Bibliographies thématiques / Stem cell heterogeneity

Littérature scientifique sur le sujet « Stem cell heterogeneity »

Auteur : Grafiati
Publié le 11 mars 2023

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Articles de revues sur le sujet "Stem cell heterogeneity"

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de Souza, Natalie. « Taming stem cell heterogeneity ». Nature Methods 9, no 7 (28 juin 2012) : 645. http://dx.doi.org/10.1038/nmeth.2094.

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Joly, Jean-Stéphane, et Vincent Tropepe. « Neural stem cell heterogeneity ». Progress in Neurobiology 170 (novembre 2018) : 1. http://dx.doi.org/10.1016/j.pneurobio.2018.09.005.

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Andersen, Marianne S., et Kim B. Jensen. « Stem cell heterogeneity revealed ». Nature Cell Biology 18, no 6 (27 mai 2016) : 587–89. http://dx.doi.org/10.1038/ncb3368.

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Krieger, T., et B. D. Simons. « Dynamic stem cell heterogeneity ». Development 142, no 8 (7 avril 2015) : 1396–406. http://dx.doi.org/10.1242/dev.101063.

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Bayin, N. Sumru, Rajeev Sen, Sheng Si, Aram S. Modrek, Valerio Ortenzi, David Zagzag, Matija Snuderl et al. « STEM-04DEFINING GLIOBLASTOMA STEM CELL HETEROGENEITY ». Neuro-Oncology 17, suppl 5 (novembre 2015) : v208.4—v209. http://dx.doi.org/10.1093/neuonc/nov234.04.

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Eaves, Allen. « Stem cell heterogeneity (discussion&rpar ; ». Stem Cells 15, S2 (avril 1997) : 217–20. http://dx.doi.org/10.1002/stem.5530150829.

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Andreotti, Julia P., Walison N. Silva, Alinne C. Costa, Caroline C. Picoli, Flávia C. O. Bitencourt, Leda M. C. Coimbra-Campos, Rodrigo R. Resende et al. « Neural stem cell niche heterogeneity ». Seminars in Cell & ; Developmental Biology 95 (novembre 2019) : 42–53. http://dx.doi.org/10.1016/j.semcdb.2019.01.005.

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Yang, Seungbok, Yoonjae Cho et Jiwon Jang. « Single cell heterogeneity in human pluripotent stem cells ». BMB Reports 54, no 10 (31 octobre 2021) : 505–15. http://dx.doi.org/10.5483/bmbrep.2021.54.10.094.

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Miller, Paul H., David J. H. F. Knapp et Connie J. Eaves. « Heterogeneity in hematopoietic stem cell populations ». Current Opinion in Hematology 20, no 4 (juillet 2013) : 257–64. http://dx.doi.org/10.1097/moh.0b013e328360aaf6.

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Bonnet, Dominique. « Human Normal Haematopoetic Stem Cell Heterogeneity ». Experimental Hematology 64 (août 2018) : S25. http://dx.doi.org/10.1016/j.exphem.2018.06.010.

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Thèses sur le sujet "Stem cell heterogeneity"

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Carr, Jonathon M. « Heterogeneity within the stem cell compartment : impact on fate determination of human pluripotent stem cells ». Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/20386/.

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Benavente, Diaz Maria. « Investigation of the molecular diversity defining muscle stem cell heterogeneity ». Electronic Thesis or Diss., Sorbonne université, 2020. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2020SORUS072.pdf.

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Le muscle squelettique adulte a une capacité de régénération remarquable, pouvant guérir après des traumatismes répétés. Cette propriété dépend de la présence de cellules souches musculaires (SCMu), qui sont pour la plupart quiescentes dans des conditions homéostatiques mais qui s'activent après une blessure, réintègrent le cycle cellulaire et prolifèrent pour donner naissance à des myoblastes qui fusionneront pour restaurer les fibres endommagées. De nombreuses études ont étudié les états transitoires que les SCMu empruntent de l'entrée du cycle cellulaire à la différenciation. Malgré le fait que plusieurs souris rapportrices génétiquement modifiées aient été générées pour examiner ces événements, l'initiation de la différenciation, qui est généralement définie par l'expression du facteur de régulation myogénique Myogenin, est difficilement appréciable à cause du manque de souris rapportrice fiable. Par conséquent, nous avons développé une nouvelle lignée rapportrice où la différenciation des cellules myogéniques exprimant le facteur de transcription Myogenin peut être marquée par l'expression d'une protéine fluorescente tdTomato. Cette nouvelle lignée de souris knock-in nous a permis d'analyser la cinétique de l'expression de Myogenin lors de la différenciation cellulaire in vitro et d'effectuer des expériences préliminaires in vivo par imagerie intravitale. De plus, bien que toutes les SCMu de souris soient caractérisées par l'expression du facteur de transcription Pax7, plusieurs études ont décrit des différences de prolifération, de capacité de transplantation et de sensibilité à la maladie entre les SCMu des muscles crâniens et des membres. Pour étudier les réseaux de régulation des gènes qui régissent cette hétérogénéité fonctionnelle, nous avons combiné des analyses transcriptomiques sur cellules uniques avec des approches de biologie cellulaire utilisant des lignées de souris rapportrices pour identifier les régulateurs clés qui confèrent des propriétés distinctes aux SCMu à haute-performance (extraoculaires) et à faible-performance (tibialis antérieur) en quiescence et lors de l'activation. Nous avons identifié un retard dans la différenciation des SCMu extraoculaires en culture, accompagné par l'expression de facteurs de remodelage de la matrice extracellulaire et de récepteurs membranaires distincts et nous avons validé l'expression de certains de ces candidats au niveau protéique. Des analyses informatiques avancées ont mis en évidence la dynamique sous-jacente au maintien d'une population de progéniteurs dans les SCMu extraoculaires, contrôlée par un réseau singulier de facteurs de transcription formant un module de molécules co-régulées. En conclusion, ces études apportent de nouvelles informations sur les mécanismes qui octroient des propriétés différentes des cellules souches musculaires venant d'emplacements anatomiques distincts
Adult skeletal muscle has a remarkable regenerative capacity, being able to recover after repeated trauma. This property depends on the presence of muscle stem cells (MuSCs), which are mostly quiescent in homeostatic conditions, re-enter the cell cycle after injury and proliferate to give rise to committed myoblasts that will eventually fuse to restore the damaged fibres. Numerous studies have investigated the cell state transitions that MuSCs undergo from cell cycle entry to differentiation. Although several genetically modified reporter mice have been generated to study these events, detailed studies on the initiation of differentiation, which is generally defined by expression of the myogenic regulatory factor Myogenin, have been hampered by the lack of a reliable reporter mouse. Therefore, we developed a fluorescent reporter line where differentiating myogenic cells expressing Myogenin are marked by the expression of a tdTomato fluorescent protein. This novel knock-in mouse line allowed us to monitor the kinetics of Myogenin expression during cell differentiation in vitro, and perform preliminary experiments on the behaviour of myogenic cells in vivo by intravital imaging. Although all mouse MuSCs are characterised by the expression of the transcription factor Pax7 and they share several properties, some studies have reported differences in proliferation, engraftment ability, and sensitivity to disease of MuSCs from cranial and limb muscles. To investigate the gene regulatory networks that govern this functional heterogeneity, we have integrated single-cell transcriptomic analyses with cell biology approaches using mouse reporter lines to identify key regulators that confer distinct properties to high performing (extraocular muscles) and lower performing (limb, Tibialis anterior muscle) MuSCs in quiescence and activated states. We identified a delayed lineage progression of extraocular MuSCs in culture that was accompanied with the expression of distinct extracellular matrix remodelling factors and membrane receptors, and we validated the expression of some of these candidates at the protein level. Advanced computational analyses highlighted the dynamics underlying the maintenance of a stem-like progenitor population in extraocular MuSCs, controlled by a singular network of transcription factors acting as a co-regulating module. Taken together, these studies provide novel insights into the mechanisms underlying the differential properties of muscle stem cells in distinct anatomical locations
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Boumahdi, Soufiane. « Identification of molecular mechanisms regulating cancer stem cell functions and tumor heterogeneity in skin squamous cell carcinoma ». Doctoral thesis, Universite Libre de Bruxelles, 2017. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/250375.

