Статті в журналах: "Tumour environment"

1

Bennaceur, Karim, Jessica Chapman, Leila Brikci-Nigassa, Kamel Sanhadji, Jean-louis Touraine, and Jacques Portoukalian. "Dendritic cells dysfunction in tumour environment." Cancer Letters 272, no. 2 (December 2008): 186–96. http://dx.doi.org/10.1016/j.canlet.2008.05.017.

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2

Shahriyari, Leili. "Cell dynamics in tumour environment after treatments." Journal of The Royal Society Interface 14, no. 127 (February 2017): 20160977. http://dx.doi.org/10.1098/rsif.2016.0977.

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Most cancer treatments cause necrotic cell deaths in the tumour microenvironment. Necrotic cells send signals to immune cells to start the wound healing process in the tissue. Therefore, we assume after stopping treatments there is a wound that needs to be healed. We develop a simple computational model to investigate cell dynamics during the wound healing process after treatments. The model predicts that the involvement of high-fitness cancer cells in the wound healing leads to fast relapse, and cancer cells outside of the wound can cause a slow recurrence of the tumour. Therefore, the absence of relapse after treatments may imply a slow-developing tumour that might not reach an observable size in the patients' lifetime. Additionally, the model indicates that the location of remaining cancer cells after treatments is an important factor in the recurrence time. The fastest recurrence happens when high-fitness cancer cells remain inside of the wound. However, the longest time to recurrence corresponds to cancer cells located outside of the wound. Note that this model is the first attempt to study cell dynamics in the wound healing process after cancer treatments, and it has some limitations that might influence the results. Experiments are needed to validate the results.

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3

Sinha, Sweta, Paramjeet Singh, and Mehmet Emir Koksal. "Mathematical and Numerical Modelling of Interference of Immune Cells in the Tumour Environment." Discrete Dynamics in Nature and Society 2023 (January 3, 2023): 1–18. http://dx.doi.org/10.1155/2023/9006678.

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In this article, the behaviour of tumour growth and its interaction with the immune system have been studied using a mathematical model in the form of partial differential equations. However, the development of tumours and how they interact with the immune system make up an extremely complex and little-understood system. A new mathematical model has been proposed to gain insight into the role of immune response in the tumour microenvironment when no treatment is applied. The resulting model is a set of partial differential equations made up of four variables: the population density of tumour cells, two different types of immune cells (CD4+ helper T cells and CD8+ cytotoxic T cells), and nutrition content. Such kinds of systems also occur frequently in science and engineering. The interaction of tumour and immune cells is exemplified by predator-prey models in ecology, in which tumour cells act as prey and immune cells act as predators. The tumour-immune cell interaction is expressed via Holling’s Type-III and Beddington-DeAngelis functional responses. The combination of finite volume and finite element method is used to approximate the system numerically because these approximations are more suitable for time-dependent systems having diffusion. Finally, numerical simulations show that the methods perform well and depict the behaviour of the model.

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4

Schumacher, Neele, Stefan Rose-John, and Dirk Schmidt-Arras. "ADAM-Mediated Signalling Pathways in Gastrointestinal Cancer Formation." International Journal of Molecular Sciences 21, no. 14 (July 20, 2020): 5133. http://dx.doi.org/10.3390/ijms21145133.

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Tumour growth is not solely driven by tumour cell-intrinsic mechanisms, but also depends on paracrine signals provided by the tumour micro-environment. These signals comprise cytokines and growth factors that are synthesized as trans-membrane proteins and need to be liberated by limited proteolysis also termed ectodomain shedding. Members of the family of A disintegrin and metalloproteases (ADAM) are major mediators of ectodomain shedding and therefore initiators of paracrine signal transduction. In this review, we summarize the current knowledge on how ADAM proteases on tumour cells but also on cells of the tumour micro-environment contribute to the formation of gastrointestinal tumours, and discuss how these processes can be exploited pharmacologically.

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5

Inácio Pinto, Nelson, June Carnier, Lila M. Oyama, Jose Pinhata Otoch, Paulo Sergio Alcântara, Flavio Tokeshi, and Claudia M. Nascimento. "Cancer as a Proinflammatory Environment: Metastasis and Cachexia." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/791060.

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The development of the syndrome of cancer cachexia and that of metastasis are related with a poor prognostic for cancer patients. They are considered multifactorial processes associated with a proinflammatory environment, to which tumour microenvironment and other tissues from the tumour bearing individuals contribute. The aim of the present review is to address the role of ghrelin, myostatin, leptin, HIF, IL-6, TNF-α, and ANGPTL-4 in the regulation of energy balance, tumour development, and tumoural cell invasion. Hypoxia induced factor plays a prominent role in tumour macro- and microenvironment, by modulating the release of proinflammatory cytokines.

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6

David, E., F. Blanchard, M. F. Heymann, G. De Pinieux, F. Gouin, F. Rédini, and D. Heymann. "The Bone Niche of Chondrosarcoma: A Sanctuary for Drug Resistance, Tumour Growth and also a Source of New Therapeutic Targets." Sarcoma 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/932451.

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Chondrosarcomas are malignant cartilage-forming tumours representing around 20% of malignant primary tumours of bone and affect mainly adults in the third to sixth decade of life. Unfortunately, the molecular pathways controlling the genesis and the growth of chondrosarcoma cells are still not fully defined. It is well admitted that the invasion of bone by tumour cells affects the balance between early bone resorption and formation and induces an “inflammatory-like” environment which establishes a dialogue between tumour cells and their environment. The bone tumour microenvironment is then described as a sanctuary that contributes to the drug resistance patterns and may control at least in part the tumour growth. The concept of “niche” defined as a specialized microenvironment that can promote the emergence of tumour stem cells and provide all the required factors for their development recently emerges in the literature. The present paper aims to summarize the main evidence sustaining the existence of a specific bone niche in the pathogenesis of chondrosarcomas.

