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Interaction of Immune and Cancer Cells pp 1–57Cite as

Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors

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Part of the book series: Experientia Supplementum ((EXS,volume 113))

Abstract

Emphasizing the dynamic processes between cancer and host immune system, the initially discovered concept of cancer immunosurveillance has been replaced by the current concept of cancer immunoediting consisting of three phases: elimination, equilibrium, and escape. Solid tumors composed of both cancer and host stromal cells are an example how the three phases of cancer immunoediting functionally evolve and how tumor shaped by the host immune system gets finally resistant phenotype. The elimination, equilibrium, and escape have been described in this chapter in details, including the role of immune surveillance, cancer dormancy, disruption of the antigen-presenting machinery, tumor-infiltrating immune cells, resistance to apoptosis, as well as the function of tumor stroma, microvesicles, exosomes, and inflammation.

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Abbreviations

AKT:

protein kinase B

APCs:

antigen-presenting cells

BMP:

bone morphogenetic protein

CAFs:

cancer-associated fibroblasts

CCR:

C-C chemokine receptor

COX:

cyclooxygenase

CSCs:

cancer stem cells

CSF-1:

colony-stimulating factor-1

CTCs:

circulating tumor cells

CTLA-4:

cytotoxic T lymphocyte-associated antigen-4

CTLs:

cytotoxic T lymphocytes

CXCR:

C-X-C motif chemokine receptor

DCs:

dendritic cells

DTCs:

disseminated tumor cells

ECM:

extracellular matrix

EMT:

epithelial-to-mesenchymal transition

ERK:

extracellular signal-regulated kinase

FAK:

focal adhesion kinase

FasL:

Fas ligand

FGF:

fibroblast growth factor

GITR:

glucocorticoid-induced tumor necrosis factor receptor

GLI:

glioma-associated oncogene homolog

GM-CSF:

granulocyte-macrophage colony stimulating factor

Hh:

hedgehog signaling

HIF-1α:

hypoxia-inducible factor-1α

HLA:

human leukocyte antigen

HSP:

heat-shock protein

IAPs:

inhibitor of apoptosis proteins

IDO:

indoleamine 2,3-dioxygenase

IFN:

interferon

IGF:

insulin-like growth factor

IL:

interleukin

ILT:

immunoglobulin-like transcript

JAK:

Janus kinase

JNK:

c-Jun N-terminal kinases

MAPK:

mitogen-activated protein kinases

MCP-1:

monocyte chemotactic protein-1

M-CSF:

macrophage colony stimulating factor

mDCs:

mature dendritic cells

MDCs:

myeloid dendritic cells

MDSCs:

myeloid-derived suppressor cells

MICs:

metastasis-initiating cells

MMPs:

metalloproteinases

mTOR:

mammalian target of rapamycin

NF-κB:

nuclear factor kappa-light-chain-enhancer of activated B cells

NK:

natural killer cells

NKG2D:

activating receptor of NK cells

NKT:

natural killer T cells

NO:

nitric oxide

NOTCH:

neurogenic locus notch homolog protein

NR2F1:

nuclear receptor subfamily-2 group-F member-1

PD-1:

programmed death-1

PDCs:

plasmacytoid dendritic cells

PD-L1:

programmed death-1 ligand (also called B7-H1)

PGE2:

prostaglandin E2

PI3K:

phosphatidylinositol 3-kinase/phosphatase

RANTES:

Regulated on Activation, Normal T-cell Expressed and Secreted (CCL5)

RNS:

reactive nitrogen species

ROI/ROS:

reactive oxygen intermediates/species

STAT:

signal transducer and activator of transcription

TAA:

tumor-associated antigen

TAMs:

tumor-associated macrophages

TANs:

tumor-associated neutrophils

TCR:

T-cell receptor

TEMs:

tie-2-expressing monocytes/macrophages

TGF-β:

transforming growth factor-β

TILs:

tumor-infiltrating lymphocytes

TLR:

toll-like receptor

TNF-α:

tumor necrosis factor-α

Tr1 cells:

type 1 regulatory T cells

TRAIL:

TNF-related apoptosis-inducing ligand

Tregs:

T regulatory cells

uPAR:

urokinase plasminogen activator receptor

VEGF:

vascular-endothelial growth factor

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Authors and Affiliations

  1. Department of Gynecologic Surgery and Gynecologic Oncology, Medical University of Lodz, Lodz, Poland

    Jacek R. Wilczyński

  2. Department of Operative Gynecology and Gynecologic Oncology, Polish Mother’s Memorial Hospital—Research Institute, Lodz, Poland

    Marek Nowak

  3. Department of Operative and Endoscopic Gynecology, Medical University of Lodz, Lodz, Poland

    Marek Nowak

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  1. Jacek R. Wilczyński
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Correspondence to Jacek R. Wilczyński .

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  1. Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland

    Magdalena Klink

  2. Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland

    Izabela Szulc-Kielbik

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Wilczyński, J.R., Nowak, M. (2022). Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors. In: Klink, M., Szulc-Kielbik, I. (eds) Interaction of Immune and Cancer Cells. Experientia Supplementum, vol 113. Springer, Cham. https://doi.org/10.1007/978-3-030-91311-3_1

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