Relevant bibliographies by topics / Cancer cell microenvironment

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Cancer cell microenvironment'

Author: Grafiati
Published: 2 November 2024

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Journal articles on the topic "Cancer cell microenvironment"

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Shive, Heather R., John S. House, Jordan L. Ferguson, Dereje D. Jima, Aubrie A. Selmek, and Dillon T. Lloyd. "Abstract PR011: Characterization of the precancerous and cancer microenvironment in a zebrafish sarcoma model." Clinical Cancer Research 28, no. 18_Supplement (September 15, 2022): PR011. http://dx.doi.org/10.1158/1557-3265.sarcomas22-pr011.

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Abstract Contributions of the microenvironment to soft tissue sarcoma progression are relatively undefined, representing a major impediment to identifying essential regulatory networks in sarcomagenesis. Furthermore, genetic and molecular characteristics that distinguish precancerous versus cancerous microenvironments are not well known across human cancer types. While animal models have the potential to reveal these complex processes, significant impediments to such inquiries include (1) the difficulty in distinguishing microenvironmental cells from precancerous or cancer cells in tissue specimens; and (2) the challenge in defining a discrete tissue with known cancer predilection that represents a precancerous microenvironment. We developed a unique zebrafish model that allows segregation of microenvironmental, precancerous, and cancerous cell populations by fluorescence-activated cell sorting. This model exhibits high predilection for malignant peripheral nerve sheath tumor (MPNST), a type of soft tissue sarcoma with a particularly poor prognosis due to aggressive growth, limited response to conventional treatment, and ineffective targeted therapy options. Using RNA-seq, we profiled the transcriptomes of microenvironmental cells from our zebrafish MPNST model and determined that the precancerous and cancerous microenvironments exhibit broad activation of inflammatory and immune-associated signaling networks. Markers for both M1 and M2 macrophage polarization were upregulated in precancerous and cancerous microenvironments, suggesting the presence of a mixed macrophage population during sarcomagenesis. Patterns of ligand and receptor expression based on a previously defined human ligand-receptor network identified significant upregulation of multiple tumor-promoting ligands in both precancerous and cancerous microenvironments. We also identified specific ligand-receptor pairs that may mediate key signaling events during sarcoma initiation and progression. Together this work provide new insight into distinguishing characteristics of the cancer-prone cellular microenvironment that may promote MPNST initiation and progression in vertebrates. Citation Format: Heather R. Shive, John S. House, Jordan L. Ferguson, Dereje D. Jima, Aubrie A. Selmek, Dillon T. Lloyd. Characterization of the precancerous and cancer microenvironment in a zebrafish sarcoma model [abstract]. In: Proceedings of the AACR Special Conference: Sarcomas; 2022 May 9-12; Montreal, QC, Canada. Philadelphia (PA): AACR; Clin Cancer Res 2022;28(18_Suppl):Abstract nr PR011.
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Campbell, Caroline J., and Brian W. Booth. "The Influence of the Normal Mammary Microenvironment on Breast Cancer Cells." Cancers 15, no. 3 (January 18, 2023): 576. http://dx.doi.org/10.3390/cancers15030576.

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The tumor microenvironment is recognized as performing a critical role in tumor initiation, progression, and metastasis of many cancers, including breast cancer. The breast cancer microenvironment is a complex mixture of cells consisting of tumor cells, immune cells, fibroblasts, and vascular cells, as well as noncellular components, such as extracellular matrix and soluble products. The interactions between the tumor cells and the tumor microenvironment modulate tumor behavior and affect the responses of cancer patients to therapies. The interactions between tumor cells and the surrounding environment can include direct cell-to-cell contact or through intercellular signals over short and long distances. The intricate functions of the tumor microenvironment in breast cancer have led to increased research into the tumor microenvironment as a possible therapeutic target of breast cancer. Though expanded research has shown the clear importance of the tumor microenvironment, there is little focus on how normal mammary epithelial cells can affect breast cancer cells. Previous studies have shown the normal breast microenvironment can manipulate non-mammary stem cells and tumor-derived cancer stem cells to participate in normal mammary gland development. The tumorigenic cells lose their tumor-forming capacity and are “redirected” to divide into “normal”, non-tumorigenic cells. This cellular behavior is “cancer cell redirection”. This review will summarize the current literature on cancer cell redirection and the normal mammary microenvironment’s influence on breast cancer cells.
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Gibson, Spencer, Tricia Choquette, Elizabeth S. Henson, Xioyan Yang, and James B. Johnston. "Abstract 2516: Analysis of CLL Celllular Environment and Response (ACCER) is a novel method to understand the microenvironment in CLL." Cancer Research 83, no. 7_Supplement (April 4, 2023): 2516. http://dx.doi.org/10.1158/1538-7445.am2023-2516.

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Abstract Microenvironments such as lymph nodes and bone marrow allow chronic lymphocytic leukemia (CLL) cells to survive after drug treatments. There are limited methods to study the to study the contribution of the microenvironment. We have adapted a solid tumour microenvironment cell culture system that provides elements of the CLL microenvironment called Analysis of CLL Cellular Environment and Response (ACCER). We optimized the cell number for patient’s primary CLL cells and HS-5 human bone marrow stromal cell line that will give sufficient cell number and viability with the ACCER. We then determined the amount of collagen type 1 to give the best extracellular matrix to seed CLL cells to the membrane. Finally, we determined that ACCER provide CLL cell protection against cell death following treatment with fludarabine and ibrutinib compared to co-culture conditions. This describes novel microenvironment model to investigate factors that promote drug resistance and cell survival in CLL. In the future, this will further validate new treatment strategies to overcome microenvironmental CLL cell survival signals. Citation Format: Spencer Gibson, Tricia Choquette, Elizabeth S. Henson, Xioyan Yang, James B. Johnston. Analysis of CLL Celllular Environment and Response (ACCER) is a novel method to understand the microenvironment in CLL [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 2516.
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Aber, Etan R., Cristina F. Contreras, Mohd Omar Sikder, Kathy P. Li, Greta E. Forbes, Vishaka Gopalan, Sridhar Hannenhalli, and Rosandra N. Kaplan. "Abstract LB308: Transcriptional profiling uncovers a unified program underlying the human metastatic and adjacent microenvironments." Cancer Research 84, no. 7_Supplement (April 5, 2024): LB308. http://dx.doi.org/10.1158/1538-7445.am2024-lb308.

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Abstract Metastasis is the primary cause of death in patients with solid tumors, yet the treatment-refractory metastatic microenvironment is poorly characterized. To gain a comprehensive understanding of microenvironmental regulation of human metastasis, we performed single-cell RNA sequencing covering endothelial, stromal, myeloid, lymphoid, and malignant cells from 28 lung and liver samples of the metastatic microenvironment and metastasis-free adjacent microenvironment from patients with metastatic adrenocortical carcinoma compared to healthy donors for a total of 275,903 cells. We discovered that the adjacent microenvironment in patients with metastatic cancer is significantly different from healthy tissue without cancer: The adjacent microenvironment has many immunosuppressive and pro-tumorigenic features similar to primary tumor and metastatic tissue. As adjacent tissues are potential sites for subsequent metastasis, the shared changes between the adjacent and metastatic microenvironments suggest that these elements of the treatment-refractory metastatic microenvironment may dictate metastasis. Importantly, these pathologic features of the adjacent and metastatic microenvironments associate with poor outcomes for patients and may be targetable. Lastly, we identify a mechanism by which tumor cells may be remotely driving and coordinating these changes in both the metastatic and adjacent microenvironments. Taken together, our study identifies shared and microenvironment-specific changes underlying a global program of metastasis. Citation Format: Etan R. Aber, Cristina F. Contreras, Mohd Omar Sikder, Kathy P. Li, Greta E. Forbes, Vishaka Gopalan, Sridhar Hannenhalli, Rosandra N. Kaplan. Transcriptional profiling uncovers a unified program underlying the human metastatic and adjacent microenvironments [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB308.
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Bischoff, Philip, Alexandra Trinks, Benedikt Obermayer, Jan Patrick Pett, Jennifer Wiederspahn, Florian Uhlitz, Xizi Liang, et al. "Single-cell RNA sequencing reveals distinct tumor microenvironmental patterns in lung adenocarcinoma." Oncogene 40, no. 50 (October 18, 2021): 6748–58. http://dx.doi.org/10.1038/s41388-021-02054-3.

