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At least 217 records · Page 12Linked to original sources
PubMed1995

Expression of p53 protein related to human papillomavirus and DNA ploidy in superficial esophageal carcinoma.

We examined the p53 protein and human papilloma virus (HPV) by immunohistochemistry and DNA ploidy by cytofluorometry in paraffin-embedded esophageal carcinoma tissue specimens. Sixty-one patients with superficial esophageal carcinoma were operated on between 1983 and 1991 without any prior treatment. Immunostaining of the anti-p53 protein antibody (CM1) was positive in 32 carcinomas (52%). Patients with p53-positive tumors had a poorer outcome than those with p53-negative tumors (P < 0.05). In addition, patients with p53-positive tumors did not have any characteristic site of relapse. Only 5 of the 61 patients (8.2%) had HPV-positive tumors. One of these 5 carcinomas expressed both p53 protein and HPV. Three patients with HPV-positive tumors which had invaded the submucosal layer died of relapse. A determination of DNA ploidy revealed 30 patients with aneuploid tumors, 13 with polyploid tumors and 18 with diploid tumors. The outcome of the patients with aneuploid tumors was worse than that of the patients with diploid tumor (P < 0.05). p53 protein expression was not associated with DNA ploidy; however, the 16 patients who had both p53-positive and aneuploid tumors had a worse prognosis than patients with p53-negative and aneuploid tumors (P < 0.01). These findings suggest that p53 protein expression in conjunction with DNA ploidy may be a useful indicator in evaluating the prognosis of patients with superficial esophageal carcinoma.

Adult↗
PubMed1983

Analysis of retinoblastoma for human adenovirus type 12 genome.

Adenovirus type 12 has high oncogenic potential in newborn rodents. Moreover, adenovirus 12 induces retinoblastoma-like tumours in baboons and transforms in vitro human embryo retinoblasts. Since adenovirus-transformed cells contain adenovirus transforming gene sequences, the detection of adenovirus 12 transforming gene in tumour cell DNA can provide evidence for or against a possible aetiological role of adenovirus 12 in retinoblastoma. In this experiment, cell DNAs from six retinoblastomas were assayed for adenovirus 12 transforming gene sequences by spot hybridization and Southern blot hybridization, using the labelled EcoRI-C fragment of adenovirus 12 DNA as a probe (the far left 16.5% of the viral genome). No adenovirus 12 transforming gene sequences were detected at the level of 0.1 or 0.5 copy of the probe per diploid cell DNA in all of six retinoblastomas.

Adenoviruses, Human↗
PubMed1991

Detection of human papillomavirus in head and neck tumors with DNA hybridization and immunohistochemical analysis.

The presence of human papillomavirus (HPV) DNA in oral, sinus, pharynx, and larynx lesions of Japanese patients was studied by Southern blot hybridization under less stringent (25% formamide, 42 degrees C) and stringent (50% formamide, 42 degrees C) conditions. Three samples from 10 benign tumors, and 3 of 30 malignant tumors, contained HPV DNA or HPV-related sequences. The HPV DNAs harbored in three laryngeal papillomas were HPV-11, -6, and -6 or -11, respectively. The HPV DNA and viral capsid antigens were easily detected by in situ hybridization, Western blotting, and peroxidase-antiperoxidase staining. However, neither the typical restriction pattern of HPV DNA nor viral antigen was identified in the malignant tumors, suggesting that subgenomic fragments remained integrated in the host cell DNA.

Antigens, Viral↗
PubMed1987

A rare common integration site of proviruses of the mouse mammary tumor virus in P-type mammary tumors of mouse strain GR.

The mouse mammary tumor virus (MMTV) can induce mammary tumors in mice by proviral activation of the cellular oncogenes int-1 or int-2. Activation of these genes, however, is observed in only a few hormone- and pregnancy-dependent mammary tumors of the mouse strain GR. To study the possible involvement of other oncogenes we cloned three MMTV proviral-host fragments (MT 40, 42, and 53) from different mammary tumors of GR with a single acquired MMTV provirus. From a genomic library of normal mouse DNA we isolated phages with insert DNAs that covered 20-30 kb of the uninterrupted regions. Suitable probes devoid of repetitive DNA sequences were isolated in order to screen other mammary tumors for MMTV proviral integrations in these regions. Only two mammary tumors, MT 40 and 42, showed integration of extra MMTV proviruses within the same region. The integrations occurred only 60 bp apart. The other mammary tumors, however, did not contain MMTV proviral integrations in this region, nor in the MT 53 region. Using mouse-hamster somatic cell hybrid DNA, the MT 40/42 integration region was assigned to mouse chromosome 7, and the second region, MT 53, to chromosome 16. The two regions bear no homology to known cellular oncogenes. We did not observe any mRNA being expressed from these cloned segments either in tumors or in normal mammary glands. These findings indicate that plaque(P)-type mammary tumors in mouse strain GR do not originate from MMTV provirus insertions in a particularly favored integration region, but that there may be a variety of integration sites in these tumors.

