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Artykuły w czasopismach na temat „Niche tumorale”

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Data publikacji: 25 maja 2024

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1

Grassi, Elisa Stellaria, Viola Ghiandai i Luca Persani. "Thyroid Cancer Stem-Like Cells: From Microenvironmental Niches to Therapeutic Strategies". Journal of Clinical Medicine 10, nr 7 (1.04.2021): 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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Onuchic, Ana Cláudia, i Roger Chammas. "Câncer e o microambiente tumoral". Revista de Medicina 89, nr 1 (19.03.2010): 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, i 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 i in. "Splenectomy reduces lung metastases and tumoral and metastatic niche inflammation". International Journal of Cancer 145, nr 9 (listopad 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 i Manish Aghi. "TMIC-57. PRO-TUMORAL EFFECTS OF INTRA-TUMORAL NEUTROPHILS IN THE GLIOBLASTOMA MICROENVIRONMENT". Neuro-Oncology 21, Supplement_6 (listopad 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 i in. "TMIC-36. SPATIAL ARCHITECTURE OF HIGH-GRADE GLIOMA REVEALS TUMOR HETEROGENEITY WITHIN DISTINCT DOMAINS". Neuro-Oncology 25, Supplement_5 (1.11.2023): 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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7

Chung, Hyewon, Sang Wha Kim i 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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8

Garcia-Mazas, Carla, Noemi Csaba i Marcos Garcia-Fuentes. "Biomaterials to suppress cancer stem cells and disrupt their tumoral niche". International Journal of Pharmaceutics 523, nr 2 (maj 2017): 490–505. http://dx.doi.org/10.1016/j.ijpharm.2016.12.013.

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9

Jansen, Caroline S., Nataliya Prokhnevska, Viraj A. Master, Martin G. Sanda, Jennifer W. Carlisle, Mehmet Asim Bilen, Maria Cardenas i in. "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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10

Uribe, Daniel, Ignacio Niechi, Gorjana Rackov, José I. Erices, Rody San Martín i Claudia Quezada. "Adapt to Persist: Glioblastoma Microenvironment and Epigenetic Regulation on Cell Plasticity". Biology 11, nr 2 (16.02.2022): 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.

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11

Mary, Benjamin, Shima Ghoroghi, Jacky G. Goetz i Vincent Hyenne. "Les vésicules extracellulaires tumorales favorisent la formation de niches pré-métastatiques". médecine/sciences 37, nr 12 (grudzień 2021): 1116–18. http://dx.doi.org/10.1051/medsci/2021203.

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Infanger, David W., YouJin Cho, Brina S. Lopez, Sunish Mohanan, S. Chris Liu, Demirkan Gursel, John A. Boockvar i 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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Follain, Gautier, Valentin Gensbittel, Benjamin Mary, Olivier Lefebvre, Sébastien Harlepp, Vincent Hyenne i Jacky G. Goetz. "Influence de la mécanique des fluides sur la formation des métastases". médecine/sciences 36, nr 10 (październik 2020): 872–78. http://dx.doi.org/10.1051/medsci/2020158.

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La suite d’évènements menant à l’apparition de métastases est appelée « cascade métastatique ». L’étude récente de la composante biomécanique de cette cascade a révélé le rôle central des liquides biologiques dans la dissémination métastatique. Tout en participant au transport des cellules tumorales circulantes et des facteurs qu’elles sécrètent, ces liquides circulants influencent cette cascade par les forces mécaniques qu’ils génèrent. Les propriétés hémodynamiques et les contraintes topologiques de l’architecture vasculaire contrôlent la formation de niches métastatiques et le potentiel métastatique des cellules tumorales.

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14

Nicke, M., G. F. Schusser i S. Recknagel. "Diagnostische Aussagekraft der Zytologie von Bauchpunktaten bei abdominalen Tumoren des Pferdes". Tierärztliche Praxis Ausgabe G: Großtiere / Nutztiere 40, nr 02 (2012): 85–93. http://dx.doi.org/10.1055/s-0038-1623102.

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Zusammenfassung Gegenstand und Ziel: Retrospektive Analyse zur Aussagekraft der Zytologie von Bauchpunktaten (BP) hinsichtlich der Intra-vitam-Diagnostik abdominaler Neoplasien. Material und Methoden: Vorgestellt werden 10 Pferde mit histopathologisch bestätigter abdominaler Tumormanifestation, bei denen ante mortem eine Abdominozentese mit Punktatuntersuchung stattfand. Im Bauchpunktat (BP) wurden die Gesamteiweißkonzentration und die Zellzahl bestimmt. Die zytologische Beurteilung erfolgte hinsichtlich der Malignitätswahrscheinlichkeit anhand definierter Malignitätskriterien. Ergebnisse: Bei fünf der 10 Pferde konnte anhand der Zytologie des BP eine Neoplasie bestätigt werden. Das maligne Lymphom war der am häufigsten (2/3 BP) diagnostizierte Tumor. Bei 1/2 Pferden mit multiplem Myelom ergab sich ebenfalls ein positiver Befund des BP. Das maligne Melanom (2/10) wurde in einem Fall über das BP diagnostiziert. Der positive Nachweis gelang ferner bei einem Pferd mit Plattenepithelkarzinom des Magens, wobei die Tumorzellmorphologie hier keine spezifische Tumordiagnose ergab, sodass eine solche nur bei 4/5 Neoplasien möglich war. Ein Adenokarzinom und ein Hämangiosarkom konnten nicht erfasst werden. Der Punktatcharakter erlaubte keinen Rückschluss auf die Tumorart. Das Vorliegen abnormer Mitosen hatte einen größeren diagnostischen Wert als die Mitoserate. Schlussfolgerung: Die Anwendung nukleärer Malignitätskriterien ermöglicht eine akzeptable Identifizierung von Tumorzellen bei Kenntnis der morphologischen Variabilität von Mesothelzellen. Das Fehlen maligner Zellen schließt jedoch eine Neoplasie nicht aus. Klinische Relevanz: Die zytologische Untersuchung des BP ist wertvoller Bestandteil des diagnostischen Vorgehens bei Verdacht auf eine abdominale Tumorose.

