The great escape: Is immune evasion required for tumor progression?

10.1038/11311 ◽  
1999 ◽  
Vol 5 (8) ◽  
pp. 874-875 ◽  
Author(s):  
Andreas Villunger ◽  
Andreas Strasser
Keyword(s):  
Tumor Progression ◽  
Immune Evasion

scholarly journals Tumor progression by immune evasion in melanoma

Cancer ◽  
2010 ◽  
Vol 116 (7) ◽  
pp. 1623-1625 ◽  
Author(s):  
Mohammed Kashani-Sabet
Keyword(s):  
Tumor Progression ◽  
Immune Evasion

scholarly journals CAFs Interacting With TAMs in Tumor Microenvironment to Enhance Tumorigenesis and Immune Evasion

2021 ◽  
Vol 11 ◽  
Author(s):  
Gurcan Gunaydin
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Progression ◽  
Tumor Cells ◽  
Immune Evasion ◽  
Poor Prognosis ◽  
Cancer Associated Fibroblasts ◽  
Mutual Relationship ◽  
Complex Interplay ◽  
Tumor Immune Evasion ◽  
Mechanisms Of Carcinogenesis

Cancer associated fibroblasts (CAFs) and tumor associated macrophages (TAMs) are among the most important and abundant players of the tumor microenvironment. CAFs as well as TAMs are known to play pivotal supportive roles in tumor growth and progression. The number of CAF or TAM cells is mostly correlated with poor prognosis. Both CAFs and TAMs are in a reciprocal communication with the tumor cells in the tumor milieu. In addition to such interactions, CAFs and TAMs are also involved in a dynamic and reciprocal interrelationship with each other. Both CAFs and TAMs are capable of altering each other’s functions. Here, the current understanding of the distinct mechanisms about the complex interplay between CAFs and TAMs are summarized. In addition, the consequences of such a mutual relationship especially for tumor progression and tumor immune evasion are highlighted, focusing on the synergistic pleiotropic effects. CAFs and TAMs are crucial components of the tumor microenvironment; thus, they may prove to be potential therapeutic targets. A better understanding of the tri-directional interactions of CAFs, TAMs and cancer cells in terms of tumor progression will pave the way for the identification of novel theranostic cues in order to better target the crucial mechanisms of carcinogenesis.

scholarly journals Epithelial-mesenchymal plasticity: How have quantitative mathematical models helped improve our understanding?

2017 ◽  
Author(s):  
Mohit Kumar Jolly ◽  
Satyendra C Tripathi ◽  
Jason A Somarelli ◽  
Samir M Hanash ◽  
Herbert Levine
Keyword(s):  
Phenotypic Plasticity ◽  
Mathematical Models ◽  
Tumor Progression ◽  
Immune Evasion ◽  
Molecular Mechanisms ◽  
Invasion And Metastasis ◽  
Hallmarks Of Cancer ◽  
Mesenchymal Phenotype ◽  
Extracellular Signals ◽  
Clinical Challenge

AbstractPhenotypic plasticity, the ability of cells to reversibly alter their phenotypes in response to signals, presents a significant clinical challenge to treating solid tumors. Tumor cells utilize phenotypic plasticity to evade therapies, metastasize, and colonize distant organs. As a result, phenotypic plasticity can accelerate tumor progression. A well-studied example of phenotypic plasticity is the bidirectional conversions among epithelial, mesenchymal, and hybrid epithelial/mesenchymal phenotype(s). These conversions can alter a repertoire of cellular traits associated with multiple hallmarks of cancer, such as metabolism, immune-evasion, and invasion and metastasis. To tackle the complexity and heterogeneity of these transitions, mathematical models have been developed that seek to capture the experimentally-verified molecular mechanisms and act as ‘ hypothesis-generating machines’. Here, we discuss how these quantitative mathematical models have helped us explain existing experimental data, guided further experiments, and provided an improved conceptual framework for understanding how multiple intracellular and extracellular signals can drive epithelial-mesenchymal plasticity at both the single-cell and population levels. We also discuss the implications of this plasticity in driving multiple aggressive facets of tumor progression.

scholarly journals Circular RNA circ_0020710 drives tumor progression and immune evasion by regulating the miR-370-3p/CXCL12 axis in melanoma

