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Start Over Descriptor "stroma cell" Topic tumor microenvironment
7 results on '"stroma cell"'

1. Tumor microenvironment complexity and therapeutic implications at a glance.

Author

Baghban R, Roshangar L, Jahanban-Esfahlan R, Seidi K, Ebrahimi-Kalan A, Jaymand M, Kolahian S, Javaheri T, and Zare P

Subjects
Animals, Humans, Neoplasms metabolism, Stromal Cells cytology, Carcinogenesis metabolism, Cell Communication, Extracellular Matrix metabolism, Stromal Cells metabolism, Tumor Microenvironment
Abstract

The dynamic interactions of cancer cells with their microenvironment consisting of stromal cells (cellular part) and extracellular matrix (ECM) components (non-cellular) is essential to stimulate the heterogeneity of cancer cell, clonal evolution and to increase the multidrug resistance ending in cancer cell progression and metastasis. The reciprocal cell-cell/ECM interaction and tumor cell hijacking of non-malignant cells force stromal cells to lose their function and acquire new phenotypes that promote development and invasion of tumor cells. Understanding the underlying cellular and molecular mechanisms governing these interactions can be used as a novel strategy to indirectly disrupt cancer cell interplay and contribute to the development of efficient and safe therapeutic strategies to fight cancer. Furthermore, the tumor-derived circulating materials can also be used as cancer diagnostic tools to precisely predict and monitor the outcome of therapy. This review evaluates such potentials in various advanced cancer models, with a focus on 3D systems as well as lab-on-chip devices. Video abstract.

Published
2020
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2. Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms.

Author

Dumontet, Erwan, Mancini, Stéphane J. C., and Tarte, Karin

Subjects
DIFFUSE large B-cell lymphomas, B cells, BONE marrow, DRUG resistance in cancer cells, CANCER cells
Abstract

B-cell non-Hodgkin lymphoma (B-NHL) evolution and treatment are complicated by a high prevalence of relapses primarily due to the ability of malignant B cells to interact with tumor-supportive lymph node (LN) and bone marrow (BM) microenvironments. In particular, progressive alterations of BM stromal cells sustain the survival, proliferation, and drug resistance of tumor B cells during diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and chronic lymphocytic leukemia (CLL). The current review describes how the crosstalk between BM stromal cells and lymphoma tumor cells triggers the establishment of the tumor supportive niche. DLBCL, FL, and CLL display distinct patterns of BM involvement, but in each case tumor-infiltrating stromal cells, corresponding to cancer-associated fibroblasts, exhibit specific phenotypic and functional features promoting the recruitment, adhesion, and survival of tumor cells. Tumor cell-derived extracellular vesicles have been recently proposed as playing a central role in triggering initial induction of tumor-supportive niches, notably within the BM. Finally, the disruption of the BM stroma reprogramming emerges as a promising therapeutic option in B-cell lymphomas. Targeting the crosstalk between BM stromal cells and malignant B cells, either through the inhibition of stroma-derived B-cell growth factors or through the mobilization of clonal B cells outside their supportive BM niche, should in particular be further evaluated as a way to avoid relapses by abrogating resistance niches. [ABSTRACT FROM AUTHOR]

Published
2021
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3. Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms

Author

Erwan Dumontet, Stéphane J. C. Mancini, and Karin Tarte

Subjects
B-cell non-Hodgkin lymphomas, cancer-associated fibroblasts, extracellular vesicles, tumor microenvironment, stroma cell, Immunologic diseases. Allergy, RC581-607
Abstract

