Academic literature on the topic 'Tumour-promoting stroma'
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Journal articles on the topic "Tumour-promoting stroma"
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Tone, Tatjana, Elīna Tauvēna, Ilze Štrumfa, and Jānis Gardovskis. "Inflammatory Cells in Gastric Cancer: Promoting the Tumour or Protecting the Host?" Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 74, no. 2 (April 1, 2020): 111–17. http://dx.doi.org/10.2478/prolas-2020-0018.
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AbstractThe study represents a comprehensive retrospective morphological profiling of gastric carcinoma in order to reveal associations between certain tumour-infiltrating inflammatory cells and clinical and/or pathological parameters. Patients’ age and gender, the extent of local tumour spread (pT), presence of metastases in regional lymph nodes (pN), tumour grade (G) as well as type according to World Health Organisation (WHO) and Lauren classifications were assessed in 211 consecutive surgically resected gastric carcinomas. Tumour-infiltrating inflammatory cells including eosinophils, neutrophils and lymphocytes were counted within the cancer stroma in five randomly selected high-power fields representative of the tumour. Descriptive statistics, Mann–Whitney and Kruskal–Wallis tests were applied; p < 0.05 was considered significant. Higher number of stromal eosinophils was associated with absence of metastases in regional lymph nodes (pN0) and histological structure of adenocarcinoma by WHO classification (p = 0.005 and p = 0.002, respectively). Higher count of stromal neutrophils showed significant associations with younger age (less than 65 years), and intestinal type by Lauren classification (p = 0.029 and p = 0.007, respectively). The density of stromal lymphocytes lacked any statistically significant association with the evaluated clinical or morphological parameters. In conclusion, the current study highlights the links between certain innate immune system cells and morphological features of gastric carcinoma.
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Seufferlein, Thomas, Michel Ducreux, Manuel Hidalgo, Gerald Prager, and Eric Van Cutsem. "More than a Gel & Hyaluronic Acid, a Central Component in the Microenvironment of Pancreatic Cancer." European Oncology & Haematology 14, no. 1 (2018): 40. http://dx.doi.org/10.17925/eoh.2018.14.1.40.
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Hyaluronic acid or hyaluronan (HA) is a major stromal component and its accumulation has been shown to play a central role in promoting tumourigenesis and progression of disease. Thus, overexpression of HA in tumours is associated with poor prognosis. Therapeutic targeting of HA is therefore an attractive strategy, particularly in pancreatic ductal adenocarcinoma (PDA), which is associated with an extremely poor prognosis and less sensitivity towards chemotherapy. PDA is characterised by a high stromal content. The accumulation of dense, fibrotic extracellular matrix components within the stroma, termed desmoplasia, results in increased tumour interstitial fluid pressure and vascular compression that impair the delivery and efficacy of therapeutic agents. While some elements of the stroma may be protective for the patient and prevent a more aggressive phenotype of PDA, a pegylated recombinant human hyaluronidase (pegvorhyaluronidase alfa) has been found to inhibit tumour growth in preclinical studies. In a clinical phase II randomised trial, the addition of pegvorhyaluronidase alfa to nab-paclitaxel and gemcitabine suggested significantly longer progression-free survival in patients with advanced PDA compared with nab-paclitaxel and gemcitabine alone. This benefit was even more pronounced in a subgroup of patients who expressed high levels of tumour HA.
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Ketteler, Julia, Andrej Panic, Henning Reis, Alina Wittka, Patrick Maier, Carsten Herskind, Ernesto Yagüe, Verena Jendrossek, and Diana Klein. "Progression-Related Loss of Stromal Caveolin 1 Levels Mediates Radiation Resistance in Prostate Carcinoma via the Apoptosis Inhibitor TRIAP1." Journal of Clinical Medicine 8, no. 3 (March 12, 2019): 348. http://dx.doi.org/10.3390/jcm8030348.
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Tumour resistance to chemo- and radiotherapy, as well as molecularly targeted therapies, limits the effectiveness of current cancer treatments. We previously reported that the radiation response of human prostate tumours is critically regulated by CAV1 expression in stromal fibroblasts and that loss of stromal CAV1 expression in advanced tumour stages may contribute to tumour radiotherapy resistance. Here we investigated whether fibroblast secreted anti-apoptotic proteins could induce radiation resistance of prostate cancer cells in a CAV1-dependent manner and identified TRIAP1 (TP53 Regulated Inhibitor of Apoptosis 1) as a resistance-promoting CAV1-dependent factor. TRIAP1 expression and secretion was significantly higher in CAV1-deficient fibroblasts and secreted TRIAP1 was able to induce radiation resistance of PC3 and LNCaP prostate cancer cells in vitro, as well as of PC3 prostate xenografts derived from co-implantation of PC3 cells with TRIAP1-expressing fibroblasts in vivo. Immunohistochemical analyses of irradiated PC3 xenograft tumours, as well as of human prostate tissue specimen, confirmed that the characteristic alterations in stromal-epithelial CAV1 expression were accompanied by increased TRIAP1 levels after radiation in xenograft tumours and within advanced prostate cancer tissues, potentially mediating resistance to radiation treatment. In conclusion, we have determined the role of CAV1 alterations potentially induced by the CAV1-deficient, and more reactive, stroma in radio sensitivity of prostate carcinoma at a molecular level. We suggest that blocking TRIAP1 activity and thus avoiding drug resistance may offer a promising drug development strategy for inhibiting resistance-promoting CAV1-dependent signals.
