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1.
Mund Kiefer Gesichtschir ; 6(6): 410-4, 2002 Nov.
Article in German | MEDLINE | ID: mdl-12447653

ABSTRACT

OBJECTIVE: The aim of this study was to determine the prevalence of mutations of the tumour suppressor gene TP53 in oral leukoplakias. MATERIAL AND METHOD: Brush biopsy specimens of 43 oral leukoplakias, 26 oral squamous cell carcinomas (OSCC) for reference, and the oral mucosa of 4 clinically normal volunteers were collected. DNA of the critical exons 5-8 was analysed by temperature gradient gel electrophoresis (TGGE). RESULTS: The prevalence of mutations was 57.7% in OSCC, 39.5% in leukoplakias and 0% in controls. The highest frequency of mutations was found in exon 5 (46.2%) in OSCC and in exon 6 (23.3%) in leukoplakia. More than one mutation was detected in 26.9% of OSCC and 7% of leukoplakia specimens. At least one mutation was found in 37.5% of T1 OSCC and 100% of T4 OSCC specimens and in 37.1% of the L1 leukoplakia and 100% of L3 leukoplakia specimens. CONCLUSIONS: TP53 mutations could be a useful prognostic indicator in precancerous oral lesions. Although the brush biopsy technique appears simple clinically, further investigations are necessary to specify the implications of genetic analysis.


Subject(s)
Carcinoma, Squamous Cell/genetics , Chromosome Deletion , Genes, p53/genetics , Leukoplakia, Oral/genetics , Mouth Mucosa/pathology , Mouth Neoplasms/genetics , Precancerous Conditions/genetics , Biopsy , Carcinoma, Squamous Cell/pathology , DNA Mutational Analysis , Exons , Female , Humans , Leukoplakia, Oral/pathology , Male , Middle Aged , Mouth Neoplasms/pathology , Neoplasm Staging , Precancerous Conditions/pathology
2.
Prostate ; 45(3): 216-24, 2000 Nov 01.
Article in English | MEDLINE | ID: mdl-11074523

ABSTRACT

BACKGROUND: Previously it was demonstrated that in prostate tumors, angiogenesis measured as microvessel density (MVD) is associated with tumor stage as well as WHO grade and is an independent predictor of clinical outcome. Vascular endothelial growth factor (VEGF) is a major inducer of angiogenesis. There is some evidence that P53 mutations cause overexpression of VEGF. We studied VEGF expression, p53 overexpression, and P53 mutations in prostate cancer (PCA) to investigate the role of VEGF as an angiogenic marker and the possible deregulation of VEGF as a result of P53 mutations in PCA. METHODS: Immunohistochemical staining with a polyclonal VEGF antibody was performed in 55 paraffin-embedded PCA, in which MVD had previously been determined, as well as in 5 prostatic adenomas (PA) and 20 adjacent normal prostate tissues. In addition, 37 PCA and 5 PAs were examined for p53 expression by immunohistochemistry. Temperature gradient gel electrophoresis (TGGE) was performed in 13 of these PCA to screen for P53 mutations. VEGF expression, p53 expression, and mutations were then correlated with tumor stage, grade, MVD, and clinical outcome. RESULTS: While PA and normal prostate tissue generally showed no or only low VEGF expression, there was a significant increase in VEGF expression with tumor stage, grade, and MVD in PCA. During clinical follow-up (mean, 31.9 months), 9 of 55 patients had tumor progression. Significant differences in VEGF expression were found between patients with tumor progression and those without (P = 0.0004). Of the 37 PCA evaluated for p53 expression, 12 exhibited p53 overexpression. TGGE revealed P53 mutations in 3 of 13 PCA. However, there was no correlation between VEGF expression, p53 overexpression, and P53 mutation, respectively. CONCLUSIONS: VEGF seems to be an important, clinically relevant inducer of angiogenesis in PCA. VEGF expression was shown to correlate positively with tumor stage, grade, MVD, and clinical outcome. However, regulation of VEGF in PCA appears to be independent of p53 expression.


