Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum and cervical secretions were collected from patients with cervical dysplasia, carcinoma-in-situ (CIS), squamous cell carcinoma (cervical SCC), and controls with normal cervices, attending clinics within the West Lambeth Health District, London. Enzyme-linked immunosorbent assays were used to examine cervical secretory IgA (sIgA) and serum IgG and IgA antibodies to herpes simplex virus (HSV). Sexual and demographic factors were considered during data analysis, which involved fitting multiple linear or multiple logistic regressions to HSV antibody levels. Prevalence of sIgA-HSV and levels of serum antibodies to HSV in all groups were compared with those of gynaecology controls. Caucasian women with mild dysplasia had a significantly higher prevalence of sIgA-HSV. Serum IgG levels to HSV (IgG-HSV) were significantly elevated in women with mild dysplasia and severe dysplasia/CIS. Serum IgA levels to HSV1 (IgG-HSV1) were significantly higher in women with cervical SCC (after adjusting for smoking habits) and other genital tumours. Significantly higher levels of serum IgA to HSV2 (IgA-HSV2) were also found among Caucasian women with cervical SCC. The possible role of HSV as a co-factor in cervical carcinogenesis is discussed.
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PMID:Class-specific herpes simplex virus antibodies in sera and cervical secretions from patients with cervical neoplasia: a multi-group comparison. 283 5

In previous studies, carcinoma of the uterine cervix of the mouse was induced by repeated vaginal exposure to inactivated herpes simplex viruses, type 1 or 2. To determine if the mouse nasopharynx is also susceptible to the carcinogenic effects of these viruses, animals were inoculated intranasally with suspensions of formaldehyde-inactivated herpes simplex viruses, type 1 or 2, or control material, four to five times a week. After exposure periods of 12, 20, and 32 weeks, groups of animals were killed randomly and the nasopharynx, along with the larynx, trachea, bronchi, and lungs, were examined histologically. No preinvasive or invasive lesions were detected. These data suggest that the nasopharynx and cervix of the mouse differ in susceptibility to induction of carcinogenesis by inactivated herpes simplex viruses.
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PMID:Resistance of mouse nasopharynx to induction of neoplasia by herpes simplex virus. 283 52

We have demonstrated that the human cytochrome P1-450 gene can be transfected into the AHH-1 human lymphoblastoid cell line using the pHEBo vector and hygromycin selection. The transfected gene was expressed when regulatory sequences derived from the herpes simplex virus thymidine kinase gene were incorporated in appropriate orientations. Gene expression was monitored at the enzyme level using assays for 7-ethoxyresorufin deethylase, 7-ethoxycoumarin deethylase and benzo[a]pyrene hydroxylase activities. Bulk transformed cell populations had 2- to 3-fold more of these enzyme activities compared with control populations. Subclones of the bulk population expressing still higher levels of 7-ethoxyresorufin deethylase activity were also obtained. Expression of the transfected cytochrome P1-450 gene was stable for 20-30 days in the presence of hygromycin B. The transformed cell populations were found to be suitable for use in gene locus mutation assays and the mutagenicity of aflatoxin-B1 and 2-acetylaminofluorene (AAF) were examined. Aflatoxin-B1 was found to be 2-3 times more mutagenic to cells bearing the transfected cytochrome P1-450 activity as compared with control cells. In contrast, no difference in AAF mutagenicity was observed. Analysis of the AAF metabolite profile indicated that cells expressing the transfected cytochrome P1-450 gene produced 8-fold more N- and 7-hydroxy-AAF than control cells. The similarity in mutagenic responses between control cells and cells bearing the transfected cytochrome P1-450 gene may be due to the low deacetylase activity of AHH-1 cells. These observations indicate that this vector and expression system are suitable for introducing novel metabolic activities into the AHH-1 cell line.
Carcinogenesis 1989 Feb
PMID:Transfection of a human cytochrome P-450 gene into the human lymphoblastoid cell line, AHH-1, and use of the recombinant cell line in gene mutation assays. 291 81

