ReviewTheoretical biology & medical modelling2007
Does the immune reaction cause malignant transformation by disrupting cell-to-cell or cell-to-matrix communications?
Review in Theoretical biology & medical modelling, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Tumor inhibitory T cell immunity may be largely a transplantation artifact not necessarily dependent upon a lack of Tregs.Theoretical biology & medical modelling · 2013Article
- A new kink in an old theory of carcinogenesis.Theoretical biology & medical modelling · 2013Article
- Immunoediting: evidence of the multifaceted role of the immune system in self-metastatic tumor growth.Theoretical biology & medical modelling · 2012Article
- Immunogenicity of premalignant lesions is the primary cause of general cytotoxic T lymphocyte unresponsiveness.The Journal of experimental medicine · 2008Article
- Emerging concepts in CD8(+) T regulatory cells.Current opinion in immunology · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
tumor progressionIn many (perhaps in all) tumor systems, a malignant cancer is preceded by a benign lesion. Most benign lesions do not transform to malignancy and many regress. The final transformative step to malignancy differs from the preceding steps in, among other things, that it often occurs in the absence of the original carcinogenic stimulus. MECHANISM OF IMMUNOSTIMULATION: Relatively low titers of specific immune reactants are known to stimulate, but cell-to-cell or cell-to-matrix interactions appear to be major inhibitors of tumor-growth. Therefore, it seems reasonable to hypothesize that the mechanism of immunostimulation may be an interference with cell-to-cell or cell-to-matrix communication by a sub-lethal immune-reaction. DISCUSSION: While the above hypothesis remains unproven, some evidence suggests that immunity may have a major facilitating effect on tumor growth especially at the time of malignant transformation. There is even some evidence suggesting that transformation in vivo may seldom occur in the absence of immunostimulation of the premalignant lesion. Positive selection by the immune reaction may be the reason that tumors are immunogenic.
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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.