Subject(s)
Endothelial Growth Factors/pharmacology , Gene Expression Regulation, Neoplastic , Genes, p53/genetics , Lymphokines/pharmacology , Neovascularization, Pathologic , Prostatic Neoplasms/blood supply , Prostatic Neoplasms/genetics , Adult , Endothelial Growth Factors/biosynthesis , Humans , Lymphokines/biosynthesis , Male , Neoplasm Staging , Prognosis , Vascular Endothelial Growth Factor A , Vascular Endothelial Growth Factors
3.
Eur Urol ; 38(4): 426-33, 2000 Oct.
Article in English | MEDLINE | ID: mdl-11025381

ABSTRACT

OBJECTIVES: Longitudinal study of Tp53 mutation in urine sediments of 26 patients with mutated primary transitional cell carcinoma (TCC) of the urinary bladder at different time periods after transurethral resection of the bladder (TURB), i.e. before and after the first TURB, prior to the control resection and before treatment of a recurrence. METHODS: DNA of the critical Tp53 exons 5-8 was anaylzed by temperature gradients (TGGE) and sequence. RESULTS: (1) In 11 of 12 patients (91.7%) mutation reoccurred with the detection of recurrence of the disease. The mutation frequency in patients without any recurrence was 1 in 8 (12.5%) after a follow-up period of 4-16 months. (2) In 7 of 10 patients, the mutation was no longer detectable in the urine sediment after TURB. (3) The mutation frequency at the control resection 6 weeks after the first TURB was 5 in 7 (71.4%) in patients found to have residual and 1 in 7 (14.2%) in the tumor-free patients. (4) In 9 of 10 samples identical mutations were found by sequence in the recurrent tumor. These results show a significant correlation between the detection of a Tp53 mutation in the urine sediments and tumor recurrence or residual. CONCLUSIONS: (1) Tp53 mutations in the urine sediment could be a useful indicator of tumor recurrence or tumor residual in patients ( approximately 40%) with primary mutated bladder cancer tissue. (2) These results support the monoclonal seeding theory. (3) The finding of identical mutations at different times indicate that the tumor was never totally removed.


Subject(s)
Carcinoma, Transitional Cell/genetics , Carcinoma, Transitional Cell/urine , Genes, p53/genetics , Neoplasm Recurrence, Local/genetics , Neoplasm Recurrence, Local/urine , Tumor Suppressor Protein p53/genetics , Tumor Suppressor Protein p53/urine , Urinary Bladder Neoplasms/genetics , Urinary Bladder Neoplasms/urine , Adult , Aged , Aged, 80 and over , DNA Mutational Analysis , Female , Humans , Male , Middle Aged , Mutation
4.
Cancer Detect Prev ; 24(1): 24-32, 2000.
Article in English | MEDLINE | ID: mdl-10757120

ABSTRACT

The relationship between expression of p53 protein in bladder cancer and tumor progression is known. In this paper, we attempt to study this phenomenon by molecular-genetic techniques. One hundred thirty-seven bladder tumor tissues were obtained from transurethral resection (TURB). Urine sediments were collected from 72 patients suffering from transitional cell carcinoma and tumor recurrence. These patients were followed up for at least three months. Separate polymerase chain reactions (PCR) were carried out for exons 5, 6, 7, and 8 of the Tp53 gene. Temperature gradient gel electrophoresis (TGGE) was used to screen mutations in the PCR products. Sequencing from reamplified mutant and wildtype bands was excised from the TGGE. Tp53 mutation frequency is 43.1% in 137 bladder cancer specimens, but already 32.7% of Ta-tumors (16/49) were Tp53 mutated. Four of 25 patients with Tp53 wild-type tumors suffered from progression. In the group of patients with Tp53 mutated cancer, seven of 12 had a tumor progression. In 11 of 14 patients with Tp53 mutation in cancer tissue, the same mutation was also found in urine sediments. In such patients, successful tumor treatment by TURB results in loss of their Tp53 mutation in urine sediment, and tumor recurrency resulted in reappearance.


