Joint Nordic prospective study on human herpesvirus 8 and multiple myeloma risk

Tedeschi, Rosamaria; Luostarinen, Tapio; Paoli, Paolo De; Gislefoss, Randi Elin; Tenkanen, Leena; Virtamo, Jarmo; Koskela, Pentti; Hallmans, Göran; Lehtinen, Matti; Dillner, Joakim

doi:10.1038/sj.bjc.6602751

Cited by 18 publications

(15 citation statements)

References 22 publications

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“…Helicobacter pylori and stomach cancer, 31 EpsteinBarr virus and Hodgkin's lymphoma, 32 non-Hodgkin's lymphoma 33 and nasopharyngeal carcinoma 34 as well as papillomaviruses and cervical, 35 anal, 36 vulvar/vaginal 37 and oropharyngeal cancer. 38 Equally important, the biobank-based prospective seroepidemiological study design has also provided clear negative results for several claimed virus-tumour associations such as herpes simplex and cervical cancer, 39 human herpes virus 8 and myeloma 40 or BKV polyomavirus and neuroblastoma. 41 Our previous negative findings regarding BKV and neuroblastoma are of relevance to the present study, as the strength of evidence associating BKV with neuroblastoma was rather similar to the evidence associating JCV with colon cancer.…”

Section: Discussionmentioning

confidence: 99%

No excess risk for colorectal cancer among subjects seropositive for the JC polyomavirus

Lundstig

Stattin

Persson

et al. 2007

Intl Journal of Cancer

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The human polyomaviruses JC virus (JCV) and BK virus (BKV) are oncogenic in experimental systems and commonly infect humans. JCV DNA has been reported to be present in human colon mucosa and in colorectal cancers. To investigate whether the risk for colorectal cancer is associated with JCV or BKV infection, we performed a case-control study nested in the Janus biobank, a cohort of 330,000 healthy Norwegian subjects. A 30-year prospective follow-up using registry linkages identified 386 men with colorectal cancer who had baseline serum samples taken >3 months before diagnosis. Control subjects were matched for sex, age and date of blood sampling and county of residence. Seropositivity for JCV or BKV had high (97-100%) sensitivity for detection of viral DNA-positive subjects and discriminated the different polyomaviruses. Seropositivity was mostly stable over time in serial samples. The relative risk for colorectal cancer among JCV seropositive subjects was 0.9 (95% CI: 0.7-1.3) and the BKV-associated relative risk was 1.1 (95% CI: 0.8-1.5). Determining seropositivity using alternative cutoffs also found no evidence of excess risk. In summary, this prospective study found no association between JCV or BKV infections and excess risk for colorectal cancer. 1 Initial infection rarely causes clinical disease, although respiratory symptoms or urinary tract disease is sometimes found in the case of BKV.2 JCV and BKV can be detected in tonsillar tissue, suggesting that the respiratory tract is the primary site of infection.3 JC viral particles are found in urban sewage, suggesting that virus-contaminated water and food may be a source of infection. 4 After primary infection, both BKV and JCV persist as latent infections in kidney epithelial cells and B lymphocytes. 1,5 Under conditions of severe immunosuppression such as leukaemia, acquired immunodeficiency syndrome (AIDS) and organ transplantation both viruses may be reactivated and cause disease. BKV reactivation is related to urinary tract diseases such as haemorrhagic cystitis and ureteric stenosis, 6,7 whereas JCV reactivation can induce progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system. 8About 70-90% of healthy adults are seropositive for BKV and JCV. Seroconversion for BK infection occurs in early childhood and JC seroconversion occurs in late childhood. 5BKV seropositivity increases rapidly with increasing age, reaching 98% seroprevalence at 7-9 years of age, followed by a minor decrease. JCV seroprevalence increases more slowly with age, reaching 50% positivity among children between 9 and 11 years. The human polyomaviruses have in vitro transforming abilities, similar to the mouse polyomavirus and simian virus 40 (SV40). 6 The virally encoded T antigens of both BKV and JCV are essential for transformation and bind to the p53 and pRb tumour suppressor proteins.10,11 Both BK and JC virus infections can induce chromosomal aberrations in human cells. [12][13][14] Possible associations of polyomaviruses wit...