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Heuberger, Schneider i Bodis. "Stellenwert der Radiotherapie beim Nicht-kleinzelligen Bronchuskarzinom". Praxis 91, nr 33 (1.08.2002): 1307–14. http://dx.doi.org/10.1024/0369-8394.91.33.1307.

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Le cancer du poumon est la cause la plus fréquente de mort par cancer en Suisse. Environ 80% de tous les cancers du poumon en Suisse sont des carcinomes bronchiques autres que des tumeurs à petites cellules. Malgré les progrès diagnostiques et thérapeutiques, le taux de guérison des cancers autres que ceux à petites cellules n'est pas satisfaisant. Le traitement multimodal (chirurgie, radiothérapie, chimiothérapie) représente une amélioration thérapeutique très prometteuse. Ce travail présente, pour chaque stade tumoral (stade I–IV) du cancer pulmonaire autre que celui à petites cellules la valeur de la radiothérapie primaire radicale ou adjuvante (postopératoire).

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Turpin, Anthony, Ariane Sharif, Luc Stoven, Serge Blond, Claude-Alain Maurage i Émilie Le Rhun. "La niche des cellules souches tumorales dans le glioblastome : des aspects fondamentaux au ciblage thérapeutique". Bulletin du Cancer 102, nr 1 (styczeń 2015): 24–33. http://dx.doi.org/10.1016/j.bulcan.2014.07.001.

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Xiang, Lisha, i 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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Quiroz-Reyes, Adriana G., Jose F. Islas, Paulina Delgado-Gonzalez, Hector Franco-Villarreal i Elsa N. Garza-Treviño. "Therapeutic Approaches for Metastases from Colorectal Cancer and Pancreatic Ductal Carcinoma". Pharmaceutics 13, nr 1 (14.01.2021): 103. http://dx.doi.org/10.3390/pharmaceutics13010103.

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Metastasis is the process of dissemination of a tumor, whereby cells from the primary site dislodge and find their way to other tissues where secondary tumors establish. Metastasis is the primary cause of death related to cancer. This process warrants changes in original tumoral cells and their microenvironment to establish a metastatic niche. Traditionally, cancer therapy has focused on metastasis prevention by systematic treatments or direct surgical re-sectioning. However, metastasis can still occur. More recently, new therapies direct their attention to targeting cancer stem cells. As they propose, these cells could be the orchestrators of the metastatic niche. In this review, we describe conventional and novel developments in cancer therapeutics for liver and lung metastasis. We further discuss the resistance mechanisms of targeted therapy, the advantages, and disadvantages of diverse treatment approaches, and future novel strategies to enhance cancer prognosis.

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Vanmechelen, Maxime, Jan Beckervordersandforth, Jon Pey, Asier Antoranz, Pouya Nasari, daniele Pantano, Sien Bevers i in. "PATH-20. SPATIAL MAPPING OF THERAPY-INDUCED, PATHOLOGICAL CHANGES IN GLIOBLASTOMA AT SINGLE-CELL RESOLUTION". Neuro-Oncology 23, Supplement_6 (2.11.2021): vi119. http://dx.doi.org/10.1093/neuonc/noab196.472.

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Abstract Glioblastoma (GBM) remains a highly malignant, intrinsically resistant and inevitably recurring brain tumor with dismal prognosis. The aggressiveness and lack of effective GBM treatments can be attributed to the highly heterogeneous and plastic nature of GBM tumor cells, which easily confer resistance to standard-of-care (SOC) therapy. While tumor progression has also been attributed to interactions with the tumor microenvironment, quantitative data describing these interactions are still largely missing. Here, we used high-dimensional, multiplexed immunohistochemistry to map evolutions in the spatial, single-cell tissue architecture of 120 paired adult GBM tumor samples derived from 60 patients at diagnosis (ND) and upon recurrence (REC) following SOC treatment. We mapped the spatial distribution of a multitude of GBM tumoral subtypes across this multicentric cohort, through which we identified a high level of heterogeneity defined by specific tumoral niches within and across patients and which evolved when subjected to SOC therapy. In addition, we describe the relationship of the various tumoral niches with their local immune-infiltrates, highlighting an even more immunosuppressive environment following SOC resistance. Finally, by aligning these findings to the observed genomic aberrations and the clinical data of the patients, we are now able to more precisely describe the heterogeneous landscape of glioblastoma and how it evolves under SOC treatment at spatial, single-cell resolution.

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Hussain, Zainab, Jeremy Nigri i Richard Tomasini. "The Cellular and Biological Impact of Extracellular Vesicles in Pancreatic Cancer". Cancers 13, nr 12 (18.06.2021): 3040. http://dx.doi.org/10.3390/cancers13123040.

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Deciphering the interactions between tumor and stromal cells is a growing field of research to improve pancreatic cancer-associated therapies and patients’ care. Indeed, while accounting for 50 to 90% of the tumor mass, many pieces of evidence reported that beyond their structural role, the non-tumoral cells composing the intra-tumoral microenvironment influence tumor cells’ proliferation, metabolism, cell death and resistance to therapies, among others. Simultaneously, tumor cells can influence non-tumoral neighboring or distant cells in order to shape a tumor-supportive and immunosuppressive environment as well as influencing the formation of metastatic niches. Among intercellular modes of communication, extracellular vesicles can simultaneously transfer the largest variety of signals and were recently reported as key effectors of cell–cell communication in pancreatic cancer, from its development to its evolution as well as its ability to resist available treatments. This review focuses on extracellular vesicles-mediated communication between different cellular components of pancreatic tumors, from the modulation of cellular activities and abilities to their biological and physiological relevance. Taking into consideration the intra-tumoral microenvironment and its extracellular-mediated crosstalk as main drivers of pancreatic cancer development should open up new therapeutic windows.

