Thematische Bibliographien / Tumoral Niche

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  1. Zeitschriftenartikel
  2. Dissertationen
  3. Bücher
  4. Buchteile
  5. Konferenzberichte
  6. Berichte der Organisationen

Auswahl der wissenschaftlichen Literatur zum Thema „Tumoral Niche“

Autor: Grafiati
Veröffentlicht am 25. Mai 2024

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Zeitschriftenartikel zum Thema "Tumoral Niche"

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Grassi, Elisa Stellaria, Viola Ghiandai und Luca Persani. „Thyroid Cancer Stem-Like Cells: From Microenvironmental Niches to Therapeutic Strategies“. Journal of Clinical Medicine 10, Nr. 7 (01.04.2021): 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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Shah, Sumedh, Garima Yagnik, Alan Nguyen, Harsh Wadhwa, Jordan Spatz, Michael Safaee, Justin Cheng und 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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Jandial, Rahul, und Khairul I Ansari. „Peri-tumoral neural niche in brain metastasis from breast cancer“. Integrative Cancer Science and Therapeutics 3, Nr. 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, Nr. 9 (November 2019): 2509–20. http://dx.doi.org/10.1002/ijc.32378.

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Chung, Hyewon, Sang Wha Kim und Seung Hyeok Seok. „Abstract B009: Tumoral activation of endothelium drives macrophages-mediated metastatic niche formation and promotes lung metastasis“. Cancer Research 83, Nr. 2_Supplement_2 (15.01.2023): 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 und Marcos Garcia-Fuentes. „Biomaterials to suppress cancer stem cells and disrupt their tumoral niche“. International Journal of Pharmaceutics 523, Nr. 2 (Mai 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, Nr. 7787 (11.12.2019): 465–70. http://dx.doi.org/10.1038/s41586-019-1836-5.

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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 (01.11.2023): 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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Infanger, David W., YouJin Cho, Brina S. Lopez, Sunish Mohanan, S. Chris Liu, Demirkan Gursel, John A. Boockvar und Claudia Fischbach. „Glioblastoma Stem Cells Are Regulated by Interleukin-8 Signaling in a Tumoral Perivascular Niche“. Cancer Research 73, Nr. 23 (11.10.2013): 7079–89. http://dx.doi.org/10.1158/0008-5472.can-13-1355.

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Xiang, Lisha, und Daniele Gilkes. „The Contribution of the Immune System in Bone Metastasis Pathogenesis“. International Journal of Molecular Sciences 20, Nr. 4 (25.02.2019): 999. http://dx.doi.org/10.3390/ijms20040999.

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Bone metastasis is associated with significant morbidity for cancer patients and results in a reduced quality of life. The bone marrow is a fertile soil containing a complex composition of immune cells that may actually provide an immune-privileged niche for disseminated tumor cells to colonize and proliferate. In this unique immune milieu, multiple immune cells including T cells, natural killer cells, macrophages, dendritic cells, myeloid-derived suppressor cells, and neutrophils are involved in the process of bone metastasis. In this review, we will discuss the crosstalk between immune cells in bone microenvironment and their involvement with cancer cell metastasis to the bone. Furthermore, we will highlight the anti-tumoral and pro-tumoral function of each immune cell type that contributes to bone metastasis. We will end with a discussion of current therapeutic strategies aimed at sensitizing immune cells.
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Dissertationen zum Thema "Tumoral Niche"

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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 germinatif
For 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 efficace
Macrophages 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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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 sains
Primary 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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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 CSH
In 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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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-angiogéniques
At 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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Dagdelen, Olcay. „Nicht-invasive Dignitätsbestimmung von HNO-Tumoren mittels Positronenemissionstomographie“. Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-27595.

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Vahedi, Nadine. „Früh- und Langzeitergebnisse nach Resektion von Lebermetastasen nicht-kolorektaler Tumoren“. Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-100951.