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AbstractRecent developments in immuno-oncology demonstrate that not only cancer cells, but also the tumor microenvironment can guide precision medicine. A comprehensive and in-depth characterization of the tumor microenvironment is challenging since its cell populations are diverse and can be important even if scarce. To identify clinically relevant microenvironmental and cancer features, we applied single-cell RNA sequencing to ten human lung adenocarcinomas and ten normal control tissues. Our analyses revealed heterogeneous carcinoma cell transcriptomes reflecting histological grade and oncogenic pathway activities, and two distinct microenvironmental patterns. The immune-activated CP²E microenvironment was composed of cancer-associated myofibroblasts, proinflammatory monocyte-derived macrophages, plasmacytoid dendritic cells and exhausted CD8+ T cells, and was prognostically unfavorable. In contrast, the inert N³MC microenvironment was characterized by normal-like myofibroblasts, non-inflammatory monocyte-derived macrophages, NK cells, myeloid dendritic cells and conventional T cells, and was associated with a favorable prognosis. Microenvironmental marker genes and signatures identified in single-cell profiles had progonostic value in bulk tumor profiles. In summary, single-cell RNA profiling of lung adenocarcinoma provides additional prognostic information based on the microenvironment, and may help to predict therapy response and to reveal possible target cell populations for future therapeutic approaches.
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AbdelFattah, HebatAllah Samy, Mayar Tarek Ibrahim, Mostafa Mahmoud Nasr, and Shaimaa Nasr Nasr Amin. "Cell Signaling in Cancer Microenvironment." International Journal of Advanced Biomedicine 2, no. 2 (May 1, 2017): 47–51. http://dx.doi.org/10.18576/ab/020204.

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Loberg, Robert D., Christopher J. Logothetis, Evan T. Keller, and Kenneth J. Pienta. "Pathogenesis and Treatment of Prostate Cancer Bone Metastases: Targeting the Lethal Phenotype." Journal of Clinical Oncology 23, no. 32 (November 10, 2005): 8232–41. http://dx.doi.org/10.1200/jco.2005.03.0841.

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Traditionally, prostate cancer treatment, as well as all cancer treatment, has been designed to target the tumor cell directly via various hormonal and chemotherapeutic agents. Recently, the realization that cancer cells exist in complex microenvironments that are essential for the tumorigenic and metastatic potential of the cancer cells is starting the redefine the paradigm for cancer therapy. The propensity of prostate cancer cells to metastasize to bone is leading to the design of novel therapies targeting both the cancer cell as well as the bone microenvironment. Tumor cells in the bone interact with the extracellular matrix, stromal cells, osteoblasts, osteoclasts, and endothelial cells to promote tumor-cell survival and proliferation leading to a lethal phenotype that includes increased morbidity and mortality for patients with advanced prostate cancer. Several strategies are being developed that target these complex tumor cell–microenvironment interactions and target the signal transduction pathways of other cells important to the development of metastases, including the osteoclasts, osteoblasts, and endothelial cells of the bone microenvironment. Current and new therapies in metastatic prostate cancer will comprise a multitargeted approach aimed at both the tumor cell and the tumor microenvironment. Here, we review the current therapeutic strategies for targeting the prostate cancer–bone microenvironment and several single- and multiagent targeted approaches to the treatment of advanced prostate cancer that are under development.
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Kim, Jaehong. "Regulation of Immune Cell Functions by Metabolic Reprogramming." Journal of Immunology Research 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/8605471.

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Recent findings show that the metabolic status of immune cells can determine immune responses. Metabolic reprogramming between aerobic glycolysis and oxidative phosphorylation, previously speculated as exclusively observable in cancer cells, exists in various types of immune and stromal cells in many different pathological conditions other than cancer. The microenvironments of cancer, obese adipose, and wound-repairing tissues share common features of inflammatory reactions. In addition, the metabolic changes in macrophages and T cells are now regarded as crucial for the functional plasticity of the immune cells and responsible for the progression and regression of many pathological processes, notably cancer. It is possible that metabolic changes in the microenvironment induced by other cellular components are responsible for the functional plasticity of immune cells. This review explores the molecular mechanisms responsible for metabolic reprogramming in macrophages and T cells and also provides a summary of recent updates with regard to the functional modulation of the immune cells by metabolic changes in the microenvironment, notably the tumor microenvironment.
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Garre, Elena, Anna Gustafsson, Maria Carmen Leiva, Joakim Håkansson, Anders Ståhlberg, Anikó Kovács, and Göran Landberg. "Breast Cancer Patient-Derived Scaffolds Can Expose Unique Individual Cancer Progressing Properties of the Cancer Microenvironment Associated with Clinical Characteristics." Cancers 14, no. 9 (April 26, 2022): 2172. http://dx.doi.org/10.3390/cancers14092172.

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Breast cancer is a heterogeneous disease in terms of cellular and structural composition, and besides acquired aggressive properties in the cancer cell population, the surrounding tumor microenvironment can affect disease progression and clinical behaviours. To specifically decode the clinical relevance of the cancer promoting effects of individual tumor microenvironments, we performed a comprehensive test of 110 breast cancer samples using a recently established in vivo-like 3D cell culture platform based on patient-derived scaffolds (PDSs). Cell-free PDSs were recellularized with three breast cancer cell lines and adaptation to the different patient-based microenvironments was monitored by quantitative PCR. Substantial variability in gene expression between individual PDS cultures from different patients was observed, as well as between different cell lines. Interestingly, specific gene expression changes in the PDS cultures were significantly linked to prognostic features and clinical information from the original cancer. This link was even more pronounced when ERα-status of cell lines and PDSs matched. The results support that PDSs cultures, including a cancer cell line of relevant origin, can monitor the activity of the tumor microenvironment and reveal unique information about the malignancy-inducing properties of the individual cancer niche and serve as a future complementary diagnostic tool for breast cancer.
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Leach, Damien, Alison Buxton, Gilberto Serrano de Almeida, Grant Buchanan, and Charlotte Lynne Bevan. "Androgen Activity in the Primary and Metastatic Prostate Cancer Microenvironments Influences Disease Progression and Patient Outcomes." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A1011. http://dx.doi.org/10.1210/jendso/bvab048.2068.

