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L Gissmann

Publications and source records attributed to L Gissmann.

At least 109 records · Page 6Linked to original sources
PubMed1987

Occurrence of HPV genomes in penile smears of healthy men.

Penile smears of 530 males without any clinically detectable genital papillomavirus infection were subjected to molecular in situ hybridization on filters with different 32P-labeled HPV-DNAs. HPV genomes were identified in 31 cases (5.8%). Eight smears reacted with HPV 6/HPV 11 DNA and 5 specimens with HPV 16 and HPV 18 DNA exclusively; in 18 cases HPV 6/HPV 11 and HPV 16/HPV 18 were found in coexistence. With regard to the different age groups, HPV-DNA was found in only 1.7% of smears obtained from persons over 35 years of age, while 7.9% of the samples from men aged 15 to 35 gave positive results. This age distribution indicates that the occurrence of HPV genomes in epithelial cells of the glans may be due to infections by sexual contact rather than to reactivation of persisting viruses.

Adolescent↗
PubMed1987

Measurement of cell-mediated immunity against bovine papilloma virus by lymphoproliferative reactions.

To study cellular immunity towards bovine papillomavirus (BPV), calves were infected intradermally with BPV-1, and the cellular immune response was measured by the lymphocyte proliferation assay. Peripheral blood lymphocytes were obtained which in control experiments were highly reactive towards mitogen stimulation. Different batches of BPV-1 were prepared by the use of density gradients. In the first set of experiments, a nonspecific mitogenic effect of the virus preparation was observed. This effect was obviously caused by soluble molecules contained in the virion-free supernatant obtained after ultracentrifugation of the viruses. Subsequently, we obtained highly purified virions which did not share the nonspecific mitogenic effect. The data obtained with these virions showed no responses of untreated control animals but a short-lived in vitro lymphoproliferative response 2 to 3 weeks after infection. This response then disappeared and was followed by a period of non-responsiveness which lasted as long as we tested the animals.

Animals↗
PubMed1987

Papillomavirus sequences integrate near cellular oncogenes in some cervical carcinomas.

The chromosomal locations of cellular sequences flanking integrated papillomavirus DNA in four cervical carcinoma cell lines and a primary cervical carcinoma have been determined. The two human papillomavirus (HPV) 16 flanking sequences derived from the tumor were localized to chromosome regions 20pter----20q13 and 3p25----3qter, regions that also contain the protooncogenes c-src-1 and c-raf-1, respectively. The HPV 16 integration site in the SiHa cervical carcinoma-derived cell line is in chromosome region 13q14----13q32. The HPV 18 integration site in SW756 cervical carcinoma cells is in chromosome 12 but is not closely linked to the Ki-ras2 gene. Finally, in two cervical carcinoma cell lines, HeLa and C4-I, HPV 18 DNA is integrated in chromosome 8, 5' of the c-myc gene. The HeLa HPV 18 integration site is within 40 kilobases 5' of the c-myc gene, inside the HL60 amplification unit surrounding and including the c-myc gene. Additionally, steady-state levels of c-myc mRNA are elevated in HeLa and C4-I cells relative to other cervical carcinoma cell lines. Thus, in at least some genital tumors, cis-activation of cellular oncogenes by HPV may be involved in malignant transformation of cervical cells.

Attachment Sites, Microbiological↗
PubMed1987

Identification of human papillomavirus type 16 E7 protein by monoclonal antibodies.

A number of human papillomavirus (HPV) type 16 proteins have recently been identified in human cervical carcinoma cell lines using polyclonal antisera against papillomavirus gene products expressed in Escherichia coli. E7 protein has been found to be the most abundant papillomavirus protein in these cells. Here we describe a panel of monoclonal antibodies recognizing a 15K Mr non-glycosylated cytoplasmic HPV-16 E7 protein. One of the antibodies cross-reacted with HPV-18 E7 protein.

Antibodies, Monoclonal↗
PubMed1987

Molecular and cytogenetic analysis of immortalized human primary keratinocytes obtained after transfection with human papillomavirus type 16 DNA.