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Le carcinome spinocellulaire (SCC) est le 2ème cancer de la peau le plus fréquent avec plus d’un million de nouveaux patients diagnostiqués dans le monde chaque année. On retrouve également des SCCs associés à un pronostic plus sombre au niveau de la tête, du cou, de la cavité orale et de l’œsophage. Des travaux récents ont démontré l’existence de cellules souches cancéreuses (CSCs) dans les SCCs cutanés mais les mécanismes moléculaires contrôlant leurs fonctions restent indéterminés. Dans une première étude, nous avons montré que Sox2, un facteur de transcription (TF) associé aux cellules souches, est détecté de manière hétérogène dans une grande majorité des papillomes et des SCCs chez la souris et chez l’humain. La délétion conditionnelle de Sox2 dans l’épiderme réduit drastiquement l’apparition de tumeurs démontrant le rôle clé de Sox2 dans l’initiation tumorale. En utilisant une souris génétiquement modifiée Sox2-GFP knock-in, nous avons démontré que les cellules tumorales Sox2+ sont enrichies en cellules propagatrices de tumeurs dont la proportion augmente au fur et à mesure des transplantations sériées. L’ablation des cellules Sox2+ dans les papillomes et les SCCs conduit à une importante régression des tumeurs, indiquant que ces cellules ont un rôle crucial dans le maintien des tumeurs. La délétion conditionnelle de Sox2 dans des papillomes et SCCs préexistants provoque également une régression majeure des tumeurs, soulignant le rôle essentiel de Sox2 dans la régulation des fonctions des cellules tumorales. Une analyse transcriptionnelle et des expériences d’immunoprécipitation de chromatine nous ont permis de mettre en évidence un réseau de gènes associés à des fonctions essentielles des cellules tumorales et régulés par Sox2 dans les tumeurs primaires in vivo. Dans une 2ème étude, nous avons montré que les SCCs issus de l’épiderme inter-folliculaire (IFE) présentent en général un caractère différencié alors que ceux issus du follicule pileux (HF) présentent fréquemment des caractéristiques de transition épithélio-mésenchymateuse (EMT). En réalisant une analyse transcriptionnelle et épigénétique, nous avons démontré que les différentes cellules à l’origine expriment un réseau de gènes spécifiques et présentent une accessibilité différentielle à des sites de liaison d’importants TFs associés soit à un phénotype épithélial soit à l’EMT. Ces résultats démontrent que l’état transcriptionnel et épigénétique de la cellule à l’origine amorce spécifiquement les tumeurs vers le processus d’EMT. L’ensemble de ces résultats souligne des mécanismes cruciaux à l’établissement de l’hétérogénéité tumorale et seront essentiels pour parvenir à des pronostics affinés et au développement de nouvelles thérapies ciblées dans le traitement du cancer.
Skin squamous cell carcinoma (SCC) is the second most frequent skin cancer with more than a million new patients affected every year throughout the world. It is also the predominant cancer of the head, neck, oral cavity and esophagus, associated with a poor prognosis. Recent studies have identified cancer stem cells (CSCs) in skin SCC but the molecular mechanisms controlling their functions remain unclear. In a first study, we show that Sox2, a transcription factor (TF) associated with stemness, is expressed in a heterogeneous manner in the vast majority of benign and malignant skin tumors in mouse and human. Sox2 conditional deletion in the epidermis impairs tumor development showing that Sox2 plays a crucial role in tumor initiation. Using a Sox2-GFP knock-in mouse model, we show that Sox2-expressing tumor cells are greatly enriched in tumor-propagating cells, which further increase upon serial transplantations. Lineage ablation of Sox2-expressing cells in primary benign and malignant SCCs leads to tumor regression, consistent with the critical role of Sox2-expressing cells in tumor maintenance. Conditional Sox2 deletion in pre-existing skin papilloma and SCC leads to tumor regression, supporting the essential role of Sox2 in regulating cancer cells functions. Using transcriptional profiling and chromatin immunoprecipitation, we uncovered a gene network controlling many cancer hallmarks regulated by Sox2 in primary tumour cells in vivo.In a second study, by targeting the same oncogenic mutations to distinct skin compartments, we show that interfollicular epidermis (IFE)-derived SCCs are generally well-differentiated, while hair follicle stem cells (HFSCs)-derived SCCs frequently exhibit features of epithelial-mesenchymal transition (EMT). Using transcriptional and epigenetic profiling, we show that IFE and HF tumor-initiating cells harbor distinct chromatin landscapes and gene regulatory networks associated with tumorigenesis and EMT. These different chromatin landscapes correlate with the differential accessibility of key epithelial and EMT TFs binding sites in the cancer cell of origin. These findings demonstrate that cell type-specific chromatin and transcriptional states differentially prime tumours towards EMT.Altogether, these results highlight crucial mechanisms for the establishment of tumor heterogeneity which will be relevant for better prognostic assessment and the development of novel targeted therapies for cancer treatment.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
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Sakamaki, Taro. « Hoxb5 defines the heterogeneity of self-renewal capacity in the hematopoietic stem cell compartment ». Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263564.