Subject(s)
Carcinoma, Transitional Cell/genetics , Genes, p53/genetics , Mutation , Urinary Bladder Neoplasms/genetics , Urine/cytology , Adult , Aged , Aged, 80 and over , Carcinoma, Transitional Cell/pathology , DNA Mutational Analysis , DNA, Neoplasm/analysis , Disease Progression , Electrophoresis/methods , Female , Humans , Male , Middle Aged , Neoplasm Recurrence, Local , Prognosis , Temperature , Urinary Bladder Neoplasms/pathology
5.
Eur Urol ; 34(5): 433-40, 1998.
Article in English | MEDLINE | ID: mdl-9803007

ABSTRACT

OBJECTIVES: To identify and analyse point mutations in p53 tumour suppressor gene (Tp53) in benign prostatic hyperplasia (BPH) by temperature gradient gel electrophoresis (TGGE) and sequence. MATERIALS AND METHODS: 141 tissue specimens (approx. 100 mg) after transurethral resection of the prostate (TURP), 12 specimens after needle biopsy. Control samples for genetic analysis were (a) 7 prostate tissues without any sign of BPH and malignancy and (b) 103 prostate cancer (PCa) tissues. DNA of the critical Tp53 exons 5-8 was amplified and run on horizontal polyacrylamide gels under defined temperature conditions (TGGE) to yield specific gel shifts and sets of homo- and heteroduplexes in case of mutation. Sequencing with a laser-fluorescent electrophoresis unit was done from re-amplified mutant and wild-type bands. RESULTS: TGGE screening of 153 BPH samples identified 29 specimens with Tp53 mutations (5 in exon 5, 11 in exon 6, 12 in exon 7, 3 in exon 8; 1 tissue sample showed mutations in 3 exons at a time). The computed mutation frequency was 19.0%. Two patients, with mutation in BPH tissue, developed PCa 2-3 years after TURP. One patient with mutation in BPH tissue developed bladder cancer. Of 118 patients with non-mutated DNA in BPH, none is known to have a urological cancer. The Tp53 mutation frequency in 103 PCa samples was 26.2%. Significant differences of mutation frequency between BPH and PCa were detected only in lower exon 5 mutation counts in BPH. CONCLUSION: Tp53 mutation in BPH tissue may be a tumour risk factor.


Subject(s)
Adenocarcinoma/genetics , Adenocarcinoma/pathology , Genes, p53 , Prostate/pathology , Prostatic Hyperplasia/genetics , Prostatic Hyperplasia/pathology , Prostatic Neoplasms/genetics , Prostatic Neoplasms/pathology , Adenocarcinoma/surgery , Aged , Aged, 80 and over , Biopsy, Needle , Culture Techniques , DNA, Neoplasm/analysis , Diagnosis, Differential , Frameshift Mutation , Gene Frequency , Humans , Immunohistochemistry , Male , Middle Aged , Point Mutation , Polymerase Chain Reaction , Prostatectomy , Prostatic Hyperplasia/surgery , Prostatic Neoplasms/surgery , Reference Values , Sensitivity and Specificity , Sequence Analysis, DNA
6.
Mund Kiefer Gesichtschir ; 2(1): 30-4, 1998 Jan.
Article in German | MEDLINE | ID: mdl-9522570

ABSTRACT

Mutations of the p53 gene are the most commonly observed genetic alterations in malignant tumors and are often associated with a loss of the tumor suppressor function of the p53 protein. We have analyzed specimens of head and neck squamous cell carcinomas (HNSCC) from 110 patients for p53 gene mutations and 92 of them additionally for human papillomavirus (HPV) infection in order to evaluate the prognostic significance of these factors by comparison with clinical follow-up data. Using the method of polymerase chain reaction (PCR)/temperature gradient gel electrophoresis (TGGE), mutations within the exons 5 to 8 of the p53 gene were found in 48 tumors (44%). Sequencing revealed missense mutations in most cases (15/20). Frequency of p53 gene mutations was not related to the tumor stage, the grade of differentiation, the presence of lymph node metastases, or the smoking history of the patients. With the help of a highly sensitive PCR/hybridization assay, an infection with the high-risk HPV types 16 and 18 could be detected in 39/92 tumor specimens (42%). Follow-up data were obtained from 99 patients with a range of 2-112 months. No correlation of overall survival on the presence of p53 gene mutations or HPV infection could be observed. The absence of statistically significant correlations between p53 gene mutations and progressive disease, however, does not exclude its putative relevance in early phases of tumor development.