A proliferating population of human foreskin keratinocytes (presently in the sixtieth passage) has been obtained after transfection with human papillomavirus (HPV) type 16 DNA. In contrast, the control cultures did not survive beyond the sixth passage. Cytogenetic analysis of cells taken from the twelfth passage revealed a heteroploid male karyotype. In approximately 50% of the cells a common marker chromosome was found, suggesting a clonal origin for at least part of the population. This is further substantiated by Southern blot analysis of cellular DNA which revealed oligomeric HPV 16 genomes integrated at a single site within the host DNA. RNA transcribed from the early region of the HPV 16 genome was identified in the cytoplasm. The immortalizing effect of HPV 16 DNA on human keratinocytes could be reproduced in a second experiment. Such cell lines represent an unique system to study the interaction of HPV with its natural target cell in vitro.

Cell Division↗
PubMed1987

Human papillomaviruses in women with a history of abnormal Papanicolaou smears and in their male partners.

Human papillomavirus infection of the genital tract was identified by the filter in situ hybridization test. Exfoliated cervical cells were tested separately for the prevalence of human papillomavirus 6/11 and 16/18. Human papillomavirus deoxyribonucleic acid (DNA) was identified in 70 and 92% of specimens of U.S. and West German women, respectively, who showed concurrent cytologic and colposcopic abnormalities, and in 50 and 54% of women, respectively, who showed neither cytologic nor colposcopic abnormalities at the time of examination. In the cytologic categories of condyloma, mild to moderate dysplasia (cervical intraepithelial neoplasia I/II), and severe dysplasia-carcinoma in situ (cervical intraepithelial neoplasia III), the overall DNA detection rate of human papillomavirus 6/11 and 16/18 varied between 75 and 83%; but human papillomavirus 16/18 was recovered relatively more frequently from the more severe lesions. Forty-eight West German women were monitored cytologically over a period of three to 24 months; progression to carcinoma in situ (cervical intraepithelial neoplasia III) was correlated with initial isolation of human papillomavirus 16/18. The vagina and vestibule were found to be frequent sites of human papillomavirus infection with the same virus type as in the cervix. In an investigation of male partners of 40 human papillomavirus-positive women, human papillomavirus was identified in exfoliated cells from 26; in 19 instances, the males harbored the same human papillomavirus types as their female partners.

Autoradiography↗
PubMed1987

[Demonstration and organizational structure of the DNA of human papillomaviruses in laryngeal and hypopharyngeal carcinomas].

Thirty biopsy specimens from various histological types of human carcinomas of the larynx and hypopharynx were analysed for the presence of human papillomavirus (HPV) DNA: DNA from the individual specimens were tested for the presence of homologous sequences to HPV genotypes 1, 2, 4, 8, 9, 10, 11, 13, 16 and 18. One squamous cell carcinoma of the hypopharynx (postcricoideal area) contained multiple copies of DNA hybridizing under stringent conditions with HPV 16 DNA. The latter DNA has been found to be frequently associated with human genital cancer. HPV 16 DNA was found mostly episomally as oligomeric circles of 7.9 kbp size, and as larger rear-ranged circular molecules. Integration of the viral DNA in the host cell DNA seems quite likely. Integration and rearrangement of viral DNA into cellular DNA may play a role in the induction and maintenance of the transformed state. The presence of sequences reacting under semistringent conditions with HPV DNA was observed in two additional biopsy specimens of this study. This could suggest that additional laryngeal cancers are associated with papilloma virus infections.

Biopsy↗
PubMed1986

Rearranged HPV 16 molecules in an anal and in a laryngeal carcinoma.

By hybridization under stringent conditions, one out of two anal carcinomas and one out of 36 laryngeal carcinomas were shown to harbor HPV 16 DNA in high copy number. Further analysis of both tumor DNAs indicated a rearrangement of the viral DNA in the tumor cells. HPV 16 DNA in the anal carcinoma could chiefly be found episomally in two different forms: a minority as 7.9-kb oligomeric episomes with no apparent modifications; as 10.7-kb rear-ranged oligomeric episomes with a duplication of the part of the viral genome encoding the open reading frames (ORF) E7, E1 and parts of E6 and E2. In the laryngeal carcinoma, integrated and episomal HPV 16 DNA molecules of 7.9 kb were present, together with rearranged molecules of approximately 18 kb with multiple duplications of the ORF E4 and parts of the ORFs E2, E5, L1 and L2. Possible consequences for transcription of the modified viral genomes are discussed.

Anus Neoplasms↗
PubMed1986

Presence of human papillomavirus type-16 and type-18 DNA sequences and their expression in cervical cancers and cell lines from Japanese patients.

