On the mechanism of tumor ‘concomitant immunity’

Gorelik, Eliezer; Segal, Shraga; Feldman, Michaël

doi:10.1002/ijc.2910270618

Cited by 46 publications

(44 citation statements)

References 12 publications

(20 reference statements)

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“…The "concomitant immunity hypothesis" was originally suggested to explain resistance to secondary tumors or infections, particularly in animal models (10,70). As an ongoing persistent infection can protect the host from the same infection, similarly, in animal models, immunity to the original tumor can prevent growth of a comparable mass (10,71).…”

Section: Induction Of Preimmunitymentioning

confidence: 99%

“…As an ongoing persistent infection can protect the host from the same infection, similarly, in animal models, immunity to the original tumor can prevent growth of a comparable mass (10,71). Concomitant immunity was considered the result of either immunogenic factors, for example common antigenic epitopes, or nonimmunogenic factors, such as putative antimitotic components (10).…”

Section: Induction Of Preimmunitymentioning

confidence: 99%

“…The concomitant effect may be abrogated once the original tumor is removed. It has also been observed that anticancer immunity can be present after the removal of the original malignant mass, a phenomenon termed sinecomitant immunity (10,71) that can potentially be attributed to the parallel removal of tumor-induced immunosuppression.…”

Section: Induction Of Preimmunitymentioning

confidence: 99%

“…Attention is drawn to the hygiene hypothesis that attempts to explain the increased incidence of pathologies such as allergies, autoimmune diseases, and cancer in the industrial world. Several historical observations and other theories, such as hormesis (9) and concomitant immunity (10), are revisited to lend more credence to the hygiene hypothesis.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Infection and Cancer: Revaluation of the Hygiene Hypothesis

Οικονομοπούλου

Brinc

Kyriacou

et al. 2013

Clinical Cancer Research

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Several studies have shown that persistent infections and inflammation can favor carcinogenesis. At the same time, certain types of pathogens and antitumor immune responses can decrease the risk of tumorigenesis or lead to cancer regression. Infectious agents and their products can orchestrate a wide range of host immune responses, through which they may positively or negatively modulate cancer development and/or progression. The factors that direct this dichotomous influence of infection-mediated immunity on carcinogenesis are not well understood. Even though not universal, several previous reports have investigated the inverse link of pathogen-induced "benign" inflammation to carcinogenesis and various other pathologies, ranging from autoimmune diseases to allergy and cancer. Several models and ideas are discussed in this review, including the impact of decreased exposure to pathogens, as well as the influence of pathogen load, the timing of infection, and the type of instigated immune response on carcinogenesis. These phenomena should guide future investigations into identifying novel targets within the microbial and host proteome, which will assist in the development of cancer therapeutics and vaccine remedies, analogous to earlier efforts based on helminthic components for the prevention and/or treatment of several pathologies.

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Section: Induction Of Preimmunitymentioning

confidence: 99%

Section: Induction Of Preimmunitymentioning

confidence: 99%

Section: Induction Of Preimmunitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Infection and Cancer: Revaluation of the Hygiene Hypothesis

Οικονομοπούλου

Brinc

Kyriacou

et al. 2013

Clinical Cancer Research

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“…Because the LB tumour itself can both induce CI and be affected by antiinflammation, it would be expected that a primary tumour inoculum could also inhibit the growth of a secondary inoculum of the same tumour. Inhibition of experimental metastases by a primary tumour has been observed in laboratory animals (Gorelik et al, 1978) and defined as 'concomitant immunity' (Gorelik et al, 1981) or, more appropriately, 'concomitant resistance' (Meiss et al, 1986), a non-specific, rapid, dose-dependent and complex phenomenon. The molecular basis of concomitant resistance remains unknown, but it is speculated that several mechanisms may be acting either simultaneously or sequentially.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammation induced by counter-irritation or by treatment with non-steroidal agents inhibits the growth of a tumour of non-detected immunogenicity

Sordelli

Fontán²,

Meiss³

et al. 1989

Br J Cancer

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Summary Counter-irritation (CI) triggered by different non-specific irritant stimuli delayed the growth of a murine tumour of non-detected immunogenicity. The syngeneic LB tumour transplant by itself also induced CI and decreased the number of leukocytes migrating to a secondary s.c. irritant stimulus, e.g. sponge or carrageenan. On the other hand, partial inhibition of cell migration by treatment with either 0.5 mg kg' indomethacin or 0.3 mg kg-' piroxicam retarded LB tumour growth, presumably by a mechanism unrelated to inhibition of immune responses by PGE2. It is suggested that Cl may play a role in the early stages of concomitant resistance.

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Antigen-specific therapy of experimental metastases

Nomi¹,

Pellis²,

Kahan³

1985

Cancer

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In a methylcholanthrene‐induced tumor (MCA‐F) model in C3H/HeJ mice, curative resection of a progressive tumor promotes artificial lung metastases following intravenous injection of a highly metastatic cell variant designated clone 9‐4. The number of metastatic lung colonies depends upon the status of host immunity at the tumor resection: mice resected 7 or 14 days, but not 28 days after tumor inoculation display significantly retarded postoperative, experimentally induced lung metastases. The number of lung colonies in mice that had tumors resected at 14 days was three times greater than in mice that had 28‐day neoplasms resected. Neither therapy with weekly injection of 50 μg tumorspecific transplantation antigen, which had been extracted using a single phase of 2.5% 1‐butanol (CBE), nor 20 mg/kg cyclophosphamide (CY) alone prevented lung colonization. Assessment of helper‐suppressor ratios in the spleen from mice after tumor surgery showed that CBE administration decreased the ratio in mice after resection of 14‐day tumors, but not after resection of 28‐day tumors. Combined therapy with specific tumor antigen and an antisuppressor cell agent reduced metastases, regardless of the tumor size. Cancer 55:1296‐1302, 1985.

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On the mechanism of tumor ‘concomitant immunity’

Abstract: Experiments were carried out relevant to the mechanisms involved in tumor "concomitant immunity". Mice bearing 3LL, 816, EL4 or the methylcholanthrene-induced T-I0 tumors were capable of completely

Cited by 46 publications

References 12 publications

Infection and Cancer: Revaluation of the Hygiene Hypothesis

Infection and Cancer: Revaluation of the Hygiene Hypothesis

Anti-inflammation induced by counter-irritation or by treatment with non-steroidal agents inhibits the growth of a tumour of non-detected immunogenicity

Antigen-specific therapy of experimental metastases

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