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Cancers Evade Immunity Via Immunoediting

Tumor Microenvironment Cancer Immunotherapy Intercellular Communication & Diseases

Cancer immunoediting describes how immunity both suppresses tumor development and shapes cancers that later escape immune destruction. The concept reframed cancer immunosurveillance into a dynamic process with three linked phases: elimination, equilibrium, and escape. Its research history moved from controversy to renewed acceptance after mouse and human evidence showed that immune pressure can eliminate transformed cells while selecting tumor variants with reduced immunogenicity. This made immunoediting central to cancer immunity, tumor evolution, immune evasion, and immunotherapy resistance[1][2][3][4].

During elimination, innate and adaptive immune mechanisms recognize transformed cells and destroy them before clinical tumor formation. IFNγ, type I interferons, lymphocytes, perforin-mediated cytotoxicity, antigen presentation, and T-cell recognition of tumor antigens contribute to this protective phase. Equilibrium then maintains occult cancer in a controlled state, where adaptive immunity restrains tumor outgrowth while editing tumor-cell populations. Escape occurs when edited tumor cells grow progressively, become clinically apparent, and establish an immunosuppressive tumor microenvironment[3][5][6][7][8][9].

Cancer immunoediting directly informs drug discovery and cancer therapeutics because immune checkpoint blockade, neoantigen-targeted therapy, cancer vaccines, and biomarker development all depend on whether tumors remain visible to T cells. Exome analysis showed that highly antigenic mutant proteins can drive strong tumor immunogenicity and that loss of these antigens through T-cell-dependent immunoselection represents a mechanism of immunoediting. In non-small cell lung cancer, immune checkpoint blockade was associated with evolution of the neoantigen landscape during acquired resistance, linking immunoediting to clinical relapse after anti-PD-1 or anti-CTLA-4 therapy[7][10][11].

Major gaps remain in measuring immunoediting in human tumors, distinguishing immune-mediated selection from neutral tumor evolution, and determining when immunotherapy strengthens antitumor immunity versus selecting resistant clones. Future work needs integrated immunogenomics, longitudinal biopsies, neoantigen tracking, immune-contexture analysis, and rational combinations that restore antigen presentation, reverse immune suppression, or prevent escape. The strongest clinical implication is that cancer immunity should be treated as an evolutionary process, not a static biomarker state[8][9][10][11].

