: J Acquir Immune Defic Syndr 2002 Feb 1;29(2):109-16
Partial list of references: SV40 and cancer
|
: J Acquir Immune Defic Syndr 2002 Feb 1;29(2):109-16 |
Detection of polyomavirus simian virus 40
tumor antigen DNA in AIDS-related systemic non-Hodgkin lymphoma.
Vilchez RA, Lednicky JA, Halvorson SJ, White ZS, Kozinetz CA, Butel JS.
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
rvilchez@bcm.tmc.edu
Systemic non-Hodgkin lymphoma (S-NHL) is a common malignancy during HIV
infection, and it is hypothesized that infectious agents may be involved in the
etiology. Epstein-Barr virus DNA is found in <40% of patients with AIDS-related
S-NHL, suggesting that other oncogenic viruses, such as polyomaviruses, may play
a role in pathogenesis. We analyzed AIDS-related S-NHL samples, NHL samples from
HIV-negative patients, peripheral blood leukocytes from HIV-infected and
-uninfected patients without NHL, and lymph nodes without tumors from
HIV-infected patients. Specimens were examined by polymerase chain reaction
analysis with use of primers specific for an N-terminal region of the
oncoprotein large tumor antigen ( T-ag ) gene conserved among all three
polyomaviruses (simian virus 40 [SV40], JC virus, and BK virus).
Polyomavirus T-ag DNA sequences, proven to be
SV40-specific, were detected more frequently in AIDS-related S-NHL samples (6 of
26) than in peripheral blood leukocytes from HIV-infected patients (6 of 26 vs.
0 of 69; p =.0001), NHL samples from HIV-negative patients (6 of 26 vs. 0 of 10;
p =.09), or lymph nodes (6 of 26 vs. 0 of 7; p =.16).
Sequences of C-terminal T-ag DNA from SV40 were
amplified from two AIDS-related S-NHL samples. Epstein-Barr virus DNA
sequences were detected in 38% (10 of 26) AIDS-related S-NHL samples, 50% (5 of
10) HIV-negative S-NHL samples, and 57% (4 of 7) lymph nodes. None of the S-NHL
samples were positive for both Epstein-Barr virus DNA and SV40 DNA. Further
studies of the possible role of SV40 in the pathogenesis of S-NHL are warranted.
PMID: 11832678 [PubMed - indexed for MEDLINE]
|
Cancer Immunol Immunother 2002 Feb;50(12):682-90 |
SV40 Tag-specific cytotoxic T lymphocytes
generated from the peripheral blood of malignant pleural mesothelioma patients.
Bright RK, Kimchi ET, Shearer MH, Kennedy RC, Pass HI.
Laboratory of Prostate Cancer Biology, Robert W. Franz Cancer Research Center,
Earle A. Chiles Research Institute, and the Oregon Cancer Center, 4805 NE Glisan
Street, Portland, OR 97213, USA, rbright@providence.org
Malignant pleural mesothelioma (MPM) is an aggressive cancer, with survival of
less than one year following diagnosis and treatment with current protocols.
Recent studies have demonstrated the presence
of the simian virus 40 (SV40)-like, large tumor antigen (Tag) in nearly 60% of
MPMs. SV40 Tag is a viral-encoded tumor-specific antigen, and thus a
potential target for the induction of anti-tumor immunity and the development of
therapeutic vaccines. We describe here evidence for the existence of SV40
Tag-specific immune responses in patients with MPM whose tumors express Tag.
Humoral immunity was demonstrated by the detection of IgG titers against Tag in
serum samples from 1/3 of patients examined. CTLs were generated from the
peripheral blood of an HLA-A2(+) MPM patient with a synthetic peptide
representing an HLA-A2 binding epitope in SV40 Tag. The CTLs demonstrated
epitope fine specificity, in that other peptides from SV40 Tag and a peptide
from influenza virus were not recognized in the context of HLA-A2. Moreover, the
CTLs were capable of recognizing mesothelioma tumor cells that expressed SV40
Tag, in an MHC class I restricted manner.
PMID: 11862420 [PubMed - in process
AN: 21849853
|
Oncogene 2002 Feb 21;21(9):1434-42 |
SV40 infection induces telomerase activity in
human mesothelial cells.
Foddis R, De Rienzo A, Broccoli D, Bocchetta M, Stekala E, Rizzo P, Tosolini
A, Grobelny JV, Jhanwar SC, Pass HI, Testa JR, Carbone M.
