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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the cross-reactivity between early (E) proteins of different human papillomavirus (HPV) types, 346 serum samples were tested with E4 and E7 of HPV 16. Two hundred and sixteen of them were also tested with HPV 1 E4, 21 with HPV 11 E4 and E7, and 109 with HPV 18 E4 and E7. Viral fusion proteins were expressed in Escherichia coli and used as antigens in Western blot experiments. The sera were obtained from patients with HPV-associated genital lesions or cervical cancer, from renal transplant recipients and from patients hospitalized for reasons unrelated to HPV infections (the controls). In contrast to findings relating to HPV 16 E4 specific antibodies, the prevalence of anti-HPV 1 E4 antibodies was not greater in renal transplant recipients than in the controls. In each age group of the control population more sera reacted with HPV 1 E4 than with HPV 16 E4. Sera of patients with HPV-associated cervical diseases and cervical cancer reacted less frequently with HPV 11 E4 or E7 and HPV 18 E4 or E7, respectively, than with the corresponding HPV 16 proteins. Thirty of 117 HPV 16 E4 or E7 positive sera showed reactivity to the corresponding protein of either HPV 1, 11 or 18. As demonstrated by cross-absorption experiments performed with 26 of the double-reacting sera, 24 contained two populations of antibodies reacting with proteins of different HPV types whereas only two contained cross-reacting antibodies. We concluded that in the majority of sera antibodies to the HPV 16 E4 and E7 proteins are type-specific.
Mol Cell Probes 1992 Aug
PMID:Detection of antibodies to the E4 or E7 proteins of human papillomaviruses (HPV) in human sera by western blot analysis: type-specific reaction of anti-HPV 16 antibodies. 132 15

By means of a consensus polymerase chain reaction (PCR) method, the prevalence of HPV types was determined in cervical biopsies from 137 women referred to the gynecological outpatient clinic for colposcopy because of an abnormal cervical smear. The prevalence of HPV was 80.3%. There was a statistically highly significant rise in the prevalence of the oncogenic HPV types (16, 18, 31, 33) with increasing severity of cervical intraepithelial neoplasia (CIN I to III), indicating a role for these HPV types in the pathogenesis of cervical cancer. The prevalence of other HPV types decreased significantly with the severity of the lesion, suggesting that these HPV types play a less significant role in this process. These data indicate that HPV typing with PCR may be a valuable tool for distinguishing between high-risk and low-risk cervical lesions. Furthermore, our results suggest that the detection of HPV types by consensus PCR in the cervix of patients with an abnormal smear but without histologically detectable CIN is a useful tool for predicting which of these patients will eventually develop CIN. Finally, a relatively low percentage (3%) of HPV double infections is reported in this study.
Virchows Arch B Cell Pathol Incl Mol Pathol 1992
PMID:Detection of human papillomavirus types by the polymerase chain reaction and the differentiation between high-risk and low-risk cervical lesions. 135 17

The expression of the c-myc oncogene was studied in paraffin-embedded specimens of cervical biopsies using a monoclonal antibody which binds to the 62,000 Dalton protein encoded by the c-myc gene. A range of cervical cancers from intraepithelial neoplasia to advanced grade IV tumours were studied together with normal cervical biopsies; c-myc status was correlated to clinical progress. There was no correlation seen between the clinical stage of the disease at presentation and c-myc expression. The 15 patients with c-myc negative cervical cancers were shown to have better disease free (mean--95.4 mos) and total survival (mean 118.0--mos) compared to the 16 patients that were c-myc positive 28.4 and 48.4 mos respectively). The pattern of recurrence differed between the two groups with c-myc positive tumours more likely to develop extra pelvic metastatic disease. The c-myc status of cervical cancer offers a prognostic indicator that could be useful in guiding treatment decisions.
Mol Cell Probes 1989 Jun
PMID:c-myc oncogene expression and clinical outcome in carcinoma of the cervix. 267 79