Animals↗
PubMed1989

Analysis of somatic mutations at human minisatellite loci in tumors and cell lines.

Hypervariable human minisatellite loci show a substantial level of germline instability, and spontaneous mutation rates to new length alleles have been measured directly by pedigree analysis. We now show that mutation events altering the number of minisatellite repeat units are not restricted to the germline, but also arise in other tissues. Mutant alleles can be detected at a very low frequency in lymphoblastoid cell lines and at much higher frequencies in clonal tumor cell populations, most particularly in gastrointestinal adenocarcinomas. Mutant alleles in these tumors are usually present at a dosage equal to or greater than that of the progenitor allele, indicating that most or all of the tumor cells carry the same clonally derived mutant allele. As with germline mutation, the incidence of somatic mutations in tumors varies from locus to locus, with the same locus showing the highest level of germline and somatic instability. Most length changes, as those in the germline, are of only a few repeat units; however, very large changes are also observed, implying that such mutations can occur in the absence of meiosis.

DNA Mutational Analysis↗
PubMed1998

Human papillomavirus infection in esophageal carcinomas: a study of 121 lesions using multiple broad-spectrum polymerase chain reactions and literature review.

To elucidate the putative role of human papillomavirus (HPV) infection in the etiology of esophageal cancer, 121 formalin-fixed, paraffin-embedded specimens originating from a non-high-incidence area for this carcinoma, from Slovenia, were screened for HPV infection using eight different polymerase chain reactions (PCR). Three different HPV consensus primer sets and four primer sets specific for HPV types 6, 16, and 18 failed to detect HPV DNA sequences in any of the tumor samples. Fragments of human beta-globin gene that served as internal controls were successfully amplified from 120 of 121 specimens. Our study confirms the opinion that most esophageal cancers originating from non-high-incidence geographic areas of this cancer are not associated with HPV infection. According to the studies reviewed, it is likely that HPV infection plays a much more significant role in esophageal carcinogenesis in those areas of the world with a high incidence of ESCC.

Aged↗
PubMed1997

Investigation of oesophageal adenocarcinoma for viral genomic sequences.

Overexpression of the tumour suppressor gene product p53 is common in oesophageal adenocarcinoma. This may be due to gene mutation, but overexpression can also result from complexing between viral proteins and p53; a number of viruses are causally linked with malignancy. This study therefore investigated the prevalence in oesophageal adenocarcinoma of viruses whose gene products are capable of interacting with p53. Seventeen tumours and 17 normal oesophagi were screened for specific DNA sequences from human papilloma virus (HPV), Adenovirus type 12, Epstein-Barr Virus (EBV), and cytomegalovirus (CMV). Frozen sections were analysed by polymerase chain reaction, and results were confirmed by Southern blot hybridization. Overexpression of p53 was studied immunohistochemically. Overexpression of p53 was identified in 11 of 17 tumours. No viral sequences were detected for HPV, CMV, or Adenovirus in any tumour. EBV sequences were found in eight of 17 tumours, and eight of 17 negative controls. There is therefore no evidence of HPV 16, 18 and 33, Adenovirus 12 or CMV infection in oesophageal adenocarcinoma. EBV infection in the oesophagus is of doubtful significance, in view of the high incidence in the control population. Overexpression of p53 cannot be explained by complexing with common viral proteins, and must be related to other intracellular mechanisms.

Adenocarcinoma↗
PubMed1977

Nucleic acid sequences of primate type C viruses in normal and neoplastic human tissues.

Recent reports on the isolation of type C viruses from human cells have generated considerable controversy because of the close relationship of the viruses to the type C viruses of subhuman primates. These findings have been interpreted as evidence for contamination despite the repeated isolation of some type C viruses from separate clinical specimens or from separate frozen primary cell stocks of the same donor. Our laboratory has described a type C virus which is released from the HEL-12 strain of normal human embryonic lung fibroblasts. The HEL-12 virus is related immunologically to simian sarcoma (woolly monkey fibrosarcoma) virus (SiSV) and the endogenous type C viruses of baboons and domestic cats. To demonstrate that the HEL-12 virus is not an adventitious contaminant, fresh human tissues were examined for antigenic cross-reactivity with HEL-12 virus antigens. Some patients with myelogenous leukemia contain circulating immunoglobulins which specifically inhibit the reverse transcriptases of HEL-12 virus and primate type C viruses. In addition, the glomerular immune complexes in patients with systemic lupus erythematosus contain antigens related to HEL-12 virus proteins. Using the techniques of molecular hybridisation, we demonstrate here that HEL-12 cells contain proviral DNA sequences before antigen expression or spontaneous virus release can be detected. We also present evidence for the existence of nucleic acid sequences homologous to HEL-12 viral RNA in the DNAs from certain cancer patients.

