Academic literature on the topic 'Niche tumorale'
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Journal articles on the topic "Niche tumorale"
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Grassi, Elisa Stellaria, Viola Ghiandai, and Luca Persani. "Thyroid Cancer Stem-Like Cells: From Microenvironmental Niches to Therapeutic Strategies." Journal of Clinical Medicine 10, no. 7 (April 1, 2021): 1455. http://dx.doi.org/10.3390/jcm10071455.
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Thyroid cancer (TC) is the most common endocrine malignancy. Recent progress in thyroid cancer biology revealed a certain degree of intratumoral heterogeneity, highlighting the coexistence of cellular subpopulations with distinct proliferative capacities and differentiation abilities. Among those subpopulations, cancer stem-like cells (CSCs) are hypothesized to drive TC heterogeneity, contributing to its metastatic potential and therapy resistance. CSCs principally exist in tumor areas with specific microenvironmental conditions, the so-called stem cell niches. In particular, in thyroid cancer, CSCs’ survival is enhanced in the hypoxic niche, the immune niche, and some areas with specific extracellular matrix composition. In this review, we summarize the current knowledge about thyroid CSCs, the tumoral niches that allow their survival, and the implications for TC therapy.
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Onuchic, Ana Cláudia, and Roger Chammas. "Câncer e o microambiente tumoral." Revista de Medicina 89, no. 1 (March 19, 2010): 21–31. http://dx.doi.org/10.11606/issn.1679-9836.v89i1p21-31.
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Antes tido como um conjunto de células alteradas em proliferação, hoje o câncer é mais bem entendido como um microambiente, em que as interações entre os elementos celulares e moleculares que o compõem são determinantes na progressão tumoral. Como resultado, a compreensão do evento neoplásico ganha complexidade crescente. A dinâmica das células tumorais passa a ser avaliada como parte de um verdadeiro tecido tumoral, sujeita a condições de vascularização, de oxigenação, de pressão intersticial e de necrose tecidual, que influenciam na cinética tumoral. Estão sendo identificados novos componentes deste nicho tumoral e as suas respectivas atuações. Entre esses integrantes, encontram-se os elementos da imunidade, cuja modulação tem sido demonstrada por uma série de pesquisas aqui revisadas, tanto no sentido da vigilância imunológica, como pressão seletiva negativa, quanto no favorecimento da progressão tumoral. Esta revisão analisará a neoplasia do ponto de vista de um microambiente tumoral, focando na participação imunológica e na cinética tumoral, expondo as principais idéias e descobertas que criaram e estão aperfeiçoando o conceito de câncer
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Jandial, Rahul, and Khairul I Ansari. "Peri-tumoral neural niche in brain metastasis from breast cancer." Integrative Cancer Science and Therapeutics 3, no. 4 (2016): 509. http://dx.doi.org/10.15761/icst.1000199.
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Stöth, Manuel, Aida Freire Valls, Mingyi Chen, Sarah Hidding, Karl Knipper, Ying Shen, Johannes Klose, et al. "Splenectomy reduces lung metastases and tumoral and metastatic niche inflammation." International Journal of Cancer 145, no. 9 (November 2019): 2509–20. http://dx.doi.org/10.1002/ijc.32378.
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Shah, Sumedh, Garima Yagnik, Alan Nguyen, Harsh Wadhwa, Jordan Spatz, Michael Safaee, Justin Cheng, and Manish Aghi. "TMIC-57. PRO-TUMORAL EFFECTS OF INTRA-TUMORAL NEUTROPHILS IN THE GLIOBLASTOMA MICROENVIRONMENT." Neuro-Oncology 21, Supplement_6 (November 2019): vi260. http://dx.doi.org/10.1093/neuonc/noz175.1091.
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Abstract While macrophage enrichment and lymphocyte depletion have been described in glioblastoma, intratumoral neutrophils and their effect on glioblastoma have been under-characterized. While tumor-associated neutrophils (TANs) were initially regarded as passive bystanders due to their short-lived nature, investigation of TANs in other cancer types revealed pro-tumoral roles. Therefore, we sought to characterize TANs in the glioblastoma microenvironment using transcriptomic analysis and define their oncologic effects. Flow cytometric analysis of patient samples for neutrophils (CD11b+/CD15+/CD66b+) revealed higher percentages of TANs in glioblastoma compared to low-grade gliomas (1.76% [n=13] vs. 0.33% [n=6], p=0.03). Using the Transwell migration assay with glioblastoma tumor conditioned-media (CM), we found that recruitment of circulating neutrophils to tumor sites is mediated by leukotriene-B4 chemoattraction and that this interaction can be blocked with the addition of LtB4 receptor antagonist, LY293111. TANs were morphologically activated, unlike circulating neutrophils from GBM patients (P< 0.05) and, while not intravascular, were close to blood vessels. We performed single-cell RNA sequencing of isolated TANs and found a distinct transcriptomic profile relative to circulating neutrophils from these patients, particularly upregulated osteopontin. Osteopontin concentration was significantly higher in TAN CM than in patient-matched peripheral blood neutrophil CM (3.2ng/mL [n=3] vs. 0.02ng/mL [n=3], p< 0.05). Because osteopontin is linked to GBM stem cell-like phenotype maintenance and TANs localized to the perivascular niche where GBM stem cells reside, we investigated TAN-GBM stem cell interactions and osteopontin as a potential mediator. We found TAN CM increased proliferation and stem cell markers (Nanog, Oct4, Sox2) of stem cell-containing GBM neurospheres (p< 0.01). These effects were blocked by osteopontin-neutralizing antibodies (p< 0.01). Our work defines neutrophil-mediated pro-tumoral effects and their mechanisms and identifies a novel approach to target GBM stem cells—by disrupting the immune cell mediators that create their supportive microenvironment in the perivascular niche.
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Moffet, Joel, Oluwaseun Fatunla, James Whittle, Jones Jordan, Samuel Roberts-Thomson, Anna Pavenko, David Scoville, et al. "TMIC-36. SPATIAL ARCHITECTURE OF HIGH-GRADE GLIOMA REVEALS TUMOR HETEROGENEITY WITHIN DISTINCT DOMAINS." Neuro-Oncology 25, Supplement_5 (November 1, 2023): v286. http://dx.doi.org/10.1093/neuonc/noad179.1102.