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Vetter, Christine. "Umdenken in der klinischen Forschung: Die Biologie der Tumore besser verstehen". Onkologische Welt 01, nr 04 (2010): 152. http://dx.doi.org/10.1055/s-0038-1632827.

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Ernüchterung scheint sich derzeit hinsichtlich der zielgerichteten Therapie maligner Tumore breit zu machen: Denn in verschiedenen Phase-III-Studien konnten die getesteten innovativen Wirkstoffe nicht die in sie gesetzten Hoffnungen erfüllen. Wir haben aufgrund der Vordaten oft auf einen Durchbruch bei der Therapie gehofft, diesen aber in Studien nicht realisieren können“, berichtete Prof. Jürgen Wolf, Köln, auf einer Pressekonferenz.

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Beniwal, Angad, Saket Jain, Sumedh Shah, Sabraj Gill, Garima Yagnik, Alan Nguyen, Harsh Wadhwa, Aaron Diaz i Manish K. Aghi. "TAMI-38. TUMOR-ASSOCIATED NEUTROPHILS IN GLIOBLASTOMA PROMOTE THE PERIVASCULAR GLIOMA STEM-LIKE CELL NICHE VIA OSTEOPONTIN SECRETION". Neuro-Oncology 23, Supplement_6 (2.11.2021): vi206. http://dx.doi.org/10.1093/neuonc/noab196.822.

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Abstract Among clinical analyses, elevated neutrophil-lymphocyte ratio has been correlated with poor outcomes of glioblastoma patients independent of other prognostic factors. Additionally, our flow cytometric studies of primary patient samples found neutrophil percentage to be significantly higher in higher-grade glioma versus lower-grade glioma. Tumor-associated neutrophils (TANs) comprise less than 2% of the glioblastoma microenvironment. While TANs were initially considered passive bystanders due to their short-lived nature, investigation of TANs in other cancers revealed distinct pro-tumoral roles. Therefore, we transcriptomically characterized glioblastoma TANs and defined their oncologic effects. Transcriptomic analysis of patient-matched TANs versus peripheral blood neutrophils revealed that functionally quiescent circulating neutrophils infiltrate IDH1-wild type glioblastoma via leukotriene B4 chemoattraction, where tumor cells morphologically and transcriptomically activate them to become TANs. Single-cell RNA-sequencing of patient-matched TANs and peripheral blood neutrophils revealed a subset of tumor-activated neutrophils which adopt a pro-tumoral secretory phenotype, marked by activation of the IL-17 signaling pathway and high osteopontin production. Using immunofluorescence stains of primary patient glioblastoma sections, we demonstrated that activated, myeloperoxidase-positive TANs reside in the perivascular niche of glioblastoma in close proximity to glioblastoma stem-like cells (GSCs) and CD31-positive endothelial cells. Further analysis in culture demonstrated that TAN-secreted osteopontin drives the formation, self-renewal, and proliferation of GSC-containing neurospheres. These results were validated using a syngeneic stem cell-derived IDH1-wild type murine glioblastoma model in vivo. Thus, while TANs are rare in glioblastoma, their enrichment in the glioblastoma perivascular niche uniquely positions them to support the GSCs that are crucial to therapeutic resistance of GBM.

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Motlagh, Mohammad Arab, i Michael Rauschmann. "Knochenbildende Tumore unter besonderer Berücksichtigung des Osteoidosteoms und Osteoblastoms". Die Wirbelsäule 05, nr 04 (listopad 2021): 224–29. http://dx.doi.org/10.1055/a-1487-7578.

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ZusammenfassungOsteoidosteome und Osteoblastome sind gutartige knochenbildende Tumore, die in den ersten beiden Lebensdekaden nicht selten die Ursache von schmerzhaften Läsionen der Wirbelsäule mit schmerzbedingter skoliotischer Deformierung sind. Beide Entitäten sind sich histologisch sehr ähnlich, lassen sich jedoch durch Röntgen bzw. computertomographische Darstellung anhand ihrer Größe und morphologischen Merkmale gut differenzieren. Die Osteoblastome können durch ihre Größenzunahme und osteodestruktives Verhalten die Wirbelsäule destabilisieren oder zu neurologischen Ausfälle führen. Die Schmerzen sprechen häufig gut auf die Nicht Steroidale AntiRheumatika (NSAR), insbesondere auf Azetylsalezylsäure, an. Schmerzpersistenz und Nebenwirkungen von NSAR sowie mögliche Instabilitäten erfordern aber häufig eine interventionelle Therapie mit chirurgisch vollständiger Resektion selten in Kombination mit Stabilisierung oder perkutane Radiofrequenzablation, die je nach morphologischen Gesichtspunkten angewendet werden können.

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Arnold, Andreas W. "Der dermatologische Rundherd, nicht immer Tinea corporis". Therapeutische Umschau 76, nr 2 (sierpień 2019): 98–104. http://dx.doi.org/10.1024/0040-5930/a001062.

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Zusammenfassung. Im Allgemeinen wird in der Dermatologie unter einem Rundherd eine oft erythematöse, runde oder ovale Macula verstanden. Diese ist meist solitär, wird aber auch für multiple Rundherde bzw. Exantheme benutzt. Manchmal handelt es sich bei einem Rundherd auch um eine Plaque, also eine erhabene, grössere Fläche. Im vorliegenden Artikel wurden pigmentierte oder hypopigmentierte Maculae sowie knotige Tumore nicht eingeschlossen. Der isolierte Rundherd stellt, mehr noch wie multiple Rundherde, oft eine diagnostische Herausforderung dar und verlangt Kenntnisse der Klinik, Anamnese und Diagnostik.