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Turón, Rodrigo Gemma. « A genome editing based approach to study tumor cell heterogeneity ». Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667524.

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Colorectal tumors are not homogeneous entities but rather composed of a mixture of cells with different phenotypes, reminiscent of healthy intestinal epithelium cell types. Intestinal epithelium is one of the organs with highest self-renewal rate, maintained by a pool of highly proliferating stem cells located at the base of the crypts. Daughters of the stem cells abandon the crypts and differentiate as they move up the villi, in a process that takes no longer than six days. Recent findings suggest that colorectal cancers (CRCs), like normal intestine, rely on a stem cell hierarchy for its growth. Cancer stem cells, identified by LGR5 gene expression, are at the apex of this hierarchy, and are thought to be the drivers of CRC expansion and metastasis. This thesis is focused on characterizing the growth dynamics of the different tumor compartments and identifying the cells that fuel tumor growth. Moreover, we have also tried to elucidate which is the cell of origin of metastasis. To complete this project we have first developed new models to study human disease, as most of the previous work relied on genetically modified mouse models to reproduce the disease. Here, we have combined patient-derived organoid 3D cultures and CRISPR/Cas9 genome editing techniques to insert fluorescent reporter proteins under the control of our genes of interest. This has allowed us to visualize different tumor cell types in vivo using LGR5, KRT20 and EMP1 as markers for stemness, differentiation and invasion respectively. In addition, we have also set up a system to follow the progeny of the abovementioned populations in vivo in intact tumors. We have identified the different tumor compartments by subcutaneously injecting modified human organoids into immunosuppressed mice. Flow cytometry purification and reinjection into secondary hosts of stem-like and differentiated-like cells has enabled us to discover that cancer cells retaining stem cell characteristics are more proficient in tumor initiation than the rest of the tumor. Nevertheless, lineage tracing of the abovementioned genes in an intact tumor cell environment shows how both stem and differentiated progenies are able to give rise to long lasting clones and thus equally fuel tumor growth. Furthermore, we have observed plasticity arising from both cell types, indicative that the cellular hierarchy is disrupted during tumor progression. In addition, we have defined EMP1 as a putative gene marker for invasive cells. EMP1-High cells are a differentiated subset of tumor cells that harbor migratory properties and secrete myeloid recruiting chemokines to the tumor site. Myeloid cells have been shown to contribute to all steps of metastasis in several cancer types. We hypothesize that this EMP1+ subpopulation is the one that disseminates from the primary tumor and initiates metastasis. For metastatic studies, we have resorted to mouse derived tumor organoids that allow the growth of primary and metastatic disease in fully immunocompetent ice, and we have set up new models to study disease relapse in metastatic sites upon primary tumor removal Taken together, our data provides new insights on the mode of tumor growth in advanced human colorectal carcinomas and suggests that stem cell traits are not required for tumor growth neither metastatic spread, contrary to what was initially though based on mouse adenoma studies.
Els tumors colorectals no són una entitat homogènia sinó que estan formats per una barreja de cèl·lules de fenotips variats, reminiscents dels tipus cel·lulars de l’epiteli intestinal sa. Estudis recents suggereixen que el creixement del càncer colorectal (CCR), igual que el de l’intestí normal, està mediat per una jerarquia amb origen en cèl·lules mare. Les cèl·lules mare del càncer, identificades per l’expressió del gen LGR5, es troben a l’àpex de la jerarquia i impulsen l’expansió del CCR i la metàstasis. Aquesta tesi se centra en caracteritzar la dinàmica d’expansió dels diferents compartiments tumorals i en identificar les cèl·lules que en mantenen el creixement. També hem intentat elucidar quina és la cèl·lula d’origen de la metàstasi. Per a realitzar aquest projecte primer hem desenvolupat nous models per estudiar la malaltia humana, combinant el cultiu d’organoids derivats de pacients i l’edició genòmica mitjançant CRISPR/Cas9. Això ens ha permès visualitzar diferents tipus cel·lulars tumorals in vivo usant LGR5, KRT20 i EMP1 com a marcadors de cèl·lula mare, cèl·lula diferenciada i cèl·lula invasiva, respectivament. Addicionalment, també hem establert un sistema per seguir la progènie de les poblacions mencionades. Hem descobert que tant el compartiment de cèl·lules mare com el diferenciat són capaços de donar lloc a una progènie que persisteix en el temps, suggerint que ambdós tipus cel·lulars contribueixen al creixement tumoral. A més a més, hem observat plasticitat entre els dos compartiments, cosa que indica que la jerarquia cel·lular es perd durant el desenvolupament del tumor. Finalment, mitjançant l’ús d’EMP1 com a marcador de cèl·lules invasives hem identificat un subgrup de cèl·lules diferenciades amb propietats migratòries i amb potencial per reclutar cèl·lules mieloides. La nostra hipòtesi és que la població EMP1+ és la que dissemina del tumor primari i inicia la metàstasi. En resum , les nostres dades suposen una nova visió en l’estudi del mode de creixement del càncer de colon d’estadis avançats en humà, i suggereixen que els trets de cèl·lula mare no són necessaris per creixement tumoral ni la disseminació metastàtica, contràriament al que es pensava inicialment, degut als estudis realitzats en adenoma de ratolí.
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Luni, Camilla. « Development of cell culture technology for the expansion of homogeneous populations of human stem cells ». Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426474.