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Abstract High-grade gliomas are aggressive primary brain cancers with poor response to standard regimens, driven by immense heterogeneity. In isocitrate dehydrogenase (IDH) wild-type high-grade glioma (glioblastoma, GBM), increased intra-tumoral heterogeneity is associated with more aggressive disease. Recently, spatial technologies have emerged to dissect this complex heterogeneity within the tumor ecosystem by preserving cellular organization in situ. Here, we construct a high-resolution molecular landscape of GBM and IDH-mutant high-grade glioma patient samples to investigate the cellular subtypes and spatial communities that compose high-grade glioma using digital spatial profiling and spatial molecular imaging. This uncovered striking diversity of the tumor and immune microenvironment, that is embodied by the heterogeneity of the inferred copy-number alterations in the tumor. Reconstructing the tumor architecture revealed two distinct niches, one composed of tumor cell states that most closely resemble normal glial cells, associated with microglia; and the other niche populated by monocytes and mesenchymal tumor cells. We further reveal that communication between tumor and immune cells is underpinned by tumor-specific ligands, such as TGFb signaling in astrocyte-like tumor cells. This primary study reveals high levels of intra-tumoral heterogeneity in high-grade gliomas, associated with a diverse immune landscape within spatially localized regions.
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Chung, Hyewon, Sang Wha Kim, and Seung Hyeok Seok. "Abstract B009: Tumoral activation of endothelium drives macrophages-mediated metastatic niche formation and promotes lung metastasis." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): B009. http://dx.doi.org/10.1158/1538-7445.metastasis22-b009.
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Abstract Primary tumor induces macrophages-enriched environment to establish metastatic niche which enhances homing and colonization of circulating tumor cells. However, the molecular mechanism underlying endothelial remodeling that favors macrophages infiltration and subsequent niche formation is not fully understood. Here, we found that tumor-derived factors activated endothelial cells to increase adhesive efficacy of monocytes to the endothelium, leading to macrophage infiltration. In mouse models of pulmonary metastasis, this endothelial activation triggered formation of premetastatic niche via accumulation of macrophages in the lungs. Of note, macrophages primed the metastatic microenvironment through enhancing expression of niche-related genes including S100A8, S100A9, MMP9 and fibronectin within the premetastatic lungs and directly transmitted survival signal to tumor cells in a contact-dependent manner. Furthermore, we demonstrated that depletion of macrophages specifically during premetastatic stages reduced niche formation and also resulted in reduced metastatic burden. These findings suggest that endothelial remodeling at metastatic site is a key step for initiation of premetastatic niche formation supported by macrophages. Targeting this step could present an opportunity for therapeutic intervention of metastatic spread in patients with malignant cancers. Citation Format: Hyewon Chung, Sang Wha Kim, Seung Hyeok Seok. Tumoral activation of endothelium drives macrophages-mediated metastatic niche formation and promotes lung metastasis [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr B009.
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Garcia-Mazas, Carla, Noemi Csaba, and Marcos Garcia-Fuentes. "Biomaterials to suppress cancer stem cells and disrupt their tumoral niche." International Journal of Pharmaceutics 523, no. 2 (May 2017): 490–505. http://dx.doi.org/10.1016/j.ijpharm.2016.12.013.
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Jansen, Caroline S., Nataliya Prokhnevska, Viraj A. Master, Martin G. Sanda, Jennifer W. Carlisle, Mehmet Asim Bilen, Maria Cardenas, et al. "An intra-tumoral niche maintains and differentiates stem-like CD8 T cells." Nature 576, no. 7787 (December 11, 2019): 465–70. http://dx.doi.org/10.1038/s41586-019-1836-5.
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Uribe, Daniel, Ignacio Niechi, Gorjana Rackov, José I. Erices, Rody San Martín, and Claudia Quezada. "Adapt to Persist: Glioblastoma Microenvironment and Epigenetic Regulation on Cell Plasticity." Biology 11, no. 2 (February 16, 2022): 313. http://dx.doi.org/10.3390/biology11020313.
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Glioblastoma (GBM) is the most frequent and aggressive brain tumor, characterized by great resistance to treatments, as well as inter- and intra-tumoral heterogeneity. GBM exhibits infiltration, vascularization and hypoxia-associated necrosis, characteristics that shape a unique microenvironment in which diverse cell types are integrated. A subpopulation of cells denominated GBM stem-like cells (GSCs) exhibits multipotency and self-renewal capacity. GSCs are considered the conductors of tumor progression due to their high tumorigenic capacity, enhanced proliferation, invasion and therapeutic resistance compared to non-GSCs cells. GSCs have been classified into two molecular subtypes: proneural and mesenchymal, the latter showing a more aggressive phenotype. Tumor microenvironment and therapy can induce a proneural-to-mesenchymal transition, as a mechanism of adaptation and resistance to treatments. In addition, GSCs can transition between quiescent and proliferative substates, allowing them to persist in different niches and adapt to different stages of tumor progression. Three niches have been described for GSCs: hypoxic/necrotic, invasive and perivascular, enhancing metabolic changes and cellular interactions shaping GSCs phenotype through metabolic changes and cellular interactions that favor their stemness. The phenotypic flexibility of GSCs to adapt to each niche is modulated by dynamic epigenetic modifications. Methylases, demethylases and histone deacetylase are deregulated in GSCs, allowing them to unlock transcriptional programs that are necessary for cell survival and plasticity. In this review, we described the effects of GSCs plasticity on GBM progression, discussing the role of GSCs niches on modulating their phenotype. Finally, we described epigenetic alterations in GSCs that are important for stemness, cell fate and therapeutic resistance.
Dissertations / Theses on the topic "Niche tumorale"
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Gualtieri, Marco. "In vivo analysis and manipulation of an invasive brain tumour." Electronic Thesis or Diss., Sorbonne université, 2022. http://www.theses.fr/2022SORUS388.
