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Biomedical subjects

M Eck

Publications and source records attributed to M Eck.

At least 19 recordsLinked to original sources
PubMed2006

Increased tartrate-resistant acid phosphatase (TRAP) expression in malignant breast, ovarian and melanoma tissue: an investigational study.

BACKGROUND: Tartrate-resistant acid phosphatase (TRAP) is a metalloprotein enzyme that belongs to the acid phosphatases and is known to be expressed by osteoclasts. It has already been investigated as a marker of bone metastases in cancer patients. In this study, which examined the value of serum TRAP concentrations as a marker of bone disease in breast cancer patients, we observed high concentrations of TRAP even in patients without bone metastases. To elucidate this phenomenon, we examined the expression of TRAP in breast cancer cells and the cells of several other malignancies. METHODS: TRAP concentrations in the serum of tumor patients were determined by ELISA. The expression of TRAP in breast, ovarian, and cervical cancer and malignant melanoma was analyzed by immunohistochemistry. RT-PCR and immunocytology were used to evaluate TRAP expression in cultured tumor cells. RESULTS: A marked increase in serum TRAP concentrations was observed in patients with breast and ovarian cancer, regardless of the presence or absence of bone disease. TRAP expression was found in breast and ovarian cancers and malignant melanoma, while cervical cancer showed only minimal expression of TRAP. Expression of TRAP was absent in benign tissue or was much less marked than in the corresponding malignant tissue. TRAP expression was also demonstrated in cultured primary cancer cells and in commercially available cell lines. CONCLUSION: Overexpression of TRAP was detected in the cells of various different tumors. TRAP might be useful as a marker of progression of malignant disease. It could also be a potential target for future cancer therapies.

Acid Phosphatase↗
PubMed2005

The chemokine receptor CCR7 is expressed on epithelium of non-inflamed gastric mucosa, Helicobacter pylori gastritis, gastric carcinoma and its precursor lesions and up-regulated by H. pylori.

CCR7 chemokine-receptor expression on tumour cells of gastric carcinoma has been associated with lymph-node metastasis and is thought to play an important role in metastasis. However, so far it is unknown whether CCR7 is newly up-regulated on gastric carcinoma or already expressed in non-neoplastic gastric epithelium. Therefore, epithelial CCR7 expression was investigated in the process of gastric carcinogenesis: non-inflamed mucosa --Helicobacter pylori gastritis -- intestinal metaplasia/dysplasia -- gastric carcinoma. CCR7 was expressed by gastric epithelium in non-inflamed gastric mucosa (n = 5), H. pylori gastritis (n = 17), intestinal metaplasia (n = 10), dysplasia (n = 3) and on tumour cells in 20 of 24 patients with gastric carcinoma (13/14 intestinal-type; 7/10 diffuse-type) as tested by immunohistochemistry. As CCR7 expression by gastric epithelium was significantly stronger in H. pylori gastritis than in non-infected mucosa, the influence of H. pylori on CCR7 receptor expression of gastric epithelial cells was investigated by fluorescence activated cell sorter analysis. H. pylori strains up-regulated the CCR7 chemokine-receptor in CCR7-positive cell lines. No difference in CCR7 up-regulation between cag(+) and cag(-)H. pylori strains was found. Epithelial CCR7 up-regulation by H. pylori may alter the metastatic fate of gastric carcinoma. Additionally, CCR7 expression not only on gastric carcinoma, but also on non-neoplastic gastric epithelium, suggests a novel biological function.

Carcinoma↗
PubMed2005

A case of metastasizing invasive hydatidiform mole. Is less--less good? Review of the literature with regard to adequate treatment.

BACKGROUND: Patients with invasive hydatidiform moles (IHM) have a good prognosis. Even if disease has spread, monocytostatic treatment might be sufficient if the diagnosis has been histologically confirmed. Established classifications divide gestational trophoblastic disease (GTD) including choriocarcinoma into cases with "high" and "low" risk. Without respect to histology "high-risk" cases are recommended to obtain polychemotherapy. CASE: A 40-year-old nullipara underwent hysterectomy for persistent vaginal bleeding after she had already been treated with curettage for hydatidiform mole. An IHM was pathohistologically confirmed. There were no signs of pulmonary spread or other metastases at the time of surgery. Postsurgically persistent beta-hCG levels lead to thorough staging, which revealed multiple pulmonary metastases and a vaginal metastasis. Despite metastasizing GTD with poor prognosis criteria she was treated with single agent therapy. Eight cycles of two weekly methotrexate (MTX) were administered. All sites of metastases responded and our patient is still fine after one year of follow-up. CONCLUSION: With respect to this and other reports monochemotherapy can be a reasonable primary treatment for metastatic IHM.

Adult↗
PubMed2004

Finite element and experimental analyses of polymer-based dental bridges reinforced by ceramic bars.

Dental bridges made of polymer materials reveal only low loading capacity. This paper analyzes possible improvements of the loading capacity of polymer-based dental bridges reinforced by incorporated ceramic bars. Finite element (FE) analyses were performed to study the stress distribution caused by the mastication process in the bridge material. In the experimental part of the study, the fracture load of dental bridges with and without ceramic bar reinforcement was evaluated. Critical stresses occur in the connector area between abutment and pontic of bridges without bar reinforcement. A suitably shaped ceramic bar incorporated into the polymer-based bridge can significantly reduce these critical stresses. The fracture load of the bridge was increased from 515 to 1603N by the bar reinforcement. We conclude from our study that a ceramic bar can significantly improve the loading capacity of a polymer-based dental bridge. The FE and the experimental analyses revealed that the detailed design of the ceramic bar is of decisive importance for the effectiveness of the suggested ceramic reinforcement.

Bite Force↗
PubMed2004

Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection.

Toll-like receptors (TLRs) expressed by mucosal epithelium play an essential role in the defense against microbes by recognizing conserved bacterial molecules. For the first time TLR4, TLR5 and TLR9 have been microanatomically localized in patients with noninflamed gastric mucosa and Helicobacter pylori gastritis by immunohistochemistry. Because polarized expression of TLRs in apical and basolateral epithelial compartments is thought to modulate mucosal immunity, subcellular TLR distribution by gastric epithelium was investigated using confocