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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hamster cells, transformed in vitro by SV40, have been reported to secrete an unidentified factor(s) that inhibits thymidine uptake (TU) by various normal cell types, including activated lymphocytes. It has been postulated that this apparent antiproliferative effect may play an in vivo role in the high tumorigenic capacity of SV40-transformed hamster cells. In keeping with this hypothesis, Adenovirus type 2-transformed hamster cells, which are only weakly tumorigenic, do not inhibit TU by indicator cells in vitro. To study the biological relevance of this phenomenon, we assayed 11 cell lines derived from different fibrosarcomas, induced in Syrian hamsters by SV40, for their ability to inhibit TU by normal rabbit kidney indicator cells. In contrast to cells transformed in vitro by SV40, media conditioned by 6 of 11 tumor-derived cell lines did not inhibit TU. Our results do not support the hypothesis that an antiproliferative factor secreted by SV40-transformed cells promotes the tumor-inducing capacity of these cells. Furthermore, inhibition of TU does not appear to be due to the production of a specific antimitotic peptide, but rather to other biochemical properties of the media conditioned by transformed cells. Finally, these biochemical properties do appear to correlate with specific morphological and growth characteristics of the tumor cells, but probably as an effect and not a cause.
Cancer Res 1989 Dec 01
PMID:Biochemical properties of media conditioned by simian virus 40-induced hamster tumor cells: correlation with distinct cell phenotypes but not with oncogenicity. 255 53

Viruses are becoming increasingly recognized as a major etiological agent in the development of numerous forms of human cancer. Human papillomaviruses (HPVs) have been associated with a number of neoplastic lesions, most notably cervical cancer which is one of the major forms of cancer world wide. Of the over 50 types of identified HPVs, HPV types 16, 18, 31 and 33 are the types most commonly associated with malignant carcinomas. These viruses contain double stranded DNA which code for about eight gene products, some of which are oncogenic when introduces into cultured rodent or human cells. In particular, both the E6 and E7 gene products have different oncogenic capabilities and these genes are selectively retained within the genome of cervical carcinoma derived cells. The E7 gene product has immortalizing capabilities in primary cells and is able to cooperate with an activated ras oncogene to fully transform primary rodent cells. The E7 gene product from HPV type 16 is also capable of complexing in vitro to the anti-oncogene product, Rb. Similar complexes occur with Adenovirus E1A and SV40 large T proteins which may suggest a shared mechanism of transformation used by HPV type 16, Adenovirus and SV40. Transformation studies using primary human cells and nontumorigenic HeLa/fibroblast hybrid cells have also suggested that chromosome 11 may be important in suppressing the HPV transformed phenotype. The transformed phenotype may therefore also involve an impaired intracellular control of persisting HPV oncogenic sequences. Although there exists no solid evidence that a cytotoxic T-lymphocyte reaction is mounted against HPV transformed cells, there is evidence that both NK cells and activated macrophages can preferentially kill HPV transformed cells in vitro. Future studies are required to identify possible targets present on HPV transformed cells which are absent on normal cells.
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PMID:The cell biology of human papillomavirus transformed cells. 255 72

The records of 96 pediatric patients with aplastic anemia or a malignancy who underwent bone marrow transplantation between 1979 and 1986 at The Children's Hospital of Philadelphia were reviewed for laboratory evidence of viral infections. The most common viral diseases identified were herpes simplex virus (HSV), cytomegalovirus and adenoviruses, which were found in 19 (20%), 17 (18) and 17 (18) patients, respectively. HSV was more common in patients with than without graft vs. host disease (GVHD) (9 of 30; 30% vs. 10 of 66; 15%), but the difference did not reach statistical significance. Late or prolonged isolation of HSV occurred in patients with chronic GVHD. Cytomegalovirus was significantly more common in patients with than without GVHD (10 of 30; 33% vs. 7 of 66; 11%). The presence of pretransplant antibody to cytomegalovirus or HSV was a good predictor of subsequent infection. Adenoviruses were isolated from all 3 patients with Burkitt's lymphoma. Adenovirus type 12, a serotype uncommon in man and known to be highly tumorigenic in young hamsters, was recovered from 4 patients. Adenoviruses were not notably more common in patients with GVHD (6 of 30; 20% vs. 11 of 66; 17%). Other viral infections demonstrated included 5 parainfluenza, 4 enteroviruses, 3 human immunodeficiency virus, 1 respiratory syncytial virus, 1 influenza B and 1 rhinovirus.
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PMID:Viral infections in pediatric bone marrow transplant patients. 283 May 86

11 malignant tumours of the oral region in children under 15 years of age were diagnosed in Finland during the 20-year period from 1961 to 1980; the age adjusted annual incidence rate being 0.31 per 1,000,000 children. 5 cases were intraoral cancer and 5 cases malignant tumours of the major salivary glands. The formalin-fixed tumours were studied using the in situ DNA hybridization technique for Adenovirus, group II, Epstein-Barr and human papillomavirus, type 16. For the first time, evidence was provided for the presence of Epstein-Barr virus in a malignant salivary gland tumour, implicating a possible etiological role for this virus in salivary gland neoplasms.
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PMID:Oral cancer in children under 15 years of age. A clinicopathological and virological study. 284 81