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Les tumeurs cérébrales primaires sont extrêmement agressives, et souvent incurables. Des cellules partageant de nombreuses caractéristiques des cellules souches neurales (CSNs) ont été identifiées dans plusieurs tumeurs cérébrales primaires. Celles-ci sont appelées cellules souches cancéreuses (CSCs) et présentent un potentiel d'autorenouvellement avec une prolifération illimitée. Les tumeurs dépendent fortement de leur microenvironnement cellulaire, qui résulte en parti du remodelage de populations préexistantes, telles que les cellules gliales et les vaisseaux sanguins (la barrière hémato-encéphalique). Dans ce projet, le système nerveux central de la drosophile est utilisé comme modèle in vivo afin de suivre les tumeurs cérébrales tout au long de la vie de l’hôte. Les CSNs de la drosophile représentent un modèle de cellules souches bien caractérisé à partir duquel des tumeurs peuvent être générées au cours du développement de l’hôte, puis survivre et proliférer largement à l’âge adulte. Dans ce système, je peux distinguer différentes populations de cellules dans la niche et explorer leur comportement par rapport aux CSC pendant la croissance tumorale. Je me suis particulièrement intéressé aux mécanismes d'interaction cellulaire qui se produisent dans les cellules gliales à l'interface avec les tumeurs. Mes résultats montrent qu'une sous-population de cellules gliales (les cellules gliales du cortex) subit une apoptose lors de la croissance tumorale, un mécanisme qui semble favoriser la propagation de la tumeur. Lorsque la mort des cellules gliales du cortex est stoppée, la croissance tumorale est réduite, ce qui suggère que la tumeur a, en partie, besoin de la mort des cellules gliales afin de se développer. En retour, une apoptose précoce des cellules gliales du cortex favorise la croissance tumoral, soulignant une interaction à double sens entre ces deux populations. Une analyse transcriptionnelle des cellules gliales du cortex durant la croissance tumorale a révélé des voies de signalisation augmentées ou réduites, et dont la fonction est en train d'être testée. En parallèle, prenant avantage d'une analyse transcriptionnelle de telles tumeur déjà disponible, j'ai sélectionné plusieurs candidats potentiels servant de médiateurs des interactions entre protéines à l'interface entre la tumeur et les cellules gliales. Enfin, j'ai évalué le rôle des protéines Rab dans la croissance tumorale. Ces travaux permettront de mieux comprendre comment les tumeurs des CSN envahissent et progressent dans les tissus sainsPrimary brain tumours are extremely aggressive, and often incurable. Interestingly, cells sharing many of the features of neural stem cells (NSCs) have been identified in several primary brain tumors. These cells are coined cancer stem cells (CSCs), and display self-renewal potential with illimited proliferation. Tumours strongly depend on a cellular microenvironment, which results in part from the remodelling of pre-existing populations, such as glial cells and blood vessels (the blood-brain barrier). The project uses the Drosophila Central Nervous System as an in vivo model to track brain tumors during the entire life of the host. The fly NSCs are a well-characterised stem cell model from which tumous can be generated during development, are CSC-driven and can survive and proliferate extensively during adulthood. In this system I can discriminate between different cell populations within the niche, and explore their behavior with respect to the CSCs during tumor growth. In particular I am interested in the mechanisms of cellular interactions happening in glial cells at the interface with the tumors. My results show that a sub-population of glial cells (cortex glia) undergoes apoptosis upon tumor growth, a mechanism that appears to promote tumor propagation. Interestingly, preventing cortex glia death leads to reduced tumor growth, suggesting that the tumour is at least in part required to eliminate glia to grow. In return, precocious killing of cortex glia favors tumor growth, pinpointing a reciprocal relationship between these two cell populations. Performing a transcriptional analysis of cortex glia during tumor growth has revealed multiple signalling pathways with a changing expression, and whose functional relevance is currently being assessed. In parallel, taking advantage of a published tumor transcriptome, I have selected several potential candidates mediating protein protein interactions at the interface between the tumour and the glia cells. Finally, I have also evaluated the role of known Rab proteins in the context of tumor development. This on-going work will shed light on how CNS tumors progress within and invade the healthy tissue
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Grégoire, Murielle. "Polynucléaires neutrophiles, cellules stromales, lymphocytes B : interaction tripartite dans la niche des lymphomes B." Thesis, Rennes 1, 2014. http://www.theses.fr/2014REN1S156/document.
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Les polynucléaires neutrophiles ont longtemps été considérés comme des cellules n’intervenant que dans la réponse immune innée. Cependant, au cours de ces dernières années, de nombreuses publications suggèrent que ces cellules, retrouvées au sein du microenvironnement de nombreux cancers, pourraient également jouer un rôle dans la tumorigénèse et la progression tumorale. Ces études mettent en évidence leur fréquence comme marqueur pronostique dans différents cancers solides, mais peu de travaux se sont intéressés à la caractérisation fonctionnelle de ces cellules dans la progression tumorale. Dans de nombreux cancers dont les lymphomes B issus du centre germinatif, les cellules tumorales, qui sont incapables de proliférer et de survivre seules, sont dépendantes de leur microenvironnement de soutien. Dans cette étude, nous avons évalué la fonctionnalité des polynucléaires neutrophiles dans la croissance des lymphomes B. Ainsi, nous avons démontré pour la première fois que les polynucléaires neutrophiles soutiennent directement la croissance et la survie des cellules tumorales de lymphomes B. De plus, un dialogue bidirectionnel existe entre les polynucléaires neutrophiles et les cellules stromales. D’une part, les cellules stromales soutiennent la survie des polynucléaires neutrophiles, qui en retour induisent les caractéristiques d’un stroma lymphoïde. L’induction de ce phénotype permet aux cellules stromales d’acquérir de meilleures capacités de soutien envers les cellules tumorales. Cette étude confirme donc que les polynucléaires neutrophiles sont une composante importante du microenvironnement tumoral, et pourraient devenir une nouvelle cible thérapeutique pour le traitement des lymphomes B issus du centre germinatifFor long time, neutrophils have only been considered as cells involved in the innate immune response. More recently, in descriptive publications, neutrophils were found in the microenvironment of many solid cancers, hypothesizing that they could also play a role in tumorigenesis and cancer progression. These studies highlighted the prognostic value of their frequency, but few of them focused on the functional characterization of these cells in tumor growth. In many cancers, including germinal centre-derived B-cell lymphomas, tumor cells are dependent on their microenvironment to proliferate and survive. In this study, we focused on the role of neutrophils in the progression of B-cell lymphomas, and for the first time we demonstrated that neutrophils directly support the growth and survival of tumor Bcells. In addition, we highlighted the existence of bidirectional cooperation between neutrophils and stromal cells. In one hand stromal cells support the survival of neutrophils. On the other hand, neutrophils induce a lymphoid stroma phenotype which is well known to enhance their supportive effect on tumor cells. This study demonstrates that neutrophils are a significant component of the tumor microenvironment and may be considered as a potential therapeutic target for the treatment of B-cell lymphomas
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Laviron, Marie. "Etude de la modulation des niches de macrophages au cours du développement tumoral et en réponse à la chimiothérapie." Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS225.pdf.