B-cell non-Hodgkin lymphoma (B-NHL) evolution and treatment are complicated by a high prevalence of relapses primarily due to the ability of malignant B cells to interact with tumor-supportive lymph node (LN) and bone marrow (BM) microenvironments. In particular, progressive alterations of BM stromal cells sustain the survival, proliferation, and drug resistance of tumor B cells during diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and chronic lymphocytic leukemia (CLL). The current review describes how the crosstalk between BM stromal cells and lymphoma tumor cells triggers the establishment of the tumor supportive niche. DLBCL, FL, and CLL display distinct patterns of BM involvement, but in each case tumor-infiltrating stromal cells, corresponding to cancer-associated fibroblasts, exhibit specific phenotypic and functional features promoting the recruitment, adhesion, and survival of tumor cells. Tumor cell-derived extracellular vesicles have been recently proposed as playing a central role in triggering initial induction of tumor-supportive niches, notably within the BM. Finally, the disruption of the BM stroma reprogramming emerges as a promising therapeutic option in B-cell lymphomas. Targeting the crosstalk between BM stromal cells and malignant B cells, either through the inhibition of stroma-derived B-cell growth factors or through the mobilization of clonal B cells outside their supportive BM niche, should in particular be further evaluated as a way to avoid relapses by abrogating resistance niches.

Published
2021
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4. Sonic-hedgehog pathway inhibition normalizes desmoplastic tumor microenvironment to improve chemo- and nanotherapy

Author

Mpekris, F., Papageorgis, P., Polydorou, C., Voutouri, C., Kalli, M., Pirentis, A. P., Stylianopoulos, T., and Stylianopoulos, T. [0000-0002-3093-1696]

Subjects
Male, Pancreatic cancers, Pathology, Pyridines, medicine.medical_treatment, Diseases, fibroblast, Polyethylene Glycols, sonic hedgehog protein, Mice, Breast cancer, primary tumor, analogs and derivatives, 0302 clinical medicine, Mice, Inbred NOD, Antineoplastic Combined Chemotherapy Protocols, vismodegib, drug delivery system, Medicine, Enzyme activity, Sonic hedgehog, Tumor, pancreatic cancer cell line, gemcitabine, Hedgehog signaling pathway, 3. Good health, Nanomedicine, priority journal, Tumor microenvironment, 030220 oncology & carcinogenesis, Collagen, medicine.medical_specialty, Tumor perfusion, Hyaluronic acid, Sonic hedgehogs, Re-engineering cancer, Vismodegib, Antineoplastic Agents, pyridine derivative, anilide, SCID, doxorubicin, Article, pancreas tumor, animal tissue, 03 medical and health sciences, Pancreatic cancer, cancer combination chemotherapy, Humans, human, mouse, antagonists and inhibitors, Tumors, human cell, animal model, intracellular signaling, Fluid stress, Fibroblasts, medicine.disease, drug efficacy, Pancreatic Neoplasms, cell proliferation, 030104 developmental biology, tumor volume, Nanoparticles, Inbred NOD, Albumin-Bound Paclitaxel, hydraulic conductivity, Medical nanotechnology, 0301 basic medicine, transcription factor Gli1, transcription factor Gli2, Pharmaceutical Science, Mice, SCID, paclitaxel, Drug Delivery Systems, Blood vessels, Tumor Microenvironment, animal, Anilides, macrogol derivative, Extracellular matrices, antineoplastic agent, biology, breast tumor, nanoparticle, Extracellular Matrix, Enzyme inhibition, female, stroma cell, Female, medicine.drug, extracellular matrix, animal experiment, Breast Neoplasms, Cell Line, tissue pressure, male, Cell Line, Tumor, Chemotherapy, Animals, Young modulus, SCID mouse, controlled study, Hedgehog Proteins, drug screening, nonhuman, business.industry, nonobese diabetic mouse, tumor cell line, Cancer, Xenograft Model Antitumor Assays, tumor xenograft, pancreas adenocarcinoma, cancer associated fibroblast, Mechanical force, Doxorubicin, Drug delivery, Cancer research, biology.protein, pathology, Ki 67 antigen, Cell culture, alpha smooth muscle actin, business, metabolism
Abstract

