scholarly journals Endothelial-Tumor Cell Interaction in Brain and CNS Malignancies

2020 ◽  
Vol 21 (19) ◽  
pp. 7371
Author(s):  
Maria Peleli ◽  
Aristidis Moustakas ◽  
Andreas Papapetropoulos
Keyword(s):  
Tumor Cells ◽  
Cell Types ◽  
Cell Interaction ◽  
Intermediate Cell ◽  
Pharmacological Interventions ◽  
New Therapeutic Approaches ◽  
Antiangiogenic Therapies ◽  
Mechanisms Of Formation ◽  
Cns Malignancies

Glioblastoma and other brain or CNS malignancies (like neuroblastoma and medulloblastoma) are difficult to treat and are characterized by excessive vascularization that favors further tumor growth. Since the mean overall survival of these types of diseases is low, the finding of new therapeutic approaches is imperative. In this review, we discuss the importance of the interaction between the endothelium and the tumor cells in brain and CNS malignancies. The different mechanisms of formation of new vessels that supply the tumor with nutrients are discussed. We also describe how the tumor cells (TC) alter the endothelial cell (EC) physiology in a way that favors tumorigenesis. In particular, mechanisms of EC–TC interaction are described such as (a) communication using secreted growth factors (i.e., VEGF, TGF-β), (b) intercellular communication through gap junctions (i.e., Cx43), and (c) indirect interaction via intermediate cell types (pericytes, astrocytes, neurons, and immune cells). At the signaling level, we outline the role of important mediators, like the gasotransmitter nitric oxide and different types of reactive oxygen species and the systems producing them. Finally, we briefly discuss the current antiangiogenic therapies used against brain and CNS tumors and the potential of new pharmacological interventions that target the EC–TC interaction.

Mesenchymal Stem Cells and Cancer Stem Cells: An Overview of Tumor-Mesenchymal Stem Cell Interaction for therapeutic interventions

2021 ◽  
Vol 22 ◽  
Author(s):  
Soheila Montazersaheb ◽  
Ezzatollah Fathi ◽  
Ayoub Mamandi ◽  
Raheleh Farahzadi ◽  
Hamid Reza Heidari
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Tumor Microenvironment ◽  
Cancer Stem Cells ◽  
Tumor Cells ◽  
Cell Types ◽  
Cell Interaction ◽  
Therapeutic Interventions ◽  
Tumorigenic Potential ◽  
Different Types

: Tumors are made up of different types of cancer cells that contribute to tumor heterogeneity. Among these cells, cancer stem cells (CSCs) have a significant role in the onset of cancer and development. Like other stem cells, CSCs are characterized by the capacity for differentiation and self-renewal. A specific population of CSCs is constituted by mesenchymal stem cells (MSCs) that differentiate into mesoderm-specific cells. The pro-or anti-tumorigenic potential of MSCs on the proliferation and development of tumor cells has been reported as contradictory results. Also, tumor progression is specified by the corresponding tumor cells like the tumor microenvironment. The tumor microenvironment consists of a network of reciprocal cell types such as endothelial cells, immune cells, MSCs, and fibroblasts as well as growth factors, chemokines, and cytokines. In this review, recent findings related to the tumor microenvironment and associated cell populations, homing of MSCs to tumor sites, and interaction of MSCs with tumor cells will be discussed.

Cancer metabolism

2019 ◽  
pp. 221-238
Author(s):  
Almut Schulze ◽  
Karim Bensaad ◽  
Adrian L. Harris
Keyword(s):  
Cancer Metabolism ◽  
Krebs Cycle ◽  
Cell Types ◽  
Oxygen Limitation ◽  
Genetic Changes ◽  
New Therapeutic Approaches ◽  
Rare Mutations ◽  
Metabolic Adaptations

Abnormalities in cancer metabolism have been noted since Warburg first described the phenomenon of glycolysis in normoxic conditions. This chapter reviews the major pathways in metabolism known to be modified in cancer, including glycolysis and the Krebs cycle, the pentose shunt, and new data implicating the role of different metabolic adaptations, including oncometabolism. It highlights the genetic changes that effect metabolism including many of the commonly occurring oncogenes but also rare mutations that specifically target metabolism. Nutrient and oxygen limitation and proliferation create the microenvironmental selective stress for modifications in hypoxic metabolism, but also affect other cell types such as endothelial cells and macrophages. This range of changes provides many new therapeutic approaches. It also describes the potential value of targeting these adaptations and approaches to monitoring in vivo effects in patients to monitor therapeutic activity.

