ReviewCancer immunology, immunotherapy : CII2004
The selection of tumor variants with altered expression of classical and nonclassical MHC class I molecules: implications for tumor immune escape.
Review in Cancer immunology, immunotherapy : CII, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 290 citations in OpenAlex.
- The prognostic and predictive value of Tregs and tumor immune subtypes in postmenopausal, hormone receptor-positive breast cancer patients treated with adjuvant endocrine therapy: a Dutch TEAM study analysis.Breast cancer research and treatment · 2015Trial
- Killer cell immunoglobulin-like receptor genes in patients with breast cancer.Medical oncology (Northwood, London, England) · 2012Trial
- Long-term follow-up of patients treated by adoptive transfer of melanoma tumor-infiltrating lymphocytes as adjuvant therapy for stage III melanoma.Cancer immunology, immunotherapy : CII · 2007Trial
- Beyond KIR and NKG2A blockade: reprogramming NK-cell immunity in solid tumors.Frontiers in cell and developmental biology · 2026Review
- A novel NKG2A alpaca nanobody targeting immune checkpoint blockade for the treatment of malignant melanoma.Frontiers in veterinary science · 2025Article
- Targeting of Non-Classical Human Leukocyte Antigens as Novel Therapeutic Strategies in Cancer.Cancers · 2024Review
- Modulation of MHC expression by interferon-gamma and its influence on PBMC-mediated cytotoxicity in canine mast cell tumour cells.Scientific reports · 2024Article
- HLA-G expression associates with immune evasion muscle-invasive urothelial cancer and drives prognostic relevance.Frontiers in immunology · 2024Article
- NK cells-derived extracellular vesicles potency in the B cell lymphoma biotherapy.Frontiers in immunology · 2024Article
- Suppression of MCP-1, IFN-γ and IL-6 production of HNSCCFrontiers in immunology · 2024Article
- Defining the Basal and Immunomodulatory Mediator-Induced Phosphoprotein Signature in Pediatric B Cell Acute Lymphoblastic Leukemia (B-ALL) Diagnostic Samples.International journal of molecular sciences · 2023Article
- Cytoplasmic localization of IRF5 induces Wnt5a/E-cadherin degradation and promotes gastric cancer cells metastasis.Cancer gene therapy · 2023Article
- A non-genetic engineering platform for rapidly generating and expanding cancer-specific armed T cells.Journal of biomedical science · 2023Article
- Immune checkpoint blockade induced shifts in cytokine expression patterns in peripheral blood of head and neck cancer patients are linked to outcome.Frontiers in immunology · 2023Article
- Role of HLA-I Structural Variants and the Polyreactive Antibodies They Generate in Immune Homeostasis.Antibodies (Basel, Switzerland) · 2022Review
- HLA-G and single nucleotide polymorphism (SNP) associations with cancer in African populations: Implications in personal medicine.Genes & diseases · 2022Review
- NKG2A-checkpoint inhibition and its blockade critically depends on peptides presented by its ligand HLA-E.Immunology · 2022Article
- Nanotechnology-Based siRNA Delivery Systems to Overcome Tumor Immune Evasion in Cancer Immunotherapy.Pharmaceutics · 2022Review
- Article
- Four Faces of Cell-Surface HLA Class-I: Their Antigenic and Immunogenic Divergence Generating Novel Targets for Vaccines.Vaccines · 2022Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor immune escape variants can be identified in human and experimental tumors. A variety of different strategies are used by tumor cells to avoid recognition by different immune effector mechanisms. Among these escape routes, alteration of MHC class I cell surface expression is one of the mechanisms most widely used by tumor cells. In this review we focus our attention on the T-cell immune selection of MHC class I-deficient tumor variants. Different altered MHC class I phenotypes that originate from multiple molecular mechanisms can be identified in human tumors. MHC-deficient tumor clones can escape T-cell immune responses, but are in theory more susceptible to NK-cell-mediated lysis. In this context, we also review the controversial issue of the aberrant expression of nonclassical HLA class I molecules, particularly HLA-G, in tumors. This expression may be relevant in tumor cells that have lost the capacity to interact with NK inhibitory receptors-namely, those tumor cells with no HLA-B or HLA-C expression. Most published studies have not analyzed these possibilities and do not provide information about the complete HLA-A, HLA-B, or HLA-C molecule profiles of the tumors studied. In contrast, HLA-E has been reported to be expressed in some tumor cell lines with very low HLA-A, HLA-B, and HLA-C expression, suggesting that HLA-E may indeed, in some cases, play a role by inhibiting NK lysis of cells that otherwise would be destroyed by NK cells. Finally, we provide evidence that the status of the immune system in the tumor-bearing animal is capable of defining the MHC profile of the tumor cells. In other words, MHC class I-negative metastatic colonies are produced in immunocompetent animals, and MHC class I-positive colonies in T-cell immunodeficient individuals.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.