The complete nucleotide sequence and genomic organization of human papillomavirus type 18, associated with cervical cancer, has been established. A detailed comparative analysis was undertaken leading to the identification of a number of features specific for genital papillomaviruses and the construction of a phylogenetic tree. Genital papillomaviruses differ from other human and animal papillomaviruses as they possess a longer E1 open reading frame (ORF) and have a characteristic control region. Phylogenetically, HPV 18 is located between the benign genital viruses, HPV 6 and HPV 11, and the malignant isolates, HPV 16 and HPV 33, and may represent an evolutionary intermediate among oncogenic papillomaviruses. Viral gene products known to be involved in cellular transformation are those of ORFs E5, E6 and E7. Significant sequence variation was found between the E6 to E7 regions of different integrated forms of HPV 18. On re-examination of the E6 primary structures we noticed that the gene has evolved by successive duplications of a unit encoding 33 amino acids, which include a Cys-X-X-Cys motif. Furthermore, the E7 gene product has apparently evolved in the same manner and is related to E6. Both gene products bear a striking resemblance to the transcriptional factor IIIA of Xenopus laevis, the prototype of a new class of nucleic acid binding proteins.
J Mol Biol 1987 Feb 20
PMID:Nucleotide sequence and comparative analysis of the human papillomavirus type 18 genome. Phylogeny of papillomaviruses and repeated structure of the E6 and E7 gene products. 303 46

A stable human X human hybridoma, termed CLNH11, was produced by fusing UC 729-6, a 6-thioguanine-resistant human lymphoblastoid B-cell line, with lymphocytes obtained from a patient with squamous cell carcinoma of the cervix. CLNH11 could grow both in serum-containing and serum-free media, and produced a significantly higher titer of antibody in serum-free media. CLNH11 secreted a human monoclonal immunoglobulin G which bound to the autologous cervical carcinoma in both tissue sections and primary cultured cells, the cervical cancer cell lines Hela and CaSki, but not to normal fibroblasts.
Mol Biol Med 1983 Sep
PMID:Human X human hybridoma producing monoclonal antibody against autologous cervical carcinoma. 633 17

Of the steroid hormone receptor family members, the estrogen receptor (ER) is notable in containing a sizable (42-amino acid) C-terminal region, denoted domain F. This F region differs from its adjacent hormone-binding domain, domain E, in that it is not well conserved among different vertebrate ER species, and its role in the biological activity of the ER is not well defined. We report an important role for the F domain of the ER in modulating the magnitude of gene transcription by estrogen and antiestrogen, and in determining the effectiveness of antiestrogens in suppressing estrogen-stimulated gene transcription. Using transient transfections, we have examined, in several cell types, the transcriptional activity of the full-length wild type human ER and ER lacking the carboxy-terminal F domain (delta F ER, containing amino acids 1-554) or ER altered in the F domain by point mutations. In some cells, namely Chinese hamster ovary (CHO) cells and MDA-MB-231 human breast cancer cells expressing wild type ER or delta F ER, estradiol (E2) stimulates equally transcription of several estrogen-responsive promoter-reporter gene constructs [estrogen ca-18119 element, (ERE)2-TATA-CAT, (ERE)2-pS2-CAT, (ERE)2-progesterone receptor(distal)-CAT]; however, the antiestrogens trans-hydroxytamoxifen and ICI 164,384, which stimulate transcription of some of these reporter constructs with the wild type ER, were unable to stimulate transcription with delta F ER. In addition, these antiestrogens were more effective antagonists of E2-stimulated transcription by delta F ER than by wild type ER. By contrast, in HeLa human cervical cancer cells and 3T3 mouse fibroblast cells, the delta F ER exposed to E2 is much less effective than wild type ER in stimulating transcription, and antiestrogens were less potent in suppressing E2-stimulated transcription by the delta F ER. These differences in response of the delta F and wild type ER to estrogen or antiestrogen do not appear to be due to a change in receptor expression level, binding affinity for ligands, or binding to estrogen response element DNA. Our data support the supposition that the conformation of the receptor-ligand complex is different with estrogen vs. antiestrogen and with wild type vs. delta F ER, such that its potential for interaction with protein cofactors or transcription factors is different and is markedly influenced by cell context. Thus, the F domain of the ER has a specific modulatory function that affects the agonist/antagonist effectiveness of antiestrogens and the transcriptional activity of the liganded ER in cells.
Mol Endocrinol 1995 Jul
PMID:The carboxy-terminal F domain of the human estrogen receptor: role in the transcriptional activity of the receptor and the effectiveness of antiestrogens as estrogen antagonists. 747 65