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7

Onion, D., R. Argent, R. Kumari, S. Watson, A. Axel, and B. Hall. "158 3D tumour models for the assessment of tumour micro-environment targeted therapies." European Journal of Cancer Supplements 8, no. 7 (November 2010): 55. http://dx.doi.org/10.1016/s1359-6349(10)71863-2.

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8

Domagala-Kulawik, J., and M. Maskey-Warzecowska. "T-regulatory cells in COPD or tumour environment." European Respiratory Journal 34, no. 1 (June 30, 2009): 284. http://dx.doi.org/10.1183/09031936.00025609.

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9

Li, L., I. Spendlove, J. Morgan, and L. G. Durrant. "CD55 is over-expressed in the tumour environment." British Journal of Cancer 84, no. 1 (2001): 80–86. http://dx.doi.org/10.1054/bjoc.2000.1570.

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10

van Tienderen, Groot Koerkamp, IJzermans, van der Laan, and Verstegen. "Recreating Tumour Complexity in a Dish: Organoid Models to Study Liver Cancer Cells and their Extracellular Environment." Cancers 11, no. 11 (November 1, 2019): 1706. http://dx.doi.org/10.3390/cancers11111706.

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Primary liver cancer, consisting predominantly of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), remains one of the most lethal malignancies worldwide. This high malignancy is related to the complex and dynamic interactions between tumour cells, stromal cells and the extracellular environment. Novel in vitro models that can recapitulate the tumour are essential in increasing our understanding of liver cancer. Herein, primary liver cancer-derived organoids have opened up new avenues due to their patient-specificity, self-organizing ability and potential recapitulation of many of the tumour properties. Organoids are solely of epithelial origin, but incorporation into co-culture models can enable the investigation of the cellular component of the tumour microenvironment. However, the extracellular component also plays a vital role in cancer progression and representation is lacking within current in vitro models. In this review, organoid technology is discussed in the context of liver cancer models through comparisons to other cell culture systems. In addition, the role of the tumour extracellular environment in primary liver cancer will be highlighted with an emphasis on its importance in in vitro modelling. Converging novel organoid-based models with models incorporating the native tumour microenvironment could lead to experimental models that can better recapitulate liver tumours in vivo.

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11

Oushy, Soliman, Justin E. Hellwinkel, Mary Wang, Ger J. Nguyen, Dicle Gunaydin, Tessa A. Harland, Thomas J. Anchordoquy, and Michael W. Graner. "Glioblastoma multiforme-derived extracellular vesicles drive normal astrocytes towards a tumour-enhancing phenotype." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1737 (November 20, 2017): 20160477. http://dx.doi.org/10.1098/rstb.2016.0477.

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Glioblastoma multiforme (GBM) is a devastating tumour with abysmal prognoses. We desperately need novel approaches to understand GBM biology and therapeutic vulnerabilities. Extracellular vesicles (EVs) are membrane-enclosed nanospheres released locally and systemically by all cells, including tumours, with tremendous potential for intercellular communication. Tumour EVs manipulate their local environments as well as distal targets; EVs may be a mechanism for tumourigenesis in the recurrent GBM setting. We hypothesized that GBM EVs drive molecular changes in normal human astrocytes (NHAs), yielding phenotypically tumour-promoting, or even tumourigenic, entities. We incubated NHAs with GBM EVs and examined the astrocytes for changes in cell migration, cytokine release and tumour cell growth promotion via the conditioned media. We measured alterations in intracellular signalling and transformation capacity (astrocyte growth in soft agar). GBM EV-treated NHAs displayed increased migratory capacity, along with enhanced cytokine production which promoted tumour cell growth. GBM EV-treated NHAs developed tumour-like signalling patterns and exhibited colony formation in soft agar, reminiscent of tumour cells themselves. GBM EVs modify the local environment to benefit the tumour itself, co-opting neighbouring astrocytes to promote tumour growth, and perhaps even driving astrocytes to a tumourigenic phenotype. Such biological activities could have profound impacts in the recurrent GBM setting. This article is part of the discussion meeting issue ‘Extracellular vesicles and the tumour microenvironment’.

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12

Yatagai, Nanae, Takumi Hasegawa, Rika Amano, Izumi Saito, Satomi Arimoto, Daisuke Takeda, Yasumasa Kakei, and Masaya Akashi. "Transcutaneous Carbon Dioxide Decreases Immunosuppressive Factors in Squamous Cell Carcinoma In Vivo." BioMed Research International 2021 (July 2, 2021): 1–9. http://dx.doi.org/10.1155/2021/5568428.

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Introduction. In recent years, the tumour immunosuppressive mechanism has attracted attention as a cause of tumour chemoresistance. Although chemoresistance and immunosuppression of tumours have been reported to be associated with a hypoxic environment, effective treatments to improve hypoxia in tumours have not yet been established. We have previously applied carbon dioxide (CO2) to squamous cell carcinoma and have shown that improvement in local oxygenation has an antitumour effect. However, the effects of local CO2 administration on tumour immunosuppression, chemoresistance, and combination with chemotherapy are unknown. In this study, we investigated the effects of local CO2 administration on squamous cell carcinoma and the effects of combined use with chemotherapy, focusing on the effects on tumour immunosuppressive factors. Methods. Human oral squamous cell carcinoma (HSC-3) was transplanted subcutaneously into the back of a nude mouse, and CO2 and cisplatin were administered. After administration twice a week for a total of 4 times, tumours were collected and the expression of tumour immunosuppressive factors (PD-L1, PD-L2, and galectin-9) was evaluated using real-time polymerase chain reaction and immunostaining. Results. Compared with the control group, a significant decrease in the mRNA expression of PD-L1 was observed in both, CO2-treated and combination groups. Similarly, the expression of PD-L2 and galectin-9 decreased in the CO2-treated and combination groups. Furthermore, immunostaining also showed a significant decrease in the protein expression of tumour immunosuppressive factors in the CO2-treated and combination groups. Conclusion. It was confirmed that the tumour immunosuppressive factors decreased due to local CO2 administration to the mouse model. CO2 administration has the potential to improve the hypoxic environment in tumours, and combined use with chemotherapy may also improve tumour immunosuppression.

