ArticleThe Journal of clinical investigation1993
Lack of HLA class I antigen expression by melanoma cells SK-MEL-33 caused by a reading frameshift in beta 2-microglobulin messenger RNA.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 93 citations in OpenAlex.
- Article
- The immune-related role of beta-2-microglobulin in melanoma.Frontiers in oncology · 2022Review
- Cancer stem cells and macrophages: molecular connections and future perspectives against cancer.Oncotarget · 2021Review
- Prostate cancer health disparities: An immuno-biological perspective.Cancer letters · 2018Article
- The human application of gene therapy to re-program T-cell specificity using chimeric antigen receptors.Chinese journal of cancer · 2014Article
- Mechanisms of action underlying the immunotherapeutic activity of Allovectin in advanced melanoma.Cancer gene therapy · 2012Review
- Implication of the β2-microglobulin gene in the generation of tumor escape phenotypes.Cancer immunology, immunotherapy : CII · 2012Review
- Article
- Article
- Synthesis of beta(2)-microglobulin-free, disulphide-linked HLA-G5 homodimers in human placental villous cytotrophoblast cells.Immunology · 2007Article
- Immunosuppressive strategies that are mediated by tumor cells.Annual review of immunology · 2007Review
- Immune selection of hot-spot beta 2-microglobulin gene mutations, HLA-A2 allospecificity loss, and antigen-processing machinery component down-regulation in melanoma cells derived from recurrent metastases following immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2005Article
- Tumor antigens for cancer immunotherapy: therapeutic potential of xenogeneic DNA vaccines.Journal of translational medicine · 2004Article
- The heavy chain of neonatal Fc receptor for IgG is sequestered in endoplasmic reticulum by forming oligomers in the absence of beta2-microglobulin association.The Biochemical journal · 2002Article
- Selective histocompatibility leukocyte antigen (HLA)-A2 loss caused by aberrant pre-mRNA splicing in 624MEL28 melanoma cells.The Journal of experimental medicine · 1999Article
- Biosynthesis of HLA-C heavy chains in melanoma cells with multiple defects in the expression of HLA-A, -B, -C molecules.British journal of cancer · 1999Article
- beta2-Microglobulin mutations, HLA class I antigen loss, and tumor progression in melanoma.The Journal of clinical investigation · 1998Article
- Metastatic potential of human melanoma cells in nude mice--characterisation of phenotype, cytokine secretion and tumour-associated antigens.British journal of cancer · 1996Article
- Loss of functional beta 2-microglobulin in metastatic melanomas from five patients receiving immunotherapy.Journal of the National Cancer Institute · 1996Article
- HLA associations in the antitumor response against malignant melanoma.Journal of immunotherapy with emphasis on tumor immunology : official journal of the Society for Biological Therapy · 1995Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The lack of HLA class I antigen expression by the melanoma cell line SK-MEL-33 is caused by a unique lesion in beta 2-microglobulin (beta 2-mu). Sequencing of beta 2-mu mRNA detected a guanosine deletion at position 323 in codon 76 that causes a frameshift with a subsequent introduction of a stop codon at a position 54 base upstream of the normal position of the stop codon in the message. The loss of 18 amino acids and the change of 6 amino acids, including a cysteine at position 80 in the carboxy terminus of beta 2-mu, are likely to cause marked changes in the structure of the polypeptide. The latter may account for the inability of beta 2-mu to associate with HLA class I heavy chains and for its lack of reactivity with the anti-beta 2-mu mAb tested. HLA class I antigen expression on SK-MEL-33 cells was reconstituted after transfection with a wild-type B2m gene, therefore indicating that the abnormality of endogenous B2m gene is the only mechanism underlying lack of HLA class I antigen expression by SK-MEL-33 cells. The guanosine deletion in B2m gene was detected also in the melanoma tissue from which SK-MEL-33 cells had originated. Therefore, the molecular lesion identified in the SK-MEL-33 melanoma cell line is not caused by a mutation acquired during growth in vitro but is likely to reflect a somatic mutation during tumor progression.
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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.