scholarly journals MOLECULAR BIOLOGICAL CHARACTERISTICS OF CANCER

2015 ◽  
Vol 69 (1-2) ◽  
pp. 5-15
Author(s):  
N. E. Kushlinskii ◽  
M. V. Nemtsova
Keyword(s):  
Tumor Cells ◽  
Normal Tissue ◽  
Genome Instability ◽  
Tumor Stroma ◽  
Cell Types ◽  
Invasion And Metastasis ◽  
Normal Cells ◽  
Tumor Genome ◽  
Different Cell Types ◽  
Proliferative Signaling

The review presents the main and additional features that distinguish tumor cells from normal tissue cells. They include sustained proliferative signaling, evasion from growth suppressors, resisting cell death, enabling replicative immortality, angiogenesis induction, and invasion and metastasis activation. Basis for the formation of these features is provided by tumor genome instability. Tumors are complex tissues that consist of different cell types interacting with each other as well as with normal cells. An important characteristic of tumor cells is the ability to interact with the tumor microenvironment and the formation of tumor stroma.

scholarly journals Genes in Tumor Formation

2019 ◽  
Vol 3 (2) ◽  
pp. 18-22
Author(s):  
Isolde Riede
Keyword(s):  
Tumor Cells ◽  
Genome Instability ◽  
Tumor Formation ◽  
Normal Cells ◽  
Tumor Supressors ◽  
Somatic Pairing ◽  
Definition Of

With the definition of four gene classes, all differences between tumor cells and normal cells can be explained. Proliferative mutations induce a shortcut, forcing the cell to divide. They allow replication without control, induce somatic pairing defects of chromosomes and genome instability. Intact Tumor Supressors or mutant Switch Functions can inhibit this process. Oncogene mutations optimize the growth of the cells.

scholarly journals Single-cell transcriptome analysis of tumor and stromal compartments of pancreatic ductal adenocarcinoma primary tumors and metastatic lesions

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Wei Lin ◽  
Pawan Noel ◽  
Erkut H. Borazanci ◽  
Jeeyun Lee ◽  
Albert Amini ◽  
...  
Keyword(s):  
Single Cell ◽  
Tumor Cells ◽  
Cell Types ◽  
Ductal Adenocarcinoma ◽  
Cellular Composition ◽  
Primary Tumors ◽  
Metastatic Lesions ◽  
Tumor Tissues ◽  
Cell Type Specific ◽  
Different Cell Types

Abstract Background Solid tumors such as pancreatic ductal adenocarcinoma (PDAC) comprise not just tumor cells but also a microenvironment with which the tumor cells constantly interact. Detailed characterization of the cellular composition of the tumor microenvironment is critical to the understanding of the disease and treatment of the patient. Single-cell transcriptomics has been used to study the cellular composition of different solid tumor types including PDAC. However, almost all of those studies used primary tumor tissues. Methods In this study, we employed a single-cell RNA sequencing technology to profile the transcriptomes of individual cells from dissociated primary tumors or metastatic biopsies obtained from patients with PDAC. Unsupervised clustering analysis as well as a new supervised classification algorithm, SuperCT, was used to identify the different cell types within the tumor tissues. The expression signatures of the different cell types were then compared between primary tumors and metastatic biopsies. The expressions of the cell type-specific signature genes were also correlated with patient survival using public datasets. Results Our single-cell RNA sequencing analysis revealed distinct cell types in primary and metastatic PDAC tissues including tumor cells, endothelial cells, cancer-associated fibroblasts (CAFs), and immune cells. The cancer cells showed high inter-patient heterogeneity, whereas the stromal cells were more homogenous across patients. Immune infiltration varies significantly from patient to patient with majority of the immune cells being macrophages and exhausted lymphocytes. We found that the tumor cellular composition was an important factor in defining the PDAC subtypes. Furthermore, the expression levels of cell type-specific markers for EMT+ cancer cells, activated CAFs, and endothelial cells significantly associated with patient survival. Conclusions Taken together, our work identifies significant heterogeneity in cellular compositions of PDAC tumors and between primary tumors and metastatic lesions. Furthermore, the cellular composition was an important factor in defining PDAC subtypes and significantly correlated with patient outcome. These findings provide valuable insights on the PDAC microenvironment and could potentially inform the management of PDAC patients.