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Stem cell-based therapies have been proposed as promising for the maintenance, regeneration, or replacement of malfunctioning tissues, but suffer from limitations mainly due to scarce cell availability and clinical safety concern related to cell quality. Optimization of stem cell expansion process is an engineering challenge, besides a biological issue. Aim of the work presented is to develop the experimental technology and the rational insight to understand and control stem cell expansion in vitro, in terms of both average and distributed properties of the cell population produced. A rational analysis of the main phenomena involved in a cell culture was achieved, underlining the sources of stem cell heterogeneity in both conventional culture systems and stirred bioreactors. From an experimental point of view, two types of bioreactors were designed, developed, and prototyped. The first, a microliter bioreactor array, was designed based on thermoconvective mixing; this experimental setup is particularly convenient for multiparametric optimization of cell culture conditions. The second, a six-well suspension bioreactor with a working volume of 10 ml/well, was designed and fabricated for coarse process optimization or, alternatively, for small-scale stem cell production; an improved setup was developed to perform stem cell cultures under hypoxia conditions. Both devices were advantageously used to culture human cord blood-derived hematopoietic stem cells, which were then characterized according to the currently available biological assays. In order to rationally optimize the stem cell expansion process, a computational model, based on a population balance approach, was developed, that takes into account receptor and receptor-ligand complex distribution in the cell sample. The model fairly describes intrinsic intra- and inter-generational heterogeneity arising from the process of cell division. These findings could give interesting feedback to experimental design and to define the operative conditions for bioreactor cultures, in order to minimize extrinsic and intrinsic heterogeneity, and to make a step towards a clinically safe and reliable human hematopoietic stem cell expansion process.
E' stato prospettato l'impiego di cellule staminali per terapie volte al mantenimento, alla rigenerazione o alla sostituzione di tessuti malfunzionanti. Tuttavia non sono ancora state risolte alcune limitazioni legate principalmente alla scarsa disponibilità di cellule staminali e ai problemi di sicurezza clinica connessi alla qualità cellulare. L'ottimizzazione del processo di espansione cellulare è un sfida ingegneristica, oltre che biologica. Scopo di questa tesi è lo sviluppo di una tecnologia sperimentale e di un quadro razionale che consenta di comprendere e controllare l'espansione di cellule staminali in vitro, sia considerando le proprietà medie che la loro distribuzione nella popolazione cellulare prodotta. E' stata realizzata un'analisi razionale dei principali fenomeni coinvolti nella coltura cellulare, ponendo in evidenza le fonti di eterogeneità sia nei sistemi di coltura convenzionali che nei bioreattori mescolati. Da un punto di vista sperimentale, sono stati progettati e sviluppati due tipi di bioreattori fino a realizzarne dei prototipi. Il primo, un sistema di bioreattori di volume dell'ordine dei microlitri, è stato progettato basato su un meccanismo di termoconvezione; questo apparato sperimentale è particolarmente adatto per un'ottimizzazione multiparametrica delle condizioni di coltura. Il secondo, un bioreattore in sospensione multipozzetto con un volume operativo di 10 ml/pozzetto, è stato pensato e costruito per un'ottimizzazione di processo meno dettagliata o, alternativamente, per una produzione su piccola scala di cellule staminali; una versione più avanzata è stata sviluppata per effettuare colture di cellule staminali in condizioni di ipossia. Entrambi i dispositivi sono stati vantaggiosamente utilizzati per coltivare cellule staminali ematopoietiche, ricavate da cordone ombelicale umano, che sono poi state caratterizzate secondo i metodi di analisi biologica convenzionali. Per ottimizzare razionalmente il processo di espansione delle cellule staminali, è stato sviluppato un modello computazionale, basato su un bilancio di popolazione, che tiene conto della distribuzione di recettori e di complessi recettore-ligando nel campione cellulare. Il modello descrive ragionevolmente l'eterogeneità intrinseca, intra- e intergenerazionale, derivante dal processo di divisione cellulare. Questi risultati possono dare un riscontro positivo in fase di progettazione degli esperimenti e di definizione delle condizioni operative a cui effettuare colture in bioreattore, al fine di minimizzare l'eterogeneità estrinseca e intrinseca della popolazione cellulare e di effettuare un ulteriore avanzamento verso un processo di espansione di cellule staminali umane clinicamente sicuro ed affidabile.
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Mejetta, Stefania 1984. « 1)Jarid2 regulates mouse epidermal stem cell activation and differentiation ; 2)Tumor heterogeneity and metastasis-initiation in human squamous cell carcinoma ». Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283482.

