SV40 in human thyroid nodules

Özdarendeli, Aykut; Camcı, Celaletdin; Aygen, Erhan; Kırkıl, Cüneyt; Toroman, Z. A.; Doğru, Osman; Doymaz, Mehmet Ziya

doi:10.1016/j.jcv.2003.12.008

Cited by 9 publications

(13 citation statements)

References 18 publications

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“…As discussed above, SV40 DNA sequences have been recovered not only from the suspect cancers but at low frequencies from 10 other cancers46 and from bladder tumors 30. Others have reported SV40 DNA sequences in thyroid nodules,57 in hepatocellular carcinoma58 and in genital tract tumors 59. SV40 DNA has been reported to be present36, 53, 60, 61 or absent43, 62, 63 in kidney disease, in urine and in peripheral blood cells of normal individuals.…”

Section: Presence Of Sv40 Dna Sequences or Sv40 T Antigen In Cancers mentioning

confidence: 95%

SV40 and human cancer: A review of recent data

Shah

2006

Intl Journal of Cancer

108

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An unknown proportion of formalin-inactivated poliovirus vaccine lots administered to millions of US residents between 1955 and 1963 was contaminated with small amounts of infectious simian virus 40 (SV40), a polyomavirus of the rhesus macaque. It has been reported that mesothelioma, brain tumors, osteosarcoma and non-Hodgkin lymphoma (NHL) contain SV40 DNA sequences and that SV40 infection introduced into humans by the vaccine probably contributed to the development of these cancers. The Immunization Safety Review Committee of the Institute of Medicine (IOM) reviewed this topic in 2002. The present review of recent studies showed that the earlier results describing the recovery of SV40 DNA sequences from a large proportion of the above tumors were not reproducible and that most studies were negative. Contamination with laboratory plasmids was identified as a possible source of false positive results in some previous studies. The low-level immunoreactivity of human sera to SV40 was very likely the result of cross-reactivity with antibodies to the SV40-related human polyomaviruses BKV and JCV, rather than of authentic SV40 infection. SV40 sero-reactivity in patients with the suspect tumors was no greater than that in controls. In epidemiologic studies, the increased incidence of some of the suspect tumors in the 1970s to 1980s was not related to the risk of exposure to SV40-contaminated vaccines. In summary, the most recent evidence does not support the notion that SV40 contributed to the development of human cancers. 1 The committee recommended the development and use of sensitive and specific serologic tests for Simian virus 40 (SV40), the development and use of sensitive and specific standardized techniques for SV40 detection, and the study of the transmissibility of SV40 in humans.1 This review presents the perspective of the author who has investigated this question since the mid 1960s.2 The background of the problem is provided first and the discussion is centered primarily on studies published in 2002 and later, in order to evaluate the evidence for an etiologic role of SV40 infection for human cancer. Earlier data are referred to for context and when necessary to make a point. Three questions are addressed: (i) some of the earlier studies reported SV40 DNA sequences (and to a lesser extent SV40 T antigen) in large proportions of mesothelioma, brain tumors, osteosarcoma and non-Hodgkin lymphoma (NHL). Are these results reproducible in the most recent studies? (ii) serology is an independent marker for viral exposure. Is there serological evidence that SV40 is circulating in the human communities or that patients with the suspect cancers are more frequently exposed to SV40? and (iii) the incidence of mesothelioma, brain tumors and NHL increased in the decades following human exposure to SV40 in the contaminated vaccines. Are these 2 events related?Background

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Section: Presence Of Sv40 Dna Sequences or Sv40 T Antigen In Cancers mentioning

confidence: 95%

SV40 and human cancer: A review of recent data

Shah

2006

Intl Journal of Cancer

108

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“…To the best of our knowledge, few studies to date have investigated the association of PyVs with thyroid cancer ( 44 – 47 ), as shown in Table I . Three of these studies ( 44 – 46 ) detected sequences of simian vacuolating virus 40 (SV40), a virus that infected rhesus monkey kidney cells used for polio vaccine production ( 48 ), in thyroid gland specimens. Since SV40 has proven to be oncogenic in rodents ( 37 , 38 , 44 ) and has transforming capacity in human cells in vitro ( 44 ), the wide distribution of SV40 contaminated vaccines in the early 1960s, led to a concern for potential tumor induction in humans ( 37 ).…”

Section: Polyomavirusesmentioning

confidence: 99%

“…Most of our knowledge regarding the association of SV40 with thyroid cancer, is based on 3 studies examining the presence of SV40 DNA in thyroid specimens ( 44 – 46 ). The first study investigated the presence of SV40 sequences in 69 patients with PTCs using Southern blotting and polymerase chain reaction (PCR) ( 44 ).…”