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Les macrophages représentent la population la plus abondante dans la tumeur et leur accumulation est associée à un mauvais pronostic dans beaucoup de cancers. Ils forment un ensemble de sous-populations pouvant varier en termes d’origine, de localisation et de fonction. Ces caractéristiques, définissant l’interaction entre le macrophage et son environnement, forment la niche du macrophage. Les niches de macrophages ont été largement décrites dans les différents tissus à l’homéostasie mais leur évolution dans la tumeur est mal connue. Mon projet de thèse s’intéresse à caractériser les niches de macrophages et s’articule autour de deux projets ; l’évolution des niches de macrophages lors du développement tumoral ; et l’impact de la chimiothérapie sur les niches de macrophages, en particulier le rôle des Treg dans la polarisation de celles-ci. A travers ces projets, nous mettons en évidence que l’hétérogénéité des macrophages est directement associée à la diversité des niches spatiales définies dans la tumeur. La polarisation des macrophages est dictée par les signaux de ces niches. Nous suggérons également que la chimiothérapie favorise les interactions entre Treg et macrophages dans la tumeur, que la déplétion des Treg post-chimiothérapie conduit à une repolarisation des macrophages vers un phénotype pro-inflammatoire, associée à un contrôle de la croissance tumorale. Ce travail met en évidence l’importance de la relation du macrophage avec la tumeur dans l’induction de ses fonctions et pourrait permettre d’identifier les populations à cibler pour rétablir une réponse immunitaire anti-tumorale efficaceMacrophages represent the most abundant population within the tumor and their accumulation is associated with bad prognosis in most cancers. They form a group of sub-populations that vary in terms of origin, localization and function. Those characteristics, defining the interaction between the macrophage and its environment, constitute the macrophage niche. Macrophage niches have been described in different tissues at homeostasis but their evolution during tumor development remains to be elucidated. My thesis project aims at characterizing macrophage niches and focuses on two parts; the evolution of macrophage niches during tumor development; and the impact of chemotherapy on macrophage niches, and specifically the role of Treg on their polarization in this setting. Through those projects, we highlight that the heterogeneity of macrophages is directly linked to the diversity of tumor spatial niches. Macrophage polarization is dictated by signals derived from the niche. We also suggest that chemotherapy favors Treg and macrophage interactions, and that Treg depletion post-chemotherapy leads to the repolarization of macrophages towards a pro-inflammatory phenotype, associated with better tumor control. This work sheds light on the importance of the relationship between the macrophage and the tumor for the induction of its functions, and could identify specific populations to target to restore an efficient anti-tumor immune response
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Fahy, Lucine. "Etude des conséquences d’un environnement hypoxique sur le développement et la chimiorésistance des leucémies aiguës lymphoblastiques T (LAL-T)." Thesis, Sorbonne Paris Cité, 2019. https://theses.md.univ-paris-diderot.fr/FAHY_Lucine_2_complete_20190627.pdf.
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La leucémie aiguë lymphoblastique T (LAL-T) est une hémopathie maligne caractérisée par une prolifération exacerbée de précurseurs lymphocytaires T incapables d’achever leur maturation. Le traitement des LAL-T est efficace dans 90% des cas chez l’enfant. Cependant, les enfants présentant une rechute ont un pronostic très défavorable. La résistance à la chimiothérapie constitue donc un défi thérapeutique majeur dans le traitement des LAL-T ; résistance qui peut être au moins en partie liée aux interactions entre les cellules leucémiques et le microenvironnement qui favorisent la survie des cellules leucémiques. La moelle osseuse, site crucial de maintien et de propagation de la leucémie, est hypoxique avec des taux d’oxygène variant de 0.1% à 5%. Sachant que les cancers solides hypoxiques sont plus résistants à la chimiothérapie et à la radiothérapie, le but de mon projet a été de déterminer les effets d’un environnement hypoxique sur le développement et la chimiorésistance des LAL-T et de comprendre les mécanismes à l’origine des effets observés.Méthodes : Des LAL-T murines et de patients ont été cultivées en hypoxie (3.5% et 1% d’O2) et en normoxie (21% d’O2). Croissance, apoptose, cycle cellulaire, métabolisme et chimiorésistance ont été mesurés ainsi que développement leucémique in vivo en souris immunodéficientes afin de déterminer l’impact de faibles taux d’oxygène sur les LAL-T.Résultats : Les résultats ont montré que l’hypoxie inhibe la croissance des LAL-T en inhibant la progression dans le cycle cellulaire et le métabolisme, les rendant moins sensibles aux traitements chimiothérapeutiques et préservant leur capacité à induire la leucémie in vivo. La perte d’expression de HIF1α par knockdown (KD) a modifié les effets de l’hypoxie observés sur les LAL-T et a restauré leur chimiosensibilité. De manière intéressante, l’activation de la voie mTOR est diminuée dans les LAL-T en hypoxie et le KD de HIF1α en hypoxie a restauré son activation. De plus, l’inhibition de mTOR dans les cellules HIF1α KD a amélioré leur chimiorésistance, montrant une relation fonctionnelle entre ces deux voies.Conclusion : Ce travail a montré que des niches hypoxiques peuvent jouer un rôle protecteur pendant le traitement chimiothérapeutique des LAL-T à travers HIF1α et mTOR. L’inhibition de HIF1α et/ou l’activation de mTOR pourraient améliorer la chimiosensibilité des LAL-T en hypoxieBackground: T cell acute lymphoblastic leukemia (T-ALL) is a malignant hematological disorder characterized by an increased proliferation of T lymphocyte precursors that are unable to complete their maturation. Treatments are effective in 90% of children T-ALL cases. However, children with relapse have a very poor prognosis. Resistance to chemotherapy is thus a major therapeutic challenge in the treatment of T-ALL that can be driven by interactions between leukemic cells and the microenvironment. Bone marrow microenvironment, a crucial site of propagation and maintenance of leukemia, is hypoxic with oxygen levels varying from 0.1 to 5%. As hypoxic solid tumors are more resistant to radiotherapy and chemotherapy, the aims of the study were to investigate to which extent oxygen levels impact on leukemia development and chemoresistance and to characterize