Adenovirus type 9 was inoculated sc into newborn Wistar/Furth rats, divided into four groups: (1) six male rats, not treated further; (2) 11 male rats, castrated at 4 weeks of age; (3) 12 male rats, castrated at 4 weeks of age and subsequently treated repeatedly with estrogen; and (4) 12 female rats, not treated further. All of the rats in group 3 developed mammary hyperplasia and tumors (fibroadenomas and lipomas), in some cases with malignant histologic structure. Rats in group 4 developed similar mammary tumors, but with later appearance and significantly slower growth. A fifth group of rats, not virus inoculated but castrated and estrogen treated as in group 3, did not develop any demonstrable mammary lesions. The results show that the effects of the virus on the mammary gland are dependent upon an estrogenic background, which by itself cannot cause tumor development in males. It is suggested that viral DNA is incorporated into the cellular DNA in such a way that it influences the synthesis and/or activity of steroid receptors, triggering tumor development.
J Natl Cancer Inst 1989 Feb 15
PMID:Adenovirus type 9-induced tumorigenesis in the rat mammary gland related to sex hormonal state. 291 27

Few human cell systems have been described in which a number of different genes induce transformation. The present investigation reports on our studies using primary human embryo retinoblasts as a model system to monitor transformation and the subsequent behaviour of individual transformants in terms of establishment, the frequency of immortalization and tumourigenic potential. SV40, Adenovirus E1 and E1A, and combinations of Adenovirus E1A and activated H-ras or N-ras were examined as transforming agents. Considerable differences were observed in the ability of these genes to transform human cells, to induce immortal lines and to produce cell lines with a tumourigenic phenotype. Activated ras genes were non-transforming in this system and the degree of complementation with adenovirus E1As in transformation experiments was dependent on both the adenovirus serotype and the ras gene used. The development of tumourigenic cell lines required the expression of more than one oncogene and additional genetic events were required in some in some instances before immortal cell lines were obtained. These findings contribute to the concept that the development of cancer is a multi-step process.
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PMID:Transformation of human embryo retinoblasts with simian virus 40, adenovirus and ras oncogenes. 301 83

Adenovirus 2 (Ad2)- and simian virus 40 (SV40)-transformed hamster embryo cells differ markedly in a number of phenotypic properties including their potential for inducing tumors in hamsters. Both Ad2- and SV40-transformed cells are immortalized and readily induce tumors in immunoincompetent newborn syngeneic hamsters, but only SV40-transformed cells are highly oncogenic in both adult syngeneic and allogeneic immunocompetent hamsters. The reasons for the difference in the oncogenic potential of the Ad2- and SV40-transformed phenotypes remain elusive. However, recent studies with transforming growth factors (TGFs) indicate that these factors play an important role in determining many phenotypic characteristics of transformed cells. To determine whether TGFs secreted by Ad2- and SV40-transformed hamster embryo cells differ, we have examined the ability of media conditioned by these two transformed cell phenotypes to modulate thymidine uptake in quiescent, untransformed cells. We found that both transformed phenotypes secrete very similar TGF alpha-like mitogenic factors which inhibit binding of 125I-labeled epidermal growth factor to its receptor. Our results also show that SV40-transformed cells, but not Ad2-transformed cells, secrete a powerful mitogenic inhibitor (MI). The MI secreted by SV40-transformed cells is inhibitory for several transformed and untransformed cell types and exerts a cytostatic, not cytolytic, action on untransformed primary hamster embryo cells. MI elutes from size exclusion high-performance liquid chromatography columns with a molecular weight of 24,000. Although MI has about the same molecular weight as TGF beta, it differs from TGF beta in two important respects: it is heat labile and it has a different target specificity for antimitogenic activity. The MI secreted by SV40-transformed cells also inhibits thymidine uptake by concanavalin A-stimulated spleen lymphocytes. This finding suggests that MI might contribute to the extreme oncogenicity of SV40-transformed cells by inhibiting mobilization of immune effector cells at the site of tumor cell proliferation.
Cancer Res 1987 Aug 01
PMID:Mitogenic and antimitogenic transforming growth factors secreted by adenovirus 2- and simian virus 40-transformed hamster cells: possible roles in promoting tumorigenesis. 303 7

