An Immunostimulation Theory of Tumor Development

Prehn, Richmond T.; Lappé, Marc

doi:10.1111/j.1600-065x.1971.tb00462.x

Cited by 88 publications

(53 citation statements)

References 110 publications

(75 reference statements)

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“…It seems feasible that the role of macrophages (and bone-marrow-containing monocytemacrophage precursors) might be in antigen processing or in increased availability for effector function (specific or nonspecific), or both. In effect, a considerable body of evidence shows that the immune defect in neonates can be repaired by adult macrophages or their precursors (Argyris, 1968;Blaese, 1975 The increased frequency of tumours observed in the newborn recipients after the transfer of low numbers of spleen, neutrophils or thymus cells may be the result of a mechanism of tumour immunostimulation as proposed by Prehn (1972), Prehn and Lappe (1971). An apparently similar block or enhancement exerted by different cell numbers has been reported in several systems, both in vitro (Prehn, 1972;Klein, 1972;Fidler, 1973;Fidler, Brodey and Bech-Nielsen, 1974;Kall and Hellstrom, 1975;Nathan and Terry, 1975) and in vivo (Belayev and Gruntenko, 1972;Fidler, 1974;Carnaud et al, 1974;Umiel and Trainin, 1974).…”

Section: Discussionmentioning

confidence: 99%

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Induction of resistance or enhancement to a transplantable murine plasmacytoma by transfer of non-immune leucocytes

Giovarelli¹,

Comoglio

Forni³

1976

Br J Cancer

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Newborn mice have a lower spontaneous resistance to the growth of a syngeneic plasmacytoma (MOPC-460) as compared to adult mice. The transfer of different leucocyte populations from non-immunized adult donors to newborn mice influence in a dual way the resistance to MOPC-460 growth, depending on the number of cells transferred. The transfer of a low number of neutrophils, thymus or spleen cells enhances the MOPC-460 takes. Higher numbers of neutrophils, thymus or bone marrow cells induce an effective protenction. By contrast, macrophages over a dose of 1 X 10(4) constantly produce a reduction of tumour growth.

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Section: Discussionmentioning

confidence: 99%

“…These contrasting findings can be interpreted by the theory, advanced by Prehn, that the effect of immunity might be biphasic, that is, a mild incipient immune response may be stimulatory to tumour growth but a strong one can be inhibitory (Prehn and Lappe, 1971).…”

mentioning

confidence: 99%

Induction of resistance or enhancement to a transplantable murine plasmacytoma by transfer of non-immune leucocytes

Giovarelli¹,

Comoglio

Forni³

1976

Br J Cancer

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“…The association between inflammation and cancer has been recognized for over a century and has led some to suggest that under some circumstances, a weak immune response promotes, rather than inhibits the development of cancer [32][33][34]. Recent studies demonstrated that αβ T cell deficiency was associated with reduced progression of chemically induced cancers [35,36].…”

Section: Neither Fish Nor Foul: Tumor-promoting Cd8 + T Cells Withoutmentioning

confidence: 99%

Emerging concepts in CD8+ T regulatory cells

Niederkorn

2008

Current Opinion in Immunology

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SummaryCD8 + T regs are elicited by unique antigen presenting cells during viral infections, by manipulation of co-stimulatory molecules, or in the development of tumors. CD8 + T regs display antigenspecificity, which is most exquisitely manifested by the HLA-E-restricted cytolytic CD8 + T regs in MS. There is evidence that some CD8 + T regs also express organ specificity. In many cases, IFN-γ is required for either the induction or expression of CD8 + T regs. CD8 + T regs can produce suppression directly by killing immune cells or indirectly by co-opting other cells to elaborate endstage suppressive molecules such as TGF-β, IL-10, and indoleamine dioxygenase (IDO).

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“…His description is presumably the first report of the link between inflammation and cancer. In the 1970s, Prehn proposed that immune effector cells contributed to carcinogenesis and named the phenomenon as "immunostimulation theory of tumor development" [4]. In the 1980s, cancer epidemiological studies identified chronic infections and inflammation as the major risk factors of various types of cancer.…”

Section: Inflammation-based Carcinogenesismentioning

confidence: 99%

Molecular Mechanisms of Inflammation-Induced Carcinogenesis

Okada

Fujii

2006

J. Clin. Biochem. Nutr.

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Summary Chronic inflammation has been thought as the major risk factor for various types of human cancer. The International Agency for Research on Cancer (IARC) has estimated that approximately one-fifth of cancer cases worldwide is attributable to infectious/inflammatory diseases. While we fundamentally understand that persistent inflammation plays a role in carcinogenesis, recent advances in the molecular study of the mechanisms have revealed that reactive oxygen and nitrogen species, harmful endogenous genotoxic substances, produced by inflammatory cells are largely involved in the carcinogenic process. In this article, we review the instances demonstrating the definite link between inflammation and cancer, and shed light on the molecular mechanisms proved to be responsible for the inflammation-based carcinogenesis.

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An Immunostimulation Theory of Tumor Development

Cited by 88 publications

References 110 publications

Induction of resistance or enhancement to a transplantable murine plasmacytoma by transfer of non-immune leucocytes

Induction of resistance or enhancement to a transplantable murine plasmacytoma by transfer of non-immune leucocytes

Emerging concepts in CD8+ T regulatory cells

Molecular Mechanisms of Inflammation-Induced Carcinogenesis

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