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Elisha, Yair, Yael Sagi, Georg Klein, Ravid Straussman, and Benjamin Geiger. "Cooperativity between stromal cytokines drives the invasive migration of human breast cancer cells." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1779 (July 2019): 20180231. http://dx.doi.org/10.1098/rstb.2018.0231.
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The cross-talk between cancer cells and the stromal microenvironment plays a key role in regulating cancer invasion. Here, we employed an ex vivo invasion model system for exploring the regulation of breast cancer cells infiltration into a variety of stromal fibroblast monolayers. Our results revealed considerable variability in the stromal induction of invasiveness, with some lines promoting and others blocking invasion. It was shown that conditioned medium (CM), derived from invasion-promoting fibroblasts, can induce epithelial–mesenchymal transition-like process in the cancer cells, and trigger their infiltration into a monolayer of invasion-blocking fibroblasts. To identify the specific invasion-promoting molecules, we analysed the cytokines in stimulatory CM, screened a library of purified cytokines for invasion-promoting activity and tested the effect of specific inhibitors of selected cytokine receptors on the CM-induced invasion. Taken together, these experiments indicated that the invasiveness of BT-474 is induced by the combined action of IL1 and IL6 and that IL1 can induce IL6 secretion by invasion-blocking fibroblasts, thereby triggering cancer cell invasion into the stroma. This unexpected observation suggests that stromal regulation of cancer invasion may involve not only cross-talk between stromal and cancer cells, but also cooperation between different stromal subpopulations. This article is part of a discussion meeting issue ‘Forces in cancer: interdisciplinary approaches in tumour mechanobiology’.
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Maeda, Masahiro, Hideyuki Takeshima, Naoko Iida, Naoko Hattori, Satoshi Yamashita, Hiroshi Moro, Yoshimi Yasukawa, et al. "Cancer cell niche factors secreted from cancer-associated fibroblast by loss of H3K27me3." Gut 69, no. 2 (May 13, 2019): 243–51. http://dx.doi.org/10.1136/gutjnl-2018-317645.
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ObjectiveCancer-associated fibroblasts (CAFs), a major component of cancer stroma, can confer aggressive properties to cancer cells by secreting multiple factors. Their phenotypes are stably maintained, but the mechanisms are not fully understood. We aimed to show the critical role of epigenetic changes in CAFs in maintaining their tumour-promoting capacity and to show the validity of the epigenomic approach in identifying therapeutic targets from CAFs to starve cancer cells.DesignTwelve pairs of primary gastric CAFs and their corresponding non-CAFs (NCAFs) were established from surgical specimens. Genome-wide DNA methylation and H3K27me3 analyses were conducted by BeadArray 450K and ChIP-on-Chip, respectively. Functions of potential a therapeutic target were analysed by inhibiting it, and prognostic impact was assessed in a database.ResultsCAFs had diverse and distinct DNA methylation and H3K27me3 patterns compared with NCAFs. Loss of H3K27me3, but not DNA methylation, in CAFs was enriched for genes involved in stem cell niche, cell growth, tissue development and stromal–epithelial interactions, such asWNT5A,GREM1,NOGandIGF2. Among these, we revealed that WNT5A, which had been considered to be derived from cancer cells, was highly expressed in cancer stromal fibroblasts, and was associated with poor prognosis. Inhibition of secreted WNT5A from CAFs suppressed cancer cell growth and migration.ConclusionsH3K27me3 plays a crucial role in defining tumour-promoting capacities of CAFs, and multiple stem cell niche factors were secreted from CAFs due to loss of H3K27me3. The validity of the epigenetic approach to uncover therapeutic targets for cancer-starving therapy was demonstrated.
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Leonard, Niamh A., Eileen Reidy, Kerry Thompson, Emma McDermott, Eleonora Peerani, Elena Tomas Bort, Frances R. Balkwill, Daniela Loessner, and Aideen E. Ryan. "Stromal Cells Promote Matrix Deposition, Remodelling and an Immunosuppressive Tumour Microenvironment in a 3D Model of Colon Cancer." Cancers 13, no. 23 (November 29, 2021): 5998. http://dx.doi.org/10.3390/cancers13235998.