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Cat. No. Product Name Information Application Publication
HY-13418 Dorsomorphin dihydrochloride
Dorsomorphin (Compound C) dihydrochloride is a potent, selective and ATP-competitive AMPK inhibitor, with a Ki of 109 nM. Dorsomorphin dihydrochloride inhibits BMP pathway by targeting the type I receptors ALK2, ALK3, and ALK6. Dorsomorphin dihydrochloride can reverse autophagy activation and anti-inflammatory effect of Urolithin A (HY-100599).
Organoid   AMPK   TGF-β Receptor   Autophagy  
Colorectal Cancer   Prostate Cancer   Ovarian Cancer   Pain   Digestive System Inflammation   Obesity  
819
HY-13418A Dorsomorphin
Dorsomorphin (BML-275) is a selective and ATP-competitive AMPK inhibitor (Ki=109 nM in the absence of AMP). Dorsomorphin (BML-275) selectively inhibits BMP type I receptors ALK2, ALK3, and ALK6. Dorsomorphin can reverse autophagy activation and anti-inflammatory effect of Urolithin A (HY-100599).
Organoid   AMPK   TGF-β Receptor   Autophagy  
819
HY-10431 SB-431542
SB-431542 is a TGF-β receptor kinase inhibitor (TRKI). SB-431542 has inhibitory activity for ALK4, ALK5 and ALK7 with IC50 values of 1 μM, 0.75 μM and 2 μM, respectively. SB-431542 also inhibits TGF-β-induced transcription, gene expression, apoptosis, and growth suppression. SB-431542 can be used for the research of cancer and signal transduction pathways.
Organoid   TGF-β Receptor   Apoptosis  
Colorectal Cancer   Prostate Cancer   Pancreatic Cancer   Digestive System Inflammation   Obesity   Lung Fibrosis  
323
HY-100941 CCCP
CCCP is an oxidative phosphorylation (OXPHOS) uncoupler. CCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation.
PINK1/Parkin   Oxidative Phosphorylation   STING   IFNAR   Mitochondrial Metabolism   Bacterial   Apoptosis  
Cancer   Digestive System Disease   Bacterial Infection   Digestive System Inflammation   Parkinson's Disease   Rheumatoid Arthritis  
192
HY-10432 A 83-01
A 83-01 is a potent inhibitor of TGF-β type I receptor ALK5 kinase, type I nodal receptor ALK4 and type I nodal receptor ALK7, with IC50s of 12 nM, 45 nM and 7.5 nM against the transcription induced by ALK5, ALK4 and ALK7, respectively.
Organoid   TGF-β Receptor  
Cancer  
144
HY-13013 SIS3
SIS3 is a potent and selective inhibitor of Smad3 with an IC50 of 3 μM for Smad3 phosphorylation. SIS3 inhibits the myofibroblast differentiation of fibroblasts by TGF-β1.
TGF-beta/Smad  
Inflammation or Immune System Disease   Colorectal Cancer   Prostate Cancer   Lung Fibrosis  
113
HY-B0673 Pirfenidone
Pirfenidone (AMR69) is an antifibrotic agent that attenuates CCL2 and CCL12 production in fibrocyte cells. Pirfenidone has growth-inhibitory effect and reduces TGF-β2 protein levels in human glioma cell lines. Pirfenidone also has anti-inflammatory activities.
TGF-beta/Smad   CCR  
Colorectal Cancer   Prostate Cancer   Viral Infection   Digestive System Inflammation   SARS-CoV-2 Infection   Lung Fibrosis   Rheumatoid Arthritis  
96
HY-12071 LDN193189
LDN193189 (DM-3189) is a potent selective BMP type I receptor (BMP I) inhibitor. LDN193189 efficiently inhibits transcriptional activity of the BMP type I receptors ALK2 and ALK3 with IC50 values of 5 nM and 30 nM, respectively. LDN193189 can be used for the research of bone morphogenetic protein signalling, such as fibrodysplasia ossificans progressiva.
Organoid   TGF-β Receptor  
Breast Cancer  
95
HY-10964 Vadimezan
Vadimezan (DMXAA), the tumor vascular disrupting agent (tumor-VDA), is a murine agonist of the stimulator of interferon genes (STING) and also a potent inducer of type I IFNs and other cytokines. Vadimezan is unable to activate human STING. Vadimezan has anti-influenza virus H1N1-PR8 activities.
STING   IFNAR   Influenza Virus  
Lung Cancer   Prostate Cancer   Viral Infection   Autoimmune Disease   SARS-CoV-2 Infection  
80
HY-16141 Cilengitide
Cilengitide (EMD 121974) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC50 values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors.
Integrin   TGF-β Receptor   Apoptosis   PD-1/PD-L1   STAT   Akt   mTOR  
Melanoma   Glioblastoma  
75
HY-13226 Galunisertib
Galunisertib (LY2157299) is an oral and selective TGF-β receptor type I (TGF-βRI) kinase inhibitor with an IC50 of 56 nM.
TGF-β Receptor  
Lung Cancer   Breast Cancer   Colorectal Cancer   Prostate Cancer   Pancreatic Cancer   SARS-CoV-2 Infection   Obesity   Lung Fibrosis  
74
HY-100347A SRI-011381 hydrochloride
SRI-011381 hydrochloride is an orally active TGF-β signaling agonist, exhibits neuroprotective effects, with blood-brain barrier permeability.
TGF-beta/Smad  
Neurological, Eye or Ear Disease   Liver Cancer  
61
HY-100347 SRI-011381
SRI-011381 is an orally active TGF-β signaling agonist, exhibits neuroprotective effects.
TGF-beta/Smad  