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Ghiabi, Pegah, Jie Jiang, Jennifer Pasquier, Mahtab Maleki, Nadine Abu-Kaoud, Najeeb Halabi, Bella S. Guerrouahen, Shahin Rafii i Arash Rafii. "Breast cancer cells promote a notch-dependent mesenchymal phenotype in endothelial cells participating to a pro-tumoral niche". Journal of Translational Medicine 13, nr 1 (2015): 27. http://dx.doi.org/10.1186/s12967-015-0386-3.

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Xu, Xiaowen, Wenjun Chang, Jie Yuan, Xue Han, Xiaojie Tan, Yibo Ding, Yanxin Luo i in. "Periostin expression in intra-tumoral stromal cells is prognostic and predictive for colorectal carcinomaviacreating a cancer-supportive niche". Oncotarget 7, nr 1 (9.11.2015): 798–813. http://dx.doi.org/10.18632/oncotarget.5985.

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Mendoza-Reinoso, Veronica, Laurie K. McCauley i Pierrick G. J. Fournier. "Contribution of Macrophages and T Cells in Skeletal Metastasis". Cancers 12, nr 4 (20.04.2020): 1014. http://dx.doi.org/10.3390/cancers12041014.

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Bone is a common site for metastases with a local microenvironment that is highly conducive for tumor establishment and growth. The bone marrow is replete with myeloid and lymphoid linage cells that provide a fertile niche for metastatic cancer cells promoting their survival and growth. Here, we discuss the role of macrophages and T cells in pro- and anti-tumoral mechanisms, their interaction to support cancer cell growth, and their contribution to the development of skeletal metastases. Importantly, immunotherapeutic strategies targeting macrophages and T cells in cancer are also discussed in this review as they represent a great promise for patients suffering from incurable bone metastases.

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Hasselmann, Meier, Amann-Vesti i Thalhammer. "Blauer Strom unter dem Fingernagel". Praxis 101, nr 8 (1.04.2012): 545–47. http://dx.doi.org/10.1024/1661-8157/a000899.

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Glomustumore sind gutartige Tumore und finden sich meist akral. Sie lassen sich durch Anamnese, klinische Untersuchung, Duplexsonographie und MR-Angiographie meist nicht-invasiv diagnostizieren. Der Interventionsbedarf hängt vom Beschwerdebild ab.

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Ghiabi, Pegah, Jie Jiang, Jennifer Pasquier, Mahtab Maleki, Nadine Abu-Kaoud, Shahin Rafii i Arash Rafii. "Endothelial Cells Provide a Notch-Dependent Pro-Tumoral Niche for Enhancing Breast Cancer Survival, Stemness and Pro-Metastatic Properties". PLoS ONE 9, nr 11 (7.11.2014): e112424. http://dx.doi.org/10.1371/journal.pone.0112424.

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Messiaen, Julie, Pouya Nasari, Yannick Van Herck, Ben Verhaaren, Ivey Sebastian, Giorgia Milli, francesca Bosisio i in. "PATH-21. THE SINGLE-CELL PATHOLOGY LANDSCAPE OF PEDIATRIC GLIOMA". Neuro-Oncology 23, Supplement_6 (2.11.2021): vi119. http://dx.doi.org/10.1093/neuonc/noab196.473.

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Abstract High-grade glioma are the main cause of cancer-related death in children. Despite extensive research, their prognosis remains poor with very few treatment options. This can be attributed to the highly heterogeneous and plastic nature of glioma tumor cells and their interactions with the microenvironment, although quantitative data are still largely missing. Here, we used high-dimensional, multiplexed immunohistochemistry to map the spatial, single-cell tissue architecture of 31 pediatric glioma samples covering 9 histologic diagnoses. This novel approach allowed us to map the spatial distribution of the various tumoral subtypes, which typically occur in specific tumoral niches, and how these interact with their local immune-microenvironment. Finally, by aligning these findings to the clinical data of the patients and comparing these to adult glioblastoma, we are now able to more precisely describe the heterogeneous landscape of pediatric glioma at single-cell resolution.

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Paolillo, Mayra, Sergio Comincini i Sergio Schinelli. "In Vitro Glioblastoma Models: A Journey into the Third Dimension". Cancers 13, nr 10 (18.05.2021): 2449. http://dx.doi.org/10.3390/cancers13102449.

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Glioblastoma multiforme (GBM) is the most lethal primary brain tumor in adults, with an average survival time of about one year from initial diagnosis. In the attempt to overcome the complexity and drawbacks associated with in vivo GBM models, together with the need of developing systems dedicated to screen new potential drugs, considerable efforts have been devoted to the implementation of reliable and affordable in vitro GBM models. Recent findings on GBM molecular features, revealing a high heterogeneity between GBM cells and also between other non-tumor cells belonging to the tumoral niche, have stressed the limitations of the classical 2D cell culture systems. Recently, several novel and innovative 3D cell cultures models for GBM have been proposed and implemented. In this review, we first describe the different populations and their functional role of GBM and niche non-tumor cells that could be used in 3D models. An overview of the current available 3D in vitro systems for modeling GBM, together with their major weaknesses and strengths, is presented. Lastly, we discuss the impact of groundbreaking technologies, such as bioprinting and multi-omics single cell analysis, on the future implementation of 3D in vitro GBM models.

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Kam, Ngar Woon, Anthony Wing Ip Lo, Desmond Tae Yang Hung, Ho Ko, Ka Chun Wu, Dora Lai Wan Kwong, Ka On Lam, To Wai Leung, Chi Ming Che i Victor Ho Fun Lee. "Shift in Tissue-Specific Immune Niches and CD137 Expression in Tuberculoma of Pembrolizumab-Treated Nasopharyngeal Carcinoma Patients". Cancers 16, nr 2 (8.01.2024): 268. http://dx.doi.org/10.3390/cancers16020268.