scholarly journals Tumor Rejection by Disturbing Tumor Stroma Cell Interactions

2001 ◽  
Vol 194 (11) ◽  
pp. 1549-1560 ◽  
Author(s):  
Sabrina Ibe ◽  
Zhihai Qin ◽  
Thomas Schüler ◽  
Susanne Preiss ◽  
Thomas Blankenstein
Keyword(s):  
T Cells ◽  
Tumor Stroma ◽  
Residual Tumor ◽  
Cell Types ◽  
Cell Interactions ◽  
Tumor Rejection ◽  
Receptor Expression ◽  
Stroma Cell ◽  
Ifn Γ ◽  
Different Cell Types

The stroma of solid tumors is a complex network of different cell types. We analyzed stroma cell interactions in two tumor models during cyclophosphamide (Cy)-induced tumor rejection. In growing tumors, tumor infiltrating macrophages (TIMs) produced interleukin (IL)-10. Beginning 6 h after Cy-treatment T cells in the tumor were inactivated and TIMs switched to interferon (IFN)-γ production. Both, IL-10 production before and IFN-γ production after Cy-treatment by TIMs required T cells. With the same kinetics as TIMs started to produce IFN-γ the tumor vasculature was destroyed which required IFN-γ receptor expression on host but not tumor cells. These events preceded hemorrhagic necrosis and residual tumor cell elimination by T cells. Together, T cells regulate the function of TIMs and tumor rejection can be induced by disturbing the stroma network.

Polyamines regulate gap junction communication in connexin 43-expressing cells

2001 ◽  
Vol 357 (2) ◽  
pp. 489-495 ◽  
Author(s):  
Leonard SHORE ◽  
Pauline McLEAN ◽  
Susan K. GILMOUR ◽  
Malcolm B. HODGINS ◽  
Malcolm E. FINBOW
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Ornithine Decarboxylase ◽  
Normal Tissue ◽  
Connexin 43 ◽  
Cell Communication ◽  
Cell Types ◽  
Decarboxylase Activity ◽  
Gap Junction Communication ◽  
Different Cell Types

The control of cell–cell communication through gap junctions is thought to be crucial in normal tissue function and during various stages of tumorigenesis. However, few natural regulators of gap junctions have been found. We show here that increasing the activity of ornithine decarboxylase, or adding polyamines to the outside of cells, increases the level of gap junction communication between various epithelial cells. Conversely, reduction of ornithine decarboxylase activity decreases the level of gap junction communication. This regulation is dependent upon the expression of connexin 43 (Cx43 or Cxα1), which is a major connexin expressed in many different cell types, and involves an increase in Cx43 and its cellular re-distribution.

scholarly journals Suppression of macrophage oxidative metabolism by products of malignant and nonmalignant cells.

1982 ◽  
Vol 156 (4) ◽  
pp. 945-961 ◽  
Author(s):  
A Szuro-Sudol ◽  
C F Nathan
Keyword(s):  
Tumor Cells ◽  
Oxidative Metabolism ◽  
Normal Cell ◽  
Specific Effect ◽  
Cell Types ◽  
Myristate Acetate ◽  
Normal Cells ◽  
Similar Activity ◽  
By Products ◽  
Cell Conditioned Medium