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Abstract Background: Cancers do not exist in isolation, surrounding tumours are supportive cells, which create the microenvironment in which cancer cells reside. In the prostate cancer (PCa), androgen receptor (AR) signalling in the surrounding fibroblasts is strikingly distinct from that within PCa cells, and has specific functions to produce, maintain, and modulate the extracellular matrix (ECM) which surrounds and interacts with PCa cells. The supportive cells of metastatic sites differ from those in the primary site and produce different types of cellular microenvironments. Since the advent of second generation anti-androgen therapy there has been an increase in the presence of liver metastasis. This project investigates how AR and anti-androgen therapy affect the prostate liver microenvironment and the subsequent effects on cancer. Results: Analysis of microenvironment of primary and metastatic sites indicates transcriptional responses distinct from that seen in PCa cells. This is exemplified by proliferation responses to androgen and anti-androgens in microenvironment cells being the reverse to that seen in Pca cells. Dichotomising microdissected PCa patient material of matched cancer and stromal tissue, based on stromal AR level shows distinct transcriptional profiles in the matched cancer cells. From previous studies, we know AR status in cancer adjacent fibroblasts (CAFs) of the primary tumor inversely associates with patient outcomes. Analysis of single cell CAFs and microdissected stromal samples points to a potential sub population of CAFs with this AR status. Conditioned media from liver and prostate fibroblast cells suggests that inactivation of AR signalling produces proliferative paracrine signals that can affect cancer cell growth. AR in primary site fibroblast and liver stellate cells regulates secretome and ECM production in the primary and metastatic site. Prostates and livers from enzalutamide treated mice showed changes in collagen fibres compared to control mice, as visualised by picro-direct-red staining. We cultured PCa cells within 3D-ECM microenvironments created in vitro from prostate fibroblasts or liver cells. The different 3D-ECM were able to produce changes in PCa cells, including gene transcription, intracellular signalling pathways, and proliferation and apoptotic responses. These data suggest that the responses of primary and metastatic microenvironments to androgens and anti-androgens can influence phosphorylation of intracellular pathways leading to alterations in gene transcription. Furthermore, the transcriptional responses of cancer cells in vitro to changes in microenvironmental AR signalling can be used to predict patient outcomes. Conclusions: Our data suggests that anti-AR therapy produces organ microenvironment-specific signals that influence the response of prostate cancer to treatments and affects patient outcomes.
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Dissertations / Theses on the topic "Cancer cell microenvironment"

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YOUSAFZAI, MUHAMMAD SULAIMAN. "Cancer cell mechanics and cell microenvironment: An optical tweezers study." Doctoral thesis, Università degli Studi di Trieste, 2016. http://hdl.handle.net/11368/2908097.

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Since cancer metastasis is a complex process, lot of research has been carried out to identify different hallmarks for its diagnosis and cure. Mechanical alterations in cancer cells during cell spreading to adjacent tissues and other organs of the body emerged as a prominent hallmark in the last decade. In this thesis we employed a mechanistic approach and used stiffness (elasticity) as a marker to study cell’s mechanical response in varying microenvironmental conditions. Cell– microenvironment mechanical interaction is a blend of cell-matrix and cell-cell interactions. Therefore we adopted an approach to study cells in the presence of their neighbouring cells as well as on compliant substrates at small forces (<10pN) using optical tweezers. The elastic modulus was calculated using the Hertz-model. We considered three breast cell lines as model, showing three phases of cancer progression: MDA-MB-231, a highly aggressive cell line belonging to the Basal cell-like phenotype; MCF-7, a less aggressive cancer cell line, belonging to the Luminal A cell-like phenotype; and HBL-100, a non-neoplastic cell line, derived from the milk of a Caucasian woman, normal control for breast basal-myoepithelial cells. Cell elasticity can be locally measured by pulling membrane tethers, stretching or indenting the cell using optical tweezers. We introduce a simple approach to perform cell indentation by axially moving the cell against a trapped microbead. Our scheme is similar to the AFM vertical cell indentation approach and can help to compare the quantitative results and thus complement AFM in a low force regime and loading rates. The elasticity trend of the three cell lines in isolated conditions showed that the aggressive MDA-MB-231 cells are significantly softer as compared to HBL-100 and MCF-7 cells. We demonstrate that stiffness measurements are sensitive to the cellular sub-regions as well as the interacting microenvironment. We probed the cells at three cellular sub regions: central (above nucleus), intermediate (cytoplasm) and near the leading edge. In isolated condition, all cells showed a significant regional variation in stiffness: higher at the center and fading toward the leading edge. However, the regional variation become statistical insignificant when the cells were in contact with other neighboring cells. We found that neighboring cells significantly alter cell stiffness: MDA-MB-231 becomes stiffer when in contact, while HBL-100 and MCF-7 exhibit softer character. Furthermore, we have studied the influence of substrate stiffness on cell elasticity by seeding the cells on Collagen and Polydimethylsiloxane (PDMS) coated substrates with varying stiffnesses to mimic extracellular (ECM) rigidities in vitro. PDMS polymer to crosslinker ratio was adjusted to 15:1, 35:1 and 50:1 corresponds to 173kPa, 88kPa and 17kPa respectively. These results show that cells adapt their stiffness to that of the substrate. Flexible substrates leads to reduced cell spreading morphological changes. Cells on complaint substrates are softer as compared to stiffness substrates. Our results demonstrates that the substrate stiffness influence not only cell spreading and motility, but also cell elasticity. Finally, from the 3D tracking of the bead probe we analyzed the lateral forces arising during the vertical indentation of the cell membrane during cell-bead interaction. We calculated and compared the elastic moduli resulting from the total and vertical forces for two breast cancer cell lines: MDA-MB-231 and HBL-100, showing that the differences are important and the total force should be considered.
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Hodkinson, Philip Simon. "Tumour microenvironment interactions of small cell lung cancer." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4254.

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Small cell lung cancer (SCLC) is characterised by rapid growth, early metastatic spread and poor long-term survival. The tumour is initially sensitive to chemotherapy and thus objective response rates are high. Unfortunately, this response is often short-lived and SCLC recurs with acquired drug resistance, resulting in early patient death. Despite intensive chemo- and radiotherapy regimes survival has not improved significantly in 20 years. Prior research suggests a critical role for the tumour microenvironment in the pathogenesis of other cancers. Therefore, investigating interactions between SCLC cells and components of the tumour stroma may identify novel therapeutic targets. This thesis demonstrates that extracellular matrix (ECM) proteins present in the tumour microenvironment protect SCLC cells in vitro from chemo- and radiotherapy induced cell cycle arrest and apoptosis via cell surface β1 integrins. Pharmacological and genetic inhibition of phosphoinositol-3 kinase signalling abrogates this effect, defining a central role for this pathway in SCLC de novo drug resistance. Furthermore, the protective effect of ECM occurs without alteration in chemotherapy-induced DNA damage allowing SCLC cells to survive with new genetic defects. Integrin-mediated drug resistance has been shown to be important in other tumours and thus development of strategies to inhibit this pathway may yield new anti-cancer treatments. The design of targeted agents to down-regulate integrin-ECM interaction requires an in depth understanding of the intracellular signals that modulate integrin affinity. Two such pathways are investigated in this thesis. 1) H-Ras, a dominant suppressor of integrin affinity, acts in part through phosphorylation of Erk. Data presented here demonstrate that H-Ras also suppresses integrins through a phospholipase-C epsilon (PLCε)-dependent pathway, thus explaining discrepancies in prior data and confirming a physiological role for this recently identified phospholipase. 2) The Notch signalling pathway has been shown to have important roles in both development and cancer. It is shown here that activation of Notch signalling increases β1 integrin affinity and can protect SCLC cells from chemotherapyinduced apoptosis. However the mechanisms appear to be different; Notch-1 modulates integrin activation through the small GTPase R-Ras and Notch-2 promotes SCLC cell survival. These results define a new Notch pathway, a novel integrin modulator and a potential therapeutic target in SCLC cells. In addition to ECM proteins, the tumour microenvironment contains immune cells that may contribute to cancer growth. The cellular composition of the SCLC stroma is poorly understood. The data presented here indicate that the microenvironment of SCLC is infiltrated by lymphocytes and macrophages, the degree of which independently predicts patient survival. This suggests that the host immune system may be able to suppress SCLC growth. It is well recognised that patients with SCLC have defects in cellular immunity which correlate with survival. An in vitro coculture model was used to investigate the underpinning mechanisms, showing SCLC cells can suppress CD4+ T-cell proliferation and macrophage CD86 expression. Furthermore, preliminary data suggest a role for a soluble factor released by SCLC cells that up-regulates CD4+ T-cell production of IL-10. The work in this thesis implies a complex interaction between SCLC cells, ECM and immune cells in the tumour microenvironment. Manipulation of these pathways may have important therapeutic implications. Further investigation is required to understand the mechanisms of this interplay, which may in part be aided by prospective analysis of patient tumour samples and an in vivo model of SCLC.
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Fong, Jenna. "Breast cancer cells affect bone cell differentiation and the bone microenvironment." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104758.