Cancer Immunology Program, Department of Pathology, Cardinal Bernardin Cancer
Center, Loyola University Chicago, Maywood, Illinois, IL 60153, USA.
Mesotheliomas are malignant tumors of the pleural and peritoneal membranes which
are often associated with asbestos exposure and with Simian virus 40 (SV40)
infection. Telomerase activity is repressed in somatic cells and tissues but is
activated in immortal and malignant cells. We evaluated telomerase activity in
seven primary malignant mesothelioma biopsies and matched lung specimens and 20
mesothelioma cell lines and eight corresponding primary tumor cultures. All the
tumor biopsies, and nearly all primary cell mesothelioma cultures and cell lines
were telomerase positive. The findings in cell lines paralleled those observed
in primary cultures in cases where paired samples were available.
Next, we found that SV40, a DNA tumor virus
present in approximately 50% of mesothelioma biopsies in the USA, induced
telomerase activity in primary human mesothelial cells, but not in primary
fibroblasts. Telomerase activity became detectable as early as 72 h following
wild-type (strain 776) SV40 infection, and a clear DNA ladder was detectable 1
week after infection. The amount of telomerase activity increased during passage
in cell culture and appeared to parallel increases in the cellular amounts of
the SV40 large T-antigen. Thus, SV40 infection leads to telomerase activity
before the infected mesothelial cells become transformed and immortalized.
SV40 infection of human fibroblasts did not cause detectable telomerase
activity. We also determined that the SV40 small t-antigen (tag) plays an
important role in inducing telomerase activity because this activity was
undetectable or minimal in mesothelial cells infected and/or transformed by SV40
tag mutants. Asbestos alone did not induce telomerase activity, and asbestos did
not influence telomerase activity in mesothelial cells infected with SV40.
Induction of telomerase activity by SV40 may be related to the very high rate of
mesothelial cell immortalization that is characteristically associated with SV40
infection of mesothelial cells.
PMID: 11857086 [PubMed - indexed for MEDLINE]
AN: 21846811
|
1: Oncogene 2002 Feb 14;21(8):1141-9 |
Association of SV40 with human tumors.
Klein G, Powers A, Croce C.
Microbiology and Tumor Biology Center, Karolinska Institut, S 171-77, Stockholm,
Sweden.
In 1994, PCR and protein studies suggested that SV40 DNA sequences and proteins
were present in 29/48 (60%) USA human mesothelioma samples. Sequence analysis
confirmed that the sequences were homologous to SV40. One year later, SV40 was
also found in 5/9 human mesotheliomas, and in 1996 SV40 was also reported to be
present in 1/3 of the tumor specimens examined. These reports, in combination
with an earlier study in 1992 which had detected SV40 in human brain tumors,
raised concerns that SV40 was associated with certain types of human tumors,
specifically mesothelioma, bone, and brain tumors. These findings raised
concerns, because these tumor types are the same malignancies that had been
observed in animals injected with SV40. However, a study in 1996 and a
presentation made at the International Mesothelioma Interest Group, IMIG in 1997
failed to detect SV40 in mesotheliomas, suggesting the possibility that
laboratory artifacts, such as PCR contamination, had caused the previous
positive findings. In 1997, the FDA, the NIH, and the CDC organized an
international conference in Bethesda to review the literature and to address the
possibility that SV40 was present in, and was possibly the cause of, some human
tumors. The results of that conference were reported the same year in a meeting
review in Oncogene by Carbone and colleagues. Briefly, the consensus was that
before accepting the possibility that SV40 was present in human tumors, a
multi-laboratory study needed to be conducted. It was recommended that a blinded
multi-laboratory study be directed by an independent scientist not previously
associated with the controversial reports of SV40 in human specimens. It was
also recommended that this study include laboratories that had reported positive
findings as well as laboratories that had failed to detect SV40 in human
specimens. Since 1997, about 30 independent reports have been published on this
topic, including the multi-laboratory study. Evidence in favor and against a
possible association of SV40 with human cancer was reviewed at an international
consensus meeting at the University of Chicago on 20, 21 April 2001, entitled
"Malignant Mesothelioma: Therapeutic Options and the Role of SV40, 2001". The
main focus was the association of SV40 with mesothelioma and other human tumors.
At the end of the meeting, a panel discussion, which included independent
experts who had not published on this topic, critically reviewed the evidence
presented at the meeting. The results of the meeting and of the final panel
discussion are outlined below.
Publication Types:
· Congresses
PMID: 11850833 [PubMed - indexed for MEDLINE]
AN: 21839854
|
Semin Oncol 2002 Feb;29(1):2-17 |
The pathogenesis of mesothelioma.
Carbone M, Kratzke RA, Testa JR.
Cancer Immunology Program, Cardinal Bernardin Cancer Center, Department of
Pathology, Loyola University Chicago, USA.
About 80% of malignant mesotheliomas (MM) in the Western World develop in
individuals with higher than background exposure to asbestos. Only a fraction of
those exposed to asbestos develop mesothelioma, indicating that additional
factors play a role. Simian virus 40 (SV40), a DNA tumor virus that
preferentially causes mesothelioma in hamsters, has been detected in several
human mesotheliomas. The expression of the SV40 large tumor antigen in
mesothelioma cells, and not in nearby stromal cells, and the capacity of
antisense T-antigen treatment to arrest mesothelioma cell growth in vitro
suggest that SV40 contributes to tumor development. The capacity of T-antigen to
bind and inhibit cellular p53 and retinoblastoma (Rb)-family proteins in
mesothelioma, together with the very high susceptibility of human mesothelial
cells to SV40-mediated transformation in vitro,
supports a causative role of SV40 in the pathogenesis of mesothelioma.
Asbestos appears to increase SV40-mediated transformation of human mesothelial
cells in vitro, suggesting that asbestos and SV40 may be cocarcinogens. p53
mutations are rarely found in mesothelioma; p16, p14ARF, and NF2
mutations/losses are frequent. Recent studies revealed the existence of a
genetic factor that predisposes affected individuals to mesothelioma in the
villages of Karain and Tuzkoy, in Anatolia, Turkey. Erionite, a type of zeolite,
may be a cofactor in these same villages, where 50% of deaths are caused by
mesothelioma. Mesothelioma appears to have a complex etiology in which
environmental carcinogens (asbestos and erionite), ionizing radiation, viruses,
and genetic factors act alone or in concert to cause malignancy. Copyright 2002
by W.B. Saunders Company.
Publication Types:
· Review
· Review, Tutorial
PMID: 11836664 [PubMed - indexed for MEDLINE]
AN: 21826992
|
: J Natl Cancer Inst 2002 Feb 6;94(3):229 |
Re: Debate on the Link Between SV40 and Human
Cancer Continues.
Kops SP.
PMID: 11830616 [PubMed - in process]
AN: 21819111
|
J Natl Cancer Inst 2002 Feb 6;94(3):229-30 |
Re: Debate on the Link Between SV40 and Human
Cancer Continues.
Carbone M, Pass HI.
M. Carbone, Cardinal Bernardin Cancer Center, Loyola University Medical School
Chicago, Maywood IL.
PMID: 11830615 [PubMed - in process]
AN: 21819110
|
J Natl Cancer Inst 2001 Sep 5;93(17):1284-6 |
Debate on the link between SV40 and human
cancer continues.
Nelson NJ.
Publication Types:
· News
PMID: 11535696 [PubMed - indexed for MEDLINE]
AN: 21427132
|
J Cell Biochem 2002;84(3):455-9 |
Detection of SV40 DNA sequences in malignant
mesothelioma specimens from the United States, but not from Turkey.
De Rienzo A, Tor M, Sterman DH, Aksoy F, Albelda SM, Testa JR.
Human Genetics Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
The incidence of malignant mesothelioma (MM) shows a strong epidemiological
association with exposure to asbestos fibers. Recently, simian virus 40 (SV40)
DNA sequences have been reported in MM tumor specimens from the United States
and several European countries, and the SV40 tumor virus has been implicated as
a potential co-factor in the etiology of this disease. However, several large
studies from the US, Finland, and Turkey did not detect SV40 sequences in MM
samples. To address this discrepancy, MM specimens from Turkey and the US were
analyzed in the same laboratory under identical conditions to detect the
presence of SV40 DNA. We detected SV40 sequences in 4 of 11 specimens from the
United States, but in none of the 9 Turkish samples examined. These findings
suggest that geographical differences exist with regard to the involvement of
SV40 in human tumors. Copyright 2001 Wiley-Liss, Inc.
PMID: 11813251 [PubMed - in process]
AN: 21671407
|
Chin Med J (Engl) 2001 Apr;114(4):382-6 |
Simian virus 40 large tumor antigen forms
specific complexes with p53 and pRb in human brain tumors.
