Puzzling and ambivalent roles of malarial infections in cancer development and progression

Faure, Éric

doi:10.1017/s0031182016001591

Cited by 5 publications

(2 citation statements)

References 113 publications

(246 reference statements)

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“…The impact of selected protozoan and helminth parasites on the spread of different cancers has been widely studied [9,10]. Most of the research work has been done on the carcinogenic role of Schistosoma haematobium (Bilharz), Opisthorchis viverrini (Poirier) Stiles & Hassall, and Clonorchis sinensis (Cobbold) [9], but important knowledge is also available about the association between malaria and carcinogenesis [11], with special reference to endemic Burkitt lymphoma [12,13,14,15].…”

Section: Hypothesis 1: Infection Of Mosquito-vectored Parasites Mamentioning

confidence: 99%

Mosquitoes, Infectious Diseases, and Cancer: A Connection to Study?

Marcondes

Benelli

2019

IJERPH

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Mosquitoes (Diptera: Culicidae) are vectors of pathogens and parasites of great medical and veterinary relevance. The possible association between mosquitoes, infectious diseases, and cancer has been investigated. Despite its potential importance, there is a severe lack of research data on the topic. Herein, current knowledge, tenuous links, and related challenges on the topic were examined, grouping information under four major hypotheses. The first hypothesis is that the infection of mosquito-vectored parasites, with special reference to Plasmodium spp., may lead to cancer. The International Agency for Research on Cancer stated that being infected by Plasmodium falciparum malaria in holoendemic areas is probably carcinogenic to humans (group 2A), considering that P. falciparum infection is able to reactivate the Epstein–Barr virus, leading to endemic Burkitt lymphoma. Also, malaria was recently associated with a cancer incidence increase in the United States. The second hypothesis is that cancer may be spread directly through mosquito bites: Aedes mosquitoes transfer viable tumor cells among vertebrate hosts, even if no plausible mechanisms for these cells to develop cancer into the new host are known. As the third hypothesis, mosquito bites may lead to hypersensitivity, resulting in cancer. Hypersensitivity stimulated by mosquito bites links allergy, oncogenesis, and the Epstein–Barr virus, causing Burkitt lymphoma. One may argue that pathogens transmitted by mosquitoes, such as viruses, may be carcinogenic. However, no detailed research evidences are available to substantiate this last hypothesis. However, despite the intriguing hypotheses outlined above, there is a severe lack of data showing cancer development in organisms exposed to mosquitoes transmitting parasites or pathogens. According to One Health criteria, this benchmark is aimed to outline major questions on this public health issue, stressing the need of multidisciplinary research and discussion.

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Section: Hypothesis 1: Infection Of Mosquito-vectored Parasites Mamentioning

confidence: 99%

Mosquitoes, Infectious Diseases, and Cancer: A Connection to Study?

Marcondes

Benelli

2019

IJERPH

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“…The cohort study indicates an association between confirmed malaria cases in individuals of endemic origin and cases of lymphoid neoplasm [ 34 ]. The capacity of malaria to promote the development and evolution of cancer can be associated with chronic inflammation, modulation of the immune system in the host, change in glucose metabolism, destabilization of suppressor tumor proteins, stimulation of angiogenesis, activation of invasion and metastasis [ 35 ].…”

Section: Introductionmentioning

confidence: 99%

The Nociceptive and Inflammatory Responses Induced by the Ehrlich Solid Tumor Are Changed in Mice Healed of Plasmodium berghei Strain ANKA Infection after Chloroquine Treatment

Rodrigues Aguiar,

Guterres,

Benarrosh

et al. 2024

Journal of Parasitology Research

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Comorbidities that involve infectious and noninfectious diseases, such as malaria and cancer, have been described. Cancer and malaria induce changes in the nociceptive and inflammatory responses through similar pathophysiological mechanisms. However, it is unclear whether malaria and antimalarial treatment can change the inflammatory and nociceptive responses induced by solid cancer. Therefore, the present study experimentally evaluated the effect of infection by Plasmodium berghei strain ANKA and chloroquine treatment on the nociceptive and inflammatory responses induced by the solid Ehrlich tumor in male BALB/c mice. On the 1st experimental day, mice were infected with Plasmodium berghei and injected with tumor cells in the left hind paw. From the 7th to the 9th experimental day, mice were treated daily with chloroquine. The parasitemia was evaluated on the 7th and 10th days after infection. On the 11th experimental day, mice were evaluated on the von Frey filament test, the hot plate test, and the paw volume test. At the end of the experimental tests on the 11th day, the peripheral blood of all mice was collected for dosing of IL-1β and TNF-α. The blood parasitemia significantly increased from the 7th to the 10th day. The chloroquine treatment significantly decreased the parasitemia on the 10th day. The presence of the tumor did not significantly change the parasitemia on the 7th and 10th days in mice treated and nontreated with chloroquine. On the 11th day, the mechanical and thermal nociceptive responses significantly increased in mice with tumors. The treatment with antimalarial significantly reduced the mechanical nociceptive response induced by tumors. The hyperalgesia induced by tumors did not change with malaria. The mechanical and thermal hyperalgesia induced by the tumor was significantly reduced in mice treated and healed from malaria. On the 11th day, the volume of the paw injected by the tumor was significantly increased. The mice treated with chloroquine, infected with malaria, or healed of malaria showed reduced paw edema induced by the tumor. Mice with tumors did not show a change in IL-β and TNF-α serum levels. Mice with tumors showed a significant increase in serum levels of IL-1β but not TNF-α when treated with chloroquine, infected with malaria, or healed of malaria. In conclusion, the results show that malaria infection and chloroquine treatment can influence, in synergic form, the nociceptive and inflammatory responses induced by the solid tumor. Moreover, the mechanical antinociception, the thermal hyperalgesia, and the antiedema effect observed in mice treated with chloroquine and healed from malaria can be related to the increase in the serum level of IL-1β.

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