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 human uterine cervix offers a unique opportunity to study the early lesions of squamous cell carcinoma, i.e., carcinoma in situ and dysplasia [combined as cervical intraepithelial neoplasia (CIN)]. In vivo, the patients with CIN have the epidemiological common denominators or "markers" of early onset of coitus, multiple sexual partners, 1st delivery before age 20, and antibodies to herpes simplex virus type 2 more frequently than do controls. The lesions themselves have specific epithelial and vascular changes observable with the colposcope in addition to the usual histological markers from biopsy specimens. The chromosomes and DNA content of cells in these lesions are abnormal. In vitro, the cells from CIN have characteristics somewhat between normal and invasive carcinoma. They lack contact inhibition and may be transferred for several generations, in contrast to normal cervical epithelial cells. The fibroblasts from areas adjacent to DIN are different from normal fibroblasts. The mitotic mechanism in cells cultured from CIN has a significantly prolonged prophase and telophase when compared to similar normal cells. The surface of CIN cells, unlike normal cells, has numerous microvilli when examined by scanning electron microscopy and has characteristic differences from normal cells with numerous elongated, irregular microvilli. With the transmission electron microscope, an increase in microvilli and a decrease in desmosomes and tonofibrils are seen in CIN cells. Some of these markers are being used clinically to manage patients with CIN. Other markers are the basis for further investigation of human carcinogenesis.
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PMID:In vivo and in vitro "markers" of human cervical intraepithelial neoplasia. 5 20

The immune reactivity of patients with squamous carcinoma of the head and neck region was compared with that of patients with squamous carcinoma of the female pelvic organs and patients with adenocarcinomas, melanomas, and sarcomas. The reactivity of patients with clinically localized tumors was compared with that of cured patients and a large normal population. Patients with squamous carcinomas of the head and neck region and female pelvic organs displayed higher incidences of impaired cellular immune competence than patients with malignancies of other histologic types. Among cured patients, those previously treated for squamous carcinoma were unique in that they displayed cellular immune defects and serum suppressants of in vitro immune reactivity similar to tumor-bearing patients. Antibodies to herpes simplex virus nonvirion antigen was found in high incidence only among patients with squamous carcinomas, and the incidences in tumor-bearing and cured patients were similar. The persisting immune defects in cured squamous carcinoma patients give importance to the determination of the role of genetic and environmental factors in the induction of these tumors. The associations made between herpes virus and squamous carcinoma offer an explanation for the defects and also an approach for the definition of the factors involved in squamous carcinogenesis. The findings are clinically relevant to the isolation of population groups at high risk for the development of squamous carcinoma, as a rational basis for the development of prophylactic measures, and as a basis for more effective therapeutic regimens.
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PMID:Unique immunobiological aspects of head and neck squamous carcinoma. 16 42

In the past few years there have been a number of reports correlating a high frequency of herpes simplex virus type 2(HSV-2) infection with lesions of the uterine cervix. These studies have used a clinical history of herpetic infection or the demonstration of herpetic antibodies in the cancer patients. The present study was performed to evaluate any possible carcinogenic activity of the formalin-inoculated herpes simplex virus type 2 in the reproductive tract of the female mouse. This approach to the study was selected because of previous experience with a model system of carcinogenesis of the cervix uteri using coal tar hydrocarbons. Cytologic and histologic preparations from experimental animals and controls are presented to demonstrate the mucosal alterations and tumors observed in the animals. Noninvasive lesions of the cervix were identified in 76.8% and invasive adenocarcinoma detected in 30.2% of the mice.
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PMID:Cervical carcinogenesis with herpes simplex virus, type 2. 16 21

The central theme of this communication is the interaction of herpes simplex virus type 2 with its host. In addition to the productive infection, we are confronted by latency and, as suggested by recent studies, by cancer. The possible mechanisms of latency and the role it may play as a precursor of carcinogenesis are discussed. If virus is to coexist with its host, a defined level of molecular interaction between host and viral gene products must exist. The association of AG-4 with active tumor growth and its identification as a minor virion protein, also exposed on the surface of the infected cell, open new vistas in the understanding of the role virus-host cell interactions may play in tumor growth. The modulation of the host immune response by the results of this interaction may play a significant role in cancer control. In these terms, the observation that antibody to AG-4 is a macroglobulin and that, therefore, immunity to AG-4 may be T-cell independent, should be given further consideration.
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PMID:Herpesvirus type 2-related antigens and their relevance to humoral and cell-mediated immunity in patients with cervical cancer. 17 45

The central theme of this communication is the recognition of an immunodiagnostic potential in a herpes virus antigen, the molecular interrelationship of which with cervical tumor cells is described. In addition to the productive infection caused by herpes simplex virus type 2 (HSV-2) we are confronted by latency and, as suggested by recent studies, by cancer. These different types of virus-host cell interactions are discussed at the host, as well as at the cellular level. A defined level of molecular interaction between host and viral gene products must exist if the virus is to co-exist with the host, as is the case in latency and carcinogenesis. The molecular interpretations posit the presence, in the squamous cervical tumor cells, of a product of the expression of the viral genome that has immunodiagnostic potential. The antigen designated AG-4 fulfills these predictions and appears to have immunodiagnostic potential. AG-4 is present in cervical tumor biopsies, but not in normal cervical tissue. It is a structural component of the HSV-2 virion that, in tissue cultures infected with HSV-2, is synthesized preferentially under conditions that prevent the normal replication of the virus. In view of its structural nature it is most probably virus-coded. AG-4 antibody identified in complement fixation assays with antigen prepared in tissue culture, disappears following successful tumor removal and reappears during cancer recurrence. This antibody also potentially identifies those patients with cervical atypia that are at high risk of neoplastic progression. The clinical benefits of the assay are evident.
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PMID:Immunodiagnostic potential of a virus-coded, tumor-associated antigen (AG-4) in cervical cancer. 19 36