Targeting the rich extracellular matrix of desmoplastic tumors has been successfully shown to normalize collagen and hyaluronan levels and re-engineer intratumoral mechanical forces, improving tumor perfusion and chemotherapy. As far as targeting the abundant cancer-associated fibroblasts (CAFs) in desmoplastic tumors is concerned, while both pharmacologic inhibition of the sonic-hedgehog pathway and genetic depletion of fibroblasts have been employed in pancreatic cancers, the results between the two methods have been contradictory. In this study, we employed vismodegib to inhibit the sonic-hedgehog pathway with the aim to i) elucidate the mechanism of how CAFs depletion improves drug delivery, ii) extent and evaluate the potential use of sonic-hedgehog inhibitors to breast cancers, and iii) investigate whether sonic-hedgehog inhibition improves not only chemotherapy, but also the efficacy of the most commonly used breast cancer nanomedicines, namely Abraxane® and Doxil®. We found that treatment with vismodegib normalizes the tumor microenvironment by reducing the proliferative CAFs and in cases the levels of collagen and hyaluronan. These modulations re-engineered the solid and fluid stresses in the tumors, improving blood vessel functionality. As a result, the delivery and efficacy of chemotherapy was improved in two models of pancreatic cancer. Additionally, vismodegib treatment significantly improved the efficacy of both Abraxane and Doxil in xenograft breast tumors. Our results suggest the use of vismodegib, and sonic hedgehog inhibitors in general, to enhance cancer chemo- and nanotherapy. © 2017 Elsevier B.V. 261 105 112 105-112

Published
2017
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5. Defining the role of solid stress and matrix stiffness in cancer cell proliferation and metastasis

Author

Kalli, Maria, Stylianopoulos, Triantafyllos, Stylianopoulos, T. [0000-0002-3093-1696], and Stylianopoulos, Triantafyllos [0000-0002-3093-1696]

Subjects
0301 basic medicine, collagen, Cancer Research, transforming growth factor, Growth-induced stress, growth-induced stress, externally applied stress, medicine.disease_cause, fibroblast, Metastasis, Extracellular matrix, myosin adenosine triphosphatase, cell stress, bone morphogenetic protein, in vitro models, cancer cell, actin polymerization, Chemistry, apoptosis, cytoskeleton, In vitro models, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, tumor growth, Oncology, stroma cell, Externally applied stress, carcinogenesis, Stromal cell, Mini Review, extracellular matrix, lcsh:RC254-282, 03 medical and health sciences, Stroma, fibronectin, fibroblasts, medicine, metastasis, tumor microenvironment, Young modulus, human, protein expression, mechanotransduction, Tumor microenvironment, glioblastoma, Cancer, Fibroblasts, medicine.disease, tumor spheroid, 030104 developmental biology, cell proliferation, Tumor progression, tumor volume, Cancer research, Short Survey, Carcinogenesis
Abstract

Solid tumors are characterized by an abnormal stroma that contributes to the development of biomechanical abnormalities in the tumor microenvironment. In particular, these abnormalities include an increase in matrix stiffness and an accumulation of solid stress in the tumor interior. So far, it is not clearly defined whether matrix stiffness and solid stress are strongly related to each other or they have distinct roles in tumor progression. Moreover, while the effects of stiffness on tumor progression are extensively studied compared to the contribution of solid stress, it is important to ascertain the biological outcomes of both abnormalities in tumorigenesis and metastasis. In this review, we discuss how each of these parameters is evolved during tumor growth and how these parameters are influenced by each other. We further review the effects of matrix stiffness and solid stress on the proliferative and metastatic potential of cancer and stromal cells and summarize the in vitro experimental setups that have been designed to study the individual contribution of these parameters. © 2018 Kalli and Stylianopoulos. 8

Published
2018

6. Remodeling components of the tumor microenvironment to enhance cancer therapy

Author

Gkretsi, V., Stylianou, A., Papageorgis, P., Polydorou, C., Stylianopoulos, T., and Stylianopoulos, T. [0000-0002-3093-1696]