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13

Goggi, Julian L., Boominathan Ramasamy, Yun Xuan Tan, Siddesh V. Hartimath, Jun Rong Tang, Peter Cheng, Rasha Msallam, Ann-Marie Chacko, You Yi Hwang, and Edward G. Robins. "Granzyme B PET Imaging Stratifies Immune Checkpoint Inhibitor Response in Hepatocellular Carcinoma." Molecular Imaging 2021 (December 9, 2021): 1–8. http://dx.doi.org/10.1155/2021/9305277.

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Hepatocellular carcinoma (HCC) is a notoriously difficult cancer to treat. The recent development of immune checkpoint inhibitors has revolutionised HCC therapy; however, successful response is only observed in a small percentage of patients. Biomarkers typically used to predict treatment response in other tumour types are ineffective in HCC, which arises in an immune-suppressive environment. However, imaging markers that measure changes in tumour infiltrating immune cells may supply information that can be used to determine which patients are responding to therapy posttreatment. We have evaluated [18F]AlF-mNOTA-GZP, a radiolabeled peptide targeting granzyme B, to stratify response to ICIs in a HEPA 1-tumours, a syngeneic model of HCC. Posttherapy, in vivo tumour retention of [18F]AlF-mNOTA-GZP was correlated to changes in tumour volume and tumour-infiltrating immune cells. [18F]AlF-mNOTA-GZP successfully stratified response to immune checkpoint inhibition in the syngeneic HEPA 1-6 model. FACS indicated significant changes in the immune environment including a decrease in immune suppressive CD4+ T regulatory cells and increases in tumour-associated GZB+ NK+ cells, which correlated well with tumour radiopharmaceutical uptake. While the immune response to ICI therapies differs in HCC compared to many other cancers, [18F]AlF-mNOTA-GZP retention is able to stratify response to ICI therapy associated with tumour infiltrating GZB+ NK+ cells in this complex tumour microenvironment.

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14

Junttila, Melissa R., and Frederic J. de Sauvage. "Influence of tumour micro-environment heterogeneity on therapeutic response." Nature 501, no. 7467 (September 2013): 346–54. http://dx.doi.org/10.1038/nature12626.

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15

KUBITZA, MARION, LUCAS HICKEY, and GREGORY ROBERTS. "Influence of host microvascular environment on tumour vascular endothelium." International Journal of Experimental Pathology 80, no. 1 (December 25, 2001): 01–10. http://dx.doi.org/10.1046/j.1365-2613.1999.00100.x.

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16

Al-Rayahi, Izzat A. M., Lee R. Machado, and Cordula M. Stover. "Properdin Is a Modulator of Tumour Immunity in a Syngeneic Mouse Melanoma Model." Medicina 57, no. 2 (January 21, 2021): 85. http://dx.doi.org/10.3390/medicina57020085.

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Background and Objectives: Tumours are often low immunogenic. The role of complement, an innate immune defence system, in tumour control has begun to be elucidated, but findings are conflicting. A role for properdin, an amplifier of complement activation, in tumour control has recently been implicated. Materials and Methods: Properdin-deficient and congenic wildtype mice were injected subcutaneously with B16F10 melanoma cells. Tumour mass and chemokine profile were assessed. The frequencies of CD45+CD11b+ Gr-1+ cells were determined from tumours and spleens, and CD206+ F4/80+ cells were evaluated in spleens. Sera were analysed for C5a, sC5b-9, and CCL2. Results: Whilst there was no difference in tumour growth at study endpoint, properdin-deficient mice had significantly fewer myeloid-derived suppressor cells (MDSCs) in their tumours and spleens. Splenic M2 type macrophages and serum levels of C5a, sC5b-9, and CCL2 were decreased in properdin-deficient compared to wildtype mice. Conclusions: The presence of intact complement amplification sustains an environment that lessens potential anti-tumour responses.

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17

FRAGOYIANNIS, GEORGE, FOTEINI KARIOTOU, and PANAYIOTIS VAFEAS. "On the avascular ellipsoidal tumour growth model within a nutritive environment." European Journal of Applied Mathematics 31, no. 1 (September 18, 2018): 111–42. http://dx.doi.org/10.1017/s0956792518000499.

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The present work is part of a series of studies conducted by the authors on analytical models of avascular tumour growth that exhibit both geometrical anisotropy and physical inhomogeneity. In particular, we consider a tumour structure formed in distinct ellipsoidal regions occupied by cell populations at a certain stage of their biological cycle. The cancer cells receive nutrient by diffusion from an inhomogeneous supply and they are subject to also an inhomogeneous pressure field imposed by the tumour microenvironment. It is proved that the lack of symmetry is strongly connected to a special condition that should hold between the data imposed by the tumour’s surrounding medium, in order for the ellipsoidal growth to be realizable, a feature already present in other non-symmetrical yet more degenerate models. The nutrient and the inhibitor concentration, as well as the pressure field, are provided in analytical fashion via closed-form series solutions in terms of ellipsoidal eigenfunctions, while their behaviour is demonstrated by indicative plots. The evolution equation of all the tumour’s ellipsoidal interfaces is postulated in ellipsoidal terms and a numerical implementation is provided in view of its solution. From the mathematical point of view, the ellipsoidal system is the most general coordinate system that the Laplace operator, which dominates the mathematical models of avascular growth, enjoys spectral decomposition. Therefore, we consider the ellipsoidal model presented in this work, as the most general analytic model describing the avascular growth in inhomogeneous environment. Additionally, due to the intrinsic degrees of freedom inherited to the model by the ellipsoidal geometry, the ellipsoidal model presented can be adapted to a very populous class of avascular tumours, varying in figure and in orientation.