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Breast carcinoma is the most commonly diagnosed cancer among women worldwide, with approximately 1 in 7 expected to be affected during her lifetime. The spread of breast cancer to secondary sites is generally incurable. Bone is the preferred site of metastasis, where the development of a secondary tumour causes severe osteolysis, hypercalcemia and a considerable pain burden. However, how breast cancer cells establish supportive interactions with bone cells is not well understood. We have examined the effects of factors released from MDA-MB-231 and 4T1 breast cancer cells on the differentiation of C57BL6 mouse bone marrow cells. Treatment with cancer-derived factors resulted in a sustained 40–60% decrease in osteoblast differentiation markers, and induced an osteoclastogenic change in the ratio of receptor activator of NF-κB ligand (RANKL) to osteoprotegerin (OPG). Importantly, exposure of bone cells to breast cancer-derived factors stimulated the subsequent attachment of cancer cells to immature osteoblasts. Inhibition of γ-secretase using pharmacological inhibitors DAPT and Compound E completely reversed cancer-induced osteoclastogenesis as well as cancer-induced enhancement of cancer cell attachment, identifying γ-secretase activity as a key mediator of these effects. We next evaluated the effects of breast cancer cells on the energy metabolism of bone cells. Treatment of bone marrow cells with conditioned medium from 4T1 breast cancer cells resulted in an increase in glucose consumption by bone cells, higher mitochondrial transmembrane potential, and a 2.3-fold rise in cellular ATP content. In addition, breast cancer derived factors stimulated the expression of mRNA and protein levels of metabolic sensor, AMP-regulated protein kinase (AMPK). To assess if such change in cell bioenergetics may have consequences for cell differentiation and activity, we used defined models of osteoclastogenesis, and increased precursor metabolic activity by providing excess energy substrates. We have found that an increase in mitochondrial transmembrane potential and cellular ATP levels during osteoclastogenesis resulted in the formation of larger osteoclasts that demonstrate higher resorptive activity. Thus, we have uncovered that osteoblasts act as a critical intermediate of premetastatic signalling by breast cancer cells, and pinpointed γ-secretase as a robust target for developing therapeutics potentially capable of reducing both the homing and progression of cancer metastases to bone. In addition, we have discovered heightened energetics in bone cells exposed to breast cancer cell-released factors, which may contribute to the formation of larger, more active osteoclasts. Modification of the AMPK pathway may prove an important therapeutic target for breast cancer metastasis to bone.
Le cancer du sein est le cancer plus diagnostiqué chez les femmes. On estime qu'environ une femme sur sept en sera affectée. La diffusion du cancer du sein aux emplacements secondaires est généralement incurable. L'os est l'emplacement préféré de la métastase, où le développement d'une tumeur secondaire cause de l'osteolyse, de l'hypercalcemie, et une douleur considérable. Cependant, comment les cellules de cancer du sein établissent des interactions supportifs avec des cellules d'os n'est pas bien compris. Nous avons examiné les effets des facteurs libérés des cellules du cancer du sein MDA-MB-231 et 4T1 sur la différentiation des cellules de moelle de la souris C57BL6. Le traitement avec des facteurs cancer-dérivés a produit une diminution de 40-60% des marqueurs de différentiation d'osteoblast, comparé au traitement par l'acide ascorbique, et a induit un changement osteoclastogenique dans le rapport du RANKL/osteoprotegerin. L'exposition des cellules d'os à des facteurs dérivés du cancer du sein a ensuite stimulé l'attachement des cellules cancéreuses aux osteoblasts non mûrs. L'inhibition du γ-secretase utilisant les inhibiteurs pharmacologiques DAPT et le Compound E a complètement inversé l'osteoclastogenise cancer-induit aussi bien que le perfectionnement cancer-induit de l'attachement de cellules cancéreuses, identifiant l'activité de le γ-secretase comme étant le médiateur principal de ces effets. Nous avons ensuite évalué les effets des cellules cancereuse sur le métabolisme énergétique des cellules d'os. Le traitement des cellules de moelle avec le medium conditionné des cellules du cancer du sein 4T1 a eu comme conséquence une augmentation des mitochondries à haut-potentiel de membrane, une augmentation de 2.3 fois le contenu cellulaire de triphosphate d'adénosine, et une consommation plus rapide du glucose. Ce changement de l'énergétique a été accompagné d'une stimulation d'AMPK dans la protéine et l'ADN messagère. Pour évaluer les effets du statut de haute énergie dans les osteoclasts, nous avons élevé l'énergique des osteoclasts avec du pyruvate de sodium. Cette addition a causée une croissance des osteoclasts, avec des plus grands nucleus, et la résorption de plus de substrat. Ainsi, nous avons découvert l'osteoblast comme étant un intermédiaire clé à la signalisation prémetastatique par des cellules du cancer du sein. Nous avons aussi indiqué le γ-secretase comme cible robuste pour le developpement de thérapeutique potentiellement capable de réduire l'autoguidage et la progression des métastases de cancer à l'os. Additonellement, nous avons découvert l'énergétique intensifiée chez les cellules d'os exposées aux facteurs cellule-libérés par le cancer du sein, qui mène à une osteoclastogenesise plus active et plus importante. La modification de la voie d'AMPK peut s'avérer être une cible thérapeutique importante pour que la métastase de cancer du sein aux os.
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Daukšte, Liene. "Mathematical Modelling of Cancer Cell Population Dynamics." Thesis, University of Canterbury. Mathematics and Statistics, 2012. http://hdl.handle.net/10092/9356.

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Mathematical models, that depict the dynamics of a cancer cell population growing out of the human body (in vitro) in unconstrained microenvironment conditions, are considered in this thesis. Cancer cells in vitro grow and divide much faster than cancer cells in the human body, therefore, the effects of various cancer treatments applied to them can be identified much faster. These cell populations, when not exposed to any cancer treatment, exhibit exponential growth that we refer to as the balanced exponential growth (BEG) state. This observation has led to several effective methods of estimating parameters that thereafter are not required to be determined experimentally. We present derivation of the age-structured model and its theoretical analysis of the existence of the solution. Furthermore, we have obtained the condition for BEG existence using the Perron- Frobenius theorem. Amathematical description of the cell-cycle control is shown for one-compartment and two-compartment populations, where a compartment refers to a cell population consisting of cells that exhibit similar kinetic properties. We have incorporated into our mathematical model the required growing/aging times in each phase of the cell cycle for the biological viability. Moreover, we have derived analytical formulae for vital parameters in cancer research, such as population doubling time, the average cell-cycle age, and the average removal age from all phases, which we argue is the average cell-cycle time of the population. An estimate of the average cell-cycle time is of a particular interest for biologists and clinicians, and for patient survival prognoses as it is considered that short cell-cycle times correlate with poor survival prognoses for patients. Applications of our mathematical model to experimental data have been shown. First, we have derived algebraic expressions to determine the population doubling time from single experimental observation as an alternative to empirically constructed growth curve. This result is applicable to various types of cancer cell lines. One option to extend this model would be to derive the cellcycle time from a single experimental measurement. Second, we have applied our mathematical model to interpret and derive dynamic-depicting parameters of five melanoma cell lines exposed to radiotherapy. The mathematical result suggests there are shortcomings in the experimental methods and provides an insight into the cancer cell population dynamics during post radiotherapy. Finally, a mathematical model depicting a theoretical cancer cell population that comprises two sub-populations with different kinetic properties is presented to describe the transition of a primary culture to a cell line cell population.
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Truong, Danh, Julieann Puleo, Alison Llave, Ghassan Mouneimne, Roger D. Kamm, and Mehdi Nikkhah. "Breast Cancer Cell Invasion into a Three Dimensional Tumor-Stroma Microenvironment." NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/621806.