Subject(s)
Carcinoma, Squamous Cell/genetics , Head and Neck Neoplasms/genetics , Mutation/genetics , Papillomaviridae/genetics , Papillomavirus Infections/genetics , Tumor Suppressor Protein p53/genetics , Tumor Virus Infections/genetics , Adult , Aged , Carcinoma, Squamous Cell/pathology , Cell Transformation, Neoplastic/genetics , Cell Transformation, Neoplastic/pathology , Female , Follow-Up Studies , Head and Neck Neoplasms/pathology , Humans , Lymph Nodes/pathology , Lymphatic Metastasis , Male , Middle Aged , Neoplasm Staging , Papillomavirus Infections/pathology , Polymerase Chain Reaction , Prognosis , Tumor Virus Infections/pathology
7.
J Oral Pathol Med ; 26(7): 315-21, 1997 Aug.
Article in English | MEDLINE | ID: mdl-9250931

ABSTRACT

We analyzed specimens of head and neck squamous cell carcinomas (HNSCC) from 110 patients for p53 gene mutations, and 92 of them for human papillomavirus (HPV) infection, in order to evaluate the prognostic significance of these factors by comparison with clinical follow-up data. Mutations within the exons 5 to 8 of the p53 gene were found in 48 tumors (44%). Sequencing revealed in most cases mis-sense mutations (16/21). Frequency of p53 gene mutations was not related to the tumor stage or the presence of lymph node metastases. Of the 46 tumors that were analyzed by immunohistochemistry, 26 stained positively (56%). The number of positively stained nuclei increased slightly with decreasing differentiation of the tumors, whereas no correlation was found between tumor stage and immunoreactivity. An infection with the high-risk HPV types 16 and 18 could be detected in 39/92 tumor specimens (42%). Follow-up data were obtained from 99 patients within a range of 2 to 112 months. No dependence of overall survival on the presence of p53 gene mutations or HPV infection could be observed. The absence of statistically significant correlations between p53 gene mutation and progressive disease, however, does not deny its putative relevance in early phases of tumor development.


Subject(s)
Carcinoma, Squamous Cell/genetics , Genes, p53/genetics , Head and Neck Neoplasms/genetics , Papillomaviridae , Papillomavirus Infections/diagnosis , Tumor Virus Infections/diagnosis , Adult , Age Factors , Aged , Aged, 80 and over , Carcinoma, Squamous Cell/mortality , Electrophoresis , Female , Follow-Up Studies , Head and Neck Neoplasms/mortality , Humans , Immunohistochemistry , Male , Middle Aged , Papillomaviridae/isolation & purification , Prognosis , Sequence Analysis , Survival Rate , Tumor Suppressor Protein p53/metabolism
8.
J Urol ; 157(3): 1049-53, 1997 Mar.
Article in English | MEDLINE | ID: mdl-9072541

ABSTRACT

PURPOSE: To test the value of a recently developed screening method for the detection of p53 mutations in prostate and bladder cancers. MATERIALS AND METHODS: Tumor tissue from 24 prostate cancers and 27 bladder cancers were evaluated. DNA of the critical p53 exons 5-8 were amplified and run on horizontal polyacrylamide gels under defined temperature conditions (TGGE) to yield specific gel shifts and sets of homo- and heteroduplexes in case of mutation. Sequencing with a laser-fluorescent electrophoresis unit was done directly from polymerase chain reaction (PCR) products and/or from reamplified mutant and wild type bands excised from the gels. RESULTS: The p53 genotype predicted from the TGGE analysis was always confirmed on the excised DNA fragments, in contrast to only 50% of cases tested by direct sequencing from mixed wild type and mutant DNA present in PCR products. With this screening protocol, 6 of 24 prostate cancers (25.0%) and 11 of 27 bladder cancers (40.7%) showed p53 mutations. At stage T1, none of prostate cancers and 41.2% of bladder cancers contained mutant p53. At higher stages (> or = T2), 30.0% of prostate cancer and 50.0% of bladder cancers were mutated. Histological tumor grading was > G1 in all but two prostate/bladder cancers with mutant p53. It appears that p53 mutations can occur early in bladder carcinogenesis. CONCLUSION: TGGE fulfills the clinical need of a rapid and specific screening method, and, at the molecular level, has the advantage of sorting out the wild type and mutant alleles for consecutive sequencing.