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Vyth-Dreese, Florry, and Arjan Griffioen. "Angiostasis as a way to improve immunotherapy." Thrombosis and Haemostasis 101, no. 06 (2009): 1025–31. http://dx.doi.org/10.1160/th08-08-0552.

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SummaryTumours express tumour-associated antigens that are recognised as self-antigens precluding the induction of effective anti-tumour immune responses. Inflammatory conditions which facilitate appropriate antigen presentation and reduce the immuno-suppressive micro-milieu may break tolerance. However, tumours have evolved mechanisms to escape cytotoxic T-cell attack by expressing inhibitory molecules on their surface, secreting suppressive factors, attracting regulatory T cells to the tumour environment or downregulating MHC molecules. Induction of angiogenesis by tumours may represent another mechanism by which tumours escape from immune attack. It provides an anti-inflammatory milieu that will prevent appropriate activation and maturation of antigen presenting cells, allow tumours to secrete suppressive factors and inhibit expression of tumour endothelial adhesion receptors, such as intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin, needed for appropriate interactions with immune cells. Inhibition of angiogenesis may, apart from its direct detrimental effects on the tumour, reverse these processes and contribute to anti-tumour immune reactivity. Without trying to give a complete overview of the field, this paper reviews insights on angio-genesis inhibition in relation to tumour immune responsiveness, mainly based on the Maastricht-Amsterdam experience. This review adds to the hypothesis of improvement of immuno-directed therapies for cancer by angiostasis.

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19

Cai, Yan, Jie Wu, Shixiong Xu, and Zhiyong Li. "A Hybrid Cellular Automata Model of Multicellular Tumour Spheroid Growth in Hypoxic Microenvironment." Journal of Applied Mathematics 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/519895.

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A three-dimensional hybrid cellular automata (CA) model is developed to study the dynamic process of multicellular tumour spheroid (MTS) growth by introducing hypoxia as an important microenvironment factor which influences cell migration and cell phenotype expression. The model enables us to examine the effects of different hypoxic environments on the growth history of the MTS and to study the dynamic interactions between MTS growth and chemical environments. The results include the spatial distribution of different phenotypes of tumour cells and associated oxygen concentration distributions under hypoxic conditions. The discussion of the model system responses to the varied hypoxic conditions reveals that the improvement of the resistance of tumour cells to a hypoxic environment may be important in the tumour normalization therapy.

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20

White, Lydia G., Hannah E. Goy, Alinor J. Rose, and Alexander D. McLellan. "Controlling Cell Trafficking: Addressing Failures in CAR T and NK Cell Therapy of Solid Tumours." Cancers 14, no. 4 (February 15, 2022): 978. http://dx.doi.org/10.3390/cancers14040978.

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The precision guiding of endogenous or adoptively transferred lymphocytes to the solid tumour mass is obligatory for optimal anti-tumour effects and will improve patient safety. The recognition and elimination of the tumour is best achieved when anti-tumour lymphocytes are proximal to the malignant cells. For example, the regional secretion of soluble factors, cytotoxic granules, and cell-surface molecule interactions are required for the death of tumour cells and the suppression of neovasculature formation, tumour-associated suppressor, or stromal cells. The resistance of individual tumour cell clones to cellular therapy and the hostile environment of the solid tumours is a major challenge to adoptive cell therapy. We review the strategies that could be useful to overcoming insufficient immune cell migration to the tumour cell mass. We argue that existing ‘competitive’ approaches should now be revisited as complementary approaches to improve CAR T and NK cell therapy.

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21

Ciccocioppo, Fausta, Paola Lanuti, Marco Marchisio, and Sebastiano Miscia. "Extracellular Vesicles Involvement in the Modulation of the Glioblastoma Environment." Journal of Oncology 2020 (January 28, 2020): 1–8. http://dx.doi.org/10.1155/2020/3961735.

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Glioblastoma (GBM) is the most deadly primary brain tumour and is a paradigmatic example of heterogeneous cancer. Although expanding data propose the phenotypic plasticity exhibited by glioblastoma cells, as a critical feature involved in the tumour development and posttherapy recurrence, the central machinery responsible for their aggressiveness remains elusive. Despite decades of research, the complex biology of the glioblastoma is still unknown. Progress in genetic and epigenetic discoveries has improved diagnostic classification, prognostic information, and therapeutic planning. In the complex model of intercellular signalling, several studies have shown that extracellular vesicles have a key role in the intercellular communication among GBM cells and the tumour microenvironment modulation. The purpose of this review is to summarize the role of the EV-mediated intercellular crosstalk in the glioblastoma physiopathology.

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22

Zou, Weiping. "Immunosuppressive networks in the tumour environment and their therapeutic relevance." Nature Reviews Cancer 5, no. 4 (March 18, 2005): 263–74. http://dx.doi.org/10.1038/nrc1586.

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Stratford, I. J., G. E. Adams, J. C. M. Bremner, S. Cole, H. S. Edwards, N. Robertson, and P. J. Wood. "Manipulation and Exploitation of the Tumour Environment for Therapeutic Benefit." International Journal of Radiation Biology 65, no. 1 (January 1994): 85–94. http://dx.doi.org/10.1080/09553009414550121.

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Brown, M. "757 Hypoxic tumour environment and its implication for cancer treatment." European Journal of Cancer Supplements 1, no. 5 (September 2003): S227. http://dx.doi.org/10.1016/s1359-6349(03)90783-x.