Neurological, Eye or Ear Disease   Liver Cancer  
61
HY-100564A 2',3'-cGAMP sodium
2',3'-cGAMP sodium (2'-3'-cyclic GMP-AMP sodium) is a endogenous cGAMP in mammalian cells. 2',3'-cGAMP sodium binds to STING with a high affinity and is a potent inducer of interferon-β (IFNβ). 2',3'-cGAMP sodium is produced in mammalian cells in response to DNA in the cytoplasm.
Endogenous Metabolite   STING   IFNAR  
Metabolic or Endocrine Disease  
44
HY-100564 2',3'-cGAMP
2',3'-cGAMP (2'-3'-cyclic GMP-AMP) is a endogenous cGAMP in mammalian cells. 2',3'-cGAMP binds to STING with a high affinity and is a potent inducer of interferon-β (IFNβ). 2',3'-cGAMP is produced in mammalian cells in response to DNA in the cytoplasm.
Endogenous Metabolite   STING   IFNAR  
Metabolic or Endocrine Disease  
44
HY-117287 Deucravacitinib
Deucravacitinib (BMS-986165) is an orally active allosteric inhibitor of tyrosine kinase 2 (TYK2), with an IC50 of 0.2 nM and a Ki of 0.02 nM against the JH2 domain of TYK2, and it exhibits selectivity over other JAK subtypes and most of the kinome. Deucravacitinib blocks IL-23, IL-12, p-STAT1/3 and Type I IFN signaling, and inhibits Th17/Th1-mediated psoriasis inflammation. Deucravacitinib can be used in research related to moderate-to-severe plaque psoriasis, inflammatory bowel disease and systemic lupus erythematosus.
JAK   STAT   Interleukin Related   IFNAR  
Systemic Lupus Erythematosus   Psoriasis   Inflammatory Bowel Disease  
36
HY-16268 Kartogenin
Kartogenin (KGN) is an inducer of chondrogenic tissue formation (EC50: 100 nM). Kartogenin induces chondrogenesis by binding to fibrin A, disrupting its interaction with the transcription factor core binding factor beta subunit (CBFβ), and by modulating the CBFβ-RUNX1 transcriptional program. Kartogenin also promotes tendon-bone junction (TBJ) wound healing by stimulating collagen synthesis. Kartogenin is widely used in cell-free therapy in the field of regeneration for cartilage regeneration and protection, tendon-bone healing, wound healing and limb development. Kartogenin promotes cartilage repair, coordinates limb development, and is also used in osteoarthritis (OA) research.
TGF-beta/Smad  
Inflammation or Immune System Disease   Liver Cancer  
33
HY-13012 RepSox
RepSox (E-616452) is a potent and selective transforming growth factor-beta receptor I/activin like kinase 5 (TGF-β-RI/ALK5) inhibitor. RepSox inhibits ALK5 autophosphorylation with an IC50 value of 4 nM. RepSox can be used for the research of obesity and associated metabolic diseases such as type 2 diabetes.
Organoid   TGF-β Receptor  
Colorectal Cancer   Prostate Cancer   Pancreatic Cancer   Glucose Metabolism   Obesity   Lung Fibrosis  
23
HY-N1584 Halofuginone
Halofuginone (RU-19110), a Febrifugine derivative, is a competitive prolyl-tRNA synthetase inhibitor with a Ki of 18.3 nM. Halofuginone is a specific inhibitor of type-I collagen synthesis and attenuates osteoarthritis (OA) by inhibition of TGF-β activity. Halofuginone is also a potent pulmonary vasodilator by activating Kv channels and blocking voltage-gated, receptor-operated and store-operated Ca2+ channels. Halofuginone has anti-malaria, anti-inflammatory, anti-cancer, anti-fibrosis effects.
DNA/RNA Synthesis   TGF-beta/Smad   Parasite   Sodium Channel   Calcium Channel  
Inflammation or Immune System Disease   Ovarian Cancer   Parasitic Infection   Pulmonary Hypertension  
22
HY-N0439 Asiaticoside
Asiaticoside, a trisaccaride triterpene from Centella asiatica, suppresses TGF-β/Smad signaling through inducing Smad7 and inhibiting TGF-βRI and TGF-βRII in keloid fibroblasts; Asiaticoside shows antioxidant, anti-inflammatory, and anti-ulcer properties.
p38 MAPK   TGF-beta/Smad   Reactive Oxygen Species (ROS)   Apoptosis   Endogenous Metabolite  
Digestive System Disease   Lung Cancer   Neurodegenerative Disease   Pain   Digestive System Inflammation   Cardiovascular Disease  
19
HY-134581 Enpatoran
Enpatoran (M5049) is an orally active and selective TLR7/8 antagonist. Enpatoran inhibits the activation of the downstream type I interferon pathway. Enpatoran is used in studies of cutaneous lupus erythematosus, systemic lupus erythematosus with cutaneous manifestations, and psoriasis.
Toll-like Receptor (TLR)   IFNAR  
Systemic Lupus Erythematosus   Psoriasis  
18
HY-12273 DMH-1
DMH-1 is a selective BMP inhibitor. DMH-1 upregulates the expression of SOX1. DMH-1 increases cardiomyocyte progenitor cells and promotes the differentiation of mouse embryonic stem cells into cardiomyocytes. DMH-1 induces the differentiation of hiPSC-derived neural progenitor cells into β3-tubulin-positive neurons.
TGF-β Receptor   Organoid   Microtubule/Tubulin  
Neurological, Eye or Ear Disease   Heart Disease  
15
HY-116084 Trimethylamine N-oxide
Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway.