Subject(s)
Electrophoresis/methods , Genes, p53/genetics , Prostatic Neoplasms/genetics , Urinary Bladder Neoplasms/genetics , Adolescent , Aged , Aged, 80 and over , DNA Mutational Analysis , Exons/genetics , Humans , Male , Middle Aged , Mutation , Neoplasm Staging , Prostatic Neoplasms/pathology , Temperature , Urinary Bladder Neoplasms/pathology
9.
Int J Cancer ; 70(1): 52-6, 1997 Jan 06.
Article in English | MEDLINE | ID: mdl-8985090

ABSTRACT

The diagnostic specificity of the detection of disseminated prostatic cells by reverse-transcriptase polymerase chain reaction (RT-PCR) of PSA mRNA was investigated. A sensitive nested PCR was developed. In blood samples from 10 healthy female and 10 healthy male persons examined by RT-PCR, mRNA of PSA was detected 3 times in each group. In the groups of patients suffering from benign prostate hyperplasia and prostate cancer, 6 of 11 and 5 of 12, respectively, gave positive RT-PCR results. With increasing analytical sensitivity of the RT-PCR of PSA mRNA, the diagnostic specificity of the assay is decreased. Further development of this diagnostic method requires the introduction of the quantitative PCR which may make possible discrimination between prostatic and non-prostatic source of PSA mRNA by quantification.


Subject(s)
Neoplasm Proteins/blood , Polymerase Chain Reaction/standards , Prostate-Specific Antigen/blood , Prostatic Neoplasms/pathology , RNA, Messenger/analysis , Female , Humans , Male , Prostatic Neoplasms/blood , Sensitivity and Specificity , Transcription, Genetic
11.
Int J Cancer ; 63(5): 639-45, 1995 Nov 27.
Article in English | MEDLINE | ID: mdl-7591279

ABSTRACT

We studied 51 cervical carcinomas, among them 25 squamous-cell carcinomas (SCC) and 26 cervical adenocarcinomas (AdCa), and 40 vulvar SCC for the presence of HPV and mutant p53. HPV was detected by PCR, and p53 alterations by temperature-gradient gel electrophoresis/direct sequencing and immunohistochemistry. HPV, mostly type 16/18, was found in 80.4% of the cervical tumors (92.0% of the SCC and 69.2% of the AdCa), but in only 27.5% of vulvar carcinomas. In contrast, p53 mutations were found in 7.8% and 52.5% of cervical and vulvar tumors respectively. Mutant p53 occurred in pre-invasive vulvar lesions, indicating that this oncogenic factor is involved early in carcinogenesis. Further analysis of recurrent/metastatic lesions of 9 cervical and 14 vulvar tumors also showed remarkable differences: in cervical cancer, HPV was persistent, and p53 mutations absent, whereas in vulvar tumors, HPV was mostly absent or not persistent, and the p53 mutation rate was very high (78.6%). These observations suggest that HPV persistence is an important event for the evolution and maintenance of cervical cancer, whereas for vulvar cancers p53 mutation and not HPV activity is a central oncogenic event.