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Colorectal cancer (CRC) is the third leading cause of cancer-related deaths worldwide. CRC develops in a complex tumour microenvironment (TME) with both mesenchymal stromal cells (MSCs) and immune infiltrate, shown to alter disease progression and treatment response. We hypothesised that an accessible, affordable model of CRC that combines multiple cell types will improve research translation to the clinic and enable the identification of novel therapeutic targets. A viable gelatine-methacrloyl-based hydrogel culture system that incorporates CRC cells with MSCs and a monocyte cell line was developed. Gels were analysed on day 10 by PCR, cytokine array, microscopy and flow cytometry. The addition of stromal cells increased transcription of matrix remodelling proteins FN1 and MMP9, induced release of tumour-promoting immune molecules MIF, Serpin E1, CXCL1, IL-8 and CXCL12 and altered cancer cell expression of immunotherapeutic targets EGFR, CD47 and PD-L1. Treatment with PD153035, an EGFR inhibitor, revealed altered CRC expression of PD-L1 but only in gels lacking MSCs. We established a viable 3D model of CRC that combined cancer cells, MSCs and monocytic cells that can be used to research the role the stroma plays in the TME, identify novel therapeutic targets and improve the transitional efficacy of therapies.
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Spunde, Karina, Ksenija Korotkaja, and Anna Zajakina. "Recombinant Viral Vectors for Therapeutic Programming of Tumour Microenvironment: Advantages and Limitations." Biomedicines 10, no. 9 (August 31, 2022): 2142. http://dx.doi.org/10.3390/biomedicines10092142.
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Viral vectors have been widely investigated as tools for cancer immunotherapy. Although many preclinical studies demonstrate significant virus-mediated tumour inhibition in synergy with immune checkpoint molecules and other drugs, the clinical success of viral vector applications in cancer therapy currently is limited. A number of challenges have to be solved to translate promising vectors to clinics. One of the key elements of successful virus-based cancer immunotherapy is the understanding of the tumour immune state and the development of vectors to modify the immunosuppressive tumour microenvironment (TME). Tumour-associated immune cells, as the main component of TME, support tumour progression through multiple pathways inducing resistance to treatment and promoting cancer cell escape mechanisms. In this review, we consider DNA and RNA virus vectors delivering immunomodulatory genes (cytokines, chemokines, co-stimulatory molecules, antibodies, etc.) and discuss how these viruses break an immunosuppressive cell development and switch TME to an immune-responsive “hot” state. We highlight the advantages and limitations of virus vectors for targeted therapeutic programming of tumour immune cell populations and tumour stroma, and propose future steps to establish viral vectors as a standard, efficient, safe, and non-toxic cancer immunotherapy approach that can complement other promising treatment strategies, e.g., checkpoint inhibitors, CAR-T, and advanced chemotherapeutics.
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Petrella, Francesco, Isabella Rimoldi, Stefania Rizzo, and Lorenzo Spaggiari. "Mesenchymal Stromal Cells for Antineoplastic Drug Loading and Delivery." Medicines 4, no. 4 (November 23, 2017): 87. http://dx.doi.org/10.3390/medicines4040087.
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Mesenchymal stromal cells are a population of undifferentiated multipotent adult cells possessing extensive self-renewal properties and the potential to differentiate into a variety of mesenchymal lineage cells. They express broad anti-inflammatory and immunomodulatory activity on the immune system and after transplantation can interact with the surrounding microenvironment, promoting tissue healing and regeneration. For this reason, mesenchymal stromal cells have been widely used in regenerative medicine, both in preclinical and clinical settings. Another clinical application of mesenchymal stromal cells is the targeted delivery of chemotherapeutic agents to neoplastic cells, maximizing the cytotoxic activity against cancer cells and minimizing collateral damage to non-neoplastic tissues. Mesenchymal stem cells are home to the stroma of several primary and metastatic neoplasms and hence can be used as vectors for targeted delivery of antineoplastic drugs to the tumour microenvironment, thereby reducing systemic toxicity and maximizing antitumour effects. Paclitaxel and gemcitabine are the chemotherapeutic drugs best loaded by mesenchymal stromal cells and delivered to neoplastic cells, whereas other agents, like pemetrexed, are not internalized by mesenchymal stromal cells and therefore are not suitable for advanced antineoplastic therapy. This review focuses on the state of the art of advanced antineoplastic cell therapy and its future perspectives, emphasizing in vitro and in vivo preclinical results and future clinical applications.
