ReviewCancer2010
Killing tumor cells through their surface beta(2)-microglobulin or major histocompatibility complex class I molecules.
Review in Cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 32 citations in OpenAlex.
- Disrupted Redox Regulation and Inflammatory Response in Pyoderma Gangrenosum.Life (Basel, Switzerland) · 2025Article
- β2-microglobulin induced apoptosis of tumor cells via the ERK signaling pathway by directly interacting with HFE in HER2-overexpressing breast cancer.BMC cancer · 2024Article
- Molecular and translational biology of the blood-based VeriStrat® proteomic test used in cancer immunotherapy treatment guidance.Journal of mass spectrometry and advances in the clinical lab · 2023Article
- β2-microglobulin and colorectal cancer among inpatients: a case-control study.Scientific reports · 2023Article
- Proteomic Analysis Reveals a Novel Therapeutic Strategy Using Fludarabine for Steroid-Resistant Asthma Exacerbation.Frontiers in immunology · 2022Article
- Combined Diagnostic Significance of Preoperative Serum β2-Microglobulin and Routine Blood Test in Patients with High-grade Glioma and Solitary Brain Metastasis.Cancer management and research · 2020Article
- Reverse Signaling by MHC-I Molecules in Immune and Non-Immune Cell Types.Frontiers in immunology · 2020Review
- Promotion on NLRC5 upregulating MHC-I expression by IFN-γ in MHC-I-deficient breast cancer cells.Immunologic research · 2019Article
- MHC Class I Molecules Exacerbate Viral Infection by Disrupting Type I Interferon Signaling.Journal of immunology research · 2019Article
- SV-BR-1-GM, a Clinically Effective GM-CSF-Secreting Breast Cancer Cell Line, Expresses an Immune Signature and Directly Activates CD4Frontiers in immunology · 2018Article
- Frequent HLA class I alterations in human prostate cancer: molecular mechanisms and clinical relevance.Cancer immunology, immunotherapy : CII · 2016Article
- ATP5b and β2-microglobulin are predictive markers for the prognosis of patients with gallbladder cancer.Journal of molecular histology · 2015Article
- β2-Microglobulin-mediated signaling as a target for cancer therapy.Anti-cancer agents in medicinal chemistry · 2014Review
- Tumor necrosis factor α-induced hypoxia-inducible factor 1α-β-catenin axis regulates major histocompatibility complex class I gene activation through chromatin remodeling.Molecular and cellular biology · 2013Article
- Article
- Supernatants from lymphocytes stimulated with Bacillus Calmette-Guerin can modify the antigenicity of tumours and stimulate allogeneic T-cell responses.British journal of cancer · 2011Article
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 1 institution in 1 country.
Funding
Abstract
Targeted antibody-based therapy has been used successfully to treat cancers. Recent studies have demonstrated that tumor cells treated with antibodies specific for beta(2)-microglobulin (beta(2)M) or major histocompatibility complex (MHC) class I molecules undergo apoptosis in vitro and in vivo (mouse models). Antibodies against beta(2)M or MHC class I induce tumor cell apoptosis by 1) recruiting MHC class I molecules to lipid rafts and activating LYN kinase and the signal-transducing enzyme phospholipase C-gamma2-dependent c-Jun N-terminal kinase signaling pathway and 2) expelling interleukin 6 and insulin-like growth factor 1 receptors out of lipid rafts and inhibiting the growth and survival factor-induced activation of the phosphatidylinositol 3-kinase/Akt and extracellular signal-related kinase pathways. Consequently, mitochondrial integrity is compromised, and the caspase-9-dependent cascade is activated in treated tumor cells. However, although beta(2)M and MHC class I are expressed on normal hematopoietic cells, which is a potential safety concern, the monoclonal antibodies were selective to tumor cells and did not damage normal cells in vitro or in human-like mouse models. These findings suggest that targeting beta(2)M or MHC class I by using antibodies or other agents offers a potential therapeutic approach for beta(2)M/MHC class I-expressing malignancies. Cancer 2010. (c) 2010 American Cancer Society.
Indexed as
Identifiers
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.