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In this study, to model 3D chemotactic tumor-stroma invasion in vitro, we developed an innovative microfluidic chip allowing side-by-side positioning of 3D hydrogel-based matrices. We were able to (1) create a dual matrix architecture that extended in a continuous manner, thus allowing invasion from one 3D matrix to another, and (2) establish distinct regions of tumor and stroma cell/ECM compositions, with a clearly demarcated tumor invasion front, thus allowing us to quantitatively analyze progression of cancer cells into the stroma at a tissue or single-cell level. We showed significantly enhanced cancer cell invasion in response to a transient gradient of epidermal growth factor (EGF). 3D tracking at the single-cell level displayed increased migration speed and persistence. Subsequently, we analyzed changes in expression of EGF receptors, cell aspect ratio, and protrusive activity. These findings show the unique ability of our model to quantitatively analyze 3D chemotactic invasion, both globally by tracking the progression of the invasion front, and at the single-cell level by examining changes in cellular behavior and morphology using high-resolution imaging. Taken together, we have shown a novel model recapitulating 3D tumor-stroma interactions for studies of real-time cell invasion and morphological changes within a single platform.
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Giraldo-Castillo, Nicolas. "The Immune Microenvironment in Clear Cell Renal Cell Carcinoma : The heterogeneous immune contextures accompanying CD8+ T cell infiltration in clear cell Renal Cell Carcinoma." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066321/document.

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Dans cette étude, nous avons tenté de décrypter les mécanismes reliant l’augmentation de lymphocytes infiltrant les tumeurs (LIT) T CD8+ et un pronostic clinique défavorable dans le cancer du rein à cellules claires (ccRCC). Pour cela, nous avons déterminé 1) la relation entre le pronostic associé à l'expression d’immune checkpoints et l’infiltrat de cellules dendritiques (DC) et de LT CD8+ et 2) les caractéristiques phénotypiques des LIT T CD8+. L’expression des immune checkpoints a été déterminée par immunohistochimie dans une cohorte de 135 ccRCC. Nous avons constaté que les densités des cellules exprimant CD8, PD-1 et LAG-3 sont corrélées, et associées à une diminution de PFS et OS. Egalement, les patients dont les tumeurs présentent des densités élevées de cellules PD-1+ et PD-L1 et/ou PD-L2 +, ont le taux de survie le plus faible. Des densités élevées de DC immatures isolées dans le stroma tumoral sont associées à une forte expression d’immune checkpoints et à un faible taux de survie chez ces patients. En revanche, les patients présentant un taux de survie prolongé ont une densité élevée de lymphocytes CD8+, des DC matures au sein de structures lymphoïdes tertiaires, ainsi qu’une faible expression d’immune checkpoints. Nous avons analysé les LIT T CD8+ chez 21 patients ccRCC par Cytométrie de Flux. On a trouvé un groupe de patients (8/21) dont les tumeurs sont caractérisées par la surexpression de marqueurs inhibiteurs (PD1 et TIM3) et de d'activation (CD69 et CD38), par l'expansion des cellules T CD8 + mémoires effectrices et un plus grand potentiel d’agressivité. En résumé, nous avons démontré qu’une densité élevée de LIT T CD8+ dans les ccRCC est accompagnée d’une forte expression d’immune checkpoints et d’une réponse immunitaire mal coordonnée dans un sous-groupe de tumeurs agressives
To decipher the potential mechanisms linking increased CD8+ T cell infiltration with an adverse clinical outcome in ccRCC, in this study we determined: 1) the prognosis associated with the expression of immune checkpoints and its coordination with dendritic cell (DC) and CD8+ cell infiltration, and 2) the phenotypic traits of CD8+ tumor infiltrating lymphocytes. The prognosis associated with CD8+ and DC infiltrations, in addition to the expression of immune checkpoints were investigated in a cohort of 135 ccRCC by quantitative immunohistochemistry. We found that the densities of CD8+, PD-1+ and LAG-3+ cells were closely correlated, and independently associated with decreased PFS and OS. In addition, patients whose tumors presented both high densities of PD-1+ cells and PD-L1+ and/or L2+ tumor cells, displayed the worst clinical outcome. High densities of immature DC isolated in the tumour stroma were associated with high expression of immune checkpoints and patients’ poor clinical outcome. In contrast, the presence of mature DC within Tertiary Lymphoid Structures identified, among the tumours with high CD8+-TIL densities, those with low expression of immune checkpoints and prolonged survival. We also investigated the phenotype of freshly isolated CD8+TIL in 21 ccRCC by flow cytometry. We found a group tumors (8/21) characterised by the over-expression of inhibitory (PD-1 and TIM-3) and activation markers (CD69 and CD38), the expansion of the effector memory cell subpopulation (CCR7-CD45RA-), and a trend toward more aggressive features. In summary, we demonstrated that the infiltration with CD8+ TIL in ccRCC is accompanied by the enhanced expression of immune checkpoints and a poorly coordinated immune response in a subgroup of aggressive tumors
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Xing, Fei. "ROLE OF NOTCH SIGNALING IN BREAST CANCER METASTASIS." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/514.

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Notch signaling is often and aberrantly activated by hypoxia during tumor progression; however, the exact pathological role of hypoxia-induced Notch signaling in tumor metastasis is as yet poorly understood. In the first part of this study, we aimed to define the mechanism of Notch ligand activation by hypoxia in both primary tumor and bone stromal cells in the metastatic niche and to clarify their roles in tumor progression. We have analyzed the expression profiles of various Notch liagnds in 779 breast cancer patients in GEO database and found that the expression of Jagged2 among all five ligands is most significantly correlated with the overall- and metastasis-free survival of breast cancer patients. The results of our immunohistochemical (IHC) analysis for Jagged2 in 61 clinical samples also revealed that both Jagged2 and Notch signaling were strongly up-regulated at the hypoxic invasive front. Activation of Jagged2 by hypoxia in tumor cells induced EMT and also promoted cell survival in vitro. Notably, a ã-secretase inhibitor significantly blocked Notch-mediated invasion and survival under hypoxia by promoting expression of E-cadherin and inhibiting Akt phosphorylation. Importantly, Jagged2 was also found to be up-regulated in bone marrow stroma under hypoxia and promoted the growth of cancer stem-like cells by activating their Notch signaling. Therefore, hypoxia-induced Jagged2 activation in both tumor invasive front and normal bone stroma plays a critical role in tumor progression and metastasis, and Jagged2 is considered to be a valuable prognostic marker and may serve as a novel therapeutic target for metastatic breast cancer. In the second part of this study, the role of Notch signaling in brain metastasis was investigated. Metastatic diseases are responsible for the majority of the deaths in breast cancer patients and the brain is one of the most common metastatic sites. The metastatic tumor in the brain profoundly affects the cognitive and sensory functions as well as morbidity of patients, and the one year survival rate among these patients remains less than 20%. However, the pathological mechanism of brain metastasis is as yet poorly understood. In this report, we found that metastatic breast tumor cells in the brain highly expressed IL-1â which can "activate" astrocytes. This activation significantly augmented the expression of JAG1 in the reactive astrocytes, which in turn activated Notch signaling pathway of cancer stem-like cells (CSCs) upon direct interaction. We also found that the activated Notch signaling in CSCs up-regulated Sox2 followed by promoting self-renewal of CSCs. Furthermore, we have shown that the blood-brain barrier permeable Notch inhibitor, Compound E, can significantly suppress the brain metastasis growth in our animal model. These results represent a novel paradigm for the understanding of how metastatic breast CSCs re-establish their niche for their self-renewal in a totally different microenvironment, which opens a new avenue to identify a novel and specific target for the brain metastatic disease
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Kaira, Mustapha. "In situ molecular profilling of the microenvironment of breast carcinoma." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-265258.

