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Biomedical subjects

H Moch

Publications and source records attributed to H Moch.

119 records · Page 7Linked to original sources
PubMed1993

Diagnostic tools for differentiating between pleural mesothelioma and lung adenocarcinoma in paraffin embedded tissue. Part I: Immunohistochemical findings.

Specimens of 27 histologically definite mesotheliomas and 34 proven adenocarcinomas were examined with a panel of 14 antibodies: pan-epithelial antibody Lu-5, anti-keratin-18, anti-keratin-7, Ber-EP4, anti-Leu-M1, HEA-125, anti-carcino-embryonic antigen (CEA), anti-blood group-related antigens (anti-BGR A, B, H), B72.3, anti-placental alkaline phosphatase (PLAP), anti-vimentin and BMA-120 used to determine their value in the differentiation between pleural mesothelioma and lung adenocarcinoma. Lu-5, anti-cytokeratin-7 and -18, B 72.3 and PLAP reacted in a high percentage of cases with both mesothelioma and adenocarcinoma. Anti-CEA and anti-Leu-M1 did not react with any of the 27 mesotheliomas tested but showed a reaction in 75% (anti-CEA) and 66% (anti-Leu-M1) of the lung adenocarcinomas. Seventeen percent of the adenocarcinomas and 96% of the mesotheliomas showed a positive reaction with anti-vimentin. Ber-EP4 was demonstrated in all lung adenocarcinomas, but only in 2 mesotheliomas in a focal manner (7%). HEA-125 and anti-BGR A, B, H reacted with 83% (HEA-125) and 75% (anti-BGR A, B, H) of the lung adenocarcinomas. The statistical parameters, sensitivity and efficiency were estimated and a normogram for judging the diagnostic power of a single antibody for the differential diagnosis of mesothelioma versus adenocarcinoma was developed. According to this, Ber-EP4, HEA-125, anti-BGR A, B, H and anti-CEA were, in descending order, the most powerful discriminatory antibodies.

Adenocarcinoma↗
PubMed1993

Diagnostic tools for differentiating pleural mesothelioma from lung adenocarcinoma in paraffin embedded tissue. II. Design of an expert system and its application to the diagnosis of mesothelioma.

A panel of 14 antibodies (panepithelial antibody Lu-5, anti-keratin-18, anti-keratin-7, Ber-EP4, anti-Leu-M1, HEA-125, anti-carcinoembryonic antigen, anti-blood group-related antigens A, B, H, B72.3, anti-placental alkaline phosphatase, anti-vimentin and BMA-120), which have been evaluated for use in differentiating mesothelioma from lung adenocarcinoma, was applied to a group of 24 suspected mesotheliomas. Using the established qualitative, descriptive criteria derived from monovariate statistical analysis of the tumour control groups (definite mesotheliomas, adenocarcinomas), a definitive allocation was possible in only 25% of suspected cases. We therefore constructed two "expert systems", based on multivariate discriminant analysis with either the ALLOC 80 program for ordinal data or a newly developed analysis program for binomial data. With these two systems diagnostic allocation of suspected mesotheliomas was improved to 75% and 79%. The use of binomial data ("positive" versus "negative") in conjunction with the probability-based test system is of particular interest because the primary data are easy to record and the test results have a higher statistical probability.

Adenocarcinoma↗
PubMed1993

p53 and erbB-2 protein overexpression are associated with early invasion and metastasis in bladder cancer.

Overexpression of p53 and erbB-2 was studied by immunohistochemistry in formalin-fixed tissue samples of 179 patients with transitional cell carcinoma of the urinary bladder. p53 immunostaining was strongly correlated with tumour stage (P < 0.0001). This was driven by a marked difference in p53 expression between pTa (37% positive) and pT1 (71%) tumours, while there was no difference between pT1 and pT2-4 tumours. Similarly, a strong overall association between p53 expression and grade (P < 0.0001) was driven by a marked difference between grade 1 (28%) and grade 2 tumours (71%), and there was no significant difference between grade 2 and grade 3 tumours. Surprisingly, the frequency of erbB-2 overexpression was higher in pT1 tumours (74%) than in either pTa (49%; P = 0.0265) or pT2-T4 (56%; P = 0.0645) tumours. Both p53 and erbB-2 expression was also associated with metastasis. Metastases were found in 77% of patients with p53 positive primary tumours, but in only 50% of the patients with p53 negative primary tumours (P = 0.022). Metastases were found in 66% of patients with erbB-2 positive primaries, but in only 37% of the erbB-2 negative primaries (P = 0.020). Of 32 patients with positivity for both p53 and erbB-2, 84% developed metastases, as compared to 49% of patients with positivity for either one or neither positive (P = 0.002). We conclude that both p53 and erbB-2 overexpression are associated with early invasion in bladder cancer. Furthermore, p53 and erbB-2 may be important predictors for metastasis.