Animals↗
PubMed1993

PCR-based microsatellite polymorphisms in the detection of loss of heterozygosity in fresh and archival tumour tissue.

PCR-based microsatellite polymorphisms have proved their power in genetic linkage analysis and other identification methods, due to their high information content and even distribution over the chromosomes. In the present study we applied microsatellite polymorphisms to detect loss of heterozygosity in fresh (snap-frozen) and in archival ovarian tumour tissue. Clear allele losses were found in fresh and paraffin embedded tumour samples. Conventional Southern analysis of flanking markers on the same tumour DNA samples confirmed the observed losses detected by microsatellite polymorphisms. Titration experiments suggest that loss of heterozygosity remains detectable in tumour samples despite 60% contamination with normal DNA. This technique provides a fast and reproducible alternative to conventional Southern blotting in the detection of loss of heterozygosity, with the crucial additional advantages of minimal sample requirements, making archival material available for genetic investigation.

Adenocarcinoma↗
PubMed1995

Allelic imbalance of chromosome 6q in ovarian tumours.

Previous work has implicated putative tumour-suppressor (ts) genes at 6q27 and a broad region at 6p12-q23. Here we report the results of a coded, randomised study of allelic imbalance at 12 loci on 6q on 40 pairs of coded tumour-blood pairs from patients with ovarian tumours. Our results provide clear evidence for the involvement of different regions of 6q in tumours of different histological subtypes. The involvement in serous tumours of a ts gene at the distal site is confirmed. However, proximal 6q presents a complex picture, with possibly three further ts genes: one at 6q21-23.3 involved at high frequency in benign and endometrioid tumours, another at 6q14-q15, also involved in endometrioid tumours, and a third suggested by a smallest region of deletion at 6q16.3-q21, between D6S275 and D6S300, that appears to be involved in early stage tumours. These observations point the way to a statistical study of the involvement of 6q in tumours of different histological type and staging performed on larger cohorts of samples.

Adenocarcinoma, Mucinous↗
PubMed2001

Detection of Toxoplasma gondii DNA in primary intraocular B-cell lymphoma.

Primary intraocular lymphoma, a variant of primary central nervous system lymphoma with ocular involvement, is a large B-cell non-Hodgkin's lymphoma. Some cases of primary intraocular lymphoma have been reported to be associated with microorganisms including Epstein-Barr virus (EBV) and human herpes virus-8 (HHV-8), but not parasites. We analyzed 10 cases of primary intraocular lymphoma using microdissection and PCR. Tumor and normal cells were microdissected from ocular tissue on slides and subjected to PCR for genes from Toxoplasma gondii, EBV, and HHV-8. We detected Toxoplasma gondii, not HHV-8 or EBV, DNA in the lymphoma but not in normal cells of two cases that resembled ocular toxoplasmosis clinically. We speculate that Toxoplasma gondii may play a role in some forms of primary intraocular B-cell lymphoma.

Adult↗
PubMed2002

Expression of p21/WAF-1, status of apoptosis and p53 mutation in esophageal squamous cell carcinoma with HPV infection.

Human papilloma virus (HPV) is regarded as a causative carcinogenic agent in anogenital squamous cell carcinoma (SCC), but there is controversy about its etiologic role in esophageal SCC (ESCC). In this study, we attempted to clarify whether HPV infection plays a crucial role in the development of ESCC by analysis of multiple factors. These included: detection of HPV DNA; evaluation of immunohistochemical assays for HPV-related cell cycle regulators and apoptosis by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method; and genetic analysis of the p53 gene. Twenty of the 48 ESCC examined (42%) were found to be positive for the HPV genome by polymerase chain reaction. They comprised 16 cases with the HPV16 subtype, three with the HPV18 subtype, and one with both HPV16 and 18. Immunohistochemical analysis revealed that the expression of p21/WAF-1 was significantly decreased in HPV-positive cases (chi2 = 9.2614; P = 0.0023). Furthermore, the 10 apoptosis-negative (< or =10%) cases of HPV-positive SCC were almost exclusively p21/WAF-1-negative (chi2 = 12.1406; P = 0.0005), indicating the significance of the relationship between HPV infection and the phenotype that is expected from HPV-induced inhibition of p53. Although 14 cases possessed missense and deletion mutations of the p53 gene (of which four mutations were found in HPV-positive ESCC), no accumulation of the mutation was defined in the phenotype, suggesting that distinct mutation processes might be involved in HPV-negative and -positive ESCC. The data provide significant support for the hypothesis that HPV infection may play a crucial role in the oncogenesis of some ESCC.

Apoptosis↗