scholarly journals Clinical Significance of Circulating Tumor Cells in Gastrointestinal Carcinomas

Diagnostics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 192
Author(s):  
Leonie Konczalla ◽  
Anna Wöstemeier ◽  
Marius Kemper ◽  
Karl-Frederik Karstens ◽  
Jakob Izbicki ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Clinical Application ◽  
Liquid Biopsy ◽  
Cancer Diagnostics ◽  
Therapeutic Approaches ◽  
Primary Tumors ◽  
New Therapeutic Approaches ◽  
Tumor Dissemination

The idea of a liquid biopsy to screen, surveil and treat cancer patients is an intensively discussed and highly awaited tool in the field of oncology. Despite intensive research in this field, the clinical application has not been implemented yet and further research has to be conducted. However, one component of the liquid biopsy is circulating tumor cells (CTCs) whose potential for clinical application is evaluated in the following. CTCs can shed from primary tumors to the peripheral blood at any time point during the progress of a malignant disease. Following, one single CTC can be the origin for distant metastasis at later cancer stage. Thus, CTCs have great potential to either be used in cancer diagnostics and patient stratification or to function as a target for new therapeutic approaches to stop tumor dissemination and metastasis at the very early beginning. Due to the biological fundamental role of CTCs in tumor progression, here, we provide an overview of CTCs in gastrointestinal cancers and their potential use in the clinical setting. In particular, we discuss the usage of CTC for screening and stratifying patients’ risk. Moreover, we will discuss the potential role of CTCs for treatment specification and treatment monitoring.

scholarly journals Immunomodulatory Properties of HLA-G in Infectious Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Laurence Amiot ◽  
Nicolas Vu ◽  
Michel Samson
Keyword(s):  
Infectious Diseases ◽  
Complex Molecule ◽  
Major Histocompatibility Complex Molecule ◽  
Cell Types ◽  
Inhibitory Effect ◽  
New Therapeutic Approaches ◽  
Extravillous Cytotrophoblasts ◽  
Cellular Source ◽  
Therapeutic Tools

HLA-G is a nonclassical major histocompatibility complex molecule first described at the maternal-fetal interface, on extravillous cytotrophoblasts. Its expression is restricted to some tissues in normal conditions but increases strongly in pathological conditions. The expression of this molecule has been studied in detail in cancers and is now also beginning to be described in infectious diseases. The relevance of studies on HLA-G expression lies in the well known inhibitory effect of this molecule on all cell types involved in innate and adaptive immunity, favoring escape from immune control. In this review, we summarize the features of HLA-G expression by type of infections (i.e, bacterial, viral, or parasitic) detailing the state of knowledge for each pathogenic agent. The polymorphism, the interference of viral proteins with HLA-G intracellular trafficking, and various cytokines have been described to modulate HLA-G expression during infections. We also discuss the cellular source of HLA-G, according to the type of infection and the potential role of HLA-G. New therapeutic approaches based on synthetic HLA-G-derived proteins or antibodies are emerging in mouse models of cancer or transplantation, and these new therapeutic tools may eventually prove useful for the treatment of infectious diseases.

scholarly journals Induction of Proteases in Peritoneal Carcinomatosis, the Role of ICAM-1/CD43 Interaction

2007 ◽  
Vol 2 ◽  
pp. 117727190700200 ◽  
Author(s):  
Nawar A. Alkhamesi ◽  
Gretta Roberts ◽  
Paul Ziprin ◽  
David H. Peck ◽  
Ara W. Darzi
Keyword(s):  
Tumor Cells ◽  
Tumor Invasion ◽  
Direct Contact ◽  
Therapeutic Option ◽  
Gelatin Zymography ◽  
Cell Types ◽  
Vital Role ◽  
Indirect Contact ◽  
Clinical Issue