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High stromal PDGF receptor B expression was shown to have strong prognostic value in a studyinvolving over 600 breast cancer patients however, the molecular role of the receptor in tumordevelopment remains unclear. In this project we studied the spatial distribution and expressionlevels of a panel genes and markers associated with PDGF signaling, in breast cancer tumormicroenvironment (TME) using a newly developed technique -in situ sequencing. The techniquerelies on padlock probes which we validated with corresponding RNA sequencing, microarray,and immunohistochemistry data. Our results showed that high PDGF receptor B mRNA colocalizedwith markers of two pathways, TGFβ and Hedgehog signaling; this suggests that theymight contribute to the PDGF-receptor B-driven tumor growth. We also showed that stromalPDGF signaling is stimulated predominantly by tumor cells. Finally, further expression profilingof each individual gene revealed that CXCL14 was mainly expressed in the stroma, ACTA2expression was enriched in the tumor/stroma boundary while the stem-cell marker, OCT3, wasexpressed in the interior of the tumor cells.
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Kiyasu, Yoshiyuki. "Disruption of CCR1-mediated myeloid cell accumulation suppresses colorectal cancer progression in mice." Kyoto University, 2020. http://hdl.handle.net/2433/259008.

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Sundquist, E. (Elias). "The role of tumor microenvironment on oral tongue cancer invasion and prognosis." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526217659.

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Abstract Oral tongue squamous cell carcinoma (OTSCC) is the most common cancer of the oral cavity. The 5-year mortality of OTSCC remains at about 50%. The tumor microenvironment (TME) is now recognized as an important factor in cancer progression and metastasis, as well as a tool for prognostication. The aim of this study was to elucidate the roles of TME hypoxia and soluble factors on cancer cell migration and invasion, and the prognostic value of two extracellular matrix (ECM) molecules: tenascin-C (TNC) and fibronectin (FN). Hypoxia was studied using oral squamous cell carcinoma cells in migration and invasion assays. Invasion assays were carried out using a 3D-myoma invasion method. Similarly, the effect of soluble factors as well as ECM alterations were studied using the myoma model: the effect of soluble factors was studied by rinsing the myoma discs prior to experiments, and ECM alterations by lyophilizing and rehydrating. ECM was further studied by analyzing the prognostic value of TNC and FN from OTSCC samples. The effect of hypoxia was shown to be OTSCC cell line dependent: the effect of hypoxia on migration and invasion was increased in aggressive cell lines. Additionally, the response to hypoxia was altered in rinsed tissue. Tissue rinsing media were analyzed and factors affecting cell motility were found. The TME was found to be pivotal for cancer invasion: invasion was impaired in non-neoplastic tissue. Furthermore, changes in the ECM by lyophilization and rehydration led to a change in the invasion mechanism. High expression of stromal TNC and FN were excellent prognosticators in early-stage OTSCC. In conclusion, the present study highlighted the role of various TME components in cancer cell invasion as well as prognostication in OTSCC. Additionally, this study provided feasible tools for more precise diagnosis of early-stage OTSCC
Tiivistelmä Liikkuvan kielen levyepiteelikarsinooma (OTSCC) on suuontelon yleisin syöpä. Viiden vuoden kuolleisuus OTSCC:an on edelleen noin 50 %. Kasvaimen mikroympäristön (TME) tiedetään nykyään olevan tärkeässä roolissa syövän kehityksessä ja etäpesäkkeiden muodostuksessa, sekä tarjoavan työkaluja ennusteiden laadintaan. Tämän tutkimuksen tarkoituksena oli selvittää TME:n hypoksian ja liukoisten tekijöiden vaikutusta syöpäsolujen liikkumiseen ja invaasioon ympäröivään kudokseen, sekä tutkia kahden solunulkoisen matriksin (ECM) proteiinin, tenaskiini-C:n (TNC) ja fibronektiinin (FN), vaikutusta OTSCC:n ennusteeseen. Hypoksian vaikutusta tutkittiin käyttäen suun levyepiteelikarsinoomasoluja liikkuvuus- ja invaasiokokeissa. Invaasiokokeissa hyödynnettiin kolmiulotteista ihmisen myoomaan perustuvaa invaasiomallia. Myös liukoisten tekijöiden ja ECM:n muutosten vaikutusten tutkimisessa käytettiin myoomamallia: liukoisten tekijöiden vaikutusta tutkittiin huuhtomalla myoomakiekot ennen niiden käyttämistä, ja ECM:n muutosten vaikutusta kylmäkuivaamalla ja uudelleen nesteyttämällä myoomakiekot. ECM:ia tutkittiin myös analysoimalla TNC:n ja FN:n värjäytyvyyden merkitystä OTSCC:n ennusteessa. Hypoksian vaikutus osoittautui solulinjariippuvaiseksi: hypoksia lisäsi kielisyöpäsolujen liikkuvuutta ja invaasiota eniten aggressiivisimmilla solulinjoilla. Lisäksi solujen vaste hypoksialle oli erilainen huuhdotussa kudoksessa. Huuhteluliuos analysoitiin ja siitä löydettiin solujen liikkumiseen vaikuttavia tekijöitä. TME:n havaittiin olevan ratkaisevassa roolissa syöpäsolujen invaasiossa: syöpäsolut eivät kyenneet invasoitumaan lainkaan ei-neoplastiseen kudokseen. Lisäksi muutosten ECM:ssä havaittiin johtavan muutoksiin solujen käyttämässä invaasion mekanismissa. Strooman TNC:n ja FN:n värjäytyvyyden todettiin olevan erinomaisia ennustekijöitä aikaisen vaiheen OTSCC:ssa. Tiivistettynä voidaan todeta, että tämä tutkimus alleviivasi useiden TME:n komponenttien vaikutusta syövän invaasiolle ja ennusteelle OTSCC:ssä. Lisäksi se tarjoaa käyttökelpoiset työkalut (TNC ja FN) tarkemmalle diagnostiikalle aikaisen vaiheen OTSCC:ssä
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Books on the topic "Cancer cell microenvironment"

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Prasad, Mayuri Sinha, Pranela Rameshwar, and Cristian Pablo Pennisi. The Stem Cell Microenvironment and Its Role in Regenerative Medicine and Cancer Pathogenesis. New York: River Publishers, 2022. http://dx.doi.org/10.1201/9781003339779.

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Jamie, Goode, Chadwick Derek, Novartis Foundation, and Symposium on the Tumour Microenvironment: Causes and Consequences of Hypoxia and Acidity (2000 : London, England), eds. The tumour microenvironment: Causes and consequences of hypoxia and acidity. Chichester: Wiley, 2001.

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Gianfranco, Fiorentini, Cogle Christopher R, and SpringerLink (Online service), eds. Cancer Microenvironment and Therapeutic Implications: Tumor Pathophysiology Mechanisms and Therapeutic Strategies. Dordrecht: Springer Netherlands, 2009.

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Siemann, Dietmar W. Tumor Microenvironment. Wiley & Sons, Incorporated, John, 2011.

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Siemann, Dietmar W. Tumor Microenvironment. Wiley & Sons, Incorporated, John, 2011.

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Siemann, Dietmar W. Tumor Microenvironment. Wiley & Sons, Incorporated, John, 2010.

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Tumor microenvironment. Hoboken: Wiley, 2011.

