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N Wernert

Publications and source records attributed to N Wernert.

83 records · Page 5Linked to original sources
PubMed1986

[Malignancy grade and clinical stage T0-T3 in prostate cancer].

The frequency of malignancy grade I-III (grading system according to Böcking and Sommerkamp, 1980) and of clinical stages T0-T3 in 393 unselected prostatic carcinomas (227 punch biopsies and 166 transurethral resections) were investigated over a period of 2 years. G III carcinomas were represented most frequently in the whole material (54%) as well as in punch biopsies (62%). G I carcinomas with a favorable prognosis make up 20% of the tumors in the whole material and only 10% in punch biopsies. In contrast, 54.9% of incidental carcinomas (T0) are G I tumors, 18.6% G III carcinomas with an unfavorable prognosis. The advanced clinical stages T2 and T3 predominate in the whole material with 62.4%, compared to stages T0 and T1 comprising 37.6%. Malignancy grade and clinical stage are clearly correlated in the whole material. In incidental carcinoma, there is also a correlation between malignancy grade and histologic extension. The percentage of higher malignancy grades G II and G III increases with age. This is true for incidental carcinoma as well. The findings emphasize the prognostic significance of the grading system.

Adenocarcinoma↗
PubMed1985

Urothelial carcinoma of the prostate.

Urothelial carcinoma is a rare type of prostatic carcinoma which as a rule bears an unfavourable prognosis. In our material it comprises 4.5% of all prostatic carcinomas. It can occur isolated in the prostate as well as in connection with a urothelial carcinoma of the urinary bladder, which may have directly infiltrated the prostate. Almost one-third of our cases are combined with an ordinary carcinoma of the prostate. The majority of pure urothelial carcinomas, with or without bladder involvement, are found in stages 0-B (59 of 68 cases). When combined with an ordinary prostatic carcinoma, most urothelial carcinomas (20 of 29 cases) are present in stages C and D. Independent of bladder involvement, 24 urothelial carcinomas are grade II and 86 grade III tumours. Survival times range from 12 to 84 months (average 34.8 months) in grade II and from 1 to 103 months (average 29.5 months) in grade III carcinomas. Problems in differential diagnosis arise when urothelial carcinoma has to be distinguished from solid or, rarely, cribriform prostatic carcinoma. Diagnostic criteria for urothelial carcinoma are compact formations without stroma being sharply delineated from stroma, extensive ductal growth pattern with necroses of comedo type, high mitotic rates and perifocal inflammation.

Adenocarcinoma↗
PubMed1982

Sex dimorphism of the adrenal cortex in rats after treatment with dexamethasone.

Sex dimorphism of adrenal cortex of the rat was studied by light and electron microscopy as well as the karyometric, gravimetric, and histometric methods after treatment with dexamethasone (2.0 mg/kg over a period of 4 days). Sex dimorphism cannot be shown in dexamethasone-induced atrophy of adrenal glands. Male fasciculata cells have more and finer distributed liposomes resembling in this way female fasciculata cells. Normally present differences in adrenal weight and nuclear size of fasciculata cells between both sexes disappear; nevertheless, female fasciculata cells remain relatively bigger compared to the corresponding male cells. Annulment of sex dimorphism is thought to be the result of altered functional activity of the zona fasciculata due to failing pituitary stimulation. Higher secretion activity of female fasciculata cells probably ceases after dexamethasone treatment.

Adrenal Cortex↗
PubMedDate not supplied

Human and mouse RAD17 genes: identification, localization, genomic structure and histological expression pattern in normal testis and seminoma.