the implicated molecular mechanisms. Methods: Mouse models and patients derived samples of T-ALL were cultured in low (1% and 3.5%) and high (21%) oxygen levels. Growth, apoptosis, cell cycle, metabolism and chemoresistance were measured as well as in vivo leukemia propagation using immune deficient mice as ways to define the impact of oxygen levels on T-ALL.Results: Results show that hypoxia inhibits the growth of T-ALL by slowing down cell cycle progression and decreasing metabolism, making them less sensitive to anti-leukemic drugs and preserving their ability to initiate leukemia in vivo after treatment. Knocking down (KD) HIF1α counteracted the effects observed in hypoxic T-ALL and restored their chemosensitivity. Interestingly activation of mTOR was diminished in hypoxic leukemic cells and HIF-1α KD restored mTOR activation in these low O2 conditions. Moreover, inhibiting mTOR in HIF1aKD T-ALL enhanced their chemoresistance, indicating a functional relationship between these two pathways.Conclusion: This work shows that hypoxic niches can play a protective role during the treatment of T-ALL through a HIF1α/mTOR molecular loop. Inhibition of HIF1α and/or activation of the mTOR pathway may help suppress the chemoresistance of T-ALL in hypoxic niches
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Nor, Carolina. "Modulação da sobrevivência e proliferação de células de câncer : mecanismos relacionados ao estado da cromatina e ao nicho tumoral." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/104742.
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Câncer é a principal causa de morte nos países desenvolvidos e a segunda causa de morte nos países em desenvolvimento. O trabalho de diversos grupos de pesquisa tem sugerido que os tumores estão organizados em uma hierarquia de células, na qual uma pequena fração apresenta propriedades de células-tronco. Essas células tem se mostrado resistentes à quimioterapia convencional, dependentes da sinalização do microambiente tumoral e responsivas à terapia diferenciativa. Aqui nós mostramos que butirato sódico (NaB), um inibidor de desacetilase de histonas, diminui a proliferação celular e a formação de colônias em linhagens celulares de meduoblastoma humano. Estes efeitos foram acompanhados de um aumento da expressão de RNAm Gria2, um marcador de diferenciação neuronal, em duas das três linhagens celulares testadas. A formação de neuroesferas também foi impedida com a exposição de uma linhagem crescida em meio de cultura apropriado para células-tronco e NaB. NaB se mostrou capaz de potencializar os efeitos do quimioterápico etoposídeo e do fator neurotrófico derivado de cérebro (BDNF) na inibição da viabilidade celular de meduloblastoma. Além disso, nós observamos que o tratamento com cisplatina aumenta a proporção de células-tronco tumorais (CTT), identificadas por ALDH+CD44+, em células de carcinoma de cabeça e pescoço, quando tratadas também com interleucina 6 (IL-6), uma citocina liberada pelo nicho perivascular. O mesmo tratamento promoveu a proliferação, sobrevivência e auto-renovação de CTTs in vitro ao aumentar o número de esferas em placas de baixa aderência e a expressão de Bmi-1 em western blots. A fosforilação do transdutor de sinal e ativador de transcrição 3 (STAT3), um indicativo de propriedades de CTTs, induzida por IL-6 não foi afetada pelo tratamento com cisplatina em células de HNSCC, enquanto que a indução de fosforilação de quinases reguladas por sinais extracelulares (ERK), indicativo de processo de diferenciação, por IL-6 foi parcialmente inibido por cisplatina. Células resistentes a baixas doses de cisplatina também expressaram mais Bmi-1 do que células nunca expostas ao quimioterápico. Experimentos in vivo corroboram os achados in vitro, uma vez que tumores humanos induzidos em camundongos imunocomprometidos apresentaram aumentada proporção de células ALDH+CD44+ após tratamento dos animais com cisplatina. O anticorpo contra o receptor de IL-6 foi capaz de reverter a indução de expressão de Bmi-1 por cisplatina e IL-6. Em conjunto, esses resultados sugerem que a modulação de mecanismos epigenéticos das células tumorais e de sinais provenientes do nicho tumoral são novos alvos promissores para o desenvolvimento de terapias adjuvantes contra o câncer.Cancer is the leading cause of death in economically developed countries and the second cause of death in developing countries. Work from a number of laboratories strongly suggests that tumors are organized as a hierarchy based on a subset of cancer cells that have stem-cell properties. These cells have been shown to be resistant to conventional therapy, dependent on contextual signals within the tumor microenvironment and, to be responsive to differentiation therapy. Here we show that sodium butyrate (NaB), a histone deacetylase inhibitor, decreases cell proliferation and colony formation in human medulloblastoma cell lines. These effects were accompanied by an increased mRNA expression of Gria2, a neuronal differentiation marker, in two out of three cell lines tested. In addition, neurosphere formation was impaired by NaB exposure in a cell line submitted to stem cells proper media. NaB also may potentiate the effect of etoposide chemotherapy and BDNF (Brain-derived neurotrophic factor) on the inhibition of medulloblastoma cells viability. Moreover, we observed that cisplatin treatment increased the proportion of cancer stem cells (CSC), identified by ALDHhighCD44high cells, in head and neck squamous cell carcinoma (HNSCC), when treated together with recombinant human IL-6 (rhIL-6). The same regimen promoted proliferation, self-renewal and survival of CSC in vitro as seen by the increase in orosphere number formed in ultra-low attachment plates, and Bmi-1 expression induction in western blots. IL-6–induced signal transducer and activator of transcription 3 (STAT3) phosphorylation (indicative of stemness) was unaffected by treatment with cisplatin in HNSCC cells, whereas IL-6–induced extracellular signal-transducer kinases (ERK) phosphorylation (indicative of differentiation processes) was partially inhibited by cisplatin. Cells resistant to lower doses of cisplatin also expressed more Bmi-1. In vivo experiments corroborated in vitro findings by showing increased proportion of ALDH highCD44high cells in xenograft tumors of mice treated with cisplatin. An antibody against the receptor of IL-6 was able to revert the induction of Bmi-1 expression seen in cells treated with cisplatin plus IL-6. Taken together, these results suggest that the modulation of the epigenetic states of the cancer cell and modulation of signals provided by the niche are promising new molecular targets for the development of adjuvant therapy for cancer.