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Physics of Cancer. Cambridge University Press, 2017.

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Zapperi, Stefano, and Caterina A. M. La Porta. Physics of Cancer. Cambridge University Press, 2017.

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Zapperi, Stefano, and Caterina A. M. La Porta. Physics of Cancer. Cambridge University Press, 2017.

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Book chapters on the topic "Cancer cell microenvironment"

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Zucker, Stanley, and Jian Cao. "Matrix Metalloproteinases and Cancer Cell Invasion/Metastasis." In The Tumor Microenvironment, 531–54. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6615-5_25.

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Enders, Greg H. "Ink4a Locus: Beyond Cell Cycle." In Cancer Genome and Tumor Microenvironment, 217–29. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_10.

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Sazeides, Christos, and Anne Le. "Metabolic Relationship Between Cancer-Associated Fibroblasts and Cancer Cells." In The Heterogeneity of Cancer Metabolism, 189–204. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_14.

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AbstractCancer-associated fibroblasts (CAFs), a major component of the tumor microenvironment (TME), play an important role in cancer initiation, progression, and metastasis. Recent findings have demonstrated that the TME not only provides physical support for cancer cells but also directs cell-to-cell interactions (in this case, the interaction between cancer cells and CAFs). As cancer progresses, the CAFs also coevolve, transitioning from an inactivated state to an activated state. The elucidation and understanding of the interaction between cancer cells and CAFs will pave the way for new cancer therapies [1–3].
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Jung, Jin G., and Anne Le. "Metabolism of Immune Cells in the Tumor Microenvironment." In The Heterogeneity of Cancer Metabolism, 173–85. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_13.

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AbstractThe tumor microenvironment (TME) is a complex biological structure surrounding tumor cells and includes blood vessels, immune cells, fibroblasts, adipocytes, and extracellular matrix (ECM) [1, 2]. These heterogeneous surrounding structures provide nutrients, metabolites, and signaling molecules to provide a cancer-friendly environment. The metabolic interplay between immune cells and cancer cells in the TME is a key feature not only for understanding tumor biology but also for discovering cancer cells’ vulnerability. As cancer immunotherapy to treat cancer patients and the use of metabolomics technologies become more and more common [3], the importance of the interplay between cancer cells and immune cells in the TME is emerging with respect to not only cell-to-cell interactions but also metabolic pathways. This interaction between immune cells and cancer cells is a complex and dynamic process in which immune cells act as a determinant factor of cancer cells’ fate and vice versa. In this chapter, we provide an overview of the metabolic interplay between immune cells and cancer cells and discuss the therapeutic opportunities as a result of this interplay in order to define targets for cancer treatment. It is important to understand and identify therapeutic targets that interrupt this cancerpromoting relationship between cancer cells and the surrounding immune cells, allowing for maximum efficacy of immune checkpoint inhibitors as well as other genetic and cellular therapies.
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Bennani, N. Nora, and Stephen M. Ansell. "Tumor Microenvironment in T-Cell Lymphomas." In Cancer Treatment and Research, 69–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99716-2_3.

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Alvarez-Silva, Marcio. "Stem Cell Niche and Microenvironment." In Principles of Stem Cell Biology and Cancer, 45–64. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118670613.ch3.

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Wilke, Cailin Moira, Shuang Wei, Lin Wang, Ilona Kryczek, Jingyuan Fang, Guobin Wang, and Weiping Zou. "T Cell and Antigen-Presenting Cell Subsets in the Tumor Microenvironment." In Cancer Immunotherapy, 17–44. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4732-0_2.

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Colombatti, Alfonso, Carla Danussi, Eliana Pivetta, and Paola Spessotto. "Cancer Stem Cells and the Microenvironment." In Advances in Cancer Stem Cell Biology, 69–84. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0809-3_5.

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Brady, Donita C., Jamie K. Alan, and Adrienne D. Cox. "Rho GTPases in Regulation of Cancer Cell Motility, Invasion, and Microenvironment." In Cancer Genome and Tumor Microenvironment, 67–91. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_4.

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Crespo, Joel, Ilona Kryczek, Theodore Welling, Shuang Wei, and Weiping Zou. "T Cell Fate in the Tumor Microenvironment." In Cancer Drug Discovery and Development, 53–74. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21167-1_3.

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Conference papers on the topic "Cancer cell microenvironment"

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Kim, Taeyeon, Jisung Kwak, Yeeun Roh, Sang Jun Sim, Hyun Seok Song, and Minah Seo. "Spectroscopic Analysis of Live Cancer Cell Microenvironment with Terahertz Metasurface Biosensing Platform." In 2024 49th International Conference on Infrared, Millimeter, and Terahertz Waves (IRMMW-THz), 1–2. IEEE, 2024. http://dx.doi.org/10.1109/irmmw-thz60956.2024.10697664.

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Gileva, M. S., E. G. Ufimceva, L. F. Gulyaeva, and V. V. Kozlov. "EX VIVO CHARACTERISTICS OF NON-SMALL CELL LUNG CANCER CELLS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-308.

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The search for molecular markers for the identification of adenocarcinoma and squamous cell lung cancer remains an urgent problem. In this work, for the first time, an ex vivo method was used to isolate cells from tissue samples of patients with non-small cell lung cancer. Potential markers of this histological tumor type were analyzed, and the cellular composition of the immune microenvironment was also assessed, including depending on the smoking status of patients.
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Dereli-Korkut, Zeynep, and Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.

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We developed a functional high throughput 3D microfluidic living cell array (MLC) for anti-cancer drug screening and mechanism discovery. Contemporary drug screening methods suffer from low sample throughput and lack of abilities of mimicking the 3D microenvironment of mammalian tissues. The poor performance of anti-cancer drugs limits the efficacy at controlling the complex disease system like cancer. Systematic studies of apoptotic signaling pathways can be prominent approaches for searching active and effective treatments with less drug resistance. Hence, innovative bio-devices are needed to represent tumor microenvironment to understand the molecular signatures of apoptosis for testing new anticancer therapies targeting apoptosis. Our novel 3D MLC design is the prototype of a high-throughput drug screening platform targeting apoptotic signaling pathways.
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Musulin, Jelena, Daniel Štifanić, Ana Zulijani, and Zlatan Car. "SEMANTIC SEGMENTATION OF ORAL SQUAMOUS CELL CARCINOMA ON EPITHELLIAL AND STROMAL TISSUE." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.194m.

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Oral cancer (OC) is among the top ten cancers worlwide, with more than 90% being squamous cell carcinoma. Despite diagnostic and therapeutic development in OC patients’ mortality and morbidity rates remain high with no advancement in the last 50 years. Development of diagnostic tools in identifying pre-cancer lesions and detecting early-stage OC might contribute to minimal invasive treatment/surgery therapy, improving prognosis and survival rates, and maintaining a high quality of life of patients. For this reason, Artificial Intelligence (AI) algorithms are widely used as a computational aid in tumor classification and segmentation to help clinicians in the earlier discovery of cancer and better monitoring of oral lesions. In this paper, we propose an AI-based system for automatic segmentation of the epithelial and stromal tissue from oral histopathological images in order to assist clinicians in discovering new informative features. In terms of semantic segmentation, the proposed AI system based on preprocessing methods and deep convolutional neural networks produced satisfactory results, with 0.878 ± 0.027 mIOU and 0.955 ± 0.014 F1 score. The obtained results show that the proposed AI-based system has a great potential in diagnosing oral squamous cell carcinoma, therefore, this paper is the first step towards analysing the tumor microenvironment, specifically segmentation of the microenvironment cells.
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Levina, Vera V., Adele Marrangoni, Elieser Gorelik, Robert Edwards, and Anna Lokshin. "Abstract 3408: Ovarian cancer stem cell cytokine microenvironment." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3408.