Immunotoxins (monoclonal antibodies-ricin A-chain conjugates) directed against the tumor-associated antigen carcinoembryonic antigen (CEA) are selective in vitro cytotoxins for human adenocarcinoma cells. However, the kinetics of intoxication are relatively slow. The effects of the UV radiation-inactivated human adenovirus and the carboxylic ionophores monensin and nigericin were examined on immunotoxin cytotoxicity to the human colorectal adenocarcinoma cell line LoVo. In a 16-hour cytotoxicity assay, adenovirus reduced 33-fold the median inhibitory concentration from 3 X 10(-8) M to 9 X 10(-10) M. In timed cytotoxicity assays, 50% of control protein synthesis was reached in immunotoxin-treated cells twentyfold faster in the presence of adenovirus (0.5 hr) than in its absence (10 hr). Adenovirus produced no enhancement of immunotoxin effect on a control cell line or on a control immunotoxin on LoVo cells, demonstrating specificity of adenovirus effect. In addition, specific immunotoxin constructed with a nonreducible thioether bond, alone or with adenovirus, produced no toxicity on LoVo cells. These results suggest that both cell surface binding and presence of a reducible disulfide bond in the conjugate are necessary for adenovirus effect. Similar potentiation of the cytotoxicity of anti-CEA immunotoxins was produced by monensin and nigericin. These studies demonstrate that both adenovirus and carboxylic ionophores are potentiators of immunotoxins directed against the CEA, producing cytotoxicity equivalent to that of ricin but specific for CEA-positive adenocarcinoma cells in culture.
J Natl Cancer Inst 1987 Oct
PMID:Enhancement of the cytotoxic effect of anti-carcinoembryonic antigen immunotoxins by adenovirus and carboxylic ionophores. 349 54

The feasibility of using adenovirus 5 as an in vitro probe for chemosensitivity in short-term cultures of human tumors was evaluated using human melanoma cell lines and primary cultures of melanoma biopsies. A convenient immunoperoxidase method was developed for quantitating viral replication 2 days after infection. Two different approaches were explored: the host cell reactivation assay (HCR) using drug-treated virus; and the viral capacity assay using drug-treated cells. The HCR assay detected sensitivity to 5-(3-methyl-1-triazeno)imidazole-4-carboxamide (MTIC) in Mer- (methyl excision repair deficient) cell lines as decreased ability of the cells to replicate MTIC-treated virus. This test should be applicable to DNA-damaging agents and repair-deficient tumors. Adenovirus replicated readily in nonproliferating primary cultures of melanoma biopsies; application of the HCR assays to this material identified one Mer- sample of 11 tested. Herpes viruses were not suitable for use in HCR because herpes simplex virus type 1 failed to distinguish Mer- from Mer+ melanoma cells; and nonproductive infection of MTIC-sensitive lymphoid cells with Epstein-Barr virus yielded an MTIC-resistant cell line. The second assay (viral capacity) involved determination of the inhibition of replication of untreated virus in treated cells. This approach correctly predicted sensitivity to hydroxyurea and deoxyadenosine in melanoma cell lines when compared with clonogenic survival assay. Viral capacity was also inhibited by cytosine arabinoside, fluorouracil, vincristine, adriamycin, 6-mercaptopurine and ionising radiation, and may therefore be useful for detecting sensitivity to a wide range of antitumor agents.
Eur J Cancer Clin Oncol 1986 Apr
PMID:Adenovirus replication as an in vitro probe for drug sensitivity in human tumors. 352 82

Five human tumor cell lines of the Mer- phenotype sensitive to killing by the methylating agent 5-(3-methyl-1-triazeno)imidazole-4-carboxamide were sensitive to hydroxyurea (HU) compared with 15 cell lines resistant to methylating agents (Mer+ phenotype). In a study using fewer cell lines, Mer- cells were also sensitive to methotrexate but not to seven other agents including the antimetabolites 1-beta-D-arabinofuranosylcytosine and 5-fluorouracil. Cells sensitive to HU were designated the Hu- phenotype. Five autologous Mer+ lines, derived in vitro by treating Mer- lines with methylating agents, did not become resistant to HU or methotrexate (Mer+ Hu- phenotype). All Mer+ lines studied had enhanced ability to reactive methylated adenovirus. Adenovirus was inactivated by prolonged treatment with HU, but no enhanced reactivation of HU-treated virus was found in Mer+ cell lines. Cell survival after 5-(3-methyl-1-triazeno)imidazole-4-carboxamide treatment was not significantly decreased by HU, nor was replication of methylated adenovirus inhibited by HU in Mer- or Mer+ lines. Replication of untreated adenovirus was poor in Mer- cells treated with HU, indicating that sensitivity of cells to HU was associated with inhibition of DNA synthesis. These results suggest that cell sensitivity to deoxynucleotide depletion is linked, perhaps coincidentally, to the Mer- phenotype. The retention of HU and methotrexate sensitivity by cells after development of resistance to 5-(3-methyl-1-triazeno)imidazole-4-carboxamide may have therapeutic implications.
Cancer Res 1986 Oct
PMID:Cross-sensitivity of methylating agents, hydroxyurea, and methotrexate in human tumor cells of the Mer- phenotype. 375 62


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