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  • 1
    ISSN: 1432-2307
    Keywords: Endometriosis ; Adenomyosis ; Endometrial function ; Correlation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Hormontherapie der Adenomyose und Endometriose läßt die Beurteilungsmöglichkeit des Heilungserfolges bzw. der Heilungschancen aus dem Funktionszustand des Corpusendometrium wünschenswert erscheinen. Bei systematischer korrelierender Untersuchung von Endometrium, Adenomyose und/oder Endometriose unter dem Einfluß endogener und exogener hormoneller Stimulation ergaben sich je nach Lokalisation des ektopischen Endometrium und nach Art des hormonellen Stimulus in Zeitpunkt und Ausmaß unterschiedliche Abweichungen vom Funktionszustand des Corpusendometrium. Diese lassen sich jedoch mit genügender Sicherheit jeweils voraussagen. Die hormonelle Stimulierung der Adenomyose war der des Corpusendometrium am ähnlichsten, die Endometriose des Ovars zeigte oft, insbesondere unter Gestagenreizen, eine überschießende Stimulation, während die übrigen extrauterinen Endometriosherde nur sehr schwach auf hormonelle Reize reagierten. Aus den Ergebnissen lassen sich für die Therapie wichtige prognostische Konsequenzen ableiten.
    Notes: Summary This study was undertaken to determine whether the hormonal sensitivity of the endometrium might be a measure of the effectiveness of hormonal therapy for adenomyosis and endometriosis. Accordingly, the effects of endogenous and exogenous hormones on the endometrium, adenomyosis, and endometriosis were correlated. The results revealed that, depending on where the ectopic endometrial tissue was located and on the type (duration and intensity) of hormonal treatment, the functional response of the endometriosis varied from that of the endometrium. The variations, however, can be predicted. The response of adenomyosis to hormonal stimulation was most like that of the endometrium. Endometriosis of the ovary often revealed an excessive response to stimulation, especially after gestagens. The other types of extrauterine foci of endometriosis, however, reacted only weakly to hormonal therapy. Important prognostic consequence for therapy can be drawn from the results.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0711
    Keywords: Key words Tamoxifen ; Endometrium ; Breast cancer ; Endometrial carcinoma ; Sonography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We restudied histologically and immunohistochemically 17 endometrial carcinomas, 2 malignant mixed tumors and 180 endometria with benign changes during or after tamoxifen therapy. The carcinomas were subtyped according to the 1994 WHO-classification. Endometrial biopsies were taken only if the endometrial thickness was 〉 8 mm sonographically, when a polyp was seen, or for postmenopausal bleeding. About half of the endometrial specimens showed simple or cystic atrophy, 55–76% had cystic-atrophic polyps or regressive hyperplasia. Depending upon the dose of tamoxifen, 7–19% (30 mg) to 27– 36% (20 mg) showed moderate glandular proliferation. 20–33% had foci of mucinous, clear cell or serous-papillary metaplasia. 68–70% revealed diffuse extensive fibrosis of the endometrial stroma. None of 11 patients biopsied before starting tamoxifen therapy had advanced endometrial glandular proliferation in the second endometrial biopsy after tamoxifen treatment. None of the 19 endometrial neoplasms after tamoxifen therapy was of the endometrioid type: 11 were mucinous adenocarcinomas, 4 clear cell carcinomas, 2 serous-papillary carcinomas, one carcinosarcoma and one malignant Müllerian mixed tumor. The reasons for discrepancies between suspicious sonograms and endometrial atrophy are discussed.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Tumor suppressor gene ; Chromosome 18q ; Breast cancer ; Colorectal cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inactivation of tumor suppressor genes is thought to be a critical step in tumorigenesis. TheDCC (deleted in colorectal carcinoma) gene, located on the long arm of chromosome 18, has been shown to be frequently deleted in colorectal tumors. To investigate the involvement of allelic deletions on chromosome 18q in breast cancer tumorigenesis we analyzed 28 primary breast tumors and 28 colorectal, tumors (24 carcinomas, 4 adenomas) with four different polymorphic DNA markers detecting RFLPs on chromosome 18q. In breast cancer we found loss of heterozygosity (LOH) in 4 of 27 (15%) informative cases whereas 15 of 25 (60%) colorectal tumors showed allelic deletions. In all cases of allelic loss theDCC locus or its proximal vicinity (locus SSAV1) were involved. LOH on chromosome 18q occurs both in breast and colorectal cancer, yet the frequency of these deletions in breast tumors is lower than in colorectal tumors. Moreover, in breast cancer these mutations were only detected in large and undifferentiated tumors.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Keywords: Key words Tumor suppressor gene ; Chromosome 18q ; Breast cancer ; Colorectal cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Inactivation of tumor suppressor genes is thought to be a critical step in tumorigenesis. The DCC (deleted in colorectal carcinoma) gene, located on the long arm of chromosome 18, has been shown to be frequently deleted in colorectal tumors. To investigate the involvement of allelic deletions on chromosome 18q in breast cancer tumorigenesis we analyzed 28 primary breast tumors and 28 colorectal tumors (24 carcinomas, 4 adenomas) with four different polymorphic DNA markers detecting RFLPs on chromosome 18q. In breast cancer we found loss of heterozygosity (LOH) in 4 of 27 (15%) informative cases whereas 15 of 25 (60%) colorectal tumors showed allelic deletions. In all cases of allelic loss the DCC locus or its proximal vicinity (locus SSAV1) were involved. LOH on chromosome 18q occurs both in breast and colorectal cancer, yet the frequency of these deletions in breast tumors is lower than in colorectal tumors. Moreover, in breast cancer these mutations were only detected in large and undifferentiated tumors.
    Type of Medium: Electronic Resource
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