Zhen H, Zhang X, Zhang Z, Fei Z, He X, Liang J, Huang W, Liu X, Zhang P.
Department of Neurosurgery, Xijing Hospital, Institute of Neurosurgery of PLA,
Fourth Military Medical University, Xi'an 710032, China. zh_ha@263.net
OBJECTIVE: To study the role of simian virus 40 (SV40) early region gene coding
product large tumor antigen (Tag) expression and the interaction between Tag and
tumor suppressors p53 and pRb in human brain tumorigenesis. METHODS: Tag was
investigated by immunoprecipitation followed by silver staining and Western blot
in 65 cases of human brain tumors and 8 cases of normal brain tissues. Tag-p53
and Tag-pRb complexes were screened in 18 and 15 Tag positive tumor tissues,
respectively. RESULTS: Tag was found in all 8 ependymomas and 2 choroid plexus
papillomas, 90% of pituitary adenomas (9/10), 73% of astrocytomas (11/15), 70%
of meningiomas (7/10), 50% of glioblastomas multiforme (4/8), 33% of
medulloblastomas (2/6). 5 oligodendrogliomas, 1 pineocytoma, and 8 normal brain
tissues were negative for Tag. Tag-p53 complex was detected in all 18 Tag
positive tumors. Tag-pRb complex was found in all 15 Tag positive tumors.
CONCLUSION: SV40 Tag is expressed in human
brain tumors and can form specific complexes with tumor suppressors p53 and pRb.
The inactivation of p53 and pRb due to the formation of Tag-p53 and Tag-pRb
complexes may be an important mechanism in the etiopathogenesis of human brain
tumors.
PMID: 11780459 [PubMed - indexed for MEDLINE]
|
Cancer Epidemiol Biomarkers Prev 2001 May;10(5):523-32 |
A multicenter evaluation of assays for
detection of SV40 DNA and results in masked mesothelioma specimens.
Strickler HD; The International SV40 Working Group.
Department of Epidemiology and Social Medicine, Albert Einstein College of
Medicine, Bronx, NY 10461, USA.
This nine-laboratory multicenter investigation was designed to assess the
sensitivity, specificity, and reproducibility of previously described assays for
detection of SV40 DNA with three goals, i.e., (a) to compare methods for testing
human tissues, (b) to examine the ability of these methods to detect SV40 in
human mesotheliomas, and (c) to uncover assay differences that could explain
conflicting findings in some past investigations. Each laboratory received, in a
masked fashion, paired replicate DNA samples extracted from 25 fresh frozen
mesotheliomas (50 samples) and one from each of 25 normal human lungs.
Interspersed were masked positive (titrations of the SV40 genome) and negative
control samples. Preliminary studies confirmed the adequacy of the samples for
testing high molecular weight double-stranded linear DNA targets. All 15 PCR-based
assays detected 5,000 copies or less of the SV40 genome spiked into 2 microg of
WI-38 DNA. A high level of specificity and reproducibility was found among the
PCR assays performed in most laboratories.
However, none of the selected normal human lung tissue or the 25 mesothelioma
tumor specimens obtained from archival samples at a single center was
reproducibly positive for the presence of SV40 DNA. Further studies are needed
to reconcile these results with previous reports of detection of SV40 DNA in
tumor specimens.
Publication Types:
· Evaluation Studies
· Multicenter Study
PMID: 11352864 [PubMed - indexed for MEDLINE]
AN: 21250767
|
Dis Markers 2001;17(3):167-72 |
Increasing evidence for involvement of SV40
in human cancer.
Butel JS.
Department of Molecular Virology and Microbiology, Baylor College of Medicine,
One Baylor Plaza, Houston, TX 77030, USA. jbutel@bcm.tmc.edu
SV40, a small DNA virus, is known to possess
strong oncogenic potential. Millions of people were exposed to SV40 as an
unknown contaminant of some early poliovaccines. This article briefly summarizes
the increasing evidence of the association of SV40 with certain types of human
cancer, including mesotheliomas and brain tumors. Unanswered questions
pertaining to the pathogenesis of human infections by SV40 and the functional
role of the virus in tumor development are noted. It is concluded that SV40
should be considered a candidate human tumor virus and that vigorous efforts to
clarify the role of the virus in human disease should be supported.