Section: Polyomavirusesmentioning

confidence: 99%

“…A total of 33% (3/9) of the PTCs and 100% (8/8) of the anaplastic carcinomas were immunoreactive, and showed mainly cytoplasmic staining. The third study included 99 patients (21 males/78 females) with thyroid nodules, 8 of whom (8.08%), were diagnosed with PTCs, while 91 (91.02%) had benign thyroid nodules, 8 of which, harboured Hashimoto's thyroiditis ( 46 ). Both nodular and normal thyroid tissue was obtained from each patient.…”

Section: Polyomavirusesmentioning

confidence: 99%

“…Both nodular and normal thyroid tissue was obtained from each patient. All 198 specimens were investigated for the presence of SV40, through the amplification of Tag coding sequences, using PCR ( 46 ). Sequences of SV40 were detected in 4 out of 99 nodules, 2 of which were PTCs, while the remaining were benign thyroid nodules.…”

Section: Polyomavirusesmentioning

confidence: 99%

See 2 more Smart Citations

Herpes and polyoma family viruses in thyroid cancer

et al. 2016

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Thyroid cancer is considered the most common malignancy that affects the endocrine system. Generally, thyroid cancer derives from follicular epithelial cells, and thyroid cancer is divided into well-differentiated papillary (80% of cases) and follicular (15% of cases) carcinoma. Follicular thyroid cancer is further divided into the conventional and oncocytic (Hürthle cell) type, poorly differentiated carcinoma and anaplastic carcinoma. Both poorly differentiated and anaplastic carcinoma can arise either de novo, or secondarily from papillary and follicular thyroid cancer. The incidence of thyroid cancer has significantly increased for both males and females of all ages, particularly for females between 55–64 years of age, from 1999 through 2008. The increased rates refer to tumors of all stages, though they were mostly noted in localized disease. Recently, viruses have been implicated in the direct regulation of epithelial-mesenchymal transition (EMT) and the development of metastases. More specifically, Epstein-Barr virus (EBV) proteins may potentially lead to the development of metastasis through the regulation of the metastasis suppressor, Nm23, and the control of Twist expression. The significant enhancement of the metastatic potential, through the induction of angiogenesis and changes to the tumor microenvironment, subsequent to viral infection, has been documented, while EMT also contributes to cancer cell permissiveness to viruses. A number of viruses have been identified to be associated with carcinogenesis, and these include lymphotropic herpesviruses, namely EBV and Kaposi's sarcoma-associated herpesvirus [KSHV, also known as human herpesvirus type 8 (HHV8)]; two hepatitis viruses, hepatitis B virus (HBV) and hepatitis C virus (HCV); human papillomaviruses (HPVs); human T cell lymphoma virus (HTLV); and a new polyomavirus, Merkel cell polyomavirus identified in 2008. In this review, we examined the association between thyroid cancer and two oncogenic virus families, the herpes and polyoma family viruses, and we discuss their potential role as causative agents in thyroid carcinogenesis.

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BK polyomavirus in Iranian patients with papillary thyroid cancer: Is it a major future challenge?

Tarharoudi

Sari

Sakhaee

et al. 2022

Journal of Medical Virology

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BK polyomavirus (BKPyV) is a well-known cause of nephropathy in renal transplant recipients. It has recently received much attention from researchers as a major predisposing factor for various cancers. This study aimed to investigate how BKPyV affected the advancement of papillary thyroid carcinoma (PTC). A total of 1057 samples were tested for BKPyV DNA and RNA, comprising 645 paraffin-embedded PTC biopsy samples (PEBS), 412 fresh biopsy samples (FBS), and 1057 adjacent noncancerous samples. The BKPyV DNA was found in 511 (48.3%) of the specimens, including 347 (84.2%) FBS and 164 (25.4%) PEBS. The mean BKPyV copy number was significantly lower in patients with PEBS (0.5 × 10 −4 ± 0.1 × 10 −4 copies/cell) than in FBS (1.3 × 10 −1 ± 0.2 × 10 −1 copies/cell) and non-PTC normal samples (0.3 × 10 −5 ± 0.04 × 10 −5 copies/cell). The PEBS had lower LT-Ag RNA expression than FBS, and no VP1 gene transcript expression was detected. In conclusion, although our findings indicated the presence of BKPyV in some Iranian PTC patients, more research is needed to corroborate these findings.

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SV40 in human thyroid nodules

Cited by 9 publications

References 18 publications

SV40 and human cancer: A review of recent data

SV40 and human cancer: A review of recent data

Herpes and polyoma family viruses in thyroid cancer

BK polyomavirus in Iranian patients with papillary thyroid cancer: Is it a major future challenge?

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