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Santiago, Alina, Wolfgang Eicheler, Jan Bussink, Paul Rijken, Ala Yaromina, Bettina Beuthien-Baumann, Albert J. van der Kogel, Michael Baumann, and Mechthild Krause. "Effect of cetuximab and fractionated irradiation on tumour micro-environment." Radiotherapy and Oncology 97, no. 2 (November 2010): 322–29. http://dx.doi.org/10.1016/j.radonc.2010.07.007.

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Mueller-Klieser, W. "SP-0173 CLINICAL RELEVANCE OF TUMOUR MICRO-ENVIRONMENT AND METABOLISM." Radiotherapy and Oncology 103 (May 2012): S66—S67. http://dx.doi.org/10.1016/s0167-8140(12)70512-1.

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Alarcón, T., H. M. Byrne, and P. K. Maini. "A cellular automaton model for tumour growth in inhomogeneous environment." Journal of Theoretical Biology 225, no. 2 (November 2003): 257–74. http://dx.doi.org/10.1016/s0022-5193(03)00244-3.

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Freeman, Patrick, and Ainhoa Mielgo. "Cancer-Associated Fibroblast Mediated Inhibition of CD8+ Cytotoxic T Cell Accumulation in Tumours: Mechanisms and Therapeutic Opportunities." Cancers 12, no. 9 (September 21, 2020): 2687. http://dx.doi.org/10.3390/cancers12092687.

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The tumour microenvironment (TME) is the complex environment in which various non-cancerous stromal cell populations co-exist, co-evolve and interact with tumour cells, having a profound impact on the progression of solid tumours. The TME is comprised of various extracellular matrix (ECM) proteins in addition to a variety of immune and stromal cells. These include tumour-associated macrophages, regulatory T cells (Tregs), myeloid-derived suppressor cells, as well as endothelial cells, pericytes and cancer-associated fibroblasts (CAFs). CAFs are the most abundant stromal cell population in many tumours and support cancer progression, metastasis and resistance to therapies through bidirectional signalling with both tumour cells and other cells within the TME. More recently, CAFs have been shown to also affect the anti-tumour immune response through direct and indirect interactions with immune cells. In this review, we specifically focus on the interactions between CAFs and cytotoxic CD8+ T cells, and on how these interactions affect T cell recruitment, infiltration and function in the tumour. We additionally provide insight into the therapeutic implications of targeting these interactions, particularly in the context of cancer immunotherapy.

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Grimes, David Robert, and Frederick J. Currell. "Oxygen diffusion in ellipsoidal tumour spheroids." Journal of The Royal Society Interface 15, no. 145 (August 2018): 20180256. http://dx.doi.org/10.1098/rsif.2018.0256.

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Oxygen plays a central role in cellular metabolism, in both healthy and tumour tissue. The presence and concentration of molecular oxygen in tumours has a substantial effect on both radiotherapy response and tumour evolution, and as a result the oxygen micro-environment is an area of intense research interest. Multi-cellular tumour spheroids closely mimic real avascular tumours, and in particular they exhibit physiologically relevant heterogeneous oxygen distribution. This property has made them a vital part of in vitro experimentation. For ideal spheroids, their heterogeneous oxygen distributions can be predicted from theory, allowing determination of cellular oxygen consumption rate (OCR) and anoxic extent. However, experimental tumour spheroids often depart markedly from perfect sphericity. There has been little consideration of this reality. To date, the question of how far an ellipsoid can diverge from perfect sphericity before spherical assumptions break down remains unanswered. In this work, we derive equations governing oxygen distribution (and, more generally, nutrient and drug distribution) in both prolate and oblate tumour ellipsoids, and quantify the theoretical limits of the assumption that the spheroid is a perfect sphere. Results of this analysis yield new methods for quantifying OCR in ellipsoidal spheroids, and how this can be applied to markedly increase experimental throughput and quality.

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Kawiak, Jerzy, Grazyna Hoser, and Joanna Domagała-Kulawik. "Problems of Cancer Treatment. Part I. Theory of Treatment Based on Known Mechanisms of Anticancer Immunological Responses." Advances in Cell Biology 5, no. 1 (March 1, 2017): 72–95. http://dx.doi.org/10.1515/acb-2017-0006.

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SummaryVarious processes, taking place both in cells and in their environment, are linked to carcinogenesis. This paper aims at recalling the complex mechanisms of oncogenesis, with particular attention paid to responses of the immune system. In development of solid tumours, leukaemias and lymphomas several common stages can be noted. A neoplastic disease cannot be understood considering only phenomena of genetic mutations. Neoplastic cells are characterised by an extensive antigenic variability and resistance to apoptosis. The cells create around them a microenvironment which protects them from defensive activity of the host. In the paper we present the recognised mechanisms of anti-neoplastic defense as well as several elements allowing the solid tumours and leukaemias to escape from the immune surveillance. The generally accepted treatment of tumours aims at reducing numbers of tumour cells. Following resection of a tumour, radiotherapy or chemotherapy, the parallel or consecutive stage of treatment was found to involve an increase in number of clones of immune system cells. One of the ways in which the immune system can be activated involves autovaccination of the host with own neoplastic cells in an apoptosis. However, attempts of such a therapy frequently brought no expected results due to blocked activity of cytotoxic cells. Therefore, the subsequent stage in activation of the immune system should involve elimination of the tumor-mobilized blockade of the system. Attempts toward this aim include neutralization of the tumour-blocked cytotoxic properties of defensive cells, first of all T lymphocytes. The recognized mechanisms of blocking T cells activity in the PD-1/PD-L1 system or due to inhibition of activation by CTLA-4 molecule provided rationale for development of effective tumour immunotherapy approaches.

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31

Kissová, Viktória, Zuzana Ševčíková, Viera Revajová, Róbert Herich, and Mikuláš Levkut. "Mast cells and eosinophils in rat mammary gland tumours induced by N-Nitroso-N-methylurea." Bulletin of the Veterinary Institute in Pulawy 59, no. 3 (September 1, 2015): 411–16. http://dx.doi.org/10.1515/bvip-2015-0060.

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Abstract The aim of the study was to evaluate the distribution and number of mast cells and eosinophils in rat mammary gland tumours induced by N-Nitroso-N-methylurea. The highest density of mast cells was found in cystic papillary adenocarcinomas of grade II. Eosinophils were detected only in the cystic papillary adenocarcinoma of grades I and II, in non-invasive cribriform adenocarcinoma and comedo-type carcinoma. Mast cell populations were observed perivascularly in the tumour stroma, in the host tumour interface, as well as in necrotic areas of neoplasms. Mast cells were observed to be intact according to their morphological changes, collectively referred to as degranulation. The obtained results indicate that mast cells and eosinophils play an important role in tumour micro-environment formation. The increased density of these cells in experimentally-induced rat mammary gland tumours suggests a poor prognosis in these cancers. Our results also confirmed that rat mammary gland tumours are good models for the study of breast cancers.

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32

Grimshaw, M. J. "Endothelins and hypoxia-inducible factor in cancer." Endocrine-Related Cancer 14, no. 2 (June 2007): 233–44. http://dx.doi.org/10.1677/erc-07-0057.

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The endothelin system is a family of three similar small peptides, two G-protein-coupled receptors and two proteinases. Endothelins have several physiological roles, notably in embryonic differentiation and vascular homeostasis. Numerous types of tumour express endothelins and their regulation is often aberrant when compared with the normal tissue from which the tumour arose. However, endothelin expression is tumour-type specific, and in some instances, expression of individual members of the endothelin system will be upregulated, while in other tumour types, they may be downregulated. Endothelins have numerous potential roles in tumours including modulating angiogenesis, inducing mitogenesis and invasion of tumour cells, and protecting cells from apoptosis. Expression of endothelins is controlled by the tumour microenvironment, whilst the endothelins themselves modify that environment; a case in point is that hypoxia stimulates endothelin expression via hypoxia-inducible factor (HIF)-1, while endothelins stabilise HIF-1 leading to expression of, for instance, vascular endothelial growth factor. This review highlights the potential roles of endothelins in various cancers and describes the pre-clinical and clinical progress that has been made in several tumour types – notably prostate, ovary, melanoma and breast cancer. The interactions between the endothelin network and HIF-1 are highlighted.

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33

Flavell, Richard A., Shomyseh Sanjabi, Stephen H. Wrzesinski та Paula Licona-Limón. "The polarization of immune cells in the tumour environment by TGFβ". Nature Reviews Immunology 10, № 8 (9 липня 2010): 554–67. http://dx.doi.org/10.1038/nri2808.

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34

Kunz, Robert F., Byron J. Gaskin, Qunhua Li, Sam Davanloo-Tajbakhsh, and Cheng Dong. "Multi-scale biological and physical modelling of the tumour micro-environment." Drug Discovery Today: Disease Models 16 (2015): 7–15. http://dx.doi.org/10.1016/j.ddmod.2015.03.001.

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35

Cross, N. A., M. Papageorgiou, and C. L. Eaton. "Bone marrow stromal cells promote growth and survival of prostate cancer cells." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 698–700. http://dx.doi.org/10.1042/bst0350698.

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Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).

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Apte, Ron N., Yakov Krelin, Xiaoping Song, Shahar Dotan, Eli Recih, Moshe Elkabets, Yaron Carmi, et al. "Effects of micro-environment- and malignant cell-derived interleukin-1 in carcinogenesis, tumour invasiveness and tumour–host interactions." European Journal of Cancer 42, no. 6 (April 2006): 751–59. http://dx.doi.org/10.1016/j.ejca.2006.01.010.

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Kapoor, Simran S., and Dietmar M. W. Zaiss. "Emerging Role of EGFR Mutations in Creating an Immune Suppressive Tumour Microenvironment." Biomedicines 10, no. 1 (December 27, 2021): 52. http://dx.doi.org/10.3390/biomedicines10010052.

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Several types of tumours overexpress the Epidermal Growth Factor Receptor (EGFR) in either wild type or mutated form. These tumours are often highly aggressive and difficult to treat. The underlying mechanisms for this phenomenon have remained largely unresolved, but recent publications suggest two independent mechanisms that may contribute. According to one line of research, tumours that overexpress the EGFR grow autonomously and become “addicted” to growth factor signalling. Inhibition of this signal using EGFR inhibitors can, therefore, induce cell death in tumour cells and lead to tumour shrinkage. The other line of research, as highlighted by recent findings, suggests that the overexpression, specifically of mutant forms of the EGFR, may create an immune-suppressive and lymphocyte depleted microenvironment within tumours. Such a lymphocyte depleted microenvironment may explain the resistance of EGFR overexpressing cancers to tumour therapies, particularly to check-point inhibitor treatments. In this article, we discuss the recent data which support an immune modulatory effect of EGFR signalling and compare these published studies with the most recent data from The Cancer Genome Atlas (TCGA), in this way, dissecting possible underlying mechanisms. We thereby focus our study on how EGFR overexpression may lead to the local activation of TGFβ, and hence to an immune suppressive environment. Consequently, we define a novel concept of how the mitogenic and immune modulatory effects of EGFR overexpression may contribute to tumour resistance to immunotherapy, and how EGFR specific inhibitors could be used best to enhance the efficacy of tumour therapy.

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Schmidt-Arras, Dirk, Eithan Galun, and Stefan Rose-John. "The two facets of gp130 signalling in liver tumorigenesis." Seminars in Immunopathology 43, no. 4 (May 28, 2021): 609–24. http://dx.doi.org/10.1007/s00281-021-00861-0.

