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Accueil Cancer de la prostate Le cancer de la prostate : diagnostic et classification. Diagnostic et classification Les traitements. Sources: Les traitements du cancer de la prostate, collection Guides patients Cancer Info, INCa, novembre La prise en charge du cancer de la prostate. Boissier www. Wiley Blackwell. Epidemiology, screening, pathology and pathogenesis. Urological Oncology. National Comprehensive Cancer Network. Glossaire Antibiotique. Substance produite par la prostate qui circule dans le sang. This site complies with the HONcode standard for trustworthy health information.
This analysis was performed without knowledge of baseline characteristics. Using log rank tests on Kaplan Meier nonparametric estimates of the survival without cancer distribution, we selected variables with a P value lower than, or equal to, 0. Gender and age being potential confounding variables, they were also entered into the Cox model, no matter the significance of their relationships with death. Tobacco consumption was accounted for as currently smoking versus nonsmoking definition variables.
Therefore, when P value is less than 0. Among patients with positive CMV serology at transplant, There was a similar rate of CMV disease or infection As a whole, patients developed either CMV infection or disease. Therefore, ATG use was forced in the Cox model for further analyses. For cancer with at least four cases, the ratio exceeds three for lung, prostate, oesophagus, uterus and colon carcinomas. One hundred and three Cox regression analysis revealed that age HR, 1.
Le cancer de la prostate : diagnostic et classification
Patients included in this subanalysis did not differ from the main cohort data not shown. The proportion of CD4 T cells was similar in the two groups. As CMV is not considered to be directly oncogenic, other mechanisms may be involved to explain the association between viral exposure and cancer. Collectively, all these results suggest that CMV contributes to the increased risk of cancer in transplant patients. Loss of CD28 and gain of CD57 are well described markers of immune exhaustion [ 15 ].
Exhaustion is characterized by the progressive loss of T cell function. Functional exhaustion develops when there is a high antigenic load and is considered to be a way of limiting the magnitude of effector T cell responses. Although this may be relevant against autoimmune responses, it may also compromise effective immunity against infectious agents and tumours [ 18 , 19 ]. CMV reactivation may further stimulate immune exhaustion and increase the risk of cancer. This suggests that repeated immune challenges drive immune exhaustion, which could reduce immunity against cancer.
Other mechanisms could be involved to explain the link between CMV and cancer. A number of investigations on infected tumour cell lines has implied that CMV infection may interfere with several key cellular signalling pathways, leading to enhanced survival and angiogenesis, as well as alterations in cell motility and adhesion [ 8 ]. For instance, US28, a viral G protein, activates signalling pathways linked to cell proliferation [ 20 ].
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This virus may also be involved in mutagenesis, inhibition of apoptosis, angiogenesis, cell invasion and modulation of the host immune system [ 21 - 23 ]. However, other observations have suggested that CMV may help in antitumour immunity.
Nevertheless, the very small number of patients seriously hampers the results of this study. However, the net effect of CMV on oncogenesis may depend from different parameters.
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CMV has been described as a possible risk factor for lung cancer in the general population. Indeed, CMV has been detected in lung carcinoma [ 26 ]. CMV has been also identified in these tumours in immunocompetent patients [ 6 , 8 , 9 ].
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Our study has some limitations. Bias inherent to retrospective studies cannot be excluded. Moreover, confounding factors associated with CMV exposure cannot be ruled out even when most of those implicated in cancer occurrence after transplantation have been taken into account. We considered all types of cancer.
Mechanisms involved in carcinogenesis may vary from one cancer to another, but a defect in immune surveillance may have an impact on different types of cancer.
Whether markers of immune exhaustion could help to define the individual risk of cancer should be assessed in future studies. CC and DD: wrote the paper. PT: reviewed the manuscript.
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This study is supported by grants from the Fondation de Transplantation. Volume 25 , Issue 9. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account. If the address matches an existing account you will receive an email with instructions to retrieve your username. Transplant International Volume 25, Issue 9.
Conflicts of Interest: The authors have declared no conflicts of interests. Tools Request permission Export citation Add to favorites Track citation. Share Give access Share full text access.
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Share full text access. Please review our Terms and Conditions of Use and check box below to share full-text version of article. Patients and methods Study design and populations We analysed a prospective cohort of consecutive RTR. CMV, cytomegalovirus. CMV disease was defined by the need of treatment in a patient with viral replication.