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Koczuła, Katarzyna Malgorzata. „Real-time metabolic flux in chronic lymphocytic leukaemia cells adapting to the hypoxic niche“. Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/6067/.

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Although knowledge of metabolic adaptations in cancer has increased dramatically, little is known about the spontaneous adoptive adaptations of cancer cells to changing conditions in the body. This is particularly important for chronic lymphocytic leukaemia (CLL) cells which continually circulate between different microenvironments in the blood, bone marrow and lymph nodes. To study such metabolic adaptations, a nuclear magnetic resonance (NMR) based approach; capable of monitoring real-time metabolism in primary CLL cells was developed. Using this setup, this thesis demonstrates fast, reversible metabolic plasticity in CLL cells during transition from normoxic to hypoxic conditions, associated with elevated HIF-1α dependent glycolysis. This work also demonstrates differential utilisation of pyruvate in oxygenated and hypoxic conditions where in the latter, pyruvate was actively transported into CLL cells to protect against oxidative stress. Moreover, real-time NMR experiments provided initial evidence that CLL metabolism in hypoxia correlates with stage of disease, adding significant relevance of our method for patient stratification. Additionally, to further investigate alterations between normoxic and hypoxic metabolism, Metabolic Flux Analysis (MFA) was carried out using primary CLL cell extracts, revealing modifications in pyruvate carboxylase (PC) activity and the pentose phosphate pathway (PPP). Despite the recent advent of promising new agents, CLL currently remains incurable and new therapeutic approaches are required. Understanding CLL cell adaptation to changing oxygen availability will permit the development of therapies that interfere with disease aetiology. This study makes several significant contributions towards this goal. Moreover, the findings may be relevant to all migratory cancer cells, and may have importance for the development of strategies to prevent cancer metastasis.
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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 hypoxie
Background: 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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Kobelt, Dennis. „Klinische Studie und experimentelle Untersuchungen zur nicht-viralen Gentherapie solider Tumoren“. Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16598.

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Krebs gehört zu den häufigsten Todesursachen weltweit. Ein großer Hoffnungsträger für die Behandlung maligner Tumore ist die Gentherapie. Die nicht-virale Gentherapie gilt als sicherere Alternative zur viralen Gentherapie. Für den nicht viralen Gentransfer sind sowohl Vektor als auch Gentransfertechnologie von entscheidender Bedeutung. Im Rahmen dieser Arbeit wurde die Gentransfereffizienz und Sicherheit der Jet-Injektion in einer klinischen Phase I Gentransferstudie mit Hilfe des Swiss-Injektors untersucht. Es konnte gezeigt werden, dass diese Technologie sicher klinisch angewendet werden kann, dass jedoch die Sicherheit der Vektoren und vor allem die Gentransfereffizienz weiter optimiert werden müssen. Ausgehend von diesen Ergebnissen wurden optimierte nicht-virale Vektoren (Minicircle, MIDGE) miteinander und mit ihren parentalen Plasmiden verglichen. Mit Hilfe des MIDGE Vektors konnte die höchste Transgenexpression aufgrund einer erhöhten Transkription erzielt werden. In Vorbereitung der klinischen Anwendung des MIDGE-Vektors wurde die Kombination von hTNF-alpha Gentransfer und Vindesin Chemotherapie untersucht. Auch hier zeigte der MIDGE-Vektor eine erhöhte in vitro Genexpression, die in vitro zu einer erhöhten Zytotoxizität von Vindesin aufgrund einer verstärkten Aktivierung der Apoptose führte. Auch in vivo konnte die verbesserte hTNF-alpha-Genexpression des MIDGE-Vektors nach Jet-Injektion gezeigt werden. Dies führte in Kombination mit Vindesin zu einem signifikant reduzierten Tumorwachstum. Durch Analyse der systemischen Vektorverteilung im Blut und in den Organen sowie in einer präklinischen toxikologischen Untersuchung konnte die sichere Anwendung des MIDGE-Vektors bestätigt werden. Abschließend wurden weitere Anwendungsmöglichkeiten des MIDGE-Vektors für die stabile Genexpression und für die Verwendung in kombinierten Gentransferprotokollen untersucht.
Cancer is one leading causes of death worldwide. Gene therapy belongs to the promising options for treatment of malignant tumors. The non-viral gene therapy is known as safer alternative to the viral gene therapy. For non-viral gene transfer the vector and the transfer technology are of crucial importance. As part of this work a clinical trial was performed to assess efficiency and safety of the non-viral jet-injection. It was shown, that this technology can be used safely in a clinical setting. As a result of this clinical trial we concluded, that vector safety and especially efficiency need further improvements. Based on this optimized non-viral vectors (minicircle, MIDGE) were compared with each other and their respective parental plasmids. The MIDGE vector showed the highest transgene expression due to increased transcription. In preparation of a clinical trial the combined treatment of hTNF-alpha gene transfer and Vindesine chemotherapy was analyzed. Again, the MIDGE vector showed the highest transgene expression. This expression led to an increased cytotoxicity of Vindesine in vitro due to an elevated apoptosis signaling. Furthermore, these results could be assigned to an in vivo model. The increased hTNF-alpha expression after MIDGE vector jet-injection in combination with Vindesine led to a significant decrease in tumor growth. Detailed analysis of systemic vector distribution in the blood and organs as well as the preclinical toxicity evaluation showed the safety of the non-viral MIDGE vector. Initial experiments were performed to show further options for stable gene expression and combined gene transfer protocols using the MIDGE vector.
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Bücher zum Thema "Tumoral Niche"