Human papillomaviruses (HPVs) are the etiological agents for genital warts and contribute to the development of cervical cancer in humans. The HPV E7 gene product is expressed in these diseases, and the E7 genes from HPV types 16 and 18 contribute to transformation in mammalian cells. Mutation and deletion analysis of this gene suggests that the transforming activity of the protein product resides in the same domain as that which is directly involved in complex formation with the retinoblastoma gene product (pRB). This domain is one of two conserved regions (designated CRI and CRII) shared by E7 and other viral oncoproteins which bind pRB, including adenovirus E1A protein. Binding of HPV type 16 E7 protein to pRB has previously been shown to affect pRB's ability to bind DNA and to form complexes with other cellular proteins. In the current study, we map the functional interaction between E7 protein and pRB by monitoring the association between a 60-kDa version of the pRB, pRB60, and the cellular transcription factor E2F. We observe that CRII of E7 (amino acids 20 to 29), which completely blocks binding of full-length E7 protein, is necessary but not sufficient to inhibit E2F/pRB60 complex formation. While CRI of E1A (amino acids 37 to 55) appears to be sufficient to compete with E2F for binding to pRB60, the equivalent region of E7 is neither necessary nor sufficient. Only E7 fragments that contained both CRII and at least a portion of the zinc-binding domain (amino acids 60 to 98) inhibited E2F/pRB60 complex formation. These results suggest that pRB60 associates with E7 and E2F through overlapping but distinct domains.
Mol Cell Biol 1993 Feb
PMID:Protein domains governing interactions between E2F, the retinoblastoma gene product, and human papillomavirus type 16 E7 protein. 767 96

To study the presence of transforming sequence Bgl II N of HSV-2 in cervical cancer tissues, we developed the nested polymerase chain reaction (PCR) for detecting such a sequence in paraffin-embedded cervical tissue sections. Samples derived from 46 patients with premalignant and malignant lesions were tested. The sequence was found in 20-25% of total cases tested but not observed in any of the normal healthy controls. This study also indicates that for the detection of HSV-2 Bgl II N sequence in cervical tissue, the nested PCR may be more reliable than the in situ hybridization method.
Mol Cell Probes 1994 Dec
PMID:Detection of herpes simplex virus type 2 Bgl II N fragment in paraffin-embedded cervical tissue sections using nested polymerase chain reaction. 770 Feb 64

Specific types of human papillomaviruses (HPVs) are closely associated with the development of cervical cancer. The transforming ability of these high-risk HPV types depends on the expression of the viral E6 and E7 oncogenes. It is therefore of particular interest to elucidate the molecular mechanisms that result in the activation of E6/E7 expression during HPV-associated tumorigenesis. Recently, much progress has been made in characterizing the proteins involved in the regulation of HPV oncogene transcription. This review describes the functional significance of cellular factors involved in the transcriptional control of the E6/E7 promoter for the two most common HPV types associated with cervical cancer, HPV16 and HPV18. In addition, we discuss regulatory pathways that may contribute to the epithelial cells specificity of E6/E7 transcription. The definition of the factors that regulate HPV oncogene transcription could provide new insights into the molecular mechanisms activating viral oncogene expression during cervical carcinogenesis and forms an experimental basis for investigating the specific biochemical pathways that contribute to HPV-associated malignant cell transformation.
Mol Carcinog 1994 Jul
PMID:Cellular control of human papillomavirus oncogene transcription. 804 95

Circulating lipid peroxide, antioxidant components and the activities of defense enzymes were estimated in uterine cervical carcinoma patients (before and after radiotherapy and radiotherapy combined chemotherapy) and compared with controls. Some of the antioxidant components such as glutathione, vitamin E and selenium are reduced in cervical cancer. The reduced levels of vitamin E and glutathione were normalized after treatment. Erythrocyte lipid peroxide (E-LPx) and erythrocyte membrane lipid peroxide (EM-LPx) levels were found to be increased in all the stages of uterine cervical carcinoma. The important antioxidant enzymes such as erythrocyte superoxide dismutase (E-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) and glucose-6-phosphate dehydrogenase (G6PDH) were found to be decreased in uterine cervical carcinoma. These altered biochemical parameters were reversed to normal, of course with varied degree after different mode of therapy. Significant normalization was observed in Type II chemoradiotherapy.
Mol Cell Biochem 1996 May 10
PMID:Effect of radiotherapy and chemoradiotherapy on circulating antioxidant system of human uterine cervical carcinoma. 879 Dec 80


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