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Section: Discussionmentioning

confidence: 99%

No excess risk for colorectal cancer among subjects seropositive for the JC polyomavirus

Lundstig

Stattin

Persson

et al. 2007

Intl Journal of Cancer

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“…HHV-8 seropositivity was 12% and 15% in cases and controls, respectively. However, they could not find any association between MM and HHV-8 seropositivity [37]. In our study, HHV-8 was not observed in patients with MM by PCR method in north east Iran.…”

Section: Discussionmentioning

confidence: 59%

“…Despite these studies, other investigators published conflicting results [22,[35][36][37][38][39][40]. Olsen et al, in United States, searched for HHV-8 in MM patients by serology, PCR, and immunohistochemistry.…”

Section: Discussionmentioning

confidence: 99%

Is There Any Relationship between Human Herpesvirus-8 and Multiple Myeloma?

et al. 2013

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Background. Human herpesvirus-8 (HHV-8) is associated with some human diseases including Kaposi's sarcoma and also some B-cell lymphoproliferative disorders. Few studies have highlighted the potential role of HHV-8 in the development of multiple myeloma (MM) which is known as a malignant proliferation of plasma cells derived from a single clone. Aims. The aim of this study was to find a relationship between HHV-8 and MM using polymerase chain reaction (PCR) method. Materials and Methods. This study was conducted on 30 formalin-fixed, paraffin-embedded (FFPE) bone marrow biopsies of multiple myeloma and 30 normal FFPE bone marrow biopsies. After the sample preparation, Deoxyribonucleic acid (DNA) was extracted by nonheating procedure. PCR for HHV-8 virus was carried out with commercial kit and the PCR products were visualized by gel electrophoresis. Finally, the statistical analysis was performed. Results. HHV-8 virus was not detected by PCR from FFPE blocks of multiple myeloma samples, while only one of the controls showed DNA band of the corrected molecular weights. Fisher's exact test showed that no statistical differences were found between the two groups ( = 0.999). Conclusion. Our report adds to the body of evidence that there is no association between HHV-8 and MM against a major role of HHV-8 infection in the pathogenesis of clonal plasma cell proliferation.

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“…HHV-8 has also been reported to be present in pemphigus vulgaris, extranodal marginal zone lymphoma of salivary gland, hemophagocytic syndrome, multiple myeloma, Kikuchi lymphadenitis, and sarcoidosis. [12][13][14][15][16][17] However, the latter list of diseases is controversial as viral detection varies among studies. [18][19][20][21] Two publications by Gó mez-Román et al, 9,10 documenting HHV-8 in lesional myofibroblasts of inflammatory myofibroblastic tumor, drew attention to the possible role of the virus in the pathogenesis of this tumor.…”

Section: Discussionmentioning

confidence: 99%

Absence of human herpesvirus-8 in pulmonary inflammatory myofibroblastic tumor: immunohistochemical and molecular analysis of 20 cases

et al. 2007

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Inflammatory myofibroblastic tumors are uncommon lesions composed of spindled myofibroblasts within a variable background of collagen and inflammatory cells. Although the true nature of these lesions is not fully elucidated, identification of consistent cytogenetic alterations in the anaplastic lymphoma kinase (ALK) gene suggests that they may be neoplastic. A small number of inflammatory myofibroblastic tumors have been reported to harbor human herpesvirus-8 (HHV-8), implicating the virus in its pathogenesis. In this study, 20 cases of pulmonary inflammatory myofibroblastic tumor were analyzed for the presence of HHV-8 with immunohistochemical and molecular methods. In all cases, antibodies to the latent nuclear antigen of the virus were applied. Four open reading frames (ORFs), including ORFs K2, 16, 26, and 72, were targeted utilizing realtime polymerase chain reaction (PCR). The cohort included 9 men and 11 women with a mean age of 37 years

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Joint Nordic prospective study on human herpesvirus 8 and multiple myeloma risk

Cited by 18 publications

References 22 publications

No excess risk for colorectal cancer among subjects seropositive for the JC polyomavirus

No excess risk for colorectal cancer among subjects seropositive for the JC polyomavirus

Is There Any Relationship between Human Herpesvirus-8 and Multiple Myeloma?

Absence of human herpesvirus-8 in pulmonary inflammatory myofibroblastic tumor: immunohistochemical and molecular analysis of 20 cases

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