Investigation of leukemia cells from children with common acute lymphoblastic leukemia for genomic sequences of the primate polyomaviruses JC virus, BK virus, and Simian virus 40

Smith, Malcolm A.; Strickler, Howard D.; Granovsky, Monica; Reaman, Gregory H.; Linet, Martha S.; Daniel, Richard; Shah, Keerti V.

doi:10.1002/(sici)1096-911x(199911)33:5<441::aid-mpo1>3.0.co;2-p

Cited by 24 publications

(11 citation statements)

References 14 publications

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“…We, and others, have analyzed cALL samples for the presence of JC, and the related polyomavirus BK, with negative results. 22,23 Herpesviruses are alternative candidates. These viruses are widely distributed in nature, the timing of infection is related to living conditions, and several members of this virus family have known transforming properties, notably EBV and human herpesvirus-8 (HHV-8).…”

Section: Introductionmentioning

confidence: 99%

Screening for herpesvirus genomes in common acute lymphoblastic leukemia

et al. 2001

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There is epidemiological evidence that infection may play a role in the etiology of childhood leukemia in particular common B cell precursor acute lymphoblastic leukemia. A panel of 20 leukemic samples (panel 1) was examined for the presence of four lymphotropic herpesviruses using conventional molecular techniques. A second independent panel of 27 leukemic samples (panel 2), along with 28 control peripheral blood samples from children with other forms of cancer, was tested for the presence of the same four viruses using sensitive realtime quantitative PCR. While herpesvirus genomes were detected, they were present at very low levels; detection rates and levels were similar in the leukemic and control panels. In addition we surveyed 18 leukemic samples (five from panel 1, six from panel 2 and a further seven samples not previously analyzed) using a degenerate PCR assay capable of detecting the genomes of known herpesviruses plus putative new members of the family. No novel herpesvirus genomes were detected suggesting that a herpesvirus is unlikely to be etiologically involved as a transforming agent in common acute lymphoblastic leukemia. Leukemia (2001) 15, 415-421.

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Section: Introductionmentioning

confidence: 99%

Screening for herpesvirus genomes in common acute lymphoblastic leukemia

et al. 2001

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“…However, 17 of the hematologic malignancies were leukemias, while the most common type of neural tumor was neuroblastoma (seven cases). Laboratory studies have not identified SV40 in childhood leukemia or neuroblastoma specimens [8,34]. Conversely, considering childhood tumors with a proposed relationship to SV40, there was only one CPP child who developed ependymoma and this child's mother had not received poliovirus vaccine during pregnancy; there were no cases of choroid plexus tumor or osteosarcoma.…”

Section: Engels and Colleaguesmentioning

confidence: 99%

Cancer risk associated with receipt of vaccines contaminated with simian virus 40: epidemiologic research

Engels¹

2005

Expert Review of Vaccines

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Simian virus (SV)40 was an accidental contaminant of poliovirus vaccines used widely in the USA and other countries in 1955-1962. Exposure to SV40 via contaminated vaccines has led to concern as SV40 causes cancer in laboratory animals. In addition, some laboratories, although not all, have detected SV40 DNA in human tumors including mesothelioma, certain brain tumors, osteosarcoma and non-Hodgkin's lymphoma. This article reviews the data regarding contamination of poliovirus vaccines with SV40 and summarizes the results from epidemiologic studies of vaccine recipients. Long-term follow-up studies have not revealed recipients of SV40-contaminated poliovirus vaccines to be at an increased risk for cancer. Thus, these studies are somewhat reassuring and indicate that either SV40 does not readily infect humans or, following infection, does not cause cancer. Recognizing that the history of SV40 contamination of vaccines highlights an inherent risk of contamination of vaccines with adventitious agents, the Institute of Medicine recently called for the development of a comprehensive US plan to prevent vaccine contamination and respond to potential contamination events when they arise.

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“…Only a limited number of published investigations have directly assayed pretreatment specimens for infectious agents at the time of cALL diagnosis and few have retrospectively analyzed archived prediagnostic specimens. More specifically, several small studies failed to detect the human polyomaviruses JC virus and BK virus in leukemia cells or stored newborn (Guthrie) blood spots (MacKenzie et al 1999; McNally and Eden 2004; Perzova et al 2000; Priftakis et al 2003; Smith et al 1999); one also failed to detect simian virus 40 (Smith et al 1999). Similarly, a few case–series and case–control studies failed to associate select human herpesviruses or human parvovirus B19 with the diagnosis of ALL (Bogdanovic et al 2004; Isa et al 2004; Luppi et al 1998; MacKenzie et al 2001; McNally and Eden 2004; O’Connor and Scadden 2000).…”

Section: Direct Evidence For Infectious Etiologymentioning

confidence: 99%

Infectious Etiologies of Childhood Leukemia: Plausibility and Challenges to Proof

O’Connor

Boneva

2007

Environ Health Perspect

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Infections as well as environmental exposures are proposed determinants of childhood acute lymphoblastic leukemia (ALL), particularly common precursor B-cell ALL (cALL). Lines of investigation test hypotheses that cALL is a rarer result of common infection, that it results from uncommon infection, or that it ensues from abnormal immune development; perhaps it requires a preceding prenatal or early childhood insult. Ideally, studies should document that particular infections precede leukemia and induce malignant transformation. However, limited detection studies have not directly linked specific human or nonhuman infectious agents with ALL or cALL. Primarily based on surrogate markers of infectious exposure, indirect evidence from ecologic and epidemiologic studies varies widely, but some suggest that infancy or early childhood infectious exposures might protect against childhood ALL or cALL. Several others suggest that maternal infection during pregnancy might increase risk or that certain breast-feeding practices decrease risk. To date, evidence cannot confirm or refute whether at least one infection induces or is a major co-factor for developing ALL or cALL, or perhaps actually protects against disease. Differences in methodology and populations studied may explain some inconsistencies. Other challenges to proof include the likely time lag between infection and diagnosis, the ubiquity of many infections, the influence of age at infection, and the limitations in laboratory assays; small numbers of cases, inaccurate background leukemia rates, and difficulty tracking mobile populations further affect cluster investigations. Nevertheless, existing evidence partially supports plausibility and warrants further investigation into potential infectious determinants of ALL and cALL, particularly in the context of multifactorial or complex systems.

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Investigation of leukemia cells from children with common acute lymphoblastic leukemia for genomic sequences of the primate polyomaviruses JC virus, BK virus, and Simian virus 40

Cited by 24 publications

References 14 publications

Screening for herpesvirus genomes in common acute lymphoblastic leukemia

Screening for herpesvirus genomes in common acute lymphoblastic leukemia

Cancer risk associated with receipt of vaccines contaminated with simian virus 40: epidemiologic research

Infectious Etiologies of Childhood Leukemia: Plausibility and Challenges to Proof

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