1

Ich will nicht, dass ihr weint: Das Krebstagebuch der 16-jährigen Jenni. Augsburg: Weltbild, 2008.

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Botta, Cirino, Marco Rossi, Niels Weinhold und Niccolò Bolli, Hrsg. Targeting the Microenvironment Niche in Solid Tumors. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-772-6.

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Remagen, W., B. Spiessl, Joachim Prein und E. Uehlinger. Atlas der Tumoren des Gesichtsschädels: Odontogene und Nicht Odontogene Tumoren. Springer London, Limited, 2013.

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Günther, Sonja. Unsichere Gespräche: Zur Interaktion Von Arzt, Patienten und Nicht-Menschlichen Akteuren in der Neuroonkologie. de Gruyter GmbH, Walter, 2017.

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Günther, Sonja. Unsichere Gespräche: Zur Interaktion Von Arzt, Patienten und Nicht-Menschlichen Akteuren in der Neuroonkologie. de Gruyter GmbH, Walter, 2017.

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Günther, Sonja. Unsichere Gespräche: Zur Interaktion Von Arzt, Patienten und Nicht-Menschlichen Akteuren in der Neuroonkologie. de Gruyter GmbH, Walter, 2017.

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Buchteile zum Thema "Tumoral Niche"

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Bennewith, Kevin L., Janine T. Erler und Amato J. Giaccia. „Premetastatic Niches“. In Tumor Microenvironment, 161–82. Chichester, UK: John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470669891.ch8.

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Kornhuber, B. „Nicht organgebundene Tumoren“. In Therapie der Krankheiten des Kindesalters, 389–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-662-10467-5_10.

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McCauley, Heather A., und Géraldine Guasch. „Serial Orthotopic Transplantation of Epithelial Tumors in Single-Cell Suspension“. In Stem Cell Niche, 231–45. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-508-8_20.

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Löser, Christoph R. „Nicht-melanozytäre benigne Tumoren“. In Hauterkrankungen in der Zahnmedizin, der Mund-Kiefer-Gesichtschirurgie, der Augenheilkunde und der Hals-Nasen-Ohrenheilkunde, 149–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-66733-0_21.

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Shiozawa, Yusuke, Russell S. Taichman und Evan T. Keller. „Detection and Isolation of Human Disseminated Tumor Cells in the Murine Bone Marrow Stem Cell Niche“. In Stem Cell Niche, 207–15. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-508-8_18.

