Relationship of herpes simplex virus type-2 antibodies and squamous dysplasia to cervical carcinomain situ

Thomas, P.; Rawls, William E.

doi:10.1002/1097-0142(197812)42:6<2716::aid-cncr2820420629>3.0.co;2-1

Cited by 33 publications

(2 citation statements)

References 20 publications

(5 reference statements)

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“…There have been numerous reports that antibodies to HSVspecific proteins are found more frequently, or at higher titer, in women with CIN or cervical carcinoma than in controls (12)(13)(14) and that HSV-specific antigens can be detected in the neoplastic cells by immunofluorescent or other methods (15)(16)(17). Among the abundance ofsometimes confusing data (18,19), two series of recent reports were of interest with respect to our in situ hybridization results.…”

mentioning

confidence: 86%

Herpesvirus-specific RNA and protein in carcinoma of the uterine cervix.

McDougall¹,

Crum²,

Fenoglio³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Cloned probes of herpes simplex virus type 2 DNA were used in cytological hybridization experiments to detect herpesvirus RNA transcripts in the neoplastic cells of tumors of the uterine cervix. Virus-specific RNA was shown to represent transcription of limited regions of the genome, of which one is known to code for a DNA-binding protein that can be found by immunoperoxidase staining in the neoplastic cells of these tumors and has also been detected in cells transformed in vitro by this virus.The thesis that the continuum of disease leading to the development of uterine cervical carcinoma is associated with prior infection by herpes simplex virus type 2 (HSV-2) (1-5) has recently been tested at the molecular level by the use of in situ cytological hybridization (6-9). The use of 3H-labeled viral DNAs as probes to detect virus-specific RNA (10, 11) in cervical tissue has resulted in general agreement, based on published reports, that at least 30% ofall cervical intraepithelial neoplasia (CIN) and cervical carcinoma tissues contain cells that bind a HSV-2 [3H]DNA probe but not probes representing other viral DNAs, indicating the presence of HSV-specific RNA (7-9). The majority of these in situ hybridizations have been conducted with whole genomic DNA as the probe. In this report we summarize our studies using cloned subgenomic fragments of HSV-2 DNA as hybridization probes to define regions of the virus genome from which the detected RNA species are transcribed and correlate the findings with attempts to identify viral antigen(s) expressed in cervical carcinoma cells.There have been numerous reports that antibodies to HSVspecific proteins are found more frequently, or at higher titer, in women with CIN or cervical carcinoma than in controls (12)(13)(14) and that HSV-specific antigens can be detected in the neoplastic cells by immunofluorescent or other methods (15)(16)(17). Among the abundance ofsometimes confusing data (18,19), two series of recent reports were of interest with respect to our in situ hybridization results. First, antiserum to the major HSV-2 binding protein (20) was shown to react with human cervical carcinoma cells in two separate studies (21,22). The tumor antigens of other DNA viruses have been shown, without exception, to have DNA-binding properties (23), and a herpes simplex tumor antigen might be expected to exhibit a similar function. Second, it was demonstrated that sera from patients with cervical carcinoma precipitated two HSV-2 polypeptides (with molecular weights 38,000 and 118,000) more frequently than did sera from controls (24).The 38,000-dalton protein was ofinterest because it has been shown that a protein of this size is encoded within Bgl II fragment N of HSV-2 DNA (25, 26), which has been reported to have transforming activity in rodent cells (27,28).Rodent cells transformed in vitro by HSV-2 have been reported to express a number of HSV-specific antigens including VP143 (29), ICP10 (30), thymidine kinase (31, 32), membrane glycoproteins gA/gB (33, 34), and CP-1 (35)...

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mentioning

confidence: 86%

Herpesvirus-specific RNA and protein in carcinoma of the uterine cervix.

McDougall¹,

Crum²,

Fenoglio³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…The association of HSV with chronic inflammation [100][101][102][103] and the development of squamous dysplasia, carcinoma in situ, and cervical carcinoma has been proven since the 1860s [104][105][106][107][108][109][110][111][112]. Since 1981, a herpes classification is available [113].…”

Section: Pathogenic Stimulus By Virusmentioning

confidence: 99%

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Brücher

Jamall

2019

4open

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A pathogenic (biological or chemical) stimulus is the earliest information received by a cell that can result in the disruption of homeostasis with consequent development of disease. Chronic inflammation involves many cell types with numerous cytokines and signaling pathways, the release of different components by the cells, and the crosstalk provoked by such stimuli involving subclinical chronic inflammation and is mechanistically manifold. Exosomes secrete chemicals that trigger the epithelium to produce exosome-like nanoparticles promoting chronic inflammation. Small molecules, together with various cytokines, selectively target signaling pathways inducing crosstalk that suppress apoptosis. 16S rRNA gene sequencing has become routine to provide information on the composition and abundance of bacteria found in human tissues and in reservoirs. The deregulation of autophagy with chronic stimulation of inflammation is an early phenomenon in carcinogenesis. The disruption of cell–cell integrity enables transcellular CagA migration and triggers deregulation of autophagy with the net result being chronic inflammation. The complex and insidious nature of chronic inflammation can be seen both inside and outside the cell and even with intracellular nuclear fragments such as chromatin, which itself can elicit a chronic inflammatory response within the cytoplasm and affect autophagy. The ultimate result of unresolved chronic inflammation is fibrosis, a step before tissue remodeling results in the formation of a precancerous niche (PCN). Various pathogenic stimuli associated with different neoplasms result in persistent inflammation. This ongoing disruption of homeostasis in the micromilieu of cells, tissues, and organs is an essential preamble to carcinogenesis and occurs early in that process.

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Condyloma Acuminatum in Rochester, Minn, 1950-1978

Chuang¹

1984

Arch Dermatol

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Relationship of herpes simplex virus type-2 antibodies and squamous dysplasia to cervical carcinomain situ

Cited by 33 publications

References 20 publications

Herpesvirus-specific RNA and protein in carcinoma of the uterine cervix.

Herpesvirus-specific RNA and protein in carcinoma of the uterine cervix.

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Condyloma Acuminatum in Rochester, Minn, 1950-1978

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