ReviewOncoimmunology2013
How to exploit stress-related immunity against Hodgkin's lymphoma: Targeting ERp5 and ADAM sheddases.
Review in Oncoimmunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Melanoma RBPome identification reveals PDIA6 as an unconventional RNA-binding protein involved in metastasis.Nucleic acids research · 2022Article
- Editorial: ADAM10 in Cancer Immunology and Autoimmunity: More Than a Simple Biochemical Scissor.Frontiers in immunology · 2020Article
- Acquired Natural Killer Cell Dysfunction in the Tumor Microenvironment of Classic Hodgkin Lymphoma.Frontiers in immunology · 2018Review
- Mesenchymal Stromal Cells Can Regulate the Immune Response in the Tumor Microenvironment.Vaccines · 2016Review
- Mesenchymal stromal cells as regulators of anti-tumour immune response.The Indian journal of medical research · 2015Article
- Trial Watch: Proteasomal inhibitors for anticancer therapy.Molecular & cellular oncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress-related immunity can be activated in the course of lymphoproliferative disorders, including Hodgkin's lymphoma, upon the interaction between killer cell lectin-like receptor subfamily K, member 1 (KLRK1, best known as NKG2D) on effector lymphocytes and NKG2D ligands (NKG2DL), such as MHC class I polypeptide-related sequence A (MICA), MICB and various UL16-binding proteins (ULBPs), on lymphoma cells. However, NKG2DLs can also bind NKG2D upon shedding, thus affecting the recognition of lymphoma cells by the immune system. The proteolytic cleavage of MICA depends on protein disulfide isomerase family A, member 6 (PDIA6, a thiol isomerase best known as ERp5) as well as on the disintegrins and metalloproteinases ADAM metallopeptidase domain 10 (ADAM10) and ADAM17, which also cleave ULPBs. These enzymes can be targeted in novel therapeutic schemes to avoid the escape of malignant cells from stress-evoked immune responses.
Indexed as
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What OpenQuestion holds
Registered trials
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.