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Saw, Phei Er, und Erwei Song. „Pre-Metastatic Niche: Communication Between Local and Distal Onco-Spheres“. In Tumor Ecosystem, 249–66. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-1183-7_11.

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Zimmermann, Arthur. „Pathogenic Features of Liver Metastasis: Mechanisms Involving Platelets, Tumor Stroma, Epithelial-Mesenchymal Transition, and the Premetastatic Niche“. In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract, 1997–2017. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26956-6_113.

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Zimmermann, Arthur. „Pathogenic Features of Liver Metastasis: Mechanisms Involving Platelets, Tumor Stroma, Epithelial-Mesenchymal Transition, and the Pre-metastatic Niche“. In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract, 1–21. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26587-2_113-1.

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Linn, Jennifer, Martin Wiesmann und Hartmut Brückmann. „Tumoren und nicht neoplastische intrakranielle Raumforderungen“. In Atlas Klinische Neuroradiologie des Gehirns, 193–309. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-540-89569-5_3.

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Schäfer, Karl-Ludwig, Raihanatou Diallo, Barbara Dockhorn-Dworniczak und Christopher Poremba. „Molekulare Grundlagen organspezifischer Tumoren: Knochen- und Weichteilsarkome“. In Molekularmedizinische Grundlagen von nicht-hereditären Tumorerkrankungen, 385–403. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56297-6_13.

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Konferenzberichte zum Thema "Tumoral Niche"

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Pasquier, Jennifer, Hamda Al Thawadi, Nadine Abu Kaoud, Pegah Ghiabi, Mahtab Maleki, Bella S. Guerrouahen und 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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Filatova, A. A., L. A. Alexeeva und N. L. Mironova. „EFFECT OF CIRCULATING CELL-FREE DNA ON THE INVASIVE POTENTIAL OF MURINE MELANOMA“. In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-382.

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Tumor-derived cell-free DNA is of particular interest because it can enter normal cells and cause their transformation. cfDNA generated by cells of the tumor microenvironment is also capable of inducing changes leading to the formation of a premetastatic niche favorable for the development of metastases. In this work the effect of cfDNA derived from melanoma cells and fibroblasts, on melanoma was studied in vitro and in vivo.
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Sokolow, AJ, D. Schiltz und U. von Fritschen. „Phylloides Tumoren - selten aber nicht harmlos“. In Wissenschaftliche Abstracts zur 40. Jahrestagung der Deutschen Gesellschaft für Senologie e.V. (DGS) Interdisziplinär. Kommunikativ. Digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730226.

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Enderling, Heiko, Lynn Hlatky und Philip Hahnfeldt. „Abstract 4931: Cancer stem cells in solid tumors: Symmetric division, niche size, and invasive tumor morphology“. In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4931.

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Croucher, Peter, Weng Hua Khoo, Ryan Chai, Alex Corr, James Smith, Qihao Ren, Paul Baldock, Michelle McDonald, Sheila Stewart und Tri G. Phan. „Abstract IA015: Niche-dependent control of tumor cell dormancy“. In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-ia015.

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Min, Wang. „Abstract 129: AIP1 suppresses tumor metastasis by regulating tumor microenvironment and metastatic niche“. In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-129.

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Carpenter, Ryan, und Jungwoo Lee. „Abstract 3748: Implantable tumor attracting niche models to study disseminated tumor cell biology“. In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3748.

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Carpenter, Ryan, und Jungwoo Lee. „Abstract 3748: Implantable tumor attracting niche models to study disseminated tumor cell biology“. In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3748.

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Zhartun, E. S., und D. B. Nizheharodava. „EXTRACELLULAR VESICLES AS A MECHANISM OF INTERCELLULAR COMMUNICATION IN TUMOR PATHOPHYSIOLOGY“. In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-125-128.