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AbstractThe liver is a vital organ with multiple functions and a large regenerative capacity. Tumours of the liver are the second most frequently cause of cancer-related death and develop in chronically inflamed livers. IL-6-type cytokines are mediators of inflammation and almost all members signal via the receptor subunit gp130 and the downstream signalling molecule STAT3. We here summarize current knowledge on how gp130 signalling and STAT3 in tumour cells and cells of the tumour micro-environment drives hepatic tumorigenesis. We furthermore discuss very recent findings describing also anti-tumorigenic roles of gp130/STAT3 and important considerations for therapeutic interventions.

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Sas-Chen, Aldema, Swati Srivastava, and Yosef Yarden. "The short and the long: non-coding RNAs and growth factors in cancer progression." Biochemical Society Transactions 45, no. 1 (February 8, 2017): 51–64. http://dx.doi.org/10.1042/bst20160131.

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A relatively well-understood multistep process enables mutation-bearing cells to form primary tumours, which later use the circulation system to colonize new locations and form metastases. However, in which way the emerging abundance of different non-coding RNAs supports tumour progression is poorly understood. Here, we review new lines of evidence linking long and short types of non-coding RNAs to signalling pathways activated in the course of cancer progression by growth factors and by the tumour micro-environment. Resolving the new dimension of non-coding RNAs in oncogenesis will probably translate to earlier detection of cancer and improved therapeutic strategies.

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Costello, P. C., D. MacDonald, W. McDonald, R. Hammond, V. Sloby, B. Faubert, and J. Megyesi. "Determination of human brain tumour therapy response using an ex vivo invasion assay provides a potential step toward individualized treatment." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 11509. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.11509.

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11509 Background: Malignant brain tumours are the 6th leading cause of pre-mature death in Ontario with over 10,000 potential years of life lost each year. Improved treatment for malignant brain tumours is needed. Models assessing chemotherapy response employ clonal malignant human tumour cells while patient responses are heterogeneous. Tumour spreading is dependent on tissue invasion and in this study, a surgical sample of each patient’s tumour was used to assess invasion and growth while exposed to a panel of clinically relevant chemotherapies. Methods: Tissue specimens were placed into a nutrient-rich collagen gel that mimics the tumour environment in the body. Chemotherapy treatments were suspended in the matrix surrounding the tumour. Growth and invasion in the presence of chemotherapies was assessed for 5 days following surgical removal in this 3 dimensional matrix and compared to control conditions using student t- test. Results: 12 patient’s individual tumour response was assessed. 4 patients tumours did not respond to any chemotherapy tested. Table 1 shows the number of responders to each therapy tested. Conclusions: Individual response to chemotherapy is highly variable both clinically and in our ex vivo assessment of tissue fragments. Several patients (8/12 or 67%) tumour assessment displayed significant (p<.05) response to one or more therapies. Results from this data will continue to be compared to patient response, The overall predictive value of the data obtained using this ex vivo model will be determined by continuing to collect information time to recurrence and survival at 3, 6, 12 and 24 months) from 90 solid tumour patients per year. Pre-assessment each patient’s responsiveness to chemotherapies could lead to more individualized and therefore more effective treatment. [Table: see text] [Table: see text]

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Lee, Hyunah. "Combination Therapy of Cancer – Escalating the Effect of Dendritic Cell-based Cancer Vaccine in the Tumour Micro-environment." European Oncology & Haematology 08, no. 04 (2012): 261. http://dx.doi.org/10.17925/eoh.2012.08.4.261.

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A key factor in initiating and operating the immune system against tumour cells, the dendritic cell (DC) has been regarded as the next possible breakthrough in new cancer therapy. However, the results of more than 15 years of clinical studies with DC vaccine revealed the difficulties fulfilling this expectation. Evidence has disclosed that the DC activation required for proper tumour-specific effector CD4+ and CD8+ T cell stimulation is inhibited in the micro-environment of tumour. Studies have further reported that DC phenotypes in tumour tissue and draining lymph nodes are mostly immature, which results in regulatory immune responses. Also, the existence of MDSCs and TAMs adversely affect both DC function and immune suppression in the cancer-environment. In this review, efforts to overcome the tumour or host-dependent hindering which inhibit the effect of cancer vaccine will be discussed. The combination therapy of cancer with DC vaccine and other immune modulators may improve the clinical efficacy.

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42

Babourina-Brooks, Ben, Martin Wilson, Theodoros N. Arvanitis, Andrew C. Peet, and Nigel P. Davies. "MRS water resonance frequency in childhood brain tumours: a novel potential biomarker of temperature and tumour environment." NMR in Biomedicine 27, no. 10 (August 14, 2014): 1222–29. http://dx.doi.org/10.1002/nbm.3177.

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43

Kariotou, Foteini, and Panayiotis Vafeas. "The Avascular Tumour Growth in the Presence of Inhomogeneous Physical Parameters Imposed from a Finite Spherical Nutritive Environment." International Journal of Differential Equations 2012 (2012): 1–25. http://dx.doi.org/10.1155/2012/175434.

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A well-known mathematical model of radially symmetric tumour growth is revisited in the present work. Under this aim, a cancerous spherical mass lying in a finite concentric nutritive surrounding is considered. The host spherical shell provides the tumor with vital nutrients, receives the debris of the necrotic cancer cells, and also transmits to the tumour the pressure imposed on its exterior boundary. We focus on studying the type of inhomogeneity that the nutrient supply and the pressure field imposed on the host exterior boundary, can exhibit in order for the spherical structure to be supported. It turns out that, if the imposed fields depart from being homogeneous, only a special type of interrelated inhomogeneity between nutrient and pressure can secure the spherical growth. The work includes an analytic derivation of the related boundary value problems based on physical conservation laws and their analytical treatment. Implementations in cases of special physical interest are examined, and also existing homogeneous results from the literature are fully recovered.