The dose response of the enhanced reactivation (ER) of herpes simplex virus type 1 has been studied in UV-irradiated normal human skin fibroblasts and fibroblasts from the following hereditary cancer-prone syndromes: retinoblastoma, aniridia, polyposis coli, neurofibromatosis type 1 and 2, dysplastic nevus syndrome, Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, and Bloom's syndrome. Surprisingly, much higher levels of ER were observed in all these genetically heterogeneous hereditary disorders than in normal human skin fibroblasts. These results suggest that loss of one allele of putative tumor suppressor genes may activate cellular processes that result in the induction of the ER response, and they support our previous observation suggesting that ER may somehow be related to the process of carcinogenesis (P. J. Abrahams et al., Cancer Res., 48: 6054-6057, 1988).
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PMID:High levels of enhanced reactivation of herpes simplex virus in skin fibroblasts from various hereditary cancer-prone syndromes. 130 28

The distribution of 1,912 breakpoints observed in a series of 148 cervical cancers was analyzed. Fifty bands were shown to be nonrandomly involved in chromosome structural rearrangements. One hundred thirty-three breaks were noted in bands known to contain a human papillomavirus integration site, and 454 breaks were noted in bands containing a herpes simplex virus breakage site. We suggest that herpes simplex viruses and, possibly, papillomaviruses play an important role in the carcinogenesis and/or development of cytogenetic abnormalities in cervical cancers.
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PMID:Herpes simplex virus and human papillomavirus sites correlate with chromosomal breakpoints in human cervical carcinoma. 131 22

Extensive epidemiological and experimental studies have suggested that some chemical agents, nutritional deficiencies, and physical factors are associated with the development of esophageal cancer (EC). Recent evidence also suggests an etiologic role of certain microorganisms in esophageal carcinogenesis either by producing carcinogens or promotors or by acting directly on the host cells. The mutagenic and carcinogenic effects of several fungi and bacteria isolated from the grains and foodstuffs in high-risk areas have been shown by in vitro and in vivo studies. Certain viruses, e.g., human papillomavirus, herpes simplex virus, cytomegalovirus, and Epstein-Barr virus, have been implicated in the pathogenesis of a variety of human cancers, and all of them are known to produce tumors in animals and cell transformation in vitro. These viruses also have been shown to infect the esophageal epithelium. Therefore, although many of the key issues of their mechanisms of action are unclear as yet, they should be considered potential etiologic agents of EC. The present review summarizes the data available on the etiology of EC, emphasizing the current evidence implicating an etiologic role of microorganisms in the pathogenesis of this malignancy.
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PMID:Infectious agents in the etiology of esophageal cancer. 132 35

Human papillomaviruses (HPV) play an important role in cervical carcinogenesis but are probably not the only factors. To assess the role of HPV 6 and 11, of herpes simplex virus (HSV) and of cytomegalovirus (CMV) as cofactors for HPV 16 and HPV 18, we used polymerase chain reaction (PCR). The genomes of these six viruses was searched for in cervical biopsies, inbred in paraffin, from 22 normal cervices, 21 low grade cervical intraepithelial neoplasia (CIN), 21 high grade CIN and 20 squamous cancers. HPV 16 DNA had the highest prevalence in cervical lesions. Its frequency reached 24% in low grade CIN, 57% in high grade CIN, 50% in cancers and 9% in normal cervices. The simultaneous presence of HPV 16 and/or HPV 18 DNA and CMV and/or HSV DNA was significantly more frequent in high grade CIN and cancers than in normal cervices. On the other hand the presence of HPV 16 and/or HPV 18 DNA in samples lacking the other viral genomes did not significantly differ between the groups. Consequently the disease-viral infection relation was not apparent when these two "potentially oncogenic" HPV are isolated without coinfection by HSV or CMV. Our results are in agreement with the hypothesis of the role of herpesviruses as cofactors in cervical carcinogenesis. These viruses may disturb the control mechanisms of cellular growth and differentiation in HPV infected cells.
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PMID:[Role of herpes virus simplex and cytomegalovirus as cofactors of papillomavirus in dysplastic and cancerous lesions of the uterine cervix]. 134 99

To study the oncogenesis of human esophageal carcinoma, the presence of DNA sequences homologous to several DNA tumor viruses and the expression of oncogenes and growth factor genes were examined in two esophageal carcinoma cell lines of Chinese origin, CE48T/VGH and CE81T/VGH. Southern blot analyses failed to detect sequences homologous to hepatitis B virus (HBV), Epstein-Barr virus (EBV), herpes simplex virus type 2 (HSV-2), cytomegalovirus (CMV) or human papilloma virus (HPV) genomes. Northern blot analyses revealed that c-myc, c-src, c-H-ras, c-abl, c-sis, and p53 genes were expressed. In addition, transcripts of transforming growth factor alpha (TGF alpha), TGF beta, and platelet derived growth factor A (PDGF A) genes were detected. These studies suggest that DNA tumor viruses may not be involved in the carcinogenesis of esophageal carcinoma. However, cooperation among different oncogenes and the production of growth factors may play an important role in that carcinogenesis.
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PMID:Absence of genomes of DNA tumor viruses and expression of oncogenes and growth factors in two esophageal carcinoma cell lines of Chinese origin. 147 73


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