Publication Types:
· Review
· Review, Tutorial
PMID: 11790883 [PubMed - indexed for MEDLINE]
AN: 21650496
|
Br J Cancer 2001 Nov 2;85(9):1295-7 |
Thirty-five year mortality following receipt
of SV40- contaminated polio vaccine during the neonatal period.
Carroll-Pankhurst C, Engels EA, Strickler HD, Goedert JJ, Wagner J, Mortimer
EA Jr.
Mandel School of Applied Social Sciences, Case Western Reserve University,
Cleveland, OH, 44106-7164, USA.
Early poliovirus vaccines, both inactivated and live attenuated, were
inadvertently contaminated with simian virus 40 (SV40), a monkey virus known to
be oncogenic for newborn hamsters. Although large epidemiologic studies have not
identified an elevated cancer risk in persons who received SV40-contaminated
vaccines, fragments of SV40 DNA have recently been identified in certain human
tumours. We report the follow-up of a cohort of 1073 persons, unique because
they received SV40-contaminated poliovirus vaccines as newborns in 1961-63. A
previous report of the status of these subjects as of 1977-79 identified 15
deaths, none due to cancer. The present study utilized the National Death Index
to identify deaths in the cohort for the years 1979-96. Expected deaths were
calculated from Cleveland area sex-, age-, race- and year-specific mortality
rates. Increased mortality from all causes was not found. 4 deaths from cancer
were found compared to 3.16 expected (P = 0.77). However, 2 deaths from
testicular cancer occurred, compared to 0.05 expected (P = 0.002), which may be
a chance finding due to multiple comparisons. There were 2 deaths due to
leukaemia, a non-significant finding, and no deaths due to tumours of the types
putatively associated with SV40. Although these results are, for the most part,
consistent with other negative epidemiologic investigations of risks from
SV40-contaminated vaccines, further study of testicular cancer may be warranted,
and it will be important to continue monitoring this cohort which is now
reaching middle-age. Copyright 2001 Cancer Research Campaign
Is a
cohort of 1073 large enough? Where is the comparison with those who did not
receive the vaccine? If the expected frequency is based on a population which
received polio vaccine, there would be no differences. If the expected
frequency includes a population which received polio vaccine, there might be no
differences.
PMID: 11720463 [PubMed - indexed for MEDLINE]
AN: 21577652
|
Semin Cancer Biol 2001 Feb;11(1):15-23 |
Cellular transformation by SV40 large T
antigen: interaction with host proteins.
Ali SH, DeCaprio JA.
Department of Adult Oncology, Dana-Farber Cancer Institute and Harvard Medical
School, Boston, MA 02115, USA.
SV40 large T antigen (TAg) is a powerful
oncoprotein capable of transforming a variety of cell types. The
transforming activity of TAg is due in large part to its perturbation of the
retinoblastoma (pRB) and p53 tumor suppressor proteins. In addition, TAg binds
to several other cellular factors, including the transcriptional co-activators
p300 and CBP, which may contribute to its transformation function. Several other
features of TAg that appear to contribute to its full transformation potential
are yet to be completely understood. Study of TAg therefore continues to provide
new insights into the mechanism of cellular transformation. Copyright 2001
Academic Press.
Publication Types:
· Review
· Review, Tutorial
PMID: 11243895 [PubMed - indexed for MEDLINE]
AN: 21139788
|
: Semin Cancer Biol 2001 Feb;11(1):23-30 |
Role of T antigen interactions with p53 in
tumorigenesis.
Pipas JM, Levine AJ.
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA
15260, USA.
SV40 induces neoplastic transformation by
disabling several key cellular growth regulatory circuits. Among these
are the Rb- and p53-families of tumor suppressors. The multifunctional,
virus-encoded large T antigen blocks the function of both Rb and p53. Large T
antigen uses multiple mechanisms to block p53 activity, and this action
contributes to tumorigenesis, in part, by blocking p53-mediated growth
suppression and apoptosis. Since the p53
pathway is inactivated in most human tumors, T antigen/p53 interactions offer a
possible mechanism by which SV40 contributes to human cancer. Copyright
2001 Academic Press.
Publication Types:
· Review
· Review, Tutorial
PMID: 11243896 [PubMed - indexed for MEDLINE]
AN: 21139789
|
Semin Cancer Biol 2001 Feb;11(1):31-8 |
SV40 and cell cycle perturbations in
malignant mesothelioma.
Testa JR, Giordano A.