Southern blot analyses of surgical specimens of cervical carcinoma from Japanese patients showed that 3/9 samples contained human papillomavirus (HPV) type-16 DNA sequences, and 2 contained HPV type-18 DNA sequences. By Northern blot analyses, RNA transcripts of HPV DNA sequences were demonstrated in some of the tissues containing HPV type-16 or HPV type-18 DNA sequences. Two cell lines established from cervical cancers of Japanese patients also contained HPV type-18 genomes and these cell lines contained HPV type-18 transcripts. Two other cervical cancer cell lines from a Japanese patient were found to contain HPV type-16 DNA sequences and their RNA transcripts.

Adenocarcinoma↗
PubMed1986

Molecular cloning of two new HPV types (HPV 37 and HPV 38) from a keratoacanthoma and a malignant melanoma.

Several benign and malignant skin tumors were analyzed for the presence of human papillomavirus (HPV) DNA. By hybridization with different HPV DNA probes under non-stringent conditions (Tm -40 degrees C), two tumors were found to contain HPV-specific DNA sequences in high copy numbers: (1) a keratoacanthoma from a patient who also suffered from a basalioma; (2) a superficial spreading malignant melanoma of an immunosuppressed patient. For further analysis of these DNA sequences genomic libraries from both tumor DNAs were constructed and, out of these, 4 different HPV DNA types have been cloned. By cross-hybridization experiments and restriction map analysis HPV 9 DNA was identified in the keratoacanthoma whereas HPV 17a DNA could be cloned from the malignant melanoma. From each tumor one additional HPV-type not identical to other known HPV-types was cloned. These isolates are closely related to HPV 9, 15, 17, 22 and 23. A physical map of both HPV DNAs was constructed. Size (7.8 kbp), co-linear alignment to HPV 16, cross-hybridization with other HPV-types under conditions of low stringency and monomeric episomal state of the HPV molecules indicate that these two DNA probes represent new HPV types that have been tentatively designated as HPV 37 (keratoacanthoma) and HPV 38 (malignant melanoma). None of these two HPV types could be found in any other of 231 tumor DNAs originating from different tissues.

Cloning, Molecular↗
PubMed1986

Persistence and expression of human papillomavirus DNA in genital cancer.

There is mounting evidence that certain types of human papillomaviruses (HPV types 16 and 18) are associated with human genital cancer. Other virus types, such as HPV-6 or HPV-11, are more regularly found in benign genital warts. Since all viruses can be present in putative precancerous lesions of the uterine cervix (dysplasia, cervical intraepithelial neoplasia) it has been postulated that individual HPV types have different 'oncogenic potential'. The molecular basis for this difference is not known. The question of the natural reservoir for the oncogenic viruses is discussed. Expression of parts of the early region of the HPV genome in cell lines established from genital cancer supports the hypothesis that papillomaviruses are involved in inducing and/or maintaining the transformed phenotype of cancer cells.

Adenocarcinoma↗
PubMed1986

The nucleotide sequence and genome organization of human papilloma virus type 11.

The complete nucleotide sequence of human papilloma virus type 11 (HPV11) DNA (7931 bp) was determined. HPV11 DNA which has been isolated from laryngeal papillomas and from genital warts (condylomata acuminata) shows a high degree of sequence homology to HPV6b (82%). The arrangement of open reading frames is very similar to HPV6b, the homology of the deduced amino acid sequences varies between 58 and 92%. Characteristic features of the noncoding region between the L1 and E6 open reading frames is an AT-rich domain of about 200 bp with extended stretches of alternating thymine-purine bases and a 12-bp inverted repeat element ACCG NNNN CGGT arranged in tandem upstream of the putative early promoter TATA box.

Amino Acid Sequence↗
PubMed1986

Molecular cloning and characterization of human papillomavirus type 7 DNA.

Human papillomavirus type 7 (HPV-7) was first described in 1981 but so far could not be molecularly cloned. It has been found almost exclusively in hand warts of butchers. We have cloned the complete genome in pBR 322, established its physical map, demonstrated the colinear genome organization with HPV-18 and analyzed the degree of homology with other HPV types and bovine papillomavirus (BPV) types. In order to investigate whether HPV-7 might be a so far unidentified bovine virus, we screened 37 bovine tumor DNAs using Southern blot analysis for its presence, with exclusively negative results. From our data we conclude that the HPV-7 genome shows all characteristics of a papillomavirus genome and that its origin is most likely human.