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Deynoux, Margaux. "Incidence de l'hypoxie sur le métabolisme oxydatif des leucémies aiguës myéloïdes : établissement et caractérisation d'un modèle in vitro de niche leucémique." Thesis, Tours, 2019. http://www.theses.fr/2019TOUR3303.
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Dans les leucémies aiguës myéloïdes (LAM), un taux élevé d’espèces réactives de l’oxygène (ROS) est connu pour favoriser la prolifération de blastes, alors qu’un niveau faible promeut la quiescence des cellules souches leucémiques. La faible oxygénation, ou hypoxie, de la niche médullaire pourrait contribuer à la chimiorésistance des LAM en diminuant le stress oxydatif. Les facteurs induits par l’hypoxie (HIF) sont impliqués dans le contrôle du métabolisme et des enzymes antioxydantes. Leur inhibition conduit à un stress et à la mort des cellules de LAM. Mon objectif était d’étudier un lien entre l’hypoxie, le métabolisme oxydatif et la chimiorésistance dans un modèle in vitro de culture de cellules de LAM. L’acquisition d’un profil hypoxique par les cellules souches hématopoïétiques (CSH), cultivées avec des cellules stromales mésenchymateuses (CSM) médullaires, a été montré. Nous avons postulé que les cellules leucémiques pouvaient également l’acquérir en coculture avec des CSM humaines. Pour le démontrer, nous avons cultivé des cellules de LAM primaires ou de la lignée MV4-11 sur des CSM humaines primaires ou de la lignée HS-27a. A l’instar des CSH, nous avons identifié trois populations leucémiques en fonction de leur capacité d’adhésion sur les CSM : en suspension, adhérentes aux CSM et nichées dans les CSM. Les cellules nichées, les plus adhérentes, ont une plus forte expression du CXCR4 que les autres. Elles sont aussi plus résistantes de 2 à 7 fois à la cytarabine. Cependant, aucune modification du phénotype souche et des capacités clonogéniques, de repopulation ou de xénogreffe, n’a pu être associée aux cellules nichées comparées aux deux autres populations. En revanche, les cellules nichées présentent un profil hypoxique, une plus faible prolifération avec une augmentation de la phase G0, et de plus faibles niveaux de ROS en lien avec une masse mitochondriale diminuée. Ceci suggère donc un lien entre la chimiorésistance et l’hypoxie ou le métabolisme, plutôt qu’avec une capacité souche. Nous avons aussi montré que l’acriflavine, un inhibiteur non spécifique des HIF, pouvait avoir un effet synergique avec la cytarabine sur les cellules nichées chimiorésistantes. Nos résultats montrent que le surnageant ou le simple contact avec les CSM ne suffisent pas à induire le changement métabolique et la résistance à la cytarabine. Nous pensons que l’hypoxie dans la niche peut moduler le métabolisme oxydatif et donc la chimiorésistance par des mécanismes directs et/ou indirects via l’expression de CXCR4, montré récemment comme impliqué dans la régulation du stress oxydatif des CSHIn acute myeloid leukemia, a high level of ROS is known to favor blasts proliferation, whereas a low level promotes stem cells quiescence. The low oxygenation, or hypoxia, of the bone marrow niche could contribute to chemoresistance of AML cells by reducing the oxidative stress. Hypoxia-inducible factors (HIF) are involved in the control of the cell metabolism and antioxidant enzymes. HIFs inhibition leads to AML cells stress and death. The purpose of this work was to study a link between hypoxia, oxidative metabolism and chemoresistance in an in vitro model of leukemic cell culture. The acquisition of a hypoxic profile by hematopoietic stem cells (HSC) cultured with medullary mesenchymal stromal cells (MSC), has been shown. We hypothesized that AML cells may also acquire such profile in a coculture with human MSCs. To demonstrate that, we cultivated primary AML cells or the MV4-11 cell line on primary human MSCs or the HS-27a cell line. Like HSCs, we identified three leukemic populations according to their adhesion capacity to MSCs: in suspension, adherent to MSCs and embedded in MSCs. Embedded cells, the most adherent, have stronger CXCR4 expression compared to the others. They are also 2- to 7-fold more resistance to cytarabine. However, no change in the stem cell phenotype profile and in the clonogenic, repopulation or xenograft capacities, could be associated with the embedded cells compared to other populations. In contrast, embedded cells present a hypoxic profile, a weak proliferation with increased G0 phase, and lower ROS level that may rely on lower mitochondrial mass. This suggests that chemoresistance mainly relies on hypoxia or cell metabolism rather than a higher stem cell capacity. Furthermore, we have shown that acriflavine, a non-specific HIF inhibitor, could synergize with the cytarabine to eliminate embedded chemoresistant cells. Our results show that the MSC supernatant or a simple contact are not sufficient to induce metabolic change and resistance to cytarabine. We assume that hypoxia in the niche may modulate the oxidative metabolism and the chemoresistance by direct mechanisms and/or indirect ones through CXCR4 expression, a chemokine receptor shown to be involved in the regulation of the oxidative stress in HSC
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Balenci, Laurent. "Etude de la protéine IQGAP1 dans un contexte physiologique de la neurogenèse adulte et dans un contexte pathologique de tumeurs cérébrales." Phd thesis, Grenoble 1, 2006. http://tel.archives-ouvertes.fr/tel-00129290.