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Jarid2 is required for the genomic recruitment of the polycomb repressive complex-2 (PRC2) in embryonic stem cells. However, its specific role during late development and adult tissues remains largely uncharacterized. In this first part of my thesis, we show that deletion of Jarid2 in mouse epidermis reduces the proliferation and potentiates the differentiation of postnatal epidermal progenitors, without affecting epidermal development. In neonatal epidermis, Jarid2 deficiency reduces H3K27 trimethylation, a chromatin repressive mark, in epidermal differentiation genes previously shown to be targets of the PRC2. However, in adult epidermis Jarid2 depletion does not affect interfollicular epidermal differentiation but results in delayed hair follicle (HF) cycling as a consequence of decreased proliferation of HF stem cells and their progeny. We conclude that Jarid2 is required for the scheduled proliferation of epidermal stem and progenitor cells necessary to maintain epidermal homeostasis. Several human and mouse solid tumors, including squamous cell carcinomas (SCC), contain a population of Cancer Stem Cells (CSCs). CSCs are characterized by their unique ability to initiate and propagate the tumor; however, very little is known about their capacity to disseminate to distant organs and give rise to metastasis. CSCs display a great functional and molecular heterogeneity, and it has been proposed that different CSC subclones might exist to either maintain the primary tumor or to metastasize in distant sites. However, the identity of these heterogeneous populations of CSCs, as well as their molecular and functional characteristics for most type of tumors remains to be elucidated. Using a novel xenograft system that we have developed to study human head and neck squamous cell carcinoma, we have identified a labelretaining (LRC) population inside the cancer stem cell pool defined by the high expression of CD44 and high activity of Aldh1. Unexpectedly, tumor LRC harbor poor initiating potential, and are more sensitive to chemotherapy than their proliferating counterparts. Intriguingly, tumor LRCs are defined by a unique transcriptome signature previously linked with bone and lung identity, two major sites of SCC metastasis, suggesting they might be involved in the colonization of distant tissues by SCC tumors. We have also identified surface molecules, including CD36 and CD37, that are uniquely expressed by tumor LRCs, that can be used as surrogate markers to isolate and characterize them from primary human SCCs. Based on this signature, we could demonstrate that the presence or absence of this population in the primary tumor of a large cohort of patients with cutaneous SCC is highly predictive of the metastatic occurrence. In addition, several markers exclusively expressed by tumor LRCs can be targeted with drugs currently in clinical trials for the treatment of other diseases. We are testing whether some of these therapeutical strategies are effective to preventing or reducing the metastatic potential of SCC tumors.
Jarid2 es necesario para la localización genómica del complejo represor polycomb repressive complex-2 (PRC2) en células stem embrionarias. Sin embargo, la función de Jarid2 en las últimas fases del desarrollo embrionario y su papel en la función de los tejidos adultos no ha sido aún caracterizada en profundidad. En esta primera parte de mi tesis doctoral, mostramos que la deleción de Jarid2 en la piel de ratón no afecta al desarrollo de la epidermis, pero reduce la proliferación y potencia la diferenciación de las células progenitoras epidermales en neonatos. La piel de los ratones neonatos Jarid2-KO muestra niveles reducidos de la marca represora de la cromatina, H3K27me3, en genes necesarios para la diferenciación de las células progenitoras. En cambio, en piel adulta la depleción de Jarid2 no afecta la diferenciación de la epidermis, pero sí que resulta en una reducción del número de células stem activas de los folículos pilosos, lo que desemboca en el retraso del crecimiento de los folículos. Por lo tanto, nuestros resultados demuestran que Jarid2 es necesario para la activación y diferenciación de diferentes células stem del compartimento queratinocítico de la piel necesarios para mantener la homeostasis epidermal. Diversos tipos de tumores sólidos humanos y de ratón, incluyendo carcinomas de células escamosas (SCCs del inglés: Squamous Cell Carcinomas), contienen una población de células madre cancerosas (CSCs del inglés Cancer Stem Cells). Las CSCs se caracterizan porque pueden iniciar y propagar el tumor; sin embargo, se conoce muy poco sobre su capacidad de alcanzar órganos lejos del tumor primario y de formar metastasis. Las CSCs pueden ser muy heterogéneas tanto a nivel funcional como molecular, y se ha propuesto que podrían existir diferentes subclones sea para mantener el tumor primario, sea para formar metástasis. No obstante, no se conoce por ahora ni la identidad de estas poblaciones heterogéneas de CSCs, ni sus características a nivel funcional o molecular. Usando un nuevo sistema de xenoinjerto que hemos desarrollado en nuestro laboratorio para estudiar SCC de cabeza y cuello, hemos identificado una población que es capaz de retener el marcaje con el tiempo (LRC de inglés: Label-retaining Cells), dentro de la población total de CSSs, definidas como células dentro del tumor que muestran alta expression de CD44 y alta actividad de Aldh1. En contra de lo que esperábamos, las LRC del tumor tienen dificultad para iniciar tumores por sí solas y son más sensibles a tratamientos de quimioterapia cuando las comparamos con otras células más proliferativas. Por otra parte, las LRC del tumor se pueden definir con un transcriptoma único que ha sido relacionado anteriormente con hueso y pulmón, que son dos de los órganos donde los SCC forman metástasis preferentemente. Esto sugiere que podrían estar involucradas en la colonización de órganos alejados del SCC primario. Hemos identificado también moléculas de superficie, incluyendo CD36 y CD37, que se expresan exclusivamente en las LRC de tumor y que se pueden usar como marcadores para aislar y caracterizar las LRC de SCCs primarios humanos. Basándonos en estos marcadores, hemos podido demostrar que la presencia o no de esta población en el tumor primario predice la formación de metástasis en pacientes con SCC cutáneos. Además, diversos marcadores que hemos identificado como únicos en LRC de tumor, son diana de fármacos ya usados en la actualidad en ensayos clínicos para tratamiento de otras enfermedades. En la actualidad estamos probando si alguno de estos tratamientos puede ser efectivo para prevenir o reducir el potencial de formar metástasis en SCC.
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Jacob, Eshtan Sarah. « Heterogeneity of the human embryonic stem cell compartment and its impact on the generation of otic progenitors ». Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/7613/.