Biomarkers, Tumor↗
PubMed1993

Comparative analysis of the expression of tenascin and established prognostic factors in human breast cancer.

Tenascin is an extracellular matrix glycoprotein expressed during morphogenesis in embryonal life. It reappears in the stroma of benign and malignant tumors. The distribution of tenascin in variants of fibrocystic disease and infiltrating breast carcinoma was assessed in cryostat sections by immunofluorescence using a polyclonal antibody. The tenascin immunoreactivity was compared with various prognostic factors. In fibrocystic disease (n = 10), tenascin appeared as periductal and periacinar bands. In infiltrating carcinomas (n = 32) the tenascin expression was markedly increased. Tenascin immunoreactivity was noted around the ducts (78%), extended into the distal stroma (56%), or was distributed in smaller (reticular) septa around and within tumor-cell nests (34%). Nineteen percent of infiltrating carcinomas did not express tenascin. None of the patterns correlated with prognostic factors such as nodal metastasis, tumor necrosis, invasion of blood vessels, or with flow cytometry results, such as ploidy and S-phase fraction. However, a significantly higher reticular and periepithelial tenascin expression was noted in cases with increased stromal inflammatory reaction. These findings indicate that the appearance of tenascin is neither an indicator of malignancy nor predictive of invasiveness or metastasis but that it is related to local inflammatory response.

Breast Neoplasms↗
PubMed1993

[Ki-67 fraction, p53 alteration and numerical chromosome aberrations (chromosomes 7 and 17) in formalin fixed bladder tumors].

p53 gene function and tumor cell proliferation are thought to be important parameters for tumor progression in bladder cancer. In this study immunohistochemistry and fluorescence in situ hybridization were used to determine the relationship between p53 alterations, tumor proliferation (Ki-67 Labeling Index), and numerical chromosomal aberrations in formalin fixed bladder tumors. p53 expression was associated with Ki-67 LI (p = 0.0014), polysomy 17 (p = 0.001) and polysomy 7 (p = 0.0241). This is further evidence for a significant role of the p53 gene in proliferation control and preservation of genomic stability.

Carcinoma, Transitional Cell↗
PubMed1993

[Demonstration of gene amplification in urinary bladder cancer by fluorescent in situ hybridization (FISH)].

Fluorescence in situ hybridization (FISH) allows visualization of chromosomes and genes in interphase nuclei. Dual labeling FISH with probes for a gene of interest and the corresponding centromere can be used to determine chromosomal deletion and gene amplification. In case of a deletion less gene signals than centromere signals are found. In case of amplification gene signal number is distinctly increased as compared to centromere signals. To study gene amplification in fresh and formalin fixed bladder cancer we used gene specific probes for erbB-2, EGF-r, and 11q13 (bcl-1, PRAD1) together with their corresponding centromere probes p17H8, p7alphaTET and plC11A. Amplification was seen in 10/140 tumors for erbB-2, in 5/107 tumors for EGF-r, and in 15/137 tumors for 11q13. Different patterns of amplification suggested that FISH allows distinction of intrachromosomal (amplified genes in clusters) and extrachromosomal amplification (diffuse distribution of signals).

Carcinoma, Transitional Cell↗
PubMed1992

Strong trans activation of the human cytomegalovirus major immediate-early enhancer by p40tax of human T-cell leukemia virus type I via two repetitive tax-responsive sequence elements.