Each of 11 tumors tested produced a factor that markedly suppressed the ability of macrophages to release H2O2 or O.2- in response to phorbol myristate acetate or zymosan. Four of seven normal cell types produced a similar activity, which was 3.5-7 times lower in titer than that in tumor cell-conditioned medium (TCM), and which was much more rapidly reversible in its effects. TCM caused 50% inhibition of H2O2 release when it was present in the medium for 48 h at a concentration of 13%, or when 100% TCM was present in the medium for 18 h. The H2O2-releasing capacity of macrophages incubated in TCM only returned to control levels by 6 d after its removal. TCM prevented augmentation of H2O2-releasing capacity by lymphokines. The titer of suppressive activity in TCM depended on both the concentration of tumor cells and the duration of their incubation. TCM did not augment the activity of catalase, myeloperoxidase, glutathione peroxidase, or glutathione reductase or the content of glutathione within macrophages, suggesting that decreased synthesis rather than increased catabolism was responsible for reduced secretion of H2O2. Suppression of the release of H2O2 or O.2- by TCM appeared to be a relatively specific effect, in that TCM increased macrophage spreading and adherence to glass while exerting little influence on rates of phagocytosis, synthesis of protein, or secretion of lysozyme, plasminogen activator, or arachidonic acid and its metabolites. Thus, tumor cells and some normal cells can secrete a factor that selectively deactivates macrophage oxidative metabolism.

scholarly journals Mechanisms of resistance of normal cells to TRAIL induced apoptosis vary between different cell types

FEBS Letters ◽  
2000 ◽  
Vol 482 (3) ◽  
pp. 193-199 ◽  
Author(s):  
Xu Dong Zhang ◽  
Tam Nguyen ◽  
Wayne D Thomas ◽  
Jayne E Sanders ◽  
Peter Hersey
Keyword(s):  
Cell Types ◽  
Mechanisms Of Resistance ◽  
Normal Cells ◽  
Induced Apoptosis ◽  
Different Cell Types

scholarly journals Tumor angiogenesis and progression are enhanced by Sema4D produced by tumor-associated macrophages

2008 ◽  
Vol 205 (7) ◽  
pp. 1673-1685 ◽  
Author(s):  
Jose Rafael Sierra ◽  
Simona Corso ◽  
Luisa Caione ◽  
Virna Cepero ◽  
Paolo Conrotto ◽  
...  
Keyword(s):  
Tumor Angiogenesis ◽  
Tumor Stroma ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Tumor Associated Macrophages ◽  
Semaphorin 4D ◽  
Vessel Maturation ◽  
Different Cell Types ◽  
Novel Therapeutic

Increased evidence suggests that cancer-associated inflammation supports tumor growth and progression. We have previously shown that semaphorin 4D (Sema4D), a ligand produced by different cell types, is a proangiogenic molecule that acts by binding to its receptor, plexin B1, expressed on endothelial cells (Conrotto, P., D. Valdembri, S. Corso, G. Serini, L. Tamagnone, P.M. Comoglio, F. Bussolino, and S. Giordano. 2005. Blood. 105:4321–4329). The present work highlights the role of Sema4D produced by the tumor microenvironment on neoplastic angiogenesis. We show that in an environment lacking Sema4D, the ability of cancer cells to generate tumor masses and metastases is severely impaired. This condition can be explained by a defective vascularization inside the tumor. We demonstrate that tumor-associated macrophages (TAMs) are the main cells producing Sema4D within the tumor stroma and that their ability to produce Sema4D is critical for tumor angiogenesis and vessel maturation. This study helps to explain the protumoral role of inflammatory cells of the tumor stroma and leads to the identification of an angiogenic molecule that might be a novel therapeutic target.

scholarly journals Mesenchymal stem cells carry and transport clusters of cancer cells

2021 ◽  
Author(s):  
Jana Zarubova ◽  
Mohammad Mahdi Hasani-Sadrabadi ◽  
Sam CP Norris ◽  
Andrea M Kasko ◽  
Song Li
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Migration ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Cell Types ◽  
Cell Clusters ◽  
Different Cell Types