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Ledaki, Ioanna I. « Heterogeneity of tumour response to hypoxia : carbonic anhydrase IX induction defines a subpopulation of hypoxic cells with stem cell properties and drug resistance ». Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:757a8e79-b20d-496c-b69b-4d6a3b7b56e3.

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Carbonic anhydrase IX (CA9) is strongly induced by hypoxia and its overexpression is associated with poor therapeutic outcome in cancer. The function of CAIX is to catalyze the reversible hydration of CO2 to bicarbonate and a proton. This helps hypoxic tumours to maintain a more neutral intracellular pH (pHi) promoting survival, but produces a more acidic extracellular (pHe) which promotes invasion and metastasis. Recent evidence has expanded on the role of hypoxia and CAIX by relating them to stem cell niches. In this study, taking advantage of the transmembrane location of CAIX, we show for the first time, a direct marked heterogeneity in response to hypoxia within each tumour cell population studied, associated with major biological differences. Based on CAIX expression pattern under hypoxic conditions, we identify, isolate and characterize two distinct populations of tumour cells, one that express CAIX and the other that does not. Interestingly, we discover that the CAIX positive population is enriched with cells expressing cancer stem cell markers. These include ALDHA1, IGF1, LIN28 and genes involved in epithelial-mesenchymal transition (EMT) and multi-drug resistance (i.e. WNT2, TWIST1, and ABCC2). Accordingly, CAIX+ve cells show higher self-renewal capacity and form tumours significantly faster compared to the CAIX-ve population. Importantly, functional suppression of CAIX in vitro and in vivo, in two breast cancer cell lines resulted in the downregulation of breast cancer stem cell signatures, suggesting that CAIX is not just a marker of stemness but also a regulator of stemness. The molecular mechanism underlying the differential expression of CAIX in the two populations is not HIF-1α-dependent, but instead driven by hypoxia-induced reorganization of chromatin structure. In line with this, we provide experimental evidence showing that the genomic locus encoding CA9 has a more “open” and transcriptionally active chromatin structure in CAIX+ve cells, and a condense and transcriptionally silent chromatin structure in the CAIX-ve cells. Given that HIF induces the transcription of CA9 by binding to hypoxia response elements (HREs) in its promoter we show a significant reduction in binding of HIF to the CA9 promoter of the negative population. We suggest that the reduce HIF binding is a result of the compact chromatin structure of CA9 promoter of the negative cells. Analysis of the transcriptome of the positive and negative populations suggests a symbiotic relationship between these two subpopulations and their environment, likely required to promote tumour growth. This is based on the following observations: Firstly, we identified that CAIX-ve cells express high levels of cytokines and based on this, we suggest that the cytokines secreted by CAIX-ve cells may transmit paracrine signals that regulate the CAIX+ve cells, thus providing a wider hypoxia tolerant microenvironment to protect the stem cell population. Secondly, we identified a metabolic heterogeneity between the CAIX+ve and CAIX-ve cells. The CAIX+ve cells show an upregulation of genes implicated in oxidative phosphorylation, TCA cycle and fatty acid synthesis. Whereas in CAIX-ve cells there is an upregulation of genes implicated in autophagy and mitophagy. Given the above together with the upregulation of oxidative phosphorylation and TCA cycle in the CAIX+ve cells, we proposed the existence of a metabolic symbiosis between the CAIX+ve and CAIX-ve cells. We postulate that the catabolic process such as autophagy and mitophagy in the CAIX-ve cells may results in the overproduction of high-energy metabolites such as lactate, glutamine and ketone bodies which in turns they are been utilized by CAIX+ve cells to fuel mitochondria respiration. Finally, we also demonstrated that in the CAIX+ve cells mTORC1 signaling is upregulated, and contributes to the regulation of CAIX expression. Given the role of mTORC1 in stem cell maintenance and EMT as well as the interdependence of mTORC1 and CAIX expression in the CAIX+ve cells we suggest that mTORC1 signaling may be the critical factor by which CAIX regulates stemness. Interestingly, the subpopulations show a differential sensitivity to HDAC inhibitors, NaBu and SAHA as treatment of MCF7 breast cancer cell line and HCT116 colon cancer cell line leads to elimination of the CAIX+ve population. This is not driven by the downregulation of HIF-1α, the major transcriptional regulator of CAIX. In contrast, we demonstrate that SAHA causes downregulation mTORC1. This suggests that SAHA-induced downregulation of CAIX expression could be due to its effect on mTORC1 pathway. Of wider significance, our findings show that tumours are not homogenous in their response to hypoxia, and distinct signal transduction networks regulate different populations of cells within the tumour. This highlights the need for the utilization of biomarkers, which reveal distinct functional hypoxia profiles of human cancers, and permit the stratification of tumours. Furthermore, the identification of epigenetic regulation of the histones in response to hypoxia for highly selective gene regulation, provides a connection between the epigenetic mechanisms under environmental stress and cancer progression, and is model for development of novel epigenetic cancer therapeutic drugs.
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Targa, Laurie. « Contribution to the study of mesenchymal stromal / stem cells heterogeneity, focus on surface markers and senescence ». Thesis, Université de Lorraine, 2019. https://docnum.univ-lorraine.fr/ulprive/DDOC_T_2019_0353_TARGA.pdf.

