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)

The neutralizing antibodies to HSV-1 and HSV-2 were determined in the sera of 128 patients. Infection was detectable in nearly 100% of the cases in each of the three investigated groups (patients with carcinoma of the cervix, female patients with chronic recurrent HSV infection in the genital area and a control group without and history of HSV infection). The percentage of patients displaying HSV-2 antibodies in the group with carcinoma of the cervix (38%) is significantly higher than in the control group (12%). The results are compared with the findings of other authors and the possible causal significance of HSV in carcinogenesis is discussed.
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PMID:[Investigations concerning the evidence of herpes simplex virus type 2 (HSV-2) antibodies in patients with carcinoma of the cervix (author's transl)]. 19 94

The familial occurrence of head and neck cancers supports the role of heredity in this disease group. The roles of environmental and genetic factors are difficult to separate. There are several well-characterized entities, however, that are associated with risk and prognosis of head and neck cancer, including Lynch-II syndrome, Bloom syndrome, Fanconi's anemia, xeroderma pigmentosum, ataxia telangiectasia, and Li-Fraumeni syndrome. Mutagen-induced chromosomal damage is associated with an increased risk of multiple primary neoplasms and upper aerodigestive tract cancers. A possible reduction of genotoxicity, mediated by micronutrients, was demonstrated in vitro. Sister chromatid exchanges and micronuclei are useful exposure and disease markers. Metabolic changes (acetylation, DBQ phenotype, and the AH locus polymorphism) have been found to be associated with cancer of the upper aerodigestive tract. Most associations between histocompatibility antigens and solid tumors are relatively weak, probably because of the masking effects of environmental factors. Infections by HPV, EBV, and HSV have a causative or predisposing role in several types of head and neck cancer. Amplification and rearrangement of oncogenes may also play a role in carcinogenesis, and oncogene amplification may be associated with aggressive tumor behavior and unfavorable clinical prognosis. Ploidy of tumors seems to be an important determinant of survival and response to therapy.
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PMID:Hereditary and environmental factors associated with risk and progression of head and neck cancer. 140 93

Infection of the cervix uteri with various types of human papillomaviruses is generally considered a necessary factor in the etiology of cancer of the cervix uteri. In many human populations throughout the world, approximately 90% of cervical carcinomas are found to harbour HPV genomes, as judged by Southern blot hybridization, while only a few percent of the cervical smears of asymptomatic individuals contain viral DNA, as assessed by filter in situ hybridization. To obtain corresponding epidemiological data from Singapore, we analysed two groups of 740 and 130 individuals by filter in situ hybridization, and found 4.1% and 6.9% of them to be HPV positive, with HPV 16 and HPV 31 being the predominant types. In consideration of the limitations of filter in situ hybridization, namely low sensitivity and a tendency to suggest false positives due to contaminants, including blood, we analysed the cervical smears of two further groups of 52 and 50 individuals by the polymerase chain reaction for infection by HPV 16 and HPV 18 respectively. With this test, 61% and 14% of the cervical smears proved to be HPV 16 and HPV 18 DNA positive respectively. We conclude that in Singapore, if not worldwide, the majority of the population the population is infected by genital HPV types, suggesting that factors other than HPV infection are ultimately rate-limiting in cervical carcinogenesis.
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PMID:Molecular diagnosis of genital HPV DNA types by polymerase chain reaction and sensitivity-standardized filter in situ hybridization in randomly sampled cohorts of Singapore women. 169 60

The denV gene from bacteriophage T4 encodes a pyrimidine dimer-specific endonuclease that has the capacity to initiate excision repair of DNA. Cells from excision repair-deficient xeroderma pigmentosum (XP) patients are able to carry out excision repair initiated by the denV gene product and introduction of the denV gene into XP cells results in the partial restoration of colony-forming ability after irradiation with UV light. In this work we have constructed a helper-independent recombinant human adenovirus, Ad5denV, which contains the denV gene. A 1.9 kb cartridge consisting of the denV gene flanked by the long terminal repeat (LTR) promoter from Rous sarcoma virus (RSV) and the simian virus 40 (SV40) polyadenylation (poly A) splice signals, was inserted into the E3 region of an E3 deletion mutant (Ad5d1E3) of adenovirus type 5. Infection of human fibroblasts and other permissive human cells with Ad5denV resulted in lytic infection and expression of the denV gene was confirmed by primer extension of infected cell RNA. The ability of the denV gene to restore the DNA repair deficiency in XP fibroblasts was examined using host cell reactivation of viral structural antigen formation for UV-irradiated adenovirus. The control virus, Ad5VSV, was also a recombinant which contained the gene for vesicular stomatitis virus glycoprotein G inserted into the E3 region of Ad5d1E3. UV survival of Ad5denV was similar to that of Ad5VSV following infection of two normal fibroblast strains and a Cockayne syndrome fibroblast strain, CS7SE, from complementation group B. In contrast, UV survival of Ad5denV was significantly greater than that for Ad5VSV after infection of three unrelated XP fibroblast strains from complementation groups A, C and E. However, UV survival of Ad5denV in the XP fibroblasts did not reach levels obtained in normal fibroblasts, indicating that restoration of the XP defect was partial.
Carcinogenesis 1991 Feb
PMID:Construction of a recombinant adenovirus containing the denV gene from bacteriophage T4 which can partially restore the DNA repair deficiency in xeroderma pigmentosum fibroblasts. 170 21