Human Genetics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
JR.Testa@fccc.edu
Although epidemiological findings have
established that exposure to asbestos fibers is the major cause of malignant
mesothelioma (MM), recent studies have implicated simian virus 40 (SV40) in the
etiology of some of these tumors. Cytogenetic and molecular genetic
evidence suggests that multiple somatic genetic events are required for
tumorigenic conversion of a mesothelial cell. As with many other types of
cancer, in MM critical oncogenic events exert their action via perturbations of
the cell cycle. Interactions between the
retinoblastoma (Rb) family of proteins and oncoproteins encoded by SV40 lead to
cell cycle alterations. Likewise, inhibition of the p53 tumor suppressor by SV40
can inactivate a crucial cell cycle checkpoint, thereby permitting cells to
undergo mitosis regardless of the presence of DNA damage. Many MMs
exhibit loss and/or inactivation of the tumor suppressors p16(INK4a)and
p14(ARF), components of the pRb and p53 cell cycle regulatory pathways,
respectively. Recent investigations have demonstrated that SV40 large T antigen,
isolated from frozen biopsies of human MM specimens, binds to and inactivates
various tumor suppressor gene products such as pRb and p53.
In this review, we discuss how SV40-oncosuppressor interactions can lead to
functional alterations of the pRb- and p53-dependent cell cycle regulatory
pathways and thereby contribute to neoplastic transformation of human
mesothelial cells. Copyright 2001 Academic Press.
Publication Types:
· Review
· Review, Tutorial
PMID: 11243897 [PubMed - indexed for MEDLINE]
AN: 21139790
|
Semin Cancer Biol 2001 Feb;11(1):39-47 |
Simian virus 40 regulatory region structural
diversity and the association of viral archetypal regulatory regions with human
brain tumors.
Lednicky JA, Butel JS.
Department of Molecular Virology and Microbiology, Baylor College of Medicine,
Houston, TX 77030, USA.
The regulatory region (RR) of simian virus 40 (SV40) contains enhancer/promoter
elements and an origin of DNA replication. Natural SV40 isolates from simian
brain or kidney tissues typically have an archetypal RR arrangement with a
single 72-basepair enhancer element. A rare simpler, shorter SV40 RR exists that
lacks a duplicated sequence in the G/C-rich region and is termed protoarchetypal.
Occasionally, SV40 strain variants arise de novo that have complex RRs, which
typically contain sequence reiterations, rearrangements, and/or deletions. These
variants replicate faster and to higher titers in tissue culture; we speculate
that such faster-growing variants were selected when laboratory strains of SV40
were initially recovered. SV40 strains with
archetypal RRs have been found in some human brain tumors. The possible
implications of these findings and a brief review of the SV40 RR structure are
presented. Copyright 2001 Academic Press.
Publication Types:
· Review
· Review, Tutorial
PMID: 11243898 [PubMed - indexed for MEDLINE]
AN: 21139791
|
J Neurosurg 2001 Jul;95(1):96-101 |
Detection of simian virus 40 DNA sequence in
human primary glioblastomas multiforme.
Kouhata T, Fukuyama K, Hagihara N, Tabuchi K.
Department of Neurosurgery, Saga Medical School, Japan.
OBJECT: Deoxyribonucleic acid oncoviruses can induce neoplastic transformation
of cells because their viral proteins interfere with antiproliferative cellular
proteins. Simian virus 40 (SV40) is a DNA virus
that induces the emergence of ependymomas, choroid plexus tumors, mesotheliomas,
osteosarcomas, sarcomas, and various tumors when injected into newborn hamsters.
Recently, approximately 60% of human ependymomas, choroid plexus tumors, and
mesotheliomas were reported to contain and express SV40 DNA sequences. In this
study the presence of SV40 DNA sequences was investigated in human brain tumors.
METHODS: Three of 32 glioblastomas mutiforme (GBMs), but none of two ependymomas
and five medulloblastomas, were found to possess SV40 DNA sequences when
examined using polymerase chain reaction (PCR). The DNA sequence analysis of PCR-amplified
fragments disclosed that the samples were identical to the regulatory region of
SV40. All three GBMs, which arose in elderly patients with wild-type p53, were
considered to be primary (de novo) tumors. Although each of the three tumors was
immunohistochemically negative for SV40 T antigen, in situ hybridization
successfully demonstrated the messenger RNA for SV40 T antigen. CONCLUSIONS:
The results of this study indicate that latent
infection of SV40 in elderly people may be implicated in the tumorigenesis of
certain primary GBMs.
