The link between MHC class I abnormalities of tumors, oncogenes, tumor suppressor genes, and transcription factors

Seliger, Barbara

doi:10.3109/1547691x.2013.875084

Cited by 33 publications

(23 citation statements)

References 21 publications

(22 reference statements)

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“…Deficiencies in components of the antigen-processing machinery in tumors have been correlated with poor prognosis and metastasis, and the urge to find therapies for these immune-escaped variants becomes urgent now that immunotherapy reaches clinical success (10,(32)(33)(34)(35)(36). The delayed tumor outgrowth of the aggressive MHC-I lo lymphoma RMA-S tumor after TEIPP T cell transfer and vaccination nicely illustrated the antitumor potency of this CD8 + T cell subset and provides us with tools to counteract tumors that have escaped from conventional immunotherapies.…”

Section: Methodsmentioning

confidence: 99%

TAP-independent self-peptides enhance T cell recognition of immune-escaped tumors

Doorduijn¹,

Sluijter²,

Querido³

et al. 2016

Journal of Clinical Investigation

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Section: Methodsmentioning

confidence: 99%

TAP-independent self-peptides enhance T cell recognition of immune-escaped tumors

Doorduijn¹,

Sluijter²,

Querido³

et al. 2016

Journal of Clinical Investigation

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“…Alterations of HLA class I APM and their significance in malignant tumors have been recently reviewed by various groups and we refer the interested reader to these reviews. [3][4][5][6][7][8] In contrast, HLA class II antigens expressed by malignant cells of solid tumors have been characterized only to a limited extent, although the aberrant expression of HLA class II antigens by melanoma cells was first described more than 30 y ago. 9 Growing evidence indicates that HLA class II antigen expression by tumor cells has a significant impact on their immunogenicity.…”

Section: Introductionmentioning

confidence: 99%

HLA class II antigen-processing pathway in tumors: Molecular defects and clinical relevance

2017

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The human leukocyte antigen (HLA) class II antigen-processing machinery (APM) presents to cognate CD4 C T-cells antigenic peptides mainly generated from exogeneous proteins in the endocytic compartment. These CD4 C T cells exert helper function, but may also act as effector cells, thereby recognizing HLA class II antigen-expressing tumor cells. Thus, HLA class II antigen expression by tumor cells influences the tumor antigen (TA)-specific immune responses and, depending on the cancer type, the clinical course of the disease. Many types of human cancers express HLA class II antigens, although with marked differences in their frequency. Some types of cancer lack HLA class II antigen expression, which could be due to structural defects or deregulation affecting different components of the complex HLA class II APM and/or from lack of cytokine(s) in the tumor microenvironment. In this review, we have summarized the information about HLA class II antigen distribution in normal tissues, the structural organization of the HLA class II APM, their expression and regulation in malignant cells, the defects, which have been identified in malignant cells, and their functional and clinical relevance.

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“…Many types of malignancies have been shown to express abnormal MHC class I, including MHC class I with structurally altered heavy chains, mutated β 2 -microglobulin and TAP1, or dysregulated antigen processing machinery, leading to reduced or absent MHC class I expression (Seliger, 2008, 2014). This dysregulation makes tumor cells susceptible to killing by NK cells, which target cells lacking MHC class I (Seliger, 2008).…”

Section: Platelets and Cancer Progressionmentioning

confidence: 99%

Cancer and Thrombosis: The Platelet Perspective

Meikle

Kelly

Garg

et al. 2017

Front. Cell Dev. Biol.

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Platelets are critical to hemostatic and immunological function, and are key players in cancer progression, metastasis, and cancer-related thrombosis. Platelets interact with immune cells to stimulate anti-tumor responses and can be activated by immune cells and tumor cells. Platelet activation can lead to complex interactions between platelets and tumor cells. Platelets facilitate cancer progression and metastasis by: (1) forming aggregates with tumor cells; (2) inducing tumor growth, epithelial-mesenchymal transition, and invasion; (3) shielding circulating tumor cells from immune surveillance and killing; (4) facilitating tethering and arrest of circulating tumor cells; and (5) promoting angiogenesis and tumor cell establishment at distant sites. Tumor cell-activated platelets also predispose cancer patients to thrombotic events. Tumor cells and tumor-derived microparticles lead to thrombosis by secreting procoagulant factors, resulting in platelet activation and clotting. Platelets play a critical role in cancer progression and thrombosis, and markers of platelet-tumor cell interaction are candidates as biomarkers for cancer progression and thrombosis risk.

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The link between MHC class I abnormalities of tumors, oncogenes, tumor suppressor genes, and transcription factors

Cited by 33 publications

References 21 publications

TAP-independent self-peptides enhance T cell recognition of immune-escaped tumors

TAP-independent self-peptides enhance T cell recognition of immune-escaped tumors

HLA class II antigen-processing pathway in tumors: Molecular defects and clinical relevance

Cancer and Thrombosis: The Platelet Perspective

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