Source: Host intestinal bacteria

Drug Metabolite   NOD-like Receptor (NLR)   Reactive Oxygen Species (ROS)   TGF-beta/Smad   Endogenous Metabolite  
Liver Cancer   Depression   Autoimmune Disease   Cardiovascular Disease  
12
HY-147124 RIG012
RIG012 is a potent RIG-I inhibitor with an IC50 of 0.71 μM using the NADH-coupled ATPase assay. RIG012 inhibits IFN-β and ISG hRsad2 expression.
IFNAR  
Cancer   Infection  
6
HY-W250978 Ovalbumins
Ovalbumins are the major proteins in egg white. Ovalbumins act as an allergen and inducer, and can be applied to mouse models of allergic diseases. Ovalbumins can induce allergic rhinitis in mice via sensitization and nasal challenge. Ovalbumins can be used to establish asthma models.
Ovalbumin, low endotoxin (HY-W250978A) is recommended for model establishment.
Interleukin Related   IFNAR  
Allergic Asthma   Allergic Rhinitis  
6
HY-P9901 Ipilimumab
Ipilimumab is a fully human monoclonal antibody IgG1κ that blocks the inhibitory receptor cytotoxic T lymphocyte antigen 4 (CTLA-4) on T cells. Ipilimumab can be used in unresectable or metastatic melanoma (MM) studies.

Species: Human

CTLA-4  
Non-Small Cell Lung Cancer   Lung Adenocarcinoma   Triple-Negative Breast Cancer   Metastatic Breast Cancer   Metastatic Melanoma  
5
HY-P99168 Anifrolumab
Anifrolumab is a type I interferon (IFN) receptor antagonist, a human monoclonal antibody. Anifrolumab blocks the activity of type I interferon. Anifrolumab can be used in systemic lupus erythematosus (SLE) research.

Species: Human

IFNAR  
Systemic Lupus Erythematosus   Rheumatoid Arthritis  
5
HY-108829A Abatacept (powder)
Abatacept (CTLA4lg; BMS-188667) powder is a soluble fusion protein consisting of the extra-cellular domain of human CTLA4 and a fragment of the Fc portion of human IgG1 (hinge and CH2 and 3 domains). Abatacept powder is a selective T-cell co-stimulation modulator and a protein agent for the autoimmune diseases.

Species: Human

CTLA-4  
Cancer   Glucose Metabolism   SARS-CoV-2 Infection   Rheumatoid Arthritis  
3
HY-P99132 Anti-Mouse CTLA-4 Antibody (9D9)
Anti-Mouse CTLA-4 Antibody (9D9) is an anti-mouse CTLA-4 IgG2b monoclonal antibody. Anti-Mouse CTLA-4 Antibody (9D9) can bind to CTLA-4 and block its binding to B7. Anti-Mouse CTLA-4 Antibody (9D9) enhances T cell function by increasing the ratio of CD8+ T cells to regulatory T cells (Tregs). Anti-Mouse CTLA-4 Antibody (9D9) can be used for research on cancer such as colon cancer and melanoma.

Species: Mouse

CTLA-4  
Inflammation or Immune System Disease   Colorectal Cancer   Melanoma  
3
HY-108829 Abatacept
Abatacept (CTLA4lg) is a soluble fusion protein consisting of the extra-cellular domain of human CTLA4 and a fragment of the Fc portion of human IgG1 (hinge and CH2 and 3 domains). Abatacept is a selective T-cell co-stimulation modulator and a protein agent for the autoimmune diseases.

