ArticleOncotarget2015
Morphometric analysis of immunoselection against hyperploid cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Impact of neoadjuvant cetuximab on liver function and tumor reduction in a murine model of selective portal vein ligation.Clinical & experimental metastasis · 2025Article
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- Mechanisms involved in selecting and maintaining neuroblastoma cancer stem cell populations, and perspectives for therapeutic targeting.World journal of stem cells · 2021Review
- Clonogenic Assays to Detect Cell Fate in Mitotic Catastrophe.Methods in molecular biology (Clifton, N.J.) · 2021Article
- eIF2α phosphorylation is pathognomonic for immunogenic cell death.Cell death and differentiation · 2018Article
- Mouse models in oncoimmunology.Nature reviews. Cancer · 2016Review
- Biomarkers of immunogenic stress in metastases from melanoma patients: Correlations with the immune infiltrate.Oncoimmunology · 2016Article
- Article
- The ratio of CD8OncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An at least transient increase of ploidy, usually by whole genome duplication, is a frequent event in oncogenesis, explaining the cytogenetic features of at least 40% of solid cancers. Here, we show that fibrosarcomas induced by the carcinogen methylcholanthrene (MCA) are distinct with respect to their ploidy status when they arise in immunocompetent wild type versus severely immunodeficient Rag2-/-γc-/- mice. MCA-induced fibrosarcomas are particularly hyperploid if they develop in an immunodeficient setting, correlating with higher DNA content, increased nuclear surface, as well as hyperphosphorylation of eukaryotic initiation factor 2α (eIF2α), a biomarker indicating endoplasmic reticulum (ER) stress. Upon transfer of such cells into wild type mice, such hyperploid, ER-stressed cells (that originated in Rag2-/-γc-/- mice) fail to proliferate and actually induce a protective anticancer immune response. In contrast, such cells do form tumors in Rag2-/-γc-/- recipients (which lack T, B and NK cells) as well as in Rag2-/- recipients (which only lack T and B lymphocytes) and conserve their hyperploidy as well as eIF2α hyperphosphorylation. To measure these parameters, we developed a morphometric analysis tool that is applicable to immunohistochemistry of formaldehyde-fixed, paraffin-embedded tissues. This software automatically identifies and quantifies the surface of nuclei and determines the intensity of eIF2α phosphorylation within a perinuclear region of interest. Comparative analyses performed on cultured cells and tissue sections validated the accuracy of this method, which can be used to investigate ploidy and ER stress in cancers in situ.
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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.