Infections with specific types of human papillomaviruses (HPV) have emerged as necessary but not sufficient factors for the development, at least, of the majority of cervical, vulvar, penile, and perianal cancers. Evidence has accumulated for their causal role in the induction of anogenital premalignant lesions. Genetic events underlying the mechanism of anogenital carcinogenesis have become increasingly understood. A host cell-mediated intracellular control down-regulating specific HPV genes (E6, E7) in replicating normal cells appears to be interrupted in cancer cells, probably due to structural modifications of the respective host cell genes acquired in the course of HPV DNA persistence. Since genital HPV infections are ubiquitous, cofactors which modify controlling host cell genes are likely to determine the different geographic rates of cervical cancer incidence.
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PMID:Papillomaviruses in anogenital cancer as a model to understand the role of viruses in human cancers. 254 12

Growth of rat liver epithelial cells (RLEC) and primary cultures of parenchymal hepatocytes is potently inhibited by TGF-beta. Transfection of a mutated Ha-ras oncogene, but not a human c-myc oncogene, into RLEC resulted in cell lines resistant to growth inhibition by TGF-beta under anchorage-dependent conditions. Infection of primary rat hepatocyte cultures with v-Ha-ras yielded a cell line likewise insensitive to inhibition by TGF-beta. Binding of [125I]TGF-beta to Ha-ras-transfected RLEC was reduced relative to control or c-myc-transfected cells. These data suggest that activation of a Ha-ras oncogene in epithelial cells may result in escape from negative growth control and hence be a critical step during carcinogenesis. However, although Ha-ras induced resistance to growth inhibition by TGF-beta under anchorage-dependent conditions, TGF-beta inhibited the spontaneous growth in soft agar of all cell lines containing the Ha-ras oncogene. This may reflect an alteration in regulation of extracellular matrix proteins and related enzymes responsible for anchorage-independent growth.
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PMID:Introduction of a Ha-ras oncogene into rat liver epithelial cells and parenchymal hepatocytes confers resistance to the growth inhibitory effects of TGF-beta. 278 73

Infection of the uterine cervix by human papilloma viruses (HPV) is a ubiquitous yet only recently recognized lesion. The morphological findings correlate with early and late gene expression. The pathological events presumably depend upon the HPV type involved and upon environmental and host factors. The recognized risk factors are those described for epithelial dysplasias and carcinomas. The prevalence is unclear: it varies among different population groups and depends upon the investigation methods employed. The natural history of the infection is unknown, although relations between cervical HPV infection and carcinogenesis are evident. Research is handicapped by the lack of suitable animal or in vitro models.
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PMID:[Human papillomavirus infections of the cervix uteri. I. Pathobiology, epidemiology and relation to cancer pathogenesis]. 282 79

Infection with 100 Opisthorchis viverrini (OP) metacercariae prior to two injections of dihydroxy-di-n-propyl nitrosamine (DHPN) (1000 mg/kg body weight) brought about significant enhancement of resultant preneoplastic lesion development in Syrian hamster liver and pancreas tissue. Thus combined treatment with carcinogen and parasite was associated with pancreatic atypical (dysplastic) foci, hepatocellular nodules, cholangiofibrosis and cholangiocarcinomas. No such lesions were observed in carcinogen alone, parasite alone or untreated control groups. In addition, parasite induced hyperplastic gall bladder epithelium was found to include areas of putative preneoplastic cells only in the DHPN-OP combined group. The results strongly suggest that pancreatitis and biliary cirrhosis associated with liver fluke infestation are responsible for the observed enhancement of carcinogenesis, and that the resultant increased proliferation plays a major role in tumorigenesis.
Carcinogenesis 1988 Jun
PMID:Enhancement of DHPN induced hepatocellular, cholangiocellular and pancreatic carcinogenesis by Opisthorchis viverrini infestation in Syrian golden hamsters. 283 5

The influence of Opisthorchis viverrini liver fluke infection on development of diethylnitrosamine (DEN)-induced hepatocellular nodules was investigated in Syrian golden hamsters. Infection with 60 metacercariae, 4 weeks prior to administration of DEN for 12 weeks in the drinking water at dose levels of 10, 20 and 40 p.p.m., resulted in a significantly increased yield of nodular lesions as compared with the group receiving carcinogen treatment alone. The results indicate an importance for parasite-associated liver injury and compensatory regeneration in hepatocarcinogenesis and suggest a possible role for Opisthorchis infestation in the generation of hepatocellular tumours in man.
Carcinogenesis 1987 Sep
PMID:Enhancement of DEN-induced hepatocellular nodule development by Opisthorchis viverrini infection in Syrian golden hamsters. 362 73

Infection by bacteria, parasites or viruses and tissue inflammation such as gastritis, hepatitis and colitis are recognized risk factors for human cancers at various sites. Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of authors' studies on liver fluke infection and cholangiocarcinoma development. A similar mechanism could apply to other suspected and known cancer-causing agents including Helicobacter pylori infection (stomach cancer) or asbestos exposure (lung mesothelioma). Studies on the type of tissue and DNA damage produced by NO and by other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.
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PMID:Chronic infections and inflammatory processes as cancer risk factors: possible role of nitric oxide in carcinogenesis. 751 36


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