Bovine papillomavirus 1↗
PubMed1986

The type of human papillomavirus present in cervical infections can be determined by the occurrence of specific marker proteins.

Four different proteins have been identified on high resolution two dimensional gels of [35S] methionine labelled human cervical biopsies whose expression correlates with the presence of papillomavirus. They are all basic proteins having molecular weights in the region of 48 to 50 kd and are normally expressed individually in different lesions unless the lesion results from a co-infection of two virus types. Comparison of the occurrence of these marker proteins with the actual HPV type present, determined by in situ filter hybridisation, has shown that two are found exclusively with HPV types 6/11 while the other two are found with types 16/18.

Antigens, Viral↗
PubMed1986

[Clinical significance of human papilloma virus (HPV) infections of the lower genital tract].

Using filter in situ hybridisation for HPV-DNA detection we found among 217 women with positive cervical cytology a positive result in 152 cases (70%). The distribution of the different HPV types showed an association of HPV 6/11 mainly with benign lesions and of HPV 16/18 with obligatory precancer and invasive cervical cancer. In 2652 swabs of cytologically negative patients HPV-DNA was identified in 9.5%. The infection rate for HPV 16/18 in pregnant women was 6.4% against 2.3% in nonpregnant women. In a number of the patients with positive cervical cytology we additionally examined smears from the vagina and vestibulum for HPV-DNA: in 42% of the cases a positive HPV result was obtained in these areas as well. In about 50% of 39 male partners peniscopy revealed penile lesions and HPV-DNA was found in penile smears. A prospective cytological and virological study of cytologically positive patients showed a clear association of HPV 16/18 with progression of cervical lesions. In a cytologically negative group, follow-up examinations revealed HPV-DNA in 31%.

Carcinoma in Situ↗
PubMed1986

[Urogenital and anal papillomavirus infections].

Recently virologists and clinicians have focused attention on infections with human papillomaviruses (HPV). This is due to the ubiquity, the increasing frequency and the possible association of these viruses with the development of squamous cell carcinomas of the skin and of the mucous membranes of the respiratory, gastrointestinal, genitourinary and anorectal tracts. HPV represent a very heterogeneous group of DNA tumor viruses. By means of molecular-biological techniques, more than 40 HPV types have been recognized. In the urogenital and anal tract, papillomaviruses have been associated with venereal warts (condylomata acuminata), which have been known and recognized as a sexually transmitted disease since the Romans. Furthermore, an association has been made recently between HPV and nonpapillomatous, sometimes macular lesions: flat condylomata of the uterine cervix and of the vagina, flat condylomatous lesions and pigmented papules. The latter are localized at the mucocutaneous borders and at the skin of the lower genital tract and of the perianal and crural region. Like epidermodysplasia verruciformis, only some virus types (HPV 16, HPV 18) are regularly found in malignant, invasive squamous cell carcinomas of the genital tract, whereas others (HPV 6, HPV 11, HPV 2, HPV 10, HPV 31) are associated preferentially with benign papillomas and dysplasias. In view of the different possible oncogenic potential of the individual genotypes, early determination of the virus type probably has not only diagnostic but also prognostic value. As HPV 16 DNA is regularly present in bowenoid papulosis (flat condylomatous lesions and pigmented papules of the male genital tract), a natural reservoir has been found from which these viruses could be transmitted to the sexual partner. Knowledge of the HPV-associated clinical pictures is therefore the prerequisite for diagnosis and treatment of both the patient and his sexual partner. Clinical observation, cytology and virus typing from genital smears of both partners represent preventive methods that may contribute to the early detection of genital cancer.

Anus Neoplasms↗
PubMed1985

[Sexual transmissibility of papillomaviruses].

Papillomavirus infections in the genitoanal region are detectable by the demonstration of type-specific HPVDNA (DNA-DNA hybridization, in situ hybridization on cell smears) or by a peroxidase-antiperoxidase assay using formalin-fixed paraffin sections for demonstration of common structural antigens of papillomaviruses. Using these methods an epidemiological study on sexual partners with genitoanal papillomavirus infections has been initiated.

Bowen's Disease↗