Recently, the human orthologue to the cell cycle checkpoint genes rad17 (Schizosaccharomyces pombe) and RAD24 (Saccharomyces cerevisiae), called HRAD17, has been isolated and localized to chromosome 4. Independently, we have isolated the HRAD17 transcript and mapped it to chromosome 5q13 between the CCNB1 and BTF2p44cen genes. Furthermore, we have identified the complete exon-intron structure of HRAD17. The gene is organized into 14 exons, the translation initiation site lies within exon 2, and the stop codon within exon 14. Two further HRAD17 pseudogenes, HRAD17P1 and HRAD17P2, were identified on chromosomes 7p21 and 13q14.3, respectively, encompassing exons 3-14 and bearing 84% and 93% homology, respectively. Additionally, we have isolated the coding region of the mouse orthologue, Mrad17, and mapped it on chromosome 13 between Ccnb1 and Btf2p44, the same two genes between which it maps in human. The predicted Mrad17 polypeptide encompasses 687 amino acids and shows 89% similarity to HRAD17. Both genes are most highly expressed in testis compared to all other tissues, as shown by Northern blot hybridization. Histological studies, based on in situ hybridization with radioactively labeled antisense HRAD17 riboprobes, showed a strong expression within the germinal epithelium of the seminiferous tubuli in normal testis whereas in testicular tumors (seminomas) only weak, diffuse signals were seen. In light of the known function of the yeast orthologue at meiotic and mitotic checkpoints, as well as the strong expression in testis and weak expression in seminomas, we suggest a putative involvement of HRAD 17 in testicular tumorigenesis.

Animals↗
PubMedDate not supplied

Neoplastic AIDS-associated Kaposi's sarcoma cell line KSY-1 cannot transdifferentiate into capillaries.

OBJECTIVE: Kaposi's sarcoma (KS) is an acquired immunodeficiency syndrome (AIDS)-defining neoplasm histologically characterized by proliferation of spindle cells, inflammatory cells, and abundant neovascularization. When the malignant cell line KSY-1 derived from an AIDS-KS tumor is transplanted subcutaneously into nude mice, prominent neovascular features develop. Using this mouse model of neoplastic KS, we set out to determine, using c-ets 1 markers specific for mouse or human tissues, whether vascular growth and inflammatory infiltrate induced by the transplanted KSY-1 cells is of host cell or transplant origin. STUDY DESIGN/METHODS: KS tumors were induced by subcutaneous inoculation of 5 x 10(6) KSY-1 cells/200 microL in immunodeficient mice, and species-specific mouse and human riboprobes of the c-ets 1 protooncogene were used for in situ hybridization to define cell of origin. RESULTS: Five different tumors were examined. Tissue sections from all cases were hybridized with radiolabeled riboprobes for the presence of both mouse and human c-ets 1 mRNA. Tumor cells were labeled with the human c-ets 1 probe, whereas neovascular and inflammatory tissues were of mouse origin. CONCLUSIONS: The finding that vascular but not tumor cells are of host origin supports the model of tumor-induced vascularization via a mechanism of tumor cell-derived cytokine-medicated pathogenesis.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Presence of genetic alterations in microdissected stroma of human colon and breast cancers.

BACKGROUND: Human carcinomas not only consist of neoplastic epithelial cells but also of tumor stroma, which may play an important role in tumor-progression. Whereas the tumor surrounding stroma is generally believed to represent a reactive component induced by tumor cell derived factors, a contribution of neoplastic cells to stroma formation via epithelium-mesenchyme transition during tumor invasion has become a novel concept in recent years. MATERIALS, METHODS AND RESULTS: We here show, by laser-assisted microdissection, that frequent genetic alterations in non-hereditary invasive human colon and breast cancers (loss of heterozygosity and TP53 mutations) occur not only in the neoplastic epithelial cells, but also in the adjacent fibroblastic stroma and that both components can share clonal features. CONCLUSION: Tumor cell-mesenchyme transitions are among the possible explanations for these findings and could actually occur during tumor invasion in vivo.

Breast Neoplasms↗
PubMedDate not supplied

Implication of the proliferation and apoptosis associated CSE1L/CAS gene for breast cancer development.

