of evidence indicates that the interaction between tumor cells and the local microenvironment at the metastatic site leads to the development of the premetastatic niche(s), which allows for the proliferation of metastatic cells during colonization.97 Tumor cells can produce various factors leading to the establishment of the premetastatic niche(s). The emerging role of exosomes in epithelial-mesenchymal-transition in cancer. Ageing Res Rev. 19, Sec. Hamburger and Salmon (1977) demonstrated in clonogenic assays that only a fraction of cells from freshly excised human tumors could form colonies in tissue culture (including myeloma, lymphoma, neuroblastoma, ovarian carcinoma, chronic lymphocytic leukemia, small cell lung cancer, and melanoma). 19.3). The stem cell theory of cancer proposes that among all cancerous cells, a few act as stem cells that reproduce themselves and sustain the cancer, much like normal stem cells normally renew and sustain our organs and tissues. MicroRNA deregulation in anaplastic thyroid cancer biology. FIGURE 13–4 Two mutually exclusive theories can be proposed to account for epigenetic tumor heterogeneity. The basics of epithelial-mesenchymal transition. Some types of resistance to chemotherapy can be accounted for by the CSC hypothesis (see Chap.

Padua Alves C, Fonseca AS, Muys BR et al, Brief report: the lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines. Tal inhibición de la regeneración del tumor llevaría final a la regresión del tumor. There are many complexities and challenges in active cancer immunotherapy (Cebon et al, 2007) but human studies of active vaccination against CSC have commenced. NOTCH4 has been shown to regulate breast CSCs and γ-secretase inhibitors of the NOTCH pathway (see Chap. Fetal cell carcinogenesis of the thyroid: a modified theory based on recent evidence. There is also heterogeneity within individual cancers, between stromal cells with a normal genome and mutated malignant cells, between differently mutated malignant clones, between epigenetically different subpopulations within clonal populations, and between cells within different microenvironments within the tumor (Fig.

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