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Biomedical subjects

E Wilander

Publications and source records attributed to E Wilander.

222 records · Page 13Linked to original sources

Silver stains in the study of endocrine cells of the gut and pancreas.

The usefulness of argentaffin (Masson) and argyrophil (Davenport, Sevier-Munger and Grimelius) staining methods for identification of endocrine cell types in the gastrointestinal tract and pancreas is discussed and comments are made on the techniques themselves. The applicability of silver impregnation methods in the histopathological investigations of endocrine tumours in the above-mentioned organs is outlined, and the chemical background of the silver reactions is briefly reviewed.

Adenoma, Islet Cell↗

Ki-67 immunostaining and DNA flow cytometry as prognostic factors in epithelial ovarian cancers.

Samples from malignant epithelial ovarian tumors were examined for expression of Ki-67, DNA ploidy and S-phase fraction (SPF). In addition, normal ovary, benign and borderline tumors were immunostained with Ki-67 to examine its role in ovarian carcinogenesis and to estimate the prognostic significance. For both Ki-67, ploidy and SFP a significant correlation to survival in malignancy was observed. Furthermore, SPF above 10% showed significant correlation to decreased survival in both stage subgroups I-II and III-IV, while for aneuploidy a decrease in survival could be detected only in localized disease. Ki-67 expression was present in tumor cells in the main part of borderline and malignant tumors and even in 2 benign counterparts, which might indicate an active state in these commonly believed dormant neoplasms. In the malignant group the Ki-67 correlation to survival seemed to be independent of staining intensity, although the observed decay in survival seemed to be faster in the strongly stained group.

Antibodies, Monoclonal↗

A novel deletion in the RET proto-oncogene found in sporadic medullary thyroid carcinoma.

Germ line point mutations in the RET proto-oncogene have been implicated in four inherited disorders: multiple endocrine neoplasia 2A (MEN 2A) and 2B (MEN 2B); familial medullary thyroid carcinoma (FMTC); and Hirschprung's disease, a congenital lack of enteric plexus neurons. Oncogenically activated RET has also been demonstrated in some sporadic medullary thyroid tumors, which show somatic missense mutations in the same regions as those found in MEN 2B. Upon screening archival sporadic MTC tumor tissue by nonradioactive single-strand conformational polymorphism analysis (SSCP), a markedly divergent exon 11 pattern was found in an unusually aggressive neoplasm. Sequencing of PCR amplified DNA revealed the deletion of nine bases encompassing a key cysteine codon at position 1831-3, often altered in MEN 2A. Normal thyroid tissue from the same patient showed a normal SSCP pattern and sequence for this exon. This novel somatic mutation further implicates the RET proto-oncogene in the development of MTC.

Amino Acid Sequence↗

Biological characteristics of adrenocortical carcinoma: a study of p53, IGF, EGF-r, Ki-67 and PCNA in 17 adrenocortical carcinomas.

Adrenocortical carcinoma (ACC) is a rare neoplasm with a poor prognosis. Prognostic factors are needed to identify patients who should be treated aggressively and those for which a less aggressive approach is warranted. As a result of advances within the field of immunohistochemistry, investigations of Ki-67, PCNA, IGF, EGF-r and p53 were performed in 17 ACC. The aim of this study was to clarify the role of Ki-67, PCNA, EGF-r, IGF and p53 in correlation to tumour behaviour and outcome. This retrospective study includes 16 patients, 10 women and 6 men, with a median age of 46 years. Nine tumours were hormonally functioning and 7 were non-functioning. The results obtained revealed that all tumours expressed PCNA and Ki-67 with median values of 59% and 14%, respectively, while p53 was negative in 88%, IGF negative in 82% and EGF-r positive in 94% of the tumours. No correlation was found between p53, IGF, EGF-r and survival rate. There was no interdependence between PCNA and Ki-67, or between PCNA, Ki-67 and the survival rate.

Adrenal Cortex Neoplasms↗

Deletion of chromosome 3p is an early event in malignant progression of cervical cancer.

BACKGROUND: Loss of chromosome 3p has been reported to be a common genetic alteration in certain types of tumors as well as in cervical cancer. To understand its role in multistep cervical carcinogenesis, we analysed the allelic loss of this chromosome region in early pre-invasive cervical neoplastic lesions. MATERIALS AND METHODS: 49 cases comprising two types of pre-invasive lesions (without and with coexisting invasive cancer) were selected. Chromosome 3p deletios in selected neoplastic lesions were detected by PCR-RFLP combined with morphologically guided microdissection technique for DNA preparation. RESULTS: DNA samples from 40 cases out of 49 were successfully amplified and found to be heterozygotes at least in one chosen chromosome marker. Of 19 cases without coexisting cancer, LOH was detected in 4 cases(21%) and 3/17(18%) precancerous lesions (1 moderate dysplasia, 2 severe dysplasias) and 1/5(20%) carcinomas-in-situ. A significantly higher rate of allelic loss was observed in pre-invasive lesions adjacent to invasive cancer, showing 29%(4/14) in precancerous lesion and 67%(2/3) in carcinoma-in-situ. Analysing the invasive cancer and synchronous pre-invasive neoplasia, LOH was found to occur at early precursor stage in the majority of cases(5/7). The most frequently lost locus in cervical cancer is the chromosome regions detected by marker D3S30(60%) and D3F15S2(47%), suggesting a candidate tumor suppressor gene, which may play a role in cervical carcinogenesis, is harboured on this chromosome region. CONCLUSIONS: Our results confirm the high frequency of chromosome 3p allelic loss in cervical cancer and suggest that this genetic alteration is an early event in the development of cervical cancer and may potentially serve as a marker of risk for progression of premalignant lesions to invasive cancer.

Chromosomes, Human, Pair 3↗