The CSEIL/CAS protein (CAS) is a Ran-binding protein with a function as a nuclear transport (export) factor. CSEIL/CAS, similar to Ran and other ran-binding proteins, plays at the same time an important role in the mitotic spindle checkpoint, which assures genomic stability during cell division. This checkpoint is frequently disturbed in neoplasms of various origin, including breast, hepatic and colonic tumors. CAS is located on chromosome 20ql3 and amplified in several cell lines, including breast, colon and bladder cancer. MEKl phosphorylation is known to be a reason for different CAS localization and activity. We evaluated the expression of CAS in 50 benign and malignant tumors of the breast by immunohistochemistry. Benign lesions of the breast (n=13) revealed a weak, predominantly cytoplasmatic CAS positivity. In ductal and lobular in situ carcinomas (n=17), 70-90% of the tumor cells were positive for anti-CAS staining which was predominantly cytoplasmatic. In invasive ductal and lobular carcinomas (n =20), 70-90% of the tumor cells stained positive with anti-CAS in a predominantly nuclear pattern. Different localization of CAS might affect its role not only for chromosome segregation, proliferation and apoptosis, but also its function in nuclear transport of proteins like retinoblastoma-gene-product, p53 and BRCAl. A different regulation in this checkpoint might contribute to the invasive potential in malignant carcinomas of the breast. Alteration of CAS-activity, possibly via MEKl-inhibition, might therefore be a possible option for breast cancer therapy.

Antibodies, Monoclonal↗
PubMedDate not supplied

Expression of the transcription factor c-Ets1 correlates with the occurrence of invasive processes during normal and pathological development.

The protein encoded by the c-ets1 proto-oncogene is a member of a new family of transcription factors. Cellular regulatory sequences responsive to the c-Ets1 proteins include a urokinase-type plasminogen activator (uPA) gene enhancer, the stromelysin 1 and the collagenase 1 gene promoters. During normal as well as pathological development, the expression of c-ets1 is associated with the occurrence of invasive processes, either in invading cells or in the invaded tissue. Since these invasive processes are thought to require the remodeling of the extracellular matrix, we investigate the relationships between c-Ets1 and the expression patterns of transcripts encoding the matrix-degrading proteases uPA, stromelysin 1 and collagenase 1, in embryos and in solid tumors.

Animals↗
PubMedDate not supplied

[Does the c-ets 1 oncogene participate in the regulation of tumor angiogenesis?].

Does the c-ets 1 protooncogene take part in the regulation of tumor angiogenesis? The formation of new blood vessels is an essential process in embryonic development and wound healing, for tumor growth and metastasis. In situ hybridization studies have revealed that the protooncogene c-ets 1 is expressed in endothelial cells at the beginning of blood vessel formation, in normal and pathological conditions. C-ets 1 encodes a transcription factor, a protein which binds specifically to DNA and which regulates the transcription of genes containing these specific binding sequences in their promotors. Thus in vitro experiments suggest that c-ets 1 may activate the transcription of genes encoding collagenase 1, stromelysine 1 and urokinase plasminogen activator, proteases involved in extracellular matrix degradation. A working hypothesis is that c-ets 1 takes part in regulating angiogenesis by controlling the transcription of these genes whose activity is necessary for the migration of endothelial cells from preexisting capillaries. This hypothesis is discussed with respect to current experimental evidences and to the complexity of the regulatory network controlling gene transcription and extracellular matrix degradation.

Cell Movement↗
PubMedDate not supplied

Pathological aspects of prostate cancer and benign nodular hyperplasia.

The aim of the study was to investigate tumor suppressor genes (TSGs) which play a role in the pathogenesis of prostate cancer. Additionally, different prostate tumors were immunohistochemically related to their potential precursor cells, the basal cells and the glandular secretory epithelium, which differ in their hormone responsiveness. By PCR-amplification of microsatellite-DNA we found allelic losses of chromosomal loci near known or putative TSGs to increase with the malignancy grade of prostate carcinoma. When investigated for numerous markers common and endometrioid carcinoma were immunohistochemically related to the secretory epithelium while the rare basal cell tumor, containing the estrogen receptor, squamous cell carcinoma and urothelial carcinoma showed features of the basal cells. In histopathological differential diagnosis high molecular weight basal cell keratins, prostatic acid phosphatase and prostate specific antigen may be of value. Stromal type nodular hyperplasia and the fetal prostate mesenchyme had common immunohistochemical features which might reflect analogous development.

Diagnosis, Differential↗