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Manandhar, Sarala, Chang-gu Kim, Su Young Oh, Sun-Hee Lee, Jiyoon Seok, Yuk-Dong Jung, Hye-Eun Lee, Young-Sun Choi, and You Mie* Lee. "Abstract B21: Exostosin 1 regulates cancer cell stemness in breast cancer cells." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-b21.

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Camargo, Luana Cristina, Joao Paulo Figueiro Longo, Karen Letycia Rodrigues de Paiva, Marina Mesquita Simões, Thais Bergmann, and Victor Carlos Mello da Silva. "Immunotherapy vaccines for triple-negative breast cancer and its influence on the tumor microenvironment." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1024.

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Objective: Cancer is still a complex and debilitating disease even though advances in treatment have occurred. Triplenegative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor prognosis and occurs more frequently in young women. Due to its metastatic features and unique tumor microenvironment, TNBC treatment is limited. In this study, we evaluated how three chemotherapy drugs could be used to produce vaccines with cells under immunogenic cell death. Methodology: For that, 4T1-luc2 cells were treated with cisplatin (100 μM), mitoxantrone (MTX) (15 μM), and doxorubicin (DOX) (50 μM) for 24 h. Then, the treated cells were injected subcutaneously in tumor-bearing Balb/c female mice, after the tumor challenge. The treatment occurred three times, once a week. During and after the treatment, primary tumor and metastatic progression were followed using the chemiluminescence technique. After 5 weeks of the tumor challenge, mice were euthanized and organs (liver, tumor, lungs, and spleen) were collected for analysis. Additionally, the spleens were processed for flow cytometry for regulatory T lymphocyte and myeloid-derived suppressor cells analysis. Results: Cisplatin and MTX vaccines slowed the primary and metastatic tumor growth as well as the decreased tumor, liver, and spleen weight, while the DOX vaccine slowed the metastatic tumor progression in the lungs but did not alter tumor and other organs’ weight. Moreover, cisplatin and MTX vaccine increased the ratio of lymphocytes in the spleen but not the DOX vaccine. All comparison was done regarding the tumor-bearing mice treated with PBS. Conclusion: Taken together, both MTX and cisplatin vaccines treated primary and secondary tumors probably by the increase of lymphocyte recruitment, and the cisplatin vaccine also has an influence on the tumor microenvironment. Finally, the therapeutical vaccine might be an interesting approach as a treatment for TNBC due to its positive effect on metastasis and tumor microenvironment, especially with cisplatin.
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Tang, Xin, Tony Cappa, Theresa B. Kuhlenschmidt, Mark S. Kuhlenschmidt, and Taher A. Saif. "Studying the Mechanical Sensitivity of Human Colon Cancer Cells Through a Novel Bio-MEMS Force Sensor." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13237.

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Cancer deaths are primarily caused by metastases, not by the parent tumor. During the metastasis, malignant cancer cells detach from the parent tumor, and spread through the patient’s circulatory system to invade new tissues and organs [1]. To study the role played by the mechanical microenvironment on the cancer cell growth and malignancy promotion, we cultured human colon carcinoma (HCT-8) cells in vitro on substrates with varied mechanical stiffness, from the physiologically relevant 1 kPa, 20 kPa to very stiff 3.5 GPa. A novel and versatile micro-electromechanical systems (Bio-MEMS) force sensor [2] is developed to quantify the strength of non-specific adhesion between living cancer cells membrane and probe, an important hallmark of cancer cell malignancy level. Immunoflurescent staining and Confocal microscopy imaging are used to visualize the cellular organelle organization and cooperate to explore the underlying mechanism.
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Abdurakhmanova, M. M., A. A. Leontieva, A. A. Yurina, T. N. Belovezhets, S. V. Kulemzin, E. V. Kuligina, V. A. Richter, and A. A. Nushtaeva. "INFLUENCE OF IL-15 AND TGFΒ ON THE PHENOTYPE OF NK CELLS WITHIN THE 3D-MODEL OF BREAST CANCER." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-284.

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NK-cell immunotherapy is a promising approach for the treatment of solid tumors. When developing such an approach, the tumor microenvironment must be taken into account. 3D cell models, represent a physiologically relevant model to evaluate the efficacy of immunotherapy in vitro. The aim of the study: to evaluate the phenotype transformation of primary NK cells derived from a healthy donor in 3D models of breast cancer upon IL-15 or TGFβ stimulation.
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Correia, Ana Luisa. "Abstract PO005: Hepatic stellate cells suppress NK cell sustained breast cancer dormancy." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-po005.

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Reports on the topic "Cancer cell microenvironment"

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Gordon, Ryan R. Identification of Cell Nonautonomous DNA Damage Responses in the Tumor Microenvironment that Contribute to Cancer Therapy Resistance. Fort Belvoir, VA: Defense Technical Information Center, March 2013. http://dx.doi.org/10.21236/ada577632.

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Gordon, Ryan R. Identification of Cell Nonautonomous DNA Damage Responses in the Tumor Microenvironment that Contribute to Cancer Therapy Resistance. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada601305.

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Mastro, Andrea M. Altering the Microenvironment to Promote Dormancy of Metastatic Breast Cancer Cell in a 3D Bone Culture System. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada604844.

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Mastro, Andrea M., and Erwin Vogler. Altering the Microenvironment to Promote Dormancy of Metastatic Breast Cancer Cell in a 3D Bone Culture System. Fort Belvoir, VA: Defense Technical Information Center, April 2015. http://dx.doi.org/10.21236/ada621382.

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Ouyang, Zhiqiang, Qian Li, Guangrong Zheng, Tengfei Ke, Jun Yang, and Chengde Liao. Radiomics for predicting tumor microenvironment phenotypes in non-small cell lung cance: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0060.

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Review question / Objective: Tumor microenvironment (TIME) phenotype is an important factor to affect the response and prognosis of immunotherapy in non-small cell lung cancer (NSCLC). Recently, accumulating studies have noninvasivly perdited the TIME phenotypes of NSCLC by using CT or PET/CT based radiomics. We will conduct this study by means of meta-analysis to eveluate the power and value of CT or PET/CT based radiomics for predicting TIME phenotypes in NSCLC patients. Condition being studied: At present, several recent prospective or retrospective cohort studies and randomized controlled studies have confirmed that CT or PET/CT-based radiomics were the potential tools to predict TIME phenotypes in NSCLC. However, this conclusion is controversial because of the difference of prediction profermance of different studies. The published and unpublished investigations will be included in this study. We will comprehensively evaluate the heterogeneity of these investigations, and the power and value of radiomics for predicting TIME phenotypes.
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She, Jingyao, Yue Chen, Chunyun Liang, Tong Chu, Jing Yu, and Peijuan Wang. Evaluating the Synergistic Impact of PD-1/PD-L1 Blockade and Platinum-Based Chemotherapy in Modulating the Tumor Microenvironment for Enhanced T Cell-Mediated Immune Responses in Advanced Endometrial Cancer: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2024. http://dx.doi.org/10.37766/inplasy2024.9.0121.

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Tang, Dean G. Microenvironment-Programmed Metastatic Prostate Cancer Stem Cells (mPCSCs). Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613324.

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Luo, Yunping, and Ralph A. Reisfeld. Priming the Tumor Immune Microenvironment Improves Immune Surveillance of Cancer Stem Cells and Prevents Cancer Recurrence. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada574527.

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Reisfeld, Ralph R., Debbie Liao, and Yunping Luo. Priming the Tumor Immune Microenvironment Improves Immune Surveillance of Cancer Stem Cells and Prevents Cancer Recurrence. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada553886.

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Lee Sohn, Lydia. Using 3D Super-Resolution Microscopy to Probe Breast Cancer Stem Cells and Their Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada609488.

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