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The use of immune checkpoint inhibitors (ICIs) in cancer treatment has shown promise but can also have unintended consequences, such as reactivating latent tuberculosis (TB). To develop treatments that address ICIs-related adverse events, it is essential to understand cellular heterogeneity across healthy and pathological tissues. We performed cross-tissue multiplexed staining analysis on samples from two patients with TB reactivation during pembrolizumab treatment for metastatic nasopharyngeal carcinoma. CD8+ T cells, rather than CD4+ T cells, accumulated preferentially in the tuberculoma and were associated with increased production of IFNγ and expression of CD137. Additionally, CD137 enrichment played a role in the spatial organization of the tuberculoma, with specific interaction limited to spatial proximal cells between IFNγ+ CD137+ CD8+ T cells and IL12+ CD137+ type-1 macrophages. This unique feature was not observed in non-tumoral or tumoral tissues. Our analysis of public transcriptomic datasets supported the notion that this cellular interaction was more prominent in patients with durable ICI responses compared to those with non-ICI-related TB. We suggest that shifts towards CD137-rich immune niches are correlated with both off-target immune-related adverse events and anti-tumor efficacy. Targeting the tumor microenvironment through conditional activation of anti-CD137 signaling in combination with ICIs can modulate the reactivity of T cells and macrophages for localized tumor killing without the potential off-target immune-related risks associated with ICIs alone.

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Kretzschmar, Alexander. "Therapie von Lebermetastasen neuroendokriner Tumore: Sunitinib nach transarterieller Embolisation erfolgreich". Onkologische Welt 02, nr 02 (2011): 83. http://dx.doi.org/10.1055/s-0038-1631225.

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Die Prognose von Patienten mit neuroendokrinen Tumoren hängt entscheidend von der Ausdehnung und dem Wachstum der Lebermetastasen ab. Eine Phase-II-Studie weist darauf hin, dass Sunitinib auch erfolgreich nach einer transarteriellen Embolisation (TAE) bei Patienten mit nicht resezierbaren Lebermetastasen neuroendokriner Tumore eingesetzt werden kann.

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Märdian, Sven, i Sabrina Morgenstern. "Megaprothesen als Femurersatz – Versorgung nach Osteosarkom". physiopraxis 20, nr 01 (styczeń 2022): 34–37. http://dx.doi.org/10.1055/a-1690-0076.

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Gelingt ein Totalersatz des Femurs, ermöglicht dies, die Beinfunktion von Menschen mit Sarkomen zu erhalten. Bei der Operation gilt es das tumoröse Gewebe zu entfernen und die Muskelansätze so zu rekonstruieren, dass die Funktion des künstlichen Hüft- und Kniegelenks gewährleistet ist. Um das Operationsergebnis nicht zu gefährden, ist auch bei der physiotherapeutischen Nachbehandlung Fingerspitzengefühl gefragt.

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Skaletz-Rorowski, A., N. H. Brockmeyer i A. Potthoff. "Krebs und HIV-Infektion". Onkologische Welt 02, nr 02 (2011): 60–62. http://dx.doi.org/10.1055/s-0038-1631214.

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ZusammenfassungTumore sind die zweithäufigste Todesursache von HIV-Patienten. Die Prävalenz von Tumorerkrankungen liegt in der nationalen Kohorte des BMBF-geförderten Kompetenznetzes HIV/ AIDS bei 8,9%. Das Kaposi-Sarkom ist mit 349 Fällen der am häufigsten dokumentierte Tumor. HHV-8 assoziierte Tumore (z. B. das Kaposi-Sarkom) werden durch molekulare Mimikry vermittelt. Die Optimierung der HIV-Therapie bleibt die wichtigste therapeutische Maßnahme. Chemotherapeutika werden bei den verschiedenen Tumorentitäten mit unterschiedlichem Erfolg eingesetzt. Während die Inzidenz des Kaposi-Sarkoms und der Non-Hodgkin-Lymphome nach Einführung der antiretroviralen Therapie deutlich abgenommen hat, nehmen nicht AIDS-definierende Tumore zu. Der häufigste nicht-AIDS definierende Tumor im Kompetenznetz ist das Analkarzinom mit 192 Fällen. HPV-Infektionen und Rauchen sind hierbei wichtige Risikofaktoren. Eine maximale Virussuppression, ein früher Beginn der antiretroviralen Therapie, Impfungen (gegen Hepatitis und HPV) und Screeningmaßnahmen (z. B. Proktoskopien) können Tumoren vorbeugen.

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Belgiovine, Cristina, Elisabeth Digifico, Clément Anfray, Aldo Ummarino i Fernando Torres Andón. "Targeting Tumor-Associated Macrophages in Anti-Cancer Therapies: Convincing the Traitors to Do the Right Thing". Journal of Clinical Medicine 9, nr 10 (8.10.2020): 3226. http://dx.doi.org/10.3390/jcm9103226.

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In the last decade, it has been well-established that tumor-infiltrating myeloid cells fuel not only the process of carcinogenesis through cancer-related inflammation mechanisms, but also tumor progression, invasion, and metastasis. In particular, tumor-associated macrophages (TAMs) are the most abundant leucocyte subset in many cancers and play a major role in the creation of a protective niche for tumor cells. Their ability to generate an immune-suppressive environment is crucial to escape the immune system and to allow the tumor to proliferate and metastasize to distant sites. Conventional therapies, including chemotherapy and radiotherapy, are often not able to limit cancer growth due to the presence of pro-tumoral TAMs; these are also responsible for the failure of novel immunotherapies based on immune-checkpoint inhibition. Several novel therapeutic strategies have been implemented to deplete TAMs; however, more recent approaches aim to use TAMs themselves as weapons to fight cancer. Exploiting their functional plasticity, the reprogramming of TAMs aims to convert immunosuppressive and pro-tumoral macrophages into immunostimulatory and anti-tumor cytotoxic effector cells. This shift eventually leads to the reconstitution of a reactive immune landscape able to destroy the tumor. In this review, we summarize the current knowledge on strategies able to reprogram TAMs with single as well as combination therapies.