Subject(s)
Adenocarcinoma/genetics , Carcinoma, Squamous Cell/genetics , Genes, p53 , Mutation , Papillomaviridae , Papillomavirus Infections/genetics , Tumor Virus Infections/genetics , Uterine Cervical Neoplasms/genetics , Vulvar Neoplasms/genetics , Adenocarcinoma/virology , Adult , Aged , Aged, 80 and over , Base Sequence , Carcinoma, Squamous Cell/virology , Female , Humans , Middle Aged , Molecular Sequence Data , Prognosis , Tumor Suppressor Protein p53/analysis , Uterine Cervical Neoplasms/virology , Vulvar Neoplasms/virology
13.
Verh Dtsch Ges Pathol ; 77: 117-8, 1993.
Article in German | MEDLINE | ID: mdl-7511267

ABSTRACT

DNA and paraffin material of more than 100 tumors of prostate, bladder and female genital organs were analyzed for p53 aberrations and compared with normal tissues by immunohistochemistry, PCR of p53 exons 5-8 and TGGE. While normal tissues, precancerous and borderline lesions, and well differentiated carcinomas usually showed wild type p53 and negative immunostaining, high grade and/or high stage carcinomas often revealed mutant p53 (rate of mutation in exon 8 >> 7 >> 6 >> 5) and/or p53 accumulation. Accumulation of p53 protein in the absence of detectable mutant p53 was recognized more often in prostate cancer than in any other tumor examined. Although p53 aberration probably represents a late molecular event in cancerogenesis, its detection may be of clinical interest as genetic footprint in recurrent and metastatic disease.


Subject(s)
Genes, p53 , Genital Neoplasms, Female/genetics , Mutation , Prostatic Neoplasms/genetics , Testicular Neoplasms/genetics , Tumor Suppressor Protein p53/biosynthesis , Urinary Bladder Neoplasms/genetics , DNA, Neoplasm/analysis , Female , Gene Expression , Genital Neoplasms, Female/pathology , Humans , Male , Ovarian Neoplasms/genetics , Ovarian Neoplasms/pathology , Prostatic Neoplasms/pathology , Testicular Neoplasms/pathology , Tumor Suppressor Protein p53/analysis , Urinary Bladder Neoplasms/pathology , Uterine Neoplasms/genetics , Uterine Neoplasms/pathology
14.
Zentralbl Bakteriol Mikrobiol Hyg A ; 268(3): 347-56, 1988 May.
Article in English | MEDLINE | ID: mdl-3043982

ABSTRACT

The specific germinating capacity of spores of Clostridium oncolyticum in tumours in vivo, and various reports on concomitant partial oncolysis (tumour lysis) have prompted us to propose a concept of equipping C. oncolyticum with genes of other organisms producing cancerostatics. As an example we used Colicin E3, whose structural genes lies in the E. coli plasmid pCo1E3-CA38. After in vitro recombination of restrictase EcoRI-fragmented pCo1E3-CA38 DNA with an uncharacterized plasmid fraction from C. concolyticum a plasmid-free strain of C. oncolyticum was infected with recombinant DNA. A special microbiological selection system allows the identification of C. oncolyticum clones with Colicin E3-similar formation of cleared haloes.


Subject(s)
Clostridium/genetics , Colicins/genetics , DNA, Recombinant , Plasmids , Transfection , Cloning, Molecular , Clostridium/physiology , DNA, Bacterial/genetics , DNA, Bacterial/ultrastructure , Electrophoresis, Agar Gel , Escherichia coli/genetics , Genetic Variation , Genetic Vectors , Microscopy, Electron , Spores, Bacterial
15.
Arch Geschwulstforsch ; 52(1): 41-8, 1982.
Article in English | MEDLINE | ID: mdl-7082130

ABSTRACT

Lysis of the UVT 15264 tumour in mice of the 17/Berlin-Buch strain as induced by intravenous injection of Clostridium butyricum H8 spores is followed by the tumour diameter and survival time. In animals thus treated, tumour regression is incomplete and the mean survival time drops below that of tumour-bearing animals not treated with spores. With concurrent antibiotic treatment survival time is prolonged to exceed that of untreated animals, without affecting ocolysis-provoked tumour regression. When spore is combined with cyclophosphamide, tumour regression is considerably improved, but the survival resembles that of untreated tumour-bearing animals; with both cyclophosphamide and antibiotic treatment survival resembles that of spore-treated animals.