The immediate-early 1 and 2 gene locus of human cytomegalovirus (HCMV) that encodes trans-activator proteins with effects on both homologous and heterologous promoters is expressed under control of a complex enhancer/promoter regulatory region. This enhancer contains four types of repetitive sequence elements with 17, 18, 19, and 21 bp that bind cellular transcription factors. Although the HCMV enhancer acts as a powerful stimulator of transcription in most cell types examined, human T cells do not support strong activity. The present study demonstrates that the tax gene product of human T-cell leukemia virus type I trans activates the major enhancer of HCMV more than 60-fold in the T-cell line Jurkat. When a series of chloramphenicol acetyltransferase expression plasmids containing synthetic oligonucleotides with the 17-, 18-, 19-, or 21-bp motif upstream of a minimal immediate-early 1 and 2 gene promoter was tested, two of the four repeat motifs could be identified as Tax-responsive elements. Both the 18- and the 19-bp motifs were able to act as strong Tax-responsive elements even when they were present as single copies. Thus, in addition to interacting with human immunodeficiency virus, HCMV is able to interact with a second retrovirus of clinical importance.

Avian Sarcoma Viruses↗
PubMed1991

[Sellar germinoma with lung metastases].

Reported in this paper is the case of a boy aged 15 years with sellar germinoma which led to one singular pulmonary metastasis, three years after subtotal surgical removal and subsequent successful irradiation of the tumor rest. The primary tumor together with the lung metastasis were characterised as germinoma with trophoblastic giant cells as additional elements. Interpretation of the pulmonary tumour was somewhat difficult, since diagnosis of the primary tumor had encouraged assumption of a chromophobic hypophyseal adenoma with polymorphic manifestation, with no relationship between the intracranial and pulmonary tumors being presumed by the surgeon. The true nature of the metastasis and, consequently, the histogenetic identity of both tumors was cleared up by immunohistochemical detection of beta-HCG in almost all syncytiotrophoblasts. Comprehensive analysis of the literature on metastasising intracranial germinomas may be helpful in disclosing possible relationships between the histological type of a primary tumor or neurosurgical action and the metastatic potential of tumors.

Adolescent↗
PubMedDate not supplied

Fluorescence in situ hybridization for detecting erbB-2 amplification in breast tumor fine needle aspiration biopsies.

OBJECTIVE: To evaluate the feasibility of erbB-2 amplification analysis of fine needle aspiration (FNA) biopsies. STUDY DESIGN: FNA smears and dissociated nuclei from 58 breast cancer samples were examined by dual-labeling fluorescence in situ hybridization (FISH) with probes for centromere 17 and the erbB-2 gene. The results were compared with the outcome of erbB-2 immunohistochemistry. RESULTS: Tumors were categorized according to the erbB-2/centromere 17 signal ratio. There were 23 tumors with high-level amplification, four cases with a low-level erbB-2 gain and 27 tumors with normal erbB-2 content. Four tumors showed an erbB-2 deletion, all in patients < or = 42 years of age. ErbB-2 amplification was strongly associated with positive erbB-2 immunostaining (P < .0001). Comparison of FISH analysis on dissociated cells and on FNA biopsies showed high correspondence (P < .0001). CONCLUSION: FISH allows reliable detection of erbB-2 gene amplification on FNA biopsies.

Adult↗
PubMedDate not supplied

Association of p27Kip1, cyclin E and c-myc expression with progression and prognosis in HPV-positive cervical neoplasms.

Recent studies demonstrated that a variety of human cancer cell lines express relatively high levels of p27Kip1 and that this might be associated with increased expression of Cyclin E. There is a feedback inhibitory loop between Cyclin E and p27Kip1, which can be counteracted by elevated c-myc activation. This study analyzed by immunohistochemistry the expression of p27Kip1, Cyclin E and c-myc in a series of HPV-positive cervical tissue samples representing various stages of cervical carcinogenesis, using 13 samples of normal epithelium, 24 low-grade CIN, 63 high-grade CIN, and 69 samples of invasive squamous cell carcinoma. To evaluate the cell proliferation, the Ki-67 Labelling Index (LI) was assessed. The presence of HPV was investigated by in situ DNA hybridization. We did not find any correlation between p27Kip1 expression and Ki-67 LI in normal and tumor tissue samples. There was evidence for an increase of p27Kip1 levels from low-grade to high-grade CIN. Cyclin E, c-myc and the Ki-67 LI were significantly increased during cervical carcinogenesis. Cyclin E and c-myc were positively correlated to cell proliferation in pre-cancerous lesions, but not related to overall survival in invasive carcinomas. Contrary to that, high levels of p27Kip1 are associated with poor overall survival in invasive cervical carcinomas of clinical stage IB. This may reflect the counteracting function of c-myc in blocking p27Kip1, thus representing the worst condition of a disturbed tumor cell cycle in cervical carcinoma, ultimately induced by HPV.

Cell Cycle Proteins↗