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Munding, Johanna, i Andrea Tannapfel. "Kurative endoskopische Therapie: Welche Läsionen eignen sich?" TumorDiagnostik & Therapie 38, nr 08 (październik 2017): 507–14. http://dx.doi.org/10.1055/s-0043-117149.

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ZusammenfassungDank flächendeckender Vorsorgeuntersuchungen werden immer mehr Tumore im Gastrointestinaltrakt so früh diagnostiziert, dass sie endoskopisch resezierbar sind. Doch nicht alle Läsionen eignen sich für eine kurative endoskopische Therapie. Abhängig ist dies vom lymphogenen Metastasierungsrisiko, das sich anhand histopathologischer Charakteristika abschätzen lässt.

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Bartlett, Alexandra Q., Nathan D. Pennock, Alex Klug i Pepper Schedin. "Immune Milieu Established by Postpartum Liver Involution Promotes Breast Cancer Liver Metastasis". Cancers 13, nr 7 (3.04.2021): 1698. http://dx.doi.org/10.3390/cancers13071698.

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In rodents, we identified a physiologic process within the normal liver that creates a pre-metastatic niche. This physiology is weaning-induced liver involution, characterized by hepatocyte cell death, immune influx, and extracellular matrix remodeling. Here, using weaning-induced liver involution as a model of a physiologically regulated pro-metastatic niche, we investigate how liver involution supports breast cancer metastasis. Liver metastases were induced in BALB/c immune competent hosts by portal vein injection of D2OR (low metastatic) or D2A1 (high metastatic) mouse mammary tumor cells. Tumor incidence and multiplicity increased in involution hosts with no evidence of a proliferation advantage. D2OR tumor cell extravasation, seeding, and early survival were not enhanced in the involuting group compared to the nulliparous group. Rather, the involution metastatic advantage was observed at 14 days post tumor cell injection. This metastatic advantage associated with induction of immune tolerance in the involution host liver, reproductive state dependent intra-tumoral immune composition, and CD8-dependent suppression of metastases in nulliparous hosts. Our findings suggest that the normal postpartum liver is in an immune suppressed state, which can provide a pro-metastatic advantage to circulating breast cancer cells. Potential relevance to women is suggested as a postpartum diagnosis of breast cancer is an independent predictor of liver metastasis.

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Álvarez Carrión, L., I. Gutiérrez Rojas, JA Ardura i V. Alonso. "Células osteogénicas afectadas por los factores solubles tumorales contribuyen a la formación del nicho pre-metastásico óseo". Revista de Osteoporosis y Metabolismo Mineral 11, nr 2 (czerwiec 2019): 64–71. http://dx.doi.org/10.4321/s1889-836x2019000200005.

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Conigliaro, Alice, i Carla Cicchini. "Exosome-Mediated Signaling in Epithelial to Mesenchymal Transition and Tumor Progression". Journal of Clinical Medicine 8, nr 1 (27.12.2018): 26. http://dx.doi.org/10.3390/jcm8010026.

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Growing evidence points to exosomes as key mediators of cell–cell communication, by transferring their specific cargo (e.g., proteins, lipids, DNA and RNA molecules) from producing to receiving cells. In cancer, the regulation of the exosome-mediated intercellular communication may be reshaped, inducing relevant changes in gene expression of recipient cells in addition to microenvironment alterations. Notably, exosomes may deliver signals able to induce the transdifferentiation process known as Epithelial-to-Mesenchymal Transition (EMT). In this review, we summarize recent findings on the role of exosomes in tumor progression and EMT, highlighting current knowledge on exosome-mediated intercellular communication in tumor-niche establishment, migration, invasion, and metastasis processes. This body of evidence suggests the relevance of taking into account exosome-mediated signaling and its multifaceted aspects to develop innovative anti-tumoral therapeutic approaches.

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Nambiar, Dhanya K., Vignesh Vignesh Viswanathan, Hongbin Cao, Weiruo Zhang, Li Guan, Manish Chamoli, Brittany Holmes i in. "Abstract 66: Galectin-1 mediated chronic tumoral-STING activation promotes metastasisthrough MDSC recruitment". Cancer Research 83, nr 7_Supplement (4.04.2023): 66. http://dx.doi.org/10.1158/1538-7445.am2023-66.

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Abstract Tumor cells alter the immune microenvironment to facilitate metastatic progression. Galectin-1 (Gal1) is a known modulator of tumor growth and progression in multiple cancer types including head and neck cancer (HNC). However, its contribution to the regulation of metastasis is poorly understood. Through this study we report a previously unknown role for Gal1 in modulating the STING pathway to regulate metastasis. The cGAS-STING pathway has paradoxical roles in cancer depending on the kinetics and strength of its induction, with chronic STING activation being linked to immune suppression and tumor progression while acute activation being associated with immune activation. However, little is known about the pathways that promote chronic STING activation. Using HNC and lung cancer models, we show that Gal-1 enhances STING protein stability, leading to sustained NF-κΒ activation and heightened chemokine-driven recruitment of myeloid derived suppressor cells (MDSCs). We show that Gal1-STING connection fosters the establishment of pre-metastatic niche through polymorphonuclear MDSCs (PMN-MDSCs), which modify the local lung microenvironment to support metastatic spread. Notably, RNA sequencing of MDSCs isolated from pre-metastatic lungs indicate the role of PMN-MDSCs in remodeling collagen and the extracellular matrix in the pre-metastatic compartment. Our findings reveal an unexpected role of STING activation in metastatic progression of HNC and lung cancer models and establish Gal1 as an endogenous positive regulator of STING. Citation Format: Dhanya K. Nambiar, Vignesh Vignesh Viswanathan, Hongbin Cao, Weiruo Zhang, Li Guan, Manish Chamoli, Brittany Holmes, Christina Kong, Rachel Hildebrand, Amanda Koong, Rie Eyben, Amato Giaccia, Lingyin Li, Edgar Engleman, Quynh Thu Le. Galectin-1 mediated chronic tumoral-STING activation promotes metastasisthrough MDSC recruitment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 66.