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Les Cellules Stromales / Souches Mésenchymateuses (CSM) ont un grand potentiel pour de nombreuses applications. Elles sont les cellules les plus utilisées pour les essais cliniques développant des thérapies cellulaires. L’efficacité thérapeutique des CSM est influencée par leur amplification in vitro et d’autres facteurs tels que les paramètres liés au donneur de cellules. Pour améliorer les thérapies à base de CSM, cette étude a ciblé l’étude de leur hétérogénéité grâce à leurs marqueurs de surface, qui permettent de mutualiser la caractérisation des cellules et la possibilité de trier des cellules vivantes. Le premier objectif de ce travail a été de décrire la variabilité des CSM entre et au sein d’échantillons venant de moelle osseuse de donneurs d’âges différents. Le deuxième objectif a été de développer une méthode de tri pour séparer les CSM selon leur expression de CD146 et de comparer les cellules triées. La troisième partie du travail a eu pour objectif de mieux connaître les marqueurs de surface des CSM sénescentes. Les résultats de cytométrie en flux sur les CSM sont soumis à de fortes fluctuations, mais certaines régularités ont pu être mises en évidence. Un ensemble de marqueurs de surface a pu être associé avec l’âge des donneurs : CD146, CD71, CD105, CD44. De plus, des liens entre l’expression de CD146, CD140b et CD71 ont été observés avec la capacité de prolifération des CSM. Des CSM de moelle osseuse provenant de donneurs d’âges différents et à différentes étapes de culture ont pu être triées avec succès selon leur expression de CD146 par une méthode immunomagnétique. Le comportement des CSM triées était encore hétérogène mais il a pu être observé que les CSM exprimant plus fortement CD146 avaient plus souvent de meilleures capacités de différentiation et de migration et étaient moins sénescentes que les cellules exprimant plus faiblement CD146. Une étude protéomique a montré que la plupart des protéines de surface détectées avaient tendance à être moins représentées sur les cellules sénescentes à l’exception de CD157. Les CSM à différentes étapes de culture jusqu’à la sénescence réplicative ont ensuite été suivies par cytométrie en flux. Cette dernière étude a révélé d’importantes fluctuations entre les différents passages, soulignant la difficulté associée à l’utilisation de ces marqueurs. Les marqueurs CD146, CD71, CD140b et CD157 méritent d’être suivis pour le contrôle qualité des CSM provenant de moelle osseuse
Mesenchymal Stromal / Stem Cells (MSC) hold great potential and are currently the most used in clinical trials with cell-based treatments. MSC quality and therapeutic effectiveness are influenced by in vitro expansion but also by other factors such as donor parameters. To ameliorate the success rate of MSC therapies, this study focused on MSC heterogeneity. To put together cell characterization and ways to act when facing cell heterogeneity, this work was oriented toward the study of surface markers that can be monitored on living cells, and can serve to sort them. The first objective was to describe initial MSC surface markers variability between and within different bone marrow MSC samples from donors of different ages. The second objective was to develop a sorting method to separate MSC according to CD146 expression and compare the sorted cells. The third objective was to widen MSC surface markers knowledge by focusing on senescent MSC. Surface markers of early passage and replicative senescent cells were compared with proteomics and flow cytometry. Flow cytometry results on MSC were shown to be submitted to strong fluctuations. However, some regularities were strong enough to stand out. A group of surface markers were found to be associated with donor age: CD146, CD71, CD105, CD44. CD146, CD140b and CD71 were also correlated with proliferation rate. CD146 expression had the particularity to be relatively stable in culture and turned out to be the most heterogeneously expressed when looking at cell population within the samples. Cultivated MSC from bone marrow coming from donor of different ages and at different culture steps were sorted successfully according to CD146 expression with immunomagnetic method. MSC behavior remained heterogeneous after sort but it could still be observed that most CD146high cells had more often better differentiation and migration capacities and were less senescent than their CD146low counterpart. Proteomics study showed that almost all surface proteins expression tended to decrease on replicative senescent MSC, except one marker that increased: CD157. MSC at different stages of culture until replicative senescence were then studied by flow cytometry. This study revealed strong fluctuation in marker expression between different passages, highlighting again the variability of MSC behavior and the difficulty to predict it. CD146, CD71, CD140b, CD157 and SSC deserve to be followed for MSC quality control
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Livres sur le sujet "Stem cell heterogeneity"

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Turksen, Kursad, dir. Stem Cell Heterogeneity. New York, NY : Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6550-2.

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Birbrair, Alexander, dir. Stem Cells Heterogeneity - Novel Concepts. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11096-3.

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Birbrair, Alexander, dir. Stem Cells Heterogeneity in Cancer. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4.

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Birbrair, Alexander, dir. Stem Cells Heterogeneity in Different Organs. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24108-7.

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Turksen, Kursad. Stem Cell Heterogeneity : Methods and Protocols. Springer New York, 2016.

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Stem Cell Heterogeneity : Methods and Protocols. Humana, 2018.

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Turksen, Kursad. Cell Biology and Translational Medicine, Volume 6 : Stem Cells : Their Heterogeneity, Niche and Regenerative Potential. Springer International Publishing AG, 2021.

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Turksen, Kursad. Cell Biology and Translational Medicine, Volume 6 : Stem Cells : Their Heterogeneity, Niche and Regenerative Potential. Springer, 2020.

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Birbrair, Alexander. Stem Cells Heterogeneity in Cancer. Springer, 2019.

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Birbrair, Alexander. Stem Cells Heterogeneity in Cancer. Springer International Publishing AG, 2020.

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Chapitres de livres sur le sujet "Stem cell heterogeneity"

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Jurecic, Roland. « Hematopoietic Stem Cell Heterogeneity ». Dans Advances in Experimental Medicine and Biology, 195–211. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24108-7_10.

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Alessandra, Salvetti, et Leonardo Rossi. « Planarian Stem Cell Heterogeneity ». Dans Advances in Experimental Medicine and Biology, 39–54. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11096-3_4.

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Hayashi, Yohei, Kiyoshi Ohnuma et Miho K. Furue. « Pluripotent Stem Cell Heterogeneity ». Dans Advances in Experimental Medicine and Biology, 71–94. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11096-3_6.

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Hatina, Jiri, Michaela Kripnerova, Katerina Houfkova, Martin Pesta, Jitka Kuncova, Jiri Sana, Ondrej Slaby et René Rodríguez. « Sarcoma Stem Cell Heterogeneity ». Dans Advances in Experimental Medicine and Biology, 95–118. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11096-3_7.