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Sevenich, Lisa, Robert L. Bowman, Steven D. Mason, Daniela F. Quail, Franck Rapaport, Benelita T. Elie, Edi Brogi, et al. "Analysis of tumour- and stroma-supplied proteolytic networks reveals a brain-metastasis-promoting role for cathepsin S." Nature Cell Biology 16, no. 9 (August 3, 2014): 876–88. http://dx.doi.org/10.1038/ncb3011.
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RIPPMANN, Jörg F., Klaus PFIZENMAIER, Ralf MATTES, Wolfgang J. RETTIG, and Dieter MOOSMAYER. "Fusion of the tissue factor extracellular domain to a tumour stroma specific single-chain fragment variable antibody results in an antigen-specific coagulation-promoting molecule." Biochemical Journal 349, no. 3 (July 25, 2000): 805–12. http://dx.doi.org/10.1042/bj3490805.
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Solid tumours growing beyond a size of 1–2mm in diameter induce supporting connective tissue structures, the tumour stroma, comprising activated fibroblasts and newly formed blood vessels, embedded in an extracellular matrix. The selective destruction of this tissue or the inhibition of its function (e.g. tumour neoangiogenesis) may result in the destruction of tumour nodules, thus providing novel opportunities for tumour therapy. Our approach aims at an antibody-mediated induction of coagulation in tumour nodules to cut off their blood supply. As a target structure the fibroblast activation protein (FAP) is used, which is specifically and abundantly expressed on the activated fibroblasts of the tumour stroma. We constructed a fusion protein comprising a single-chain module of a FAP-specific humanized antibody [single-chain fragment variable (scFv) OS4] and the extracellular domain of human tissue factor. The fusion protein, designated TFOS4, was produced in the Proteus mirabilis protoplast expression system with a yield of 15µg/ml. Biochemical characterization of TFOS4 revealed high-affinity binding to cellular FAP. Further, TFOS4 bound to factor VIIa and also exerted allosteric activation of factor VIIa. A complex of TFOS4 and factor VIIa bound to FAP-expressing cells efficiently generated activated factor X. Finally, cell-bound TFOS4 selectively induced plasma coagulation, implying its activity under physiological conditions, notably with relevant concentrations of coagulation factors and their natural inhibitors. These findings suggest that TFOS4 has the potential to increase the procoagulant state in a cell-type-specific fashion. No systemic coagulation or side effects were observed when TFOS4 was injected intravenously into normal mice, indicating the biosafety and specificity of the recombinant protein.
Dissertations / Theses on the topic "Tumour-promoting stroma"
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Gieniec, Krystyna Anna. "Investigating the Contribution of Specific Cancer-Associated Fibroblast Subsets to Colorectal Tumourigenesis." Thesis, 2020. http://hdl.handle.net/2440/130896.
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Despite colorectal cancer (CRC) remaining a prominent cause of cancer death worldwide, there is little known about how the surrounding connective tissue ‘stroma’ specifically encourages poorer prognosis. While many studies have attempted to interrogate the molecular cross-talk between the tumour and stromal cancer-associated fibroblasts (CAFs), the most important tumour-promoting interactions remain ill-defined. We are yet to adequately exploit these pathways for the prevention and treatment of CRC. In this thesis I aimed to identify and test specific CAF subsets for their putative ability to promote CRC, both in vitro and in vivo. Through RNA-sequencing, prognostic analyses and immunohistochemistry, I identified Melanoma cell adhesion molecule (MCAM) as a candidate CRC-promoting stromal factor that was significantly associated with worse patient prognosis. MCAM expression was significantly upregulated in mouse and human CRC compared to normal colon tissue and marked proliferative tumour-associated stroma comprised of both endothelial and fibroblast cell populations in vivo. Upon overexpression in primary mouse colon fibroblasts in vitro, MCAM significantly reduced contractile activity and enhanced migration. I also developed immunocompetent mouse models of primary and metastatic CRC to examine the efficacy of an inhibitor of a known CRC-promoting stromal factor, Gremlin1 (GREM1). These mouse models involved the implantation of mouse colorectal tumour organoids directly into the colon wall via colonoscope or into the liver via the portal vein, and the tumours generated represented human disease both genetically and pathologically. If we can better understand CAF biology and heterogeneity, and identify specific tumour-promoting CAF subtypes, then we can develop more targeted therapeutic strategies that inhibit both the cancer and its enhancing stroma to ultimately improve CRC patient survival.Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2021
Book chapters on the topic "Tumour-promoting stroma"
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Polanska, Urszula M., Kieran T. Mellody, and Akira Orimo. "Tumour-Promoting Stromal Myofibroblasts in Human Carcinomas." In The Tumor Microenvironment, 325–49. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6615-5_16.
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