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Les cellules souches/progénitrices sont douées d'une forte plasticité cellulaire qui leur permet de développer, de maintenir et de régénérer organes ou tissus dans lesquels elles résident. Ces processus requièrent l'intégration de signaux moléculaires et environnementaux qui influencent leur comportement et leur devenir. La perturbation de l'un de ces mécanismes régulateurs aboutit à une perte de contrôle des cellules souches/progénitrices pouvant entraîner le développement de pathologies cancéreuses. De ce fait, la connaissance des éléments cellulaires et moléculaires régulant la biologie des cellules souches/progénitrices est nécessaire pour l'emploi éventuel de ces cellules en médecine régénérative et pour une avancée dans les traitements anti-cancéreux.La protéine IQGAP1, que nous avons étudiée dans le cerveau dans un contexte physiologique et pathologique, s'est révélée être un nouveau marqueur de cellules souches/progénitrices normales et tumorales. A travers une étude comparative de souris sauvages et iqgap1-/-, nous avons analysé les propriétés et le comportement in vivo comme in vitro des cellules souches/progénitrices neurales. Nous avons démontré qu'IQGAP1 joue un rôle dans la neurogenèse adulte en régulant la migration des cellules progénitrices neurales en réponse au VEGF, facteur pléïotropique intervenant notamment dans la neurogenèse et l'angiogenèse tumorale. D'autre part, dans un contexte tumoral de gliomes humains et chimio-induits chez le rat, la caractérisation de cette protéine dans des cellules souches/progénitrices tumorales au sein de tumeurs malignes a permis d'attribuer un rôle putatif à la protéine IQGAP1 dans l'expansion tumorale par la dissémination de ces cellules cancéreuses. L'identification et la caractérisation de tous les mécanismes environnementaux régulant la motilité et la migration des précurseurs neuraux normaux pourraient s'avérer utile pour la compréhension des mécanismes d'invasion tumorale et pour le développement de thérapies anti-cancéreuses plus efficaces.
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Lim, Chetana. "Microenvironnement et angiogénèse : implications dans la stratégie onco-chirurgicale des métastases hépatiques synchrones des cancers colorectaux." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC018/document.
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Lors du diagnostic de cancer colorectal, près d’un quart des patients ont des métastases hépatiques dites synchrones. Lorsque la tumeur primitive est asymptomatique, la stratégie chirurgicale (chirurgie première de la tumeur primitive versus chirurgie première des métastases hépatiques) reste débattue. Les recommandations actuelles ne reposent que sur des accords d’experts qui elles-mêmes sont basées sur des études cliniques rétrospectives. L’étude du microenvironnement tumoral a pris ces dernières années une place majeure dans la recherche sur le cancer. Elle a permis de changer de paradigme avec une nouvelle conception du processus métastatique : une tumeur primitive peut agir sur le microenvironnement du futur site métastatique pour créer une "niche pré-métastatique". Cette niche pré-métastatique permettrait secondairement la croissance des cellules tumorales via une angiogénèse tumorale et la formation de métastases. Par une triple approche à la fois fondamentale, translationnelle et clinique, nous avons obtenu des données qui suggèrent qu’une chirurgie première de la tumeur colique ou rectale permet de moduler l’angiogénèse au sein du microenvironnement hépatique. Cette stratégie chirurgicale permettrait également d’améliorer le pronostic oncologique des malades et l’efficacité des anti-angiogéniquesAt the time of the diagnosis of colorectal cancer, nearly 25% of patients have synchronous liver metastases. When this tumor is asymptomatic, the question of surgical strategy (primary tumor first versus liver-first strategy) remains debated. Current recommendations are based on agreements of experts which are by themselves based on retrospective clinical studies. The study of the tumor microenvironment has taken in recent years a major place in the field of cancer research. It leads to new paradigm with a new conception of the metastatic process. It may be possible that the microenvironment of the metastatic sites can be modulated by the primary tumor to promote the formation of the pre-“metastatic niche”. This leads to promote the growth of cancer cells and increase the metastatic potential of primary tumor. By a multidisciplinary research including fundamental, translational and clinical approaches, we have shown that primary tumor first strategy could modulate tumor angiogenesis and liver metastatic process. It is associated with improved survival of patients and efficacy of the anti-angiogenic therapy
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Franco, Lídia Mafalda Lopes. "Potencialidade das células estaminais no tratamento do cancro." Master's thesis, 2013. http://hdl.handle.net/10451/46194.
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Trabalho Final de Mestrado Integrado, Ciências Farmacêuticas, Universidade de Lisboa, Faculdade de Farmácia, 2013Atualmente, o cancro tornou-se uma doença frequente e uma das principais causas de mortalidade em todo o mundo. Existem várias evidências que o cancro é uma doença de células estaminais. Compreender as propriedades e características das células estaminais tumorais (CETs) é crucial para a investigação na área da oncologia, nomeadamente no isolamento e identificação das CETs, no diagnóstico e na terapêutica do cancro. Os tratamentos anti-cancerígenos convencionais têm muitas vezes efeitos incompletos e temporários, diminuindo apenas o tamanho do tumor e este tende a recidivar devido, maioritariamente, aos múltiplos mecanismos de resistência existentes nas CETs. As CETs também necessitam de um microambiente particular para controlar o seu estado de auto-renovação e indiferenciação. Deste modo, as hipóteses terapêuticas que se focam em atingir as CETs e o seu nicho oferecem uma estratégia promissora no tratamento do cancro. O presente trabalho introduz a informação básica existente sobre as CETs, nomeadamente, a sua definição, origem e as principais características, incluindo a importância do nicho; descreve vários orgãos onde foi demonstrada a existência destas células; compara as diferentes técnicas utilizadas para isolar e identificar as CETs entre a população tumoral total; analisa os múltiplos mecanismos de resistência inerentes às CETs e enumera os principais alvos moleculares e de sinalização com potencial para ser utilizados no desenvolvimento futuro de terapêuticas anti-CETs. Desta forma, é dada uma visão geral do conhecimento atual acerca destas células e os potenciais agentes terapêuticos que estão atualmente em investigação.