Subjects
Cancer Research, cell migration, Vascular normalization, Review, Vessel compression, Bioinformatics, Stress alleviation, 0302 clinical medicine, Medicine, Solid tumor, in vitro models, transforming growth factor beta, 0303 health sciences, atomic force microscopy, breast tumor, apoptosis, In vitro models, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, cell invasion, vessel compression, 3. Good health, tumor growth, Oncology, colon cancer, stroma cell, 030220 oncology & carcinogenesis, tumor vessel permeability, cancer therapy, stress alleviation, liver cell carcinoma, Tumor vessel permeability, extracellular matrix, Cancer therapy, cell motility, Tumor vasculature, lcsh:RC254-282, 03 medical and health sciences, blood vessel permeability, Stroma, tumor vascularization, pancreas cancer, tumor microenvironment, human, vascular normalization, 030304 developmental biology, Tumor microenvironment, nonhuman, business.industry, vasculotropin, glioblastoma, mechanical stress, Cancer, medicine.disease, tumor spheroid, cell proliferation, Tumor progression, Cancer cell, chromosome aberration, business
Abstract

Solid tumor pathophysiology is characterized by an abnormal microenvironment that guides tumor progression and poses barriers to the efficacy of cancer therapies. Most common among tumor types are abnormalities in the structure of the tumor vasculature and stroma. Remodeling the tumor microenvironment with the aim to normalize any aberrant properties has the potential to improve therapy. In this review, we discuss structural abnormalities of the tumor microenvironment and summarize the therapeutic strategies that have been developed to normalize tumors as well as their potential to enhance therapy. Finally, we present different in vitro models that have been developed to analyze and better understand the effects of the tumor microenvironment on cancer cell behavior. � 2015 Gkretsi, Stylianou, Papageorgis, Polydorou and Stylianopoulos. 5

Published
2015

7. Atomic Force Microscopy Probing of Cancer Cells and Tumor Microenvironment Components

Author

Stylianou, A., Stylianopoulos, T., and Stylianopoulos, T. [0000-0002-3093-1696]

Subjects
0301 basic medicine, Nonlinear optics, Cytoskeleton organization, Mechanical properties, Diseases, Imaging techniques, 02 engineering and technology, Metastasis, Imaging, Extracellular matrix, Atomic force microscopy, Pathology, Biomechanics, cell interaction, Enzyme activity, Extracellular matrices, cancer cell, Cell migration, 021001 nanoscience & nanotechnology, intercellular adhesion molecule 1, Cell biology, Crosstalk (biology), Tumor microenvironment, stroma cell, protein degradation, podosome, 0210 nano-technology, Extracellular matrix, Stromal cells, Fibroblasts, Cell migration, Metastasis, Imaging, Mechanical properties, Second harmonic generation, Coupled AFM, scanning electron microscopy, Operating principles, Materials science, Stromal cell, Cells, Biomedical Engineering, Bioengineering, protein kinase Syk, Article, nerve growth factor, Extracellular matrix interactions, 03 medical and health sciences, medicine, Young modulus, exosome, Stromal cells, Tumors, Harmonic generation, piezoelectricity, cancer growth factor, Second harmonic generation, Fibroblasts, matrix attachment region binding protein, medicine.disease, 030104 developmental biology, Cancer cell, cancer research, Therapeutic strategy, Cell culture, Cytology, Coupled AFM, light related phenomena
Abstract

Cancer cells have different characteristics from normal cells in terms of morphology, cell–cell interactions, cytoskeleton organization, cell growth rates, and cell-extracellular matrix interactions. Although the clarification of these characteristics is crucial for the effective development of new therapeutic strategies, they remain poorly identified. Furthermore, tumor microenvironment plays a crucial role in cancer progression and metastasis, and thus, it is of utmost importance to decode and fully understand the crosstalk and the interactions between its different components. Atomic force microscopy (AFM) is an established and multifunctional tool in biomedical sciences with many applications in cancer research. In this review, we discuss the use of AFM in the study of cancer cells and the tumor microenvironment. We first provide a brief overview of AFM operating principles highlighting its contribution to the study of cancer and stromal cells. Next, we present research on the use of AFM in the study of cell-tumor microenvironment interactions during cancer cell migration and invasion. Finally, we discuss the development of coupled AFM modalities and the combination of different kinds of imaging with AFM that have been applied to cancer research. © 2015, Springer Science+Business Media New York. 6 33 46 33-46

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