Species: Human

CTLA-4  
Lung Cancer   Melanoma   SARS-CoV-2 Infection   Rheumatoid Arthritis  
3
HY-P99241 Ponsegromab
Ponsegromab is a Growth differentiation factor 15 (GDF15) inhibitor with human, cynomolgus monkey, and mouse target IC50 values of 0.123 nM, 0.053 nM, and 0.102 nM, respectively. Ponsegromab acts as a chemosensitizer, increases intracellular reactive oxygen species, reduces glutathione levels. Ponsegromab can be used for the research of oxaliplatin-resistant colorectal cancer.

Species: Human

TGF-beta/Smad   TGF-β Receptor  
Breast Cancer   Non-Small Cell Lung Cancer  
3
HY-P99355 Bimagrumab
Bimagrumab (Anti-ACVR2B Reference Antibody) is a human monoclonal antibody that blocks activin type II receptor (ActRII), with KDs of 1.7 pM and 434 pM for human ActRIIB and ActRIIA, respectively. Bimagrumab can be used for the research of pathological muscle loss and weakness.

Species: Human

TGF-β Receptor  
Metabolic or Endocrine Disease  
3
HY-W016562 Hippuric acid
Hippuric Acid is an orally active metabolite. Hippuric Acid can be produced by intestinal microorganisms from the metabolism of polyphenols, benzoic acid. Hippuric Acid decreases NRF2, MMP9 and leads to ROS accumulation. Hippuric Acid activates TGFβ/SMAD signaling. Hippuric Acid improves hyperuricemia and colitis. Hippuric Acid can also be used in cardiovascular disease research. .
Endogenous Metabolite   Keap1-Nrf2   MMP   Reactive Oxygen Species (ROS)   TGF-beta/Smad  
Colorectal Cancer   Cardiovascular Disease   Colitis   Hyperuricemia   Rheumatoid Arthritis  
2
HY-P99117 Cadonilimab
Cadonilimab (AK104) is a humanized tetravalent IgG1 bispecific antibody targeting PD1/CTLA4. Cadonilimab blocks both PD-1 and CTLA-4 pathways, thereby relieving their corresponding immunosuppressive effects and reversing tumor specific T cell exhaustion. Cadonilimab significantly downregulates Fc-mediated effector functions, including antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), complement dependent cytotoxicity (CDC). Cadonilimab can be used for research of metastatic cervical cancer, as well as other malignancies such as gastric cancer, GEJ adenocarcinoma and non-small cell lung cancer (NSCLC).

Species: Human

PD-1/PD-L1   CTLA-4  
Inflammation or Immune System Disease   Gastric Cancer   Non-Small Cell Lung Cancer   Triple-Negative Breast Cancer  
1
HY-P99166 Vudalimab
Vudalimab is a potent dual PD-1 and CTLA-4 inhibitor as a fully humanized bispecific monoclonal antibody. Vudalimab targets immune checkpoint receptors PD-1 and CTLA-4 and promotes tumor-selective T-cell activation.

Species: Human

PD-1/PD-L1   CTLA-4  
Cancer   Inflammation or Immune System Disease  
/
HY-P990042 Gotistobart
Gotistobart (ONC-392; BNT 316) is a humanized anti-CTLA-4 antibody with selective regulatory T cell depletion activity in the tumor microenvironment. Gotistobart can be used for the research of cancer, such as non-small cell lung cancer.

Species: Human

CTLA-4  
Inflammation or Immune System Disease   Non-Small Cell Lung Cancer  
/
HY-P990690 Volrustomig
Volrustomig (MEDI-5752) is a human IgG1 κ monoclonal antibody targeting CTLA4/PD1. The isotype control for Volrustomig is Human IgG1 kappa, Isotype Control (HY-P99001). Volrustomig anchors to the surface of T cells by binding PD-1, induces PD-1 internalization and degradation, and preferentially inhibits CTLA-4 on activated PD-1+ T cells. Volrustomig binds to tumor-infiltrating lymphocytes and a subset of PD-1+ B cells, enhances T cell function and IFNγ secretion. Volrustomig reduces the activation of non-tumor-infiltrating lymphocytes and exhibits manageable toxicity. Volrustomig can be used in research on various cancers, such as non-small cell lung cancer, gastric cancer, hepatobiliary cancer, and cervical cancer.