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Alvina, Fidelia B., Arvin M. Gouw et Anne Le. « Cancer Stem Cell Metabolism ». Dans The Heterogeneity of Cancer Metabolism, 161–72. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_12.

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AbstractCancer stem cells (CSCs), also known as tumorinitiating cells (TICs), are a group of cells found within cancer cells. Like normal stem cells, CSCs can proliferate, engage in self-renewal, and are often implicated in the recurrence of tumors after therapy [1, 2]. The existence of CSCs in various types of cancer has been proven, such as in acute myeloid leukemia (AML) [3], breast [4], pancreatic [5], and lung cancers [6], to name a few. There are two theories regarding the origin of CSCs. First, CSCs may have arisen from normal stem/progenitor cells that experienced changes in their environment or genetic mutations. On the other hand, CSCs may also have originated from differentiated cells that underwent genetic and/or heterotypic modifications [7]. Either way, CSCs reprogram their metabolism in order to support tumorigenesis.
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Prabavathy, D., et Niveditha Ramadoss. « Heterogeneity of Small Cell Lung Cancer Stem Cells ». Dans Stem Cells Heterogeneity in Cancer, 41–57. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_3.

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Hatina, Jiri, Maximilian Boesch, Sieghart Sopper, Michaela Kripnerova, Dominik Wolf, Daniel Reimer, Christian Marth et Alain G. Zeimet. « Ovarian Cancer Stem Cell Heterogeneity ». Dans Stem Cells Heterogeneity in Cancer, 201–21. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_12.

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Kripnerova, Michaela, Hamendra Singh Parmar, Martin Pesta, Michaela Kohoutova, Jitka Kuncova, Karel Drbal, Marie Rajtmajerova et Jiri Hatina. « Urothelial Cancer Stem Cell Heterogeneity ». Dans Stem Cells Heterogeneity in Cancer, 127–51. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_8.

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Qian, Xu, Xiaobo Nie, Barbara Wollenberg, Holger Sudhoff, Andreas M. Kaufmann et Andreas E. Albers. « Heterogeneity of Head and Neck Squamous Cell Carcinoma Stem Cells ». Dans Stem Cells Heterogeneity in Cancer, 23–40. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_2.

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Badeaux, Mark A., et Dean G. Tang. « Prostate Cancer Cell Heterogeneity and Prostate Cancer Stem Cells ». Dans Cancer Stem Cells, 183–91. Hoboken, NJ : John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.ch14.

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Actes de conférences sur le sujet "Stem cell heterogeneity"

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Xian, W., S. Niroula et F. Mckeon. « Airway Stem Cell Heterogeneity in Advanced Cystic Fibrosis ». Dans American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6189.

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Mckeon, F., W. Xian, S. Niroula, S. Wang, W. Rao, J. F. Engelhardt, K. R. Parekh, M. L. Metersky et K. Goller. « Lung Stem Cell Heterogeneity in Advanced Cystic Fibrosis ». Dans American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2665.

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Harris, Molly, Dong-mi Shin, Seungbum Choi, Benjamin Low, Emily Miller, Brad Rybinski, Roderick Bronson et Kyuson Yun. « Abstract 3300 : Cancer stem cell heterogeneity and cell-of-origin in medulloblastomas ». Dans 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.am2012-3300.

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Fu, Nai Yang, Anne Rios, Bhupinder Pal, Charity Law, Paul Jamieson, Francois Vaillant, Gordon K. Smyth, Matthew E. Ritchie, Geoffrey J. Lindeman et Jane E. Visvader. « Abstract 5024 : Unmasking heterogeneity within the adult mammary stem cell compartment ». Dans 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.am2017-5024.

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Miyoshi, Norikatsu, Shiki Fujino, Masaru Sasaki, Takayuki Ogino, Hidekazu Takahashi, Mamoru Uemura, Chu Matsuda, Tsunekazu Mizushima, Hidetoshi Eguchi et Yuichiro Doki. « Abstract 4962 : Tumor heterogeneity driven by cancer stem cell expressing POU5F1 ». Dans Proceedings : AACR Annual Meeting 2020 ; April 27-28, 2020 and June 22-24, 2020 ; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4962.

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Azizi, Ebrahim, Shamileh Fouladdel, Yadwinder S. Deol, Jonathan Bender, Sean McDermott, Hui Jiang, Mary Sehl, Shawn G. Clouthier, Sunitha Nagrath et Max S. Wicha. « Abstract 1943 : Exploring cancer stem cells heterogeneity via single cell multiplex gene expression analysis ». Dans 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.am2014-1943.

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Reya, Tannishtha. « Abstract IA13 : Imaging stem cell signals in cancer heterogeneity and therapy resistance ». Dans Abstracts : AACR Special Conference : Advances in Modeling Cancer in Mice : Technology, Biology, and Beyond ; September 24-27, 2017 ; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.mousemodels17-ia13.

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Scurrah, Cherie’ R., Bob Chen, Nick Markham, Alan Simmons, Austin Southard-Smith, Mary Macedonia, Eunyoung Choi et al. « Abstract PO-051 : Tumor stem cells arising from a non-stem origin maintain a differentiated phenotype and modulate T cell activity ». Dans 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-051.

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Xiong, Ying, Dayvia A. Laws et Amanda C. LaRue. « Abstract A77 : Hematopoietic stem cell-derived adipocytes promote tumor progression ». Dans Abstracts : AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment ; February 26 — March 1, 2014 ; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a77.

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Neal, Molly E. Heft, Stephanie The, John Henry J. Owen, Clifford Chang, Mark E. P. Prince, Arvind Rao et Steven B. Chinn. « Abstract PO-006 : Single cell transcriptomic analysis of primary head and neck cancer stem cells ». Dans 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-006.

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