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Bas, M. "Evidenz und Evidenzlücken für medikamentös zu behandelnde, nicht-tumoröse Erkrankungen im Gebiet der HNO-Heilkunde". Laryngo-Rhino-Otologie 95, S 01 (29.04.2016): S217—S232. http://dx.doi.org/10.1055/s-0041-108940.

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Decraene, Brecht, Asier Antoranz, Tatjana Verbeke, Maxime Vanmechelen, Pouya Nazari, Lien Solie, Nikolina Dubroja i in. "TMIC-37. SINGLE-CELL CHARACTERIZATION OF THE IMMUNE LANDSCAPE OF EXTREME LONG-TERM SURVIVORS WITH MALIGNANT GLIOMA". Neuro-Oncology 24, Supplement_7 (1.11.2022): vii279. http://dx.doi.org/10.1093/neuonc/noac209.1081.

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Abstract Glioblastoma Multiforme (GBM) remains the most common malignant primary brain tumor with a dismal prognosis that rarely exceeds beyond two years despite extensive therapy, which consists of maximal safe surgical resection, radiotherapy and/or chemotherapy. Recently, it has become clear that GBM is not one homogeneous entity and that both intra-and intertumoral heterogeneity contribute significantly to differences in tumoral behavior which may consequently be responsible for differences in survival. Strikingly and despite its dismal prognosis, small fractions of GBM patients seem to display extreme extended survival compared to the large majority of patients. The underlying mechanisms for this peculiarity remain largely unknown however, even though emerging data suggest that both cancer cell-autonomous and microenvironmental factors and their interplay probably play an important role. We used high-dimensional, multiplexed immunohistochemistry to spatially, and cytometry by time-of-flight to quantitively, characterize the cell constitution and interactions within the tumor microenvironment (TME) in 21 extreme long-term survivors (living over 10 year) and 42 deeply matched controls and therefore short-term survivors (living under 1.5 year) on a single cell level. For all tumors (epi)genetic data was also collected. We identified a high level of both inter-and intrapatient heterogeneity defined by several distinct tumoral niches, as well as described interactions within these niches and with the surrounding infiltrating immune cells of the TME in GBM. Finally, by linking patient characteristics with the heterogeneous immune composition we are able to create an immune stratification that can be linked to patient survival in GBM. Therefore, this study is an essential initial step towards strategies to alter the TME in a favorable way with a personalized modulation strategy.

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Riesterer, Oliver. "Extrakranielle stereotaktische Radiotherapie bei frühen nicht-kleinzelligen Bronchialkarzinomen und Oligometastasen". Praxis 102, nr 21 (1.10.2013): 1309–16. http://dx.doi.org/10.1024/1661-8157/a001440.

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Die extrakranielle stereotaktische Radiotherapie (ESRT) ist eine neue Bestrahlungstechnik, die Fortschritte auf dem Gebiet der Radiotherapieplanung, der Intensitätsmodulation und der Bildsteuerung integriert. Mit der ESRT ist es möglich Tumore anstelle von sechs Wochen in nur wenigen Tagen und mit ablativer Dosis zu behandeln. Prospektive Phase-II-Studien belegen die Wirksamkeit der ESRT bei der Behandlung von Patienten mit inoperablen frühen nichtkleinzelligen Bronchialkarzinomen. Die dabei erreichten Tumorkontrollraten betragen 85–95% bei akzeptabler Toxizität. In der Klinik wird die ESRT auch zunehmend zur Behandlung von Metastasen in Lunge, Leber, Retroperitoneum und im Knochen angewendet. Da mit der ESRT eine lokal kurative Dosis in kurzer Zeit verabreicht werden kann, eröffnet diese Therapieform auch neue Perspektiven für die Behandlung von Patienten mit Oligometastasen.

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Ghiabi, Pegah. "Notch-Mediated Crosstalk Between Breast Cancer Cells And Endothelial Cells Induces A Transitional Endmt Phenotype Participating To An Endothelial Pro-Tumoral Niche". Qatar Foundation Annual Research Forum Proceedings, nr 2013 (listopad 2013): BIOSP 025. http://dx.doi.org/10.5339/qfarf.2013.biosp-025.

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Castellana, Donatello, Fatiha Zobairi, Maria Carmen Martinez, Maria Antonietta Panaro, Vincenzo Mitolo, Jean-Marie Freyssinet i Corinne Kunzelmann. "Membrane Microvesicles as Actors in the Establishment of a Favorable Prostatic Tumoral Niche: A Role for Activated Fibroblasts and CX3CL1-CX3CR1 Axis". Cancer Research 69, nr 3 (20.01.2009): 785–93. http://dx.doi.org/10.1158/0008-5472.can-08-1946.

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Pasquier, Jennifer, Hamda Al Thawadi, Pegah Ghiabi, Nadine Abu-Kaoud, Mahtab Maleki, Bella S. Guerrouahen, Fabien Vidal i in. "Microparticles mediated cross-talk between tumoral and endothelial cells promote the constitution of a pro-metastatic vascular niche through Arf6 up regulation". Cancer Microenvironment 7, nr 1-2 (15.01.2014): 41–59. http://dx.doi.org/10.1007/s12307-013-0142-2.