Species: Human

PD-1/PD-L1   CTLA-4  
Gastric Cancer   Liver Cancer   Cervical Cancer   Non-Small Cell Lung Cancer  
/
HY-P990789 Anti-Mouse CTLA-4 Antibody (9H10)
Anti-Mouse CTLA-4 Antibody (9H10) is a kind of syrian hamster IgG antibody inhibitor, targeting to CTLA-4. Anti-Mouse CTLA-4 Antibody (9H10) binds mouse CTLA-4 and blocks the interaction between CTLA-4 and its ligand. Anti-Mouse CTLA-4 Antibody (9H10) shows potent anti-tumor effect in various tumor models, such as breast and colon cancer.

Species: Mouse

CTLA-4  
Breast Cancer   Prostate Cancer  
/
HY-P9918 Tremelimumab
Tremelimumab (Ticilimumab) is a fully human monoclonal antibody specific for cytotoxic T-lymphocyte antigen-4 (CTLA-4) and can be used for metastatic melanoma research.

Species: Human

CTLA-4  
Inflammation or Immune System Disease   Non-Small Cell Lung Cancer   Triple-Negative Breast Cancer   Metastatic Breast Cancer  
/
HY-P10587 Icotrokinra
Icotrokinra (JNJ-77242113) is an orally available, selective antagonist of the IL-23 receptor. Icotrokinra inhibits IL-23-induced STAT3 phosphorylation in peripheral blood mononuclear cells (IC50=5.6 pM) and inhibits IL-23-induced interferon IFN-γ production in NK cells with an IC50 of 18.4 pM. Icotrokinra exhibits anti-inflammatory activity in a rat TNBS-induced colitis model. Icotrokinra can be used in the study of psoriasis, psoriatic arthritis, and inflammatory bowel disease.
Interleukin Related   STAT   IFNAR  
Inflammation or Immune System Disease  
/

References

[1]. Dunn GP, et al. Cancer immunoediting: from immunosurveillance to tumor escape. Nat Immunol. 2002;3(11):991-998.  [Content Brief]

[2]. Dunn GP, et al. The three Es of cancer immunoediting. Annu Rev Immunol. 2004;22:329-360.  [Content Brief]

[3]. Shankaran V, et al. IFNγ and lymphocytes prevent primary tumour development and shape tumour immunogenicity. Nature. 2001;410(6832):1107-1111.  [Content Brief]

[4]. Dunn GP, et al. The immunobiology of cancer immunosurveillance and immunoediting. Immunity. 2004;21(2):137-148.  [Content Brief]

[5]. Dunn GP, et al. Interferons, immunity and cancer immunoediting. Nat Rev Immunol. 2006;6(11):836-848.  [Content Brief]

[6]. Koebel CM, et al. Adaptive immunity maintains occult cancer in an equilibrium state. Nature. 2007;450(7171):903-907.  [Content Brief]

[7]. Matsushita H, et al. Cancer exome analysis reveals a T-cell-dependent mechanism of cancer immunoediting. Nature. 2012;482(7385):400-404.  [Content Brief]

[8]. Schreiber RD, et al. Cancer immunoediting: integrating immunity's roles in cancer suppression and promotion. Science. 2011;331(6024):1565-1570.  [Content Brief]

[9]. Mittal D, et al. New insights into cancer immunoediting and its three component phases-elimination, equilibrium and escape. Curr Opin Immunol. 2014;27:16-25.  [Content Brief]

[10]. Anagnostou V, et al. Evolution of neoantigen landscape during immune checkpoint blockade in non-small cell lung cancer. Cancer Discov. 2017;7(3):264-276.  [Content Brief]

[11]. Gubin MM, et al. Clin Cancer Res. 2022;28(18):3917-3928.  [Content Brief]

Keywords

cancer immunoediting, immune evasion, elimination equilibrium escape, tumor immunogenicity, cancer immunosurveillance, neoantigen loss, immune checkpoint blockade, tumor microenvironment