Experiments were done to determine if cloned transforming sequences from herpes simplex virus type 2 (HSV-2) DNA confer upon transfected Rat-2 cells the capacity to be stimulated in phospholipase and cyclooxygenase activities following 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment. Tumor-derived Rat-2 cells transformed with sub-fragments (BamHI-E, HindIII/HpaI-ED, or PstI-C) overlapping the right-hand end of the BglII-C transforming region of HSV-2 DNA were stimulated by TPA in both phospholipase activity, measured by deacylation of arachidonic acid, and cyclooxygenase activity, measured by prostaglandin synthesis. Non-transfected Rat-2 control cells showed no increase in these enzyme activities following TPA treatment. To our knowledge, this is the first evidence that cloned HSV-2 DNA has the capacity to induce cellular functions (phospholipase and cyclooxygenase) in transformed mammalian cells.
Carcinogenesis 1987 Jan
PMID:Induction of cellular functions in spontaneously immortalized rat-2 cells transfected with cloned herpes simplex virus type 2 (HSV-2) DNA. 302 79

A prospective study of cervical dysplasia cases and control cases matched for age and parity was undertaken in search of factors related to cervical carcinogenesis. Cytologic examination of 66,736 women revealed negative findings in 28.5%, inflammation in 70.3%, dysplasia in 1.4% and carcinoma in 0.1% of the cases. Data on epidemiologic features, cytomorphologic characteristics and serologic findings of antibodies to herpes simplex virus (HSV) were collected for proven cancer patients, dysplasia cases and control subjects. Cancer patients revealed significantly elevated antibodies to HSV as compared to the controls. The analysis revealed a higher proportion of dysplasia cases with an age at consummation of marriage of less than or equal to 15 years as compared to controls, with a relative risk of 1.5 (P less than .05). Similarly, a higher proportion of women with dysplasia had HSV-II-specific antibodies as compared to control women. The relative risk was found to be 1.3, which was not statistically significant (P greater than .05). The Mantel-Haenszel summary relative risk between antibodies to HSV and the two groups (dysplasia cases and controls), adjusted for the age at consummation of marriage, worked out to be 1.38, which was also statistically not significant (P greater than .05). The overall progression rate of dysplasia to malignancy was found to be 11.7% at the end of 54 months (during a total follow-up period of 84 months). Progression to cancer was highest in severe dysplasia cases and less in mild dysplasia cases. The progression rates were also significantly higher in the group of women who revealed antibodies to HSV II. Similar differences in the progression rates were observed with regard to the age at consummation of marriage.
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PMID:Natural history of precancerous and early cancerous lesions of the uterine cervix. 303 45

Epidemiological studies relating genital herpetic infection to cervical carcinoma are reviewed. The high frequency of herpes simplex virus type 2 (HSV-2) antibodies in young women (21 years or younger) with cervical carcinoma in situ and in women with dysplasia or carcinoma in situ, matched for various sexual attributes to control women, provide support for a causal relation. However, various laboratory, histopathological, and statistical problems associated with all epidemiological studies do not yet permit a firm conclusion as to the etiological role to the genital virus in cervical carcinogenesis. With the use of herpes-related cancer antigens or purified HSV-2 type-specific antigens, and with the possible development of protective HSV-2 vaccines, the application of epidemiological approaches may be necessary to provide the most finite evidence of causality.
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PMID:Epidemiological studies relating genital herpetic infection to cervical carcinoma. 436 85