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Franzen, Achim M., Christiane Kaup Franzen i Annekatrin Coordes. "Veränderte Indikation zur Parotidektomie im nordwestlichen Brandenburg: Eine Longitudinaluntersuchung". Laryngo-Rhino-Otologie 97, nr 06 (10.04.2018): 405–9. http://dx.doi.org/10.1055/a-0596-7714.

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Zusammenfassung Hintergrund Kenntnisse über die Indikationen zu einer Parotidektomie basieren auf den Mitteilungen einzelner Kliniken, Tumor- und Krankenhausdatenbanken. Die Studie prüft die Hypothese, dass sich die Operationsindikation während der vergangenen Jahre verändert hat. Material und Methoden Wir führten eine retrospektive Beobachtungsstudie der Patienten durch, die zwischen 1975 und 2016 (Einteilung in 4 Quartilen) in einem Ausbildungskranken haus einer Medizinischen Hochschule mit Schwerpunktversorgung eine Parotidektomie erhielten. Ergebnisse 405 Männer und 366 Frauen wurden wegen eines benignen (600/78 %) oder malignen (116/15 %) Tumors oder einer Parotitis (55/7 %) operiert. Der Anteil der benignen Tumore blieb weitgehend konstant (78 %), der der malignen Tumore stieg (7 %–23 %) bei gleichzeitigem Abfall der Parotitiden (17 % – < 1 %). Bei den benignen Tumoren fiel der Anteil der pleomorphen Adenome (60 % –24 %), während Warthin Tumore häufiger auftraten (23 % –58 %). Unter den malignen Tumoren stieg der Anteil der Metastasen von 2/13 auf 31/49 (insbes. Plattenepithelkarzinomen der Haut). Diskussion Die vorliegende Studie zeigt die sinkende Bedeutung der Parotitis als Indikation für eine Parotidektomie bedingt durch verbesserte nicht-chirurgische Verfahren. Die ansteigende Prävalenz von Warthin-Tumoren in der aktuellen Arbeit war mit einem steigenden Anteil der Raucher assoziiert. Der Anstieg der Malignome war auf die steigende Prävalenz von intraparotidealen Matastasen der Plattenepithelkarzinome der Haut zurückzuführen. Die Ergebnisse der histologischen Diagnosen basieren auf der Auswertung von Krankenakten und können bisher nicht durch die Auswertungen überregionaler Tumordatenbanken oder Krankenhausstatistiken (ICD- oder DRG-Bezug) generiert werden. Hierzu befürworten die Autoren die Einrichtung eines speziellen Speicheldrüsenregisters.

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Stübinger, van der Horst i Braun. "Raumforderungen im kleinen Becken aus Sicht des Urologen". Therapeutische Umschau 64, nr 7 (1.07.2007): 395–98. http://dx.doi.org/10.1024/0040-5930.64.7.395.

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Tumore im kleinen Becken, die ihren Ursprung nicht primär im Urogenitaltrakt haben, können aufgrund der engen räumlichen Beziehung häufig zu einer sekundären Beteiligung des Harntraktes führen. Benigne Tumore (Uterus myomatosus, Ovarialzyste, Kolonadenom) führen ebenso wie maligne Tumore (z.B. Uterus-, Zervix-, Ovarial- und Kolonkarzinome) zu Verdrängungserscheinungen bzw. Infiltrationen der Harnorgane. Häufige urologische Symptome sind Blasenentleerungsstörungen, Harninkontinenz, urogenitale Entzündungen oder Harnabflussstörungen bis hin zum Nierenversagen. Dies sind oft die ersten Krankheitssymptome und erst in der weiteren Diagnostik wird dann der ursächliche Primärtumor entdeckt. Wichtig ist, dass primär urologische Tumore des Beckens – benigner als auch maligner Art – zu einer identischen Symptomatik führen können und somit ebenfalls differentialdiagnostisch miteinbezogen werden müssen. Die therapeutischen Maßnahmen richten sich zunächst nach der klinischen Symptomatik, an welche sich die Behandlung der Ursache anschließt. Kommt es beispielsweise durch einen verdrängenden Tumor im kleinen Becken zu einer akuten Abflussbehinderung des oberen oder unteren Harntraktes, ist eine sofortige interventionelle Entlastung der Harnwege mittels Nieren- oder Blasenfistelung notwendig. Erst im zweiten Schritt sollte dann die Möglichkeit der Tumorsanierung geprüft werden.

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Oppermann. "Wenn's die Kehle zuschnürt". Praxis 93, nr 3 (1.01.2004): 60–64. http://dx.doi.org/10.1024/0369-8394.93.3.60.

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Wenn es ihm die Kehle zuschnürt, versagt dem Betroffenen die Stimme, er kann nicht mehr gut schlucken oder empfindet eine Luftnot. Die Bedrohlichkeit der genannten Funktionseinschränkungen nimmt in dieser Reihenfolge zu. Organische oder auch funktionelle Störungen der Stimme gefährden nicht die Lebensfähigkeit eines Patienten, können aber seine lautsprachliche Kommunikationsfähigkeit invalidisierend beeinträchtigen. Pharyngeale Schluckstörungen können, vor allem unerkannt, zu vital bedrohlichen rezidivierenden Aspirationspneumonien führen. Obstruktionen der zervikalen Atemwege können durch Funktionsstörungen der Glottis, durch gut- und bösartige Tumore wie auch durch die Folgezustände nach deren Operation oder Bestrahlung entstehen. Zur Wiederherstellung der Stimme, des Schluckvermögens und der Atmung stehen in der Regel differenzierte palliative Massnahmen, meist als kleinere operative Eingriffe, zur Verfügung.

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