Introduction The development of peritoneal metastases is a significant clinical issue in the treatment of abdominal cancers and is associated with poor prognosis. We have previously shown that ICAM-1-CD43 interaction plays a significant role in tumor adhesion. However, an invasive phenotype is critical to establish tumor progression via cell associated and secreted proteases including matrix metalloproteinases. High metalloproteinases level significantly enhanced metastasis phenotype on tumors, a detrimental effect on surgical outcome. We investigated the role of direct and indirect signaling between the mesothelium and the tumor cells in enhancing tumor invasion and possible therapeutic intervention. Methods Mesothelial cells were enzymatically derived from human omental tissue and implanted in 24 wells plates. Colorectal cancer cells were then introduced and allowed a direct and an indirect contact with the mesothelial layer. Anti-ICAM antibodies, anti-CD43 antibodies, and heparin were used to block MMP production. Gelatin zymography was performed on the supernatant to detect MMPs activity. Results MMP production was observed in mesothelial and tumor cells. Direct contact between cell types enhanced MMP9 and 2 (p < 0.05). Indirect contact also stimulate MMPs but at a lower degree. ICAM-1 blocking antibodies attenuated MMP production in direct contact to that observed in the indirect. Heparin introduction achieved a similar outcome. Conclusions ICAM-1-CD43 interaction plays a vital role in tumor cells-peritoneum adhesion and invasion, which is manifested by the increased production of MMPs leading to tumor invasion and peritoneal loco-regional. Blocking this interaction with heparin can provide a new therapeutic option.

scholarly journals Hepatocyte-tumor cell interaction in vitro. I. Conditions for rosette formation and inhibition by anti-H-2 antibody.

1980 ◽  
Vol 151 (4) ◽  
pp. 984-989 ◽  
Author(s):  
V Schirrmacher ◽  
R Cheingsong-Popov ◽  
H Arnheiter
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Metastatic Tumor ◽  
Cell Interaction ◽  
Rosette Formation ◽  
Normal Cells ◽  
Neuraminidase Treatment

Murine hepatocytes, isolated by an in situ collagenase-perfusion technique and cultured in Petri dishes, were shown to form rosettes with liver-metastasizing syngeneic tumor cells. Pretreatment of the tumor cells with neuraminidase generally increased the binding, whereas pretreatment of the liver cells with neuraminidase abolished the binding completely. The tumor-cell binding may be mediated by the previously described lectin-like receptor of hepatocytes that also was sensitive to neuraminidase treatment and that bound desialylated cells better than normal cells. Anti-H-2 sera could efficiently inhibit the rosette formation of metastatic tumor cells with the hepatocytes, which points to a possible role of H-2 molecules in this interaction of neoplastic and normal cells.

scholarly journals The Role of Metabolism in Tumor Immune Evasion: Novel Approaches to Improve Immunotherapy

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 361
Author(s):  
Alberto Cruz-Bermúdez ◽  
Raquel Laza-Briviesca ◽  
Marta Casarrubios ◽  
Belén Sierra-Rodero ◽  
Mariano Provencio
Keyword(s):  
Tumor Cells ◽  
Immune Evasion ◽  
Building Materials ◽  
Cell Types ◽  
First Line ◽  
Tumor Immune Evasion ◽  
Novel Approaches ◽  
Metabolic Properties ◽  
Selection Of

The tumor microenvironment exhibits altered metabolic properties as a consequence of the needs of tumor cells, the natural selection of the most adapted clones, and the selfish relationship with other cell types. Beyond its role in supporting uncontrolled tumor growth, through energy and building materials obtention, metabolism is a key element controlling tumor immune evasion. Immunotherapy has revolutionized the treatment of cancer, being the first line of treatment for multiple types of malignancies. However, many patients either do not benefit from immunotherapy or eventually relapse. In this review we overview the immunoediting process with a focus on the metabolism-related elements that are responsible for increased immune evasion, either through reduced immunogenicity or increased resistance of tumor cells to the apoptotic action of immune cells. Finally, we describe the main molecules to modulate these immune evasion processes through the control of the metabolic microenvironment as well as their clinical developmental status.

scholarly journals Human platelets exert cytotoxic effects on tumor cells

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1252-1255 ◽  
Author(s):  
GM Ibele ◽  
NE Kay ◽  
GJ Johnson ◽  
HS Jacob
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Types ◽  
Human Platelets ◽  
Fixed Number ◽  
Cell Cytotoxicity ◽  
Lipoxygenase Inhibitor ◽  
Tumor Metastases