The immune system has evolved under Darwinian pressures as a defence against ubiquitous viruses. Immune surveillance against viral antigens protects the normal host. Individuals with inherited or acquired immune-deficiency disorders can become vulnerable to ubiquitous viruses and neoplasms can ensue, such as B-cell lymphoma, hepatocellular carcinoma, squamous-cell carcinoma, Kaposi's sarcoma, and carcinoma of the penis and uterine cervix. Immunodeficiency permits Epstein-Barr virus, hepatitis B virus, papillomavirus, herpes simplex virus, and cytomegalovirus to induce sustained target-cell proliferation. Each virus selects specific cellular targets bearing viral receptors and the infection leads to proliferation of the target cells rather than lysis. Various co-factors, including nutrition, exposure to tumour-promoting agents, parasitic infection, and ultraviolet light, may promote carcinogenesis. Depending on the type and severity of the immune deficiency, gradual proliferation may lead to evolution of a malignant clone. Conversion of polyclonal virally infected proliferating cells to give monoclonal malignancy is probably due to specific cytogenetic rearrangements which allow oncogene activation and endow an altered tumour cell with selective growth advantages over normal diploid cells. Prevention of viral oncogenesis may be possible by treatment of immune-deficient individuals with premalignant disorders. Immunotherapy and antiviral therapy may prevent progression of viral-induced proliferation to malignancy. The purpose of this paper is to discuss and evaluate the role of immune deficiency and viruses in the induction of malignancies commonly occurring in Africans residing in sub-Saharan Africa (Purtilo, 1976). The types of malignancies commonly occurring in this region are believed to be due to ubiquitous viruses. A failure of immune surveillance mechanisms to recognize viral antigens and abrogate proliferation of infected target cells predisposes to malignancy by increasing the chance of a proliferating cell undergoing a cytogenetic or molecular alteration which endows it with malignant characteristics. The immunological surveillance hypothesis has been elaborated during this century by Ehrlich, Thomas, Burnet, and Schwartz (reviewed by Purtilo & Linder, 1983). This hypothesis rests on several assumptions: that neoplastic cells possess unique tumour antigens: tumour antigens provoke an immune response in the host; and the immune response is protective and eliminates the tumour.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Squamous-cell carcinoma, Kaposi's sarcoma and Burkitt's lymphoma are consequences of impaired immune surveillance of ubiquitous viruses in acquired immune deficiency syndrome, allograft recipients and tropical African patients. 610 Feb 88

The paper deals with the mechanism of emergence of early virus-induced antigens in animal tumors and their association with carcinogenesis. Problems of the specificity of the antigens of tumors induced by herpes simplex virus in different animal species and their immunogenicity for the tumor carriers are discussed.
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PMID:[Antigens associated with herpes simplex viruses in human and animal tumors]. 620 15

The multivaried aspects of the herpes simplex viruses (HSV) types 1 and 2 and the infections they produce are discussed. Points emphasized are: (1) the need for considering these (and other viruses) from an evolutionary perspective; (2) the necessity of disseminating current methods for virus identification; (3) the great progress in molecular-virological aspects and in the genetics of the virus which provide new tools for epidemiological and immunological studies and define more convincingly the possible causal role of HSV-2 in cervical carcinogenesis; (4) the problems with vaccines and the therapeutic advances and failures; (5) the great psychosocial aspect of some herpetic infections and the need to be sympathetic and supportive to afflicted patients and their families; (6) the overreaction regarding HSV that currently exists among physicians, nurses, the public, and the press resulting in increased misery for those afflicted or misdiagnosed, or in poor advice or management given by some physicians pressured in part by the fear of malpractice suits. The problems then are many but the prospects for their solution are in sight as more research at all levels is being conducted today in all corners of the world on the complex herpes simplex viruses.
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PMID:Herpes simplex virus infection: problems and prospects as perceived by a peripatetic pediatrician. 624 86

An enhanced reactivation of ultraviolet-damaged (u.v. at 254 nm) unclear replicating double-stranded DNA viruses occurs when corresponding host cells are treated with radiation or carcinogens prior to infection. This phenomenon seems to be due to an induced DNA repair activity the nature of which is yet unknown. The u.v.-induced enhanced reactivation (ER) of u.v.-damaged herpes simplex virus (u.v. - HSV) was compared in dividing skin fibroblasts of 30 donors either normal or afflicted by genetic disorders, some of which confer a high risk for sunlight induced skin cancers. Cultures were exposed to a single dose of 1.0-25 J.m-2 from 0-60 h before infection with u.v.-HSV (at about 10-3 survival) and the rate of viral production was determined. ER was maximal for a 36 h time interval in all lines. The u.v. dose eliciting maximal ER was 15 J.m-2 in fibroblasts from normal donors, xeroderma pigmentosum (XP) heterozygotes, Mibelli's porokeratosis, diffused naevomatosis, Down's syndrome, xerodermoids, XP variants and epidermodysplasia verruciformis. However, in the latter 3 cases, ER was almost 10 times more pronounced than in the normal cases. The u.v. dose eliciting maximal ER was 0.1, 0.3 and 2 J.m-2 in excision deficient XP fibroblasts from groups A, D and C, respectively, 2.5 J.m-2 in 11961 fibroblasts and 5 J.m-2 in fibroblast lines from cockayne s syndrome.
Carcinogenesis 1981
PMID:Enhanced reactivation of ultraviolet-damaged herpes virus in ultraviolet pretreated skin fibroblasts of cancer prone donors. 626 75


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