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44

Peyrode, Caroline, François Gouin, Aurélien Vidal, Philippe Auzeloux, Sophie Besse, Marie-Mélanie Dauplat, Serge Askienazy, et al. "A “Proteoglycan Targeting Strategy” for the Scintigraphic Imaging and Monitoring of the Swarm Rat Chondrosarcoma Orthotopic Model." Sarcoma 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/691608.

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Our lab developed99mTc-NTP 15-5 radiotracer as targeting proteoglycans (PGs) for the scintigraphic imaging of joint. This paper reports preclinical results of99mTc-NTP 15-5 imaging of an orthotopic model of Swarm rat chondrosarcoma (SRC).99mTc-NTP 15-5 imaging of SRC-bearing and sham-operated animals was performed and quantified at regular intervals after surgery and compared to bone scintigraphy and tumoural volume. Tumours were characterized by histology and PG assay. SRC exhibited a significant99mTc-NTP 15-5 uptake at very early stage after implant (with tumour/muscle ratio of 1.61 ± 0.14), whereas no measurable tumour was evidenced. As tumour grew, mean tumour/muscle ratio was increased by 2.4, between the early and late stage of pathology. Bone scintigraphy failed to image chondrosarcoma, even at the later stage of study.99mTc-NTP 15-5 imaging provided a suitable set of quantitative criteria for thein vivocharacterization of chondrosarcoma behaviour in bone environment, useful for achieving a greater understanding of the pathology.

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45

Iafrate, M., T. Prayer Galetti, V. Bronte, F. Pagano, G. Gri, T. Kasic, and A. Viola. "155 Tumour infiltrating lymphocytes (TIL) in prostatic neoplasia of untreated patients are inhibited in their function by tumour environment." European Urology Supplements 3, no. 2 (February 2004): 41. http://dx.doi.org/10.1016/s1569-9056(04)90156-x.

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46

Coltrini, Daniela, Roberto Ronca, Mirella Belleri, Luciano Zardi, Stefano Indraccolo, Valentina Scarlato, Raffaella Giavazzi, and Marco Presta. "Impact of VEGF-dependent tumour micro-environment on EDB fibronectin expression by subcutaneous human tumour xenografts in nude mice." Journal of Pathology 219, no. 4 (December 2009): 455–62. http://dx.doi.org/10.1002/path.2626.

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47

Oosterwijk, E., and R. J. Gillies. "Targeting ion transport in cancer." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1638 (March 19, 2014): 20130107. http://dx.doi.org/10.1098/rstb.2013.0107.

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The metabolism of cancer cells differs substantially from normal cells, including ion transport. Although this phenomenon has been long recognized, ion transporters have not been viewed as suitable therapeutic targets. However, the acidic pH values present in tumours which are well outside of normal limits are now becoming recognized as an important therapeutic target. Carbonic anhydrase IX (CAIX) is fundamental to tumour pH regulation. CAIX is commonly expressed in cancer, but lowly expressed in normal tissues and that presents an attractive target. Here, we discuss the possibilities of exploiting the acidic, hypoxic tumour environment as possible target for therapy. Additionally, clinical experience with CAIX targeting in cancer patients is discussed.

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Wirta, Erkki-Ville, Säde Szeto, Ulrika Hänninen, Maarit Ahtiainen, Jan Böhm, Jukka-Pekka Mecklin, Lauri A. Aaltonen, and Toni T. Seppälä. "Prognostic Value of Immune Environment Analysis in Small Bowel Adenocarcinomas with Verified Mutational Landscape and Predisposing Conditions." Cancers 12, no. 8 (July 23, 2020): 2018. http://dx.doi.org/10.3390/cancers12082018.

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Background: Small bowel adenocarcinoma (SBA) is a rare yet insidious cancer with poor survival. The abundance of tumour-infiltrating lymphocytes is associated with improved survival, but the role of the programmed death-1/programmed death ligand-1 (PD-1/PD-L1) pathway in tumour escape is controversial. We evaluated immune cell infiltration, PD1/PD-L1 expression and their prognostic value in a series of SBAs with previously verified predisposing conditions and exome-wide somatic mutation characterization. Methods: Formalin-fixed paraffin-embedded tissue sections stained for CD3, CD8, PD-L1 and PD-1 were analysed from 94 SBAs. An immune cell score (ICS) was formed from the amount of the CD3 and CD8 positive lymphocytes from the tumour centre and invasive margin. The PD-L1 and PD-1 positive immune cells (ICs) and ICS were combined into a variable called Immunoprofile. Results: High ICS, PD-L1IC and PD-1, individually and combined as Immunoprofile, were prognostic for better patient outcome. Sixty-five (69%) SBAs expressed ≥1% positive PD-L1IC. A high tumour mutation burden was common (19%) and associated with immune markers. Immunoprofile, adjusted for TNM stage, mismatch repair status, tumour location, sex and age were independent prognostic markers for disease-specific and overall survival. Conclusions: Analysing tumoral immune contexture provides prognostic information in SBA. Combining ICS, PD-1 and PD-L1IC as Immunoprofile enhanced the prognostic performance.

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Carbone, Michele, Sarah T. Arron, Bruce Beutler, Angela Bononi, Webster Cavenee, James E. Cleaver, Carlo M. Croce, et al. "Tumour predisposition and cancer syndromes as models to study gene–environment interactions." Nature Reviews Cancer 20, no. 9 (May 29, 2020): 533–49. http://dx.doi.org/10.1038/s41568-020-0265-y.

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Morgan, J., I. Spendlove, and L. G. Durrant. "The role of CD55 in protecting the tumour environment from complement attack." Tissue Antigens 60, no. 3 (September 2002): 213–23. http://dx.doi.org/10.1034/j.1399-0039.2002.600303.x.

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