Nowadays, cancer has been a frequent disease and the first or second most common cause of death worldwide. Mounting evidence has implicated that cancer is a disease of stem cells. Understanding the properties and characteristics of cancer stem cells (CSC) are key to future study on cancer research, such as the isolation and identification of CSCs, the cancer diagnosis, and the cancer therapy. The standard oncology treatments have incomplete and temporary effects that only shrink the tumor, and the tumor tends to relapse mainly due to the multiple resistant mechanisms existing in CSCs. CSCs also require a special microenvironment to control their self-renewal and undifferentiated state. Thus, therapeutic hypothesis that focuses on targeting CSCs and their microenvironmental niche offer a promising strategy in the treatment of cancer. The present work introduces the basic information about CSCs, namely, the definition, origin, and the main characteristics, including the importance of the de CSC niche; describes different organs where it was demonstrated the existence of these cells; compare different techniques used to isolate and identify CSCs among the bulk tumors; analyze the multiple resistant mechanisms inherent in CSCs and lists the main molecular and signaling targets that have the potential to be utilized for future development of anti-CSC therapeutics. Thus, it is given an overview about the current knowledge regarding CSC and the potential therapeutic agents that are currently under investigation.
Book chapters on the topic "Niche tumorale"
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Ludwig, Wolf-Dieter, and Kerstin Noëlle Vokinger. "Hochpreisigkeit bei Onkologika." In Arzneimittel-Kompass 2021, 79–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2021. http://dx.doi.org/10.1007/978-3-662-63929-0_6.
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Zusammenfassung Zusammenfassung Onkologikasind seit mehreren Jahren die umsatzstärkste Arzneimittelgruppe in Deutschland. Während 2014 unter den 30 umsatzstärksten patentgeschützten Arzneimitteln nur drei Onkologika mit Nettokosten zwischen 184 Mio. € und 259 Mio. € je Arzneimittel waren, befinden sich unter den führenden 20 Arzneimitteln nach Nettokosten im Jahr 2020 bereits neun Onkologika. Sie sind deshalb inzwischen die mit weitem Abstand umsatzstärkste Arzneimittelgruppe mit 9,5 Mrd. € Nettokosten insgesamt. Verantwortlich hierfür sind die sehr hohen Preise, die heute von pharmazeutischen Unternehmern (pU) für neuartige Wirkstoffe zur Behandlung hämatologischer Neoplasien und solider Tumore (z. B. Proteinkinaseinhibitoren und monoklonale Antikörper) verlangt werden. Im Zusammenhang mit der Auswertung von Verordnungen ist zu berücksichtigen, dass für GKV-Patient:innen 2020 insgesamt nur 8,1 Mio. Verordnungen von Onkologika erfolgten, die nur 1,2 % aller verordneten Arzneimittel des GKV-Arzneimittelmarktes ausmachten. Anhand aktueller Untersuchungen konnte inzwischen gezeigt werden, dass die Kosten für Forschung & Entwicklung (F & E)neuer Wirkstoffe, die von pU häufig als Begründung für die sehr hohen Preise der Onkologika genannt wurden, deutlich niedriger liegen als früher behauptet (im Median circa 548 Mio. €), sodass Onkologika heute sehr hohe Erträge generieren, die die Kosten für F & E deutlich übersteigen. Darüber hinaus belegen sowohl aktuelle Studien aus den USA und Europa als auch die Ergebnisse der seit 2011 in Deutschland durchgeführten frühen Nutzenbewertung von Onkologika, dass ein Zusammenhang zwischen deren klinischem Nutzen und den Behandlungskosten meist nicht besteht.
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"Nicht tumoröse Differenzialdiagnosen." In MRT des Zentralnervensystems, edited by Michael Forsting and Olav Jansen. Stuttgart: Georg Thieme Verlag, 2014. http://dx.doi.org/10.1055/b-0034-98920.
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"26.12 Weitere nicht tumoröse Kolonerkrankungen." In Chirurgie, edited by Andreas Hirner and Kuno Weise. Stuttgart: Georg Thieme Verlag, 2004. http://dx.doi.org/10.1055/b-0034-89821.
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"26.12 Weitere nicht tumoröse Kolonerkrankungen." In Chirurgie, edited by Andreas Hirner and Kuno Weise. Stuttgart: Georg Thieme Verlag, 2008. http://dx.doi.org/10.1055/b-0034-69013.
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Carolina Monteiro, Ana, and Adriana Bonomo. "Breast-Tumor-Derived Bone Pre-Metastatic Disease: Interplay between Immune and Bone Cells within Bone Marrow Microenvironment." In Bone Tumors - A Comprehensive Review of Selected Topics [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107278.
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The bone marrow is a dynamic organ where osteogenesis and bone remodeling take place side by side with hematopoiesis and the maintenance of immunological memory. It provides a unique microenvironment favoring the colonization and outgrowth of breast cancer cells. The outcome of breast-cancer-derived bone metastases depends on the formation of a pre-metastatic niche, which is initiated through “education” of non-tumoral cells present in the primary cancerous niche. Among other participants, immune cells and their secreted factors can boost the successful seeding of the distant disease. In this chapter, we discuss the reciprocal interplay between bone and T and B cells, particularly in pathological contexts. In the first part, we are exploring the knowledge brought by the osteoimmunology field, especially from the best studied disease in this area, rheumatoid arthritis. In the second part, we summarize the latest findings on underlying cellular and molecular mechanisms for breast-cancer-derived bone pre-metastatic niche formation. In addition, we explore the concept that breast-tumor-primed T and B cells function as messengers from the periphery to the bone marrow, alter bone turnover homeostasis in favor of osteoclasts, before tumor colonization, leading to a pre-metastatic niche formation to further the development of bone metastases.
Conference papers on the topic "Niche tumorale"
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Pasquier, Jennifer, Hamda Al Thawadi, Nadine Abu Kaoud, Pegah Ghiabi, Mahtab Maleki, Bella S. Guerrouahen, and Arash Rafii. "Abstract A74: Microparticles mediate cross-talk between tumoral and endothelial cells and promote the constitution of an angiocrine pro-metastatic niche through Arf6 up regulation." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; September 18-21, 2013; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1078-0432.ovca13-a74.
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Kürten, Cornelius H. L., A. Kulkarni, L. Vujanovic, X. Chen, U. Duvvuri, S. Kim, X. Lu, AR Cillo, S. Lang, and RL Ferris. "„Heiße“ vs. „kalte“ Tumore: Unterschiede im entzündeten vs. nicht entzündeten Tumormikromilieu (TMM) von Kopf-Hals-Plattenepithelkarzinomen (HNO-PEC) mittels Einzelzell-RNA-Sequenzierung." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727790.
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