Abstract Monocytes are thought to play a role in host resistance to tumor cell growth in animals and humans. In addition, platelets are known to be involved in tumor metastases. To investigate the interaction of these two cell types and their effect on tumor cells, human monocytes and platelets were examined using an in vitro monocyte-tumor cell cytotoxicity assay. Monocytes alone resulted in 32% +/- 1.5 (mean +/- SEM) tumor cell kill. When platelets were added to monocytes in a 1:1 ratio, an increase in cytotoxicity to 61% +/- 3.2 was observed. The cytotoxicity noted when platelets were added to a fixed number of monocytes and tumor cells was dependent on the number of platelets added. A decrease in cytotoxicity from 32% +/- 1.5 to 12% +/- 2.3 was observed when contaminating platelets were removed from monocyte preparations. Platelets added to tumor cells in the absence of any monocytes were also toxic, resulting in a maximum kill of 95% at a 4:1 platelet/tumor cell ratio. Secreted products of freshly isolated platelets may be responsible for much of the observed cytotoxicity, since supernatants from the platelets were toxic for tumor cells. Platelets pretreated with a cyclooxygenase inhibitor (ASA) or a lipoxygenase inhibitor had decreased cytotoxicity compared with untreated platelets. Our results indicate that products of platelet arachidonate metabolism are toxic for tumor cell lines. They also suggest that the role of the platelet must be considered when studying monocyte-tumor cell cytotoxicity.

scholarly journals The Emerging Role of the Microenvironment in Endometrial Cancer

Cancers ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 408 ◽  
Author(s):  
Subhransu Sahoo ◽  
Xu Zhang ◽  
Hubert Hondermarck ◽  
Pradeep Tanwar
Keyword(s):  
Endometrial Cancer ◽  
Tumor Cells ◽  
Stromal Cells ◽  
Cancer Recurrence ◽  
Metastatic Potential ◽  
Cell Types ◽  
Therapeutic Interventions ◽  
Signaling Cascades ◽  
Metastatic Progression

Endometrial cancer (EC) is one of the most frequently diagnosed cancers in women, and despite recent therapeutic advances, in many cases, treatment failure results in cancer recurrence, metastasis, and death. Current research demonstrates that the interactive crosstalk between two discrete cell types (tumor and stroma) promotes tumor growth and investigations have uncovered the dual role of the stromal cells in the normal and cancerous state. In contrast to tumor cells, stromal cells within the tumor microenvironment (TME) are genetically stable. However, tumor cells modify adjacent stromal cells in the TME. The alteration in signaling cascades of TME from anti-tumorigenic to pro-tumorigenic enhances metastatic potential and/or confers therapeutic resistance. Therefore, the TME is a fertile ground for the development of novel therapies. Furthermore, disrupting cancer-promoting signals from the TME or re-educating stromal cells may be an effective strategy to impair metastatic progression. Here, we review the paradoxical role of different non-neoplastic stromal cells during specific stages of EC progression. We also suggest that the inhibition of microenvironment-derived signals may suppress metastatic EC progression and offer novel potential therapeutic interventions.

scholarly journals Human platelets exert cytotoxic effects on tumor cells

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1252-1255
Author(s):  
GM Ibele ◽  
NE Kay ◽  
GJ Johnson ◽  
HS Jacob
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Types ◽  
Human Platelets ◽  
Fixed Number ◽  
Cell Cytotoxicity ◽  
Lipoxygenase Inhibitor ◽  
Tumor Metastases

Monocytes are thought to play a role in host resistance to tumor cell growth in animals and humans. In addition, platelets are known to be involved in tumor metastases. To investigate the interaction of these two cell types and their effect on tumor cells, human monocytes and platelets were examined using an in vitro monocyte-tumor cell cytotoxicity assay. Monocytes alone resulted in 32% +/- 1.5 (mean +/- SEM) tumor cell kill. When platelets were added to monocytes in a 1:1 ratio, an increase in cytotoxicity to 61% +/- 3.2 was observed. The cytotoxicity noted when platelets were added to a fixed number of monocytes and tumor cells was dependent on the number of platelets added. A decrease in cytotoxicity from 32% +/- 1.5 to 12% +/- 2.3 was observed when contaminating platelets were removed from monocyte preparations. Platelets added to tumor cells in the absence of any monocytes were also toxic, resulting in a maximum kill of 95% at a 4:1 platelet/tumor cell ratio. Secreted products of freshly isolated platelets may be responsible for much of the observed cytotoxicity, since supernatants from the platelets were toxic for tumor cells. Platelets pretreated with a cyclooxygenase inhibitor (ASA) or a lipoxygenase inhibitor had decreased cytotoxicity compared with untreated platelets. Our results indicate that products of platelet arachidonate metabolism are toxic for tumor cell lines. They also suggest that the role of the platelet must be considered when studying monocyte-tumor cell cytotoxicity.

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