ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009
Immunodeficient mouse strains display marked variability in growth of human melanoma lung metastases.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
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- Boosting Natural Killer Cell-Mediated Targeting of Sarcoma Through DNAM-1 and NKG2D.Frontiers in immunology · 2020Article
- AZ304, a novel dual BRAF inhibitor, exerts anti-tumour effects in colorectal cancer independently of BRAF genetic status.British journal of cancer · 2018Article
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- A therapeutic T cell receptor mimic antibody targets tumor-associated PRAME peptide/HLA-I antigens.The Journal of clinical investigation · 2017Article
- Murine Tumor Models for Oncolytic Rhabdo-Virotherapy.ILAR journal · 2016Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
purposeImmunodeficient mice serve as critical hosts for transplantation of xenogeneic cells for in vivo analysis of various biological processes. Because investigators typically select one or two immunodeficient mouse strains as recipients, no comprehensive study has been published documenting differences in human tumor engraftment. Taking advantage of the increased metastatic potential of RhoC-expressing human (A375) melanoma cells, we evaluate four immunodeficient mouse strains: severe combined immunodeficiency (scid), nonobese diabetic (NOD)-scid, NOD-scid beta2m(null), and NOD-scid IL2Rgamma(null) as xenograft tumor recipients. EXPERIMENTAL
designBioluminescence, magnetic resonance imaging, and histopathology were used to monitor serial tumor growth. Natural killer (NK) cell function was examined in each mouse strain using standard (51)Chromium release assays.
resultsMelanoma metastases growth is delayed and variable in scid and NOD-scid mice. In contrast, NOD-scid beta2m(null) and NOD-scid IL2Rgamma(null) mice show rapid tumor engraftment, although tumor growth is variable in NOD-scid beta2m(null) mice. NK cells were detected in all strains except NOD-scid IL2Rgamma(null), and in vitro activated scid, NOD-scid, and NOD-scid beta2m(null) NK cells kill human melanoma lines and primary melanoma cells. Expression of human NKG2D ligands MHC class I chain-related A and B molecules renders melanoma susceptible to murine NK cell-mediated cytotoxicity and killing is inhibited by antibody blockade of murine NKG2D.
conclusionsMurine NKG2D recognition of MICA/B is an important receptor-ligand interaction used by NK cells in immunodeficient strains to limit engraftment of human tumors. The absolute NK deficiency in NOD-scid IL2Rgamma(null) animals makes this strain an excellent recipient of melanoma and potentially other human malignancies.
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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.