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In normal cells, mechanisms that prevent the development of cancer function, while in tumor cells there are defects in the regulatory chain that controls cell proliferation and its homeostasis. Intercellular communication is the exchange of information through various signaling mechanisms affecting many aspects of cell life and is crucial for morphogenesis, differentiation, interaction, homeostasis and cell growth. The study of the mechanisms of intercellular communication mediated by extracellular vesicles is important for understanding the sequential events in the cell that lead to the development of cancer. The key importance of intercellular communication of tumor cells is manifested in autocrine stimulation (increased proliferation and inhibition of apoptosis signals), suppression of immunity (tumor extracellular vesicles create an immunosuppressive environment), preparation of a metastatic niche.
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Wang, Qirui, Yanqing Anna Gong und Yi Fan. „Abstract B44: Regulation of macrophage activation by vascular niche in glioblastoma“. In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b44.

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Berichte der Organisationen zum Thema "Tumoral Niche"

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Hinch, Lindsay. Elucidating the Tumor Suppressive Role of SLITs in Maintaining the Basal Cell Niche. Fort Belvoir, VA: Defense Technical Information Center, Juli 2010. http://dx.doi.org/10.21236/ada537890.

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Hinck, Lindsay. Elucidating the Tumor Suppressive Role of SLITs in Maintaining the Basal Cell Niche. Fort Belvoir, VA: Defense Technical Information Center, Juli 2009. http://dx.doi.org/10.21236/ada515794.

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Hinck, Lindsay. Elucidating the Tumor-Suppressive Role of SLITs in Maintaining the Basal Cell Niche. Fort Belvoir, VA: Defense Technical Information Center, Oktober 2011. http://dx.doi.org/10.21236/ada561080.

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Marsden, Carolyn. Mesenchymal Stem Cells in the Bone Marrow Provide a Supportive Niche for Early Disseminated Breast Tumor-Initiating Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada552881.

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Kapulnik, Yoram, und Donald A. Phillips. Isoflavonoid Regulation of Root Bacteria. United States Department of Agriculture, Januar 1996. http://dx.doi.org/10.32747/1996.7570561.bard.

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The overall objective of this project was to develop a conceptual framework for enhancing root colonization by beneficial bacteria. To accomplish this aim we tested the hypothesis that production and excretion of the plant phytoalexin medicarpin can be used for creation of a special niche along the legume roots, where beneficial microorganism, such as rhizobium, will have a selective advantage. On the Israeli side it was shown that higher medicarpin levels are exuded following the application of Rhizobium meliloti to the rhizosphere but the specific biochemical pathway governing medicarpin production was not induced significantly enough to support a constant production and excretion of this molecule to the rhizosphere. Furthermore, pathogenic bacteria and chemical elicitors were found to induce higher levels of this phytoalexin and it became important to test its natural abundance in field grown plants. On the US side, the occurrence of flavonoids and nucleosides in agricultural soils has been evaluated and biologically significant quantities of these molecules were identified. A more virulent Agrobacterium tumefaciens strain was isolated from alfalfa (Medicago sativa L.) which forms tumors on a wide range of plant species. This isolate contains genes that increase competitive colonization abilities on roots by reducing the accumulation of alfalfa isoflavonoids in the bacterial cells. Following gene tagging efforts the US lab found that mutation in the bacterial efflux pump operons of this isolate reduced its competitive abilities. This results support our original hypothesis that detoxification activity of isoflavenoids molecules, based on bacterial gene(s), is an important selection mechanism in the rhizosphere. In addition, we focused on biotin as a regulatory element in the rhizosphere to support growth of some rhizosphere microorganisms and designed a bacterial gene construct carrying the biotin-binding protein, streptavidin. Expressing this gene in tobacco roots did not affect the biotin level but its expression in alfalfa was lethal. In conclusion, the collaborative combination of basic and applied approaches toward the understanding of rhizosphere activity yielded new knowledge related to the colonization of roots by beneficial microorganisms in the presence of biological active molecules exuded from the plant roots.
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