Subject(s)
Antibiotics, Antineoplastic/therapeutic use , Clostridium/metabolism , Cyclophosphamide/therapeutic use , Neoplasms, Experimental/drug therapy , Animals , Mice , Neoplasms, Experimental/mortality , Spores, Bacterial/metabolism
16.
Arch Geschwulstforsch ; 52(8): 613-20, 1982.
Article in German | MEDLINE | ID: mdl-7168625

ABSTRACT

An aggregation technique is used for construction of multicellular spheroids from trypsinized cell cultures of several normal and cancerous cell lines. This technique is applicable also in the presence of 1 X 10(9)/ml spores of Clostridium oncolyticum, and spores and vegetative bacterial cells can be counted by a soft agar colonization technique after trypsinization of spheroids. 24 hours after aerobic cultivation of spore-containing spheroids, germination and multiplication of Clostridium is detected by microscopy, electron-microscopy, and by bacterial cultivation technique. In this response there was no considerable difference between spheroids from tumour or from fresh cell lines. By electron microscopy many spores and vegetatively multiplying Clostridia became visible in the central necrotic part of spheroids. In the peripheral aerobic rim of spheroids, however, also few vegetative Clostridia were detectable.


Subject(s)
Clostridium/growth & development , Neoplasms/physiopathology , Cell Aggregation , Cell Line , Clostridium/ultrastructure , Humans , Microscopy, Electron , Models, Biological , Neoplasms/ultrastructure , Trypsin/pharmacology
17.
Arch Geschwulstforsch ; 51(1): 51-7, 1981.
Article in English | MEDLINE | ID: mdl-7196212

ABSTRACT

During incubation of monolayer cell cultures with clostridia spores in the presence of 1.5 per cent of oxygen vegetative bacterial rods become visible and cell necrosis occurs preferentially in tumour cell lines. After such cocultivation tumour cells show a higher amount of clostridia not elutable by washing than finite cells. Electron microscopy of associated clostridia shows vegetative rods in contact to and inside of tumour cells.


Subject(s)
Clostridium/growth & development , Neoplasms, Experimental/microbiology , Anaerobiosis , Animals , Carcinoma, Ehrlich Tumor/microbiology , Cell Line , Female , Fibrosarcoma/microbiology , Humans , Microscopy, Electron , Ovarian Neoplasms/microbiology , Spores, Bacterial
18.
Article in English | MEDLINE | ID: mdl-7032143

ABSTRACT

Clostridium butyricum was recultivated from tumour material after treatment of tumour-bearing mice with spores and counted by soft agar colony technique. The oncolytic strain Cl. butyricum H8 grows inside the tumour UVT 15264 up to 8 X 10(8)/g during 48 h. In this time part of tumour became lysed. Multiplication inside of this tumour by the tumour specific but nononcolytic strain Cl. butyricum CNRZ 528 could not be detected by application counting technique. Combination of spore treatment with antibiotic chemotherapy in dosage able to prevent oncolysis or in dosage to reduce them corresponds with loss of clostridial multiplication or with reduced vegetative multiplication respectively.


Subject(s)
Bacteriological Techniques , Clostridium/growth & development , Sarcoma, Experimental/microbiology , Skin Neoplasms/microbiology , Animals , Clostridium/drug effects , Drug Combinations/pharmacology , Mice , Neoplasms , Penicillin G/pharmacology , Penicillin G Benzathine/pharmacology , Penicillin G Procaine/pharmacology , Species Specificity , Spores, Bacterial/drug effects , Spores, Bacterial/growth & development
19.
Arch Geschwulstforsch ; 50(1): 53-7, 1980.
Article in German | MEDLINE | ID: mdl-7447631

ABSTRACT

Subcultures of Clostridium oncolyticum M55 and in a slightly modified manner of an oncolytic strain of Cl. butyricum H8 are differentiated by lysotypic reaction of the bacteriophage 5 from several tumour-selective non-oncolytic strains and subcultures of Cl. butyricum.


Subject(s)
Bacteriophages , Clostridium , Neoplasms/microbiology , Species Specificity
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