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Chuan-Yuan Wei ◽  
Meng-Xuan Zhu ◽  
Nan-Hang Lu ◽  
Jia-Qi Liu ◽  
Yan-Wen Yang ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Immune Evasion ◽  
Circular Rna

scholarly journals Stochastic modeling of tumor progression and immune evasion

2018 ◽  
Vol 458 ◽  
pp. 148-155 ◽  
Author(s):  
Jason T. George ◽  
Herbert Levine
Keyword(s):  
Tumor Progression ◽  
Stochastic Modeling ◽  
Immune Evasion

scholarly journals CD155: A Multi-Functional Molecule in Tumor Progression

2020 ◽  
Vol 21 (3) ◽  
pp. 922 ◽  
Author(s):  
Rosa Molfetta ◽  
Beatrice Zitti ◽  
Mario Lecce ◽  
Nadia Domenica Milito ◽  
Helena Stabile ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Progression ◽  
Immune Evasion ◽  
Immune Surveillance ◽  
Multiple Roles ◽  
Cancer Development ◽  
Cytotoxic Lymphocytes ◽  
Tumor Proliferation ◽  
Effector Cells ◽  
Activating Receptor

CD155 is an adhesion molecule belonging to the Nectin/Nectin-like family often overexpressed on tumor cells and involved in many different processes such as cell adhesion, migration and proliferation. In contrast to these pro-tumorigenic functions, CD155 is also a ligand for the activating receptor DNAM-1 expressed on cytotoxic lymphocytes including Natural Killer (NK) cells and involved in anti-tumor immune response. However, during tumor progression inhibitory receptors for CD155 are up-regulated on the surface of effector cells, contributing to an impairment of their cytotoxic capacity. In this review we will focus on the roles of CD155 as a ligand for the activating receptor DNAM-1 regulating immune surveillance against cancer and as pro-oncogenic molecule favoring tumor proliferation, invasion and immune evasion. A deeper understanding of the multiple roles played by CD155 in cancer development contributes to improving anti-tumor strategies aimed to potentiate immune response against cancer.

scholarly journals Upregulated glycolysis correlates with tumor progression and immune evasion in head and neck squamous cell carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hideyuki Takahashi ◽  
Reika Kawabata-Iwakawa ◽  
Shota Ida ◽  
Ikko Mito ◽  
Hiroe Tada ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Progression ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Immune Evasion ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Neck Squamous Cell Carcinoma ◽  
Glycolytic Activity

AbstractAltered metabolism is an emerging hallmark of cancer. Cancer cells preferentially utilize glycolysis for energy production, termed “aerobic glycolysis.” In this study, we performed a comprehensive analysis of the glycolytic activity in head and neck squamous cell carcinoma (HNSCC) using data obtained from The Cancer Genome Atlas database. We first divided 520 patients with HNSCC into four groups based on the mRNA expression of 16 glycolysis-related genes. The upregulated glycolytic activity positively correlated with human papillomavirus-negative tumor type, advanced T factor, and unfavorable prognosis. The gene set enrichment analysis revealed upregulation of several hallmark pathways, including interferon-alpha response, myc targets, unfolded protein response, transforming growth factor-β signaling, cholesterol homeostasis, and interleukin 6-Janus kinase-signal transducer and activator of transcription 3 signaling, in the glycolysis-upregulated groups. Immune cell enrichment analysis revealed decreased infiltration of T cells, dendritic cells, and B cells in the glycolysis-upregulated groups, suggesting impaired tumor antigen presentation, T cell activation, and antibody production in the TME. Moreover, the expression profile of immune-related genes indicated increased immune evasion in the glycolysis-upregulated tumors. Collectively, these findings suggest that transcriptome analysis of glycolytic activity of tumors has the potential as a biomarker for tumor progression and immunological status in patients with HNSCC.

Expressions of cyclooxygenase-2 (COX-2) and prostaglandin E receptors (EPs) in gallbladder carcinoma (GBca)-association with tumor progression

2001 ◽  
Vol 120 (5) ◽  
pp. A573-A573
Author(s):  
J SHODA ◽  
T ASANO ◽  
T KAWAMOTO ◽  
Y MATSUZAKI ◽  
N TANAKA ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Gallbladder Carcinoma ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Cox 2
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