AbstractCell clusters that collectively migrate from primary tumors appear to be far more potent in forming distant metastases than single cancer cells. A better understanding of collective cell migration phenomenon and the involvement of different cell types during this process is needed. Here, we utilize a micropatterned surface composed of a thousand of low-adhesive microwells to screen motility of spheroids containing different cell types by analyzing their ability to move from the bottom to the top of the microwells. Mesenchymal stem cells (MSCs) spheroid migration was efficient in contrast to cancer cell only spheroids. In spheroids with both cell types mixed together, MSCs were able to carry the low-motile cancer cells during migration. As the percentage of MSCs increased in the spheroids, more migrating spheroids were detected. Extracellular vesicles secreted by MSCs also contributed to the pro-migratory effect exerted by MSCs. However, the transport of cancer cells was more efficient when MSCs were physically present in the cluster. Similar results were obtained when cell clusters were encapsulated within a micropatterned hydrogel, where collective migration was guided by micropatterned matrix stiffness. These results suggest that stromal cells facilitate the migration of cancer cell clusters, which is contrary to the general belief that malignant cells metastasize independently.SignificanceDuring metastasis, tumor cells may migrate as a cluster, which exhibit higher metastatic capacity compared to single cells. However, whether and how non-cancer cells contained in tumor cluster regulate it’s migration is not clear. Here, we utilize two unique approaches to study collective tumor cell migration in vitro: first, in low-adhesive microwells and second, in micropatterned hydrogels to analyze migration in 3D microenvironment. Our results indicate that MSCs in tumor cell clusters could play an important role in the dissemination of cancer cells by actively transporting low-motile cancer cells. In addition, MSC-released paracrine factors also increase the motility of tumor cells. These findings reveal a new mechanism of cancer cell migration and may lead to new approaches to suppress metastases.

scholarly journals The Microenvironment in Epstein–Barr Virus-Associated Malignancies

Pathogens ◽  
2018 ◽  
Vol 7 (2) ◽  
pp. 40 ◽  
Author(s):  
Geok Tan ◽  
Lydia Visser ◽  
Lu Tan ◽  
Anke Berg ◽  
Arjan Diepstra
Keyword(s):  
Tumor Cells ◽  
Epstein Barr Virus ◽  
Immune Escape ◽  
Cell Types ◽  
Barr Virus ◽  
Adaptive Immune Cells ◽  
Associated Malignancy ◽  
Epstein Barr ◽  
Immune Escape Mechanisms ◽  
Different Cell Types

The Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the tumor cells. In fact, latent EBV-infected tumor cells utilize several specific mechanisms to form and shape the TME to their own benefit. These mechanisms have been studied largely in the context of EBV+ Hodgkin lymphoma, undifferentiated nasopharyngeal carcinoma, and EBV+ gastric cancer. This review describes the composition, immune escape mechanisms, and tumor cell promoting properties of the TME in these three malignancies. Mechanisms of susceptibility which regularly involve genes related to immune system function are also discussed, as only a small proportion of EBV-infected individuals develops an EBV-associated malignancy.

scholarly journals Dissecting the Role of Bone Marrow Stromal Cells on Bone Metastases

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Denise Buenrostro ◽  
Serk In Park ◽  
Julie A. Sterling
Keyword(s):  
Bone Marrow ◽  
Bone Metastases ◽  
Tumor Cells ◽  
Bone Marrow Cells ◽  
Current Knowledge ◽  
Metastatic Cancer ◽  
Cell Types ◽  
Bone Microenvironment ◽  
Or Gene ◽  
Different Cell Types

Tumor-induced bone disease is a dynamic process that involves interactions with many cell types. Once metastatic cancer cells reach the bone, they are in contact with many different cell types that are present in the cell-rich bone marrow. These cells include the immune cells, myeloid cells, fibroblasts, osteoblasts, osteoclasts, and mesenchymal stem cells. Each of these cell populations can influence the behavior or gene expression of both the tumor cells and the bone microenvironment. Additionally, the tumor itself can alter the behavior of these bone marrow cells which further alters both the microenvironment and the tumor cells. While many groups focus on studying these interactions, much remains unknown. A better understanding of the interactions between the tumor cells and the bone microenvironment will improve our knowledge on how tumors establish in bone and may lead to improvements in diagnosing and treating bone metastases. This review details our current knowledge on the interactions between tumor cells that reside in bone and their microenvironment.

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