PMID: 11453404 [PubMed - indexed for MEDLINE]
AN: 21345940
|
Semin Cancer Biol 2001 Feb;11(1):49-61 |
Association of SV40 with human tumours.
Jasani B, Cristaudo A, Emri SA, Gazdar AF, Gibbs A, Krynska B, Miller C,
Mutti L, Radu C, Tognon M, Procopio A.
Immunocytochemistry and Molecular Pathology Unit, Department of Pathology,
University of Wales College of Medicine, CF14 4XN, Cardiff, UK.
SV40 was discovered as a contaminant of poliovirus vaccines that were
inadvertently administered to millions of people in Europe and the United States
between 1955 and 1963. Shortly afterwards, SV40 was proven to be oncogenic in
rodents and capable of transforming human and animal cells in vitro. The
possibility that SV40 might cause tumours in humans thus became a subject of
scientific and public interest and scrutiny. However, largely due to a lack of
significant epidemiological evidence, interest in assessing SV40's potential
carcinogenic role in humans diminished.
Recently, many laboratories have reported the presence of SV40-like DNA in a
high proportion of human mesotheliomas, ependymomas and osteosarcoma (the three
main types of tumours caused by virus in hamsters), renewing the question
whether SV40 might be a human tumour virus. Molecular data from these studies
are reviewed to re-evaluate the potential role of SV40 as a human carcinogen.
Copyright 2001 Academic Press.
Included in this reference list is some of the epidemiological evidence in favor of there being a relationship between SV40 and cancer. To the extent to which there is not more, to what extent is it due to the question not being adequately studied? (To adequately assess the risk, comparisons between those vaccinated with polio vaccine, other vaccines, and NO vaccines would have had to have been made.)
Publication Types:
· Review
· Review, Tutorial
PMID: 11243899 [PubMed - indexed for MEDLINE]
AN: 21139792
|
Semin Cancer Biol 2001 Feb;11(1):5-13 |
The role of the SV40 ST antigen in cell
growth promotion and transformation.
Rundell K, Parakati R.
Department of Microbiology-Immunology, Northwestern University, and The Robert
H. Lurie Comprehensive Cancer Center, Chicago, IL 60611, USA. krundell@northwestern.edu
The simian virus 40 small-t (ST) antigen plays
a key role in permissive and nonpermissive infections, increasing virus yields
in lytic cycles of primate cells and enhancing the ability of large-T (LT) to
transform rodent or even human cells. In the absence of ST, tumors in
rodent model systems appear primarily in lymphoid and other proliferative
tissues and transformation is reduced in several in vitro systems. The functions
of ST largely reflect its binding and inhibition of protein phosphatase 2A,
although a recently described dnaJ domain also contributes to its biology. The
dnaJ domain is present in LT and a third early gene product, the 17kT protein,
for which a potential role in transformation deserves further evaluation.
Copyright 2001 Academic Press.
Publication Types:
· Review
· Review, Tutorial
PMID: 11243894 [PubMed - indexed for MEDLINE]
AN: 21139787
|
Semin Cancer Biol 2001 Feb;11(1):63-71 |
SV40 and the pathogenesis of mesothelioma.
Rizzo P, Bocchetta M, Powers A, Foddis R, Stekala E, Pass HI, Carbone M.
Cancer Immunology Program, Cardinal Bernardin Cancer Center, Department of
Pathology, Loyola University Chicago, Maywood, IL 60153, USA.
Malignant mesothelioma, a tumor of the pleura,
pericardium, and peritoneum, is presently a worldwide problem. Current therapy
is ineffective in slowing the course of the disease, and median survival from
the time of diagnosis is rarely greater than 1 year. While the tumor was almost
unknown prior to the second half of the twentieth century, it is presently
responsible for more than 2000 deaths per year in the US alone. Mesothelioma is
frequently associated with exposure to asbestos, but the incidence of cases
involving individuals with low levels of asbestos exposure is increasing. For
this reason, there has been much interest in studying whether there are
alternative factors that act alone or in conjunction with asbestos in producing
this malignancy. In the last decade, simian virus 40 (SV40) has become the most
notable suspected agent. Copyright 2001 Academic Press.
Publication Types:
· Review
· Review, Tutorial
PMID: 11243900 [PubMed - indexed for MEDLINE]
AN: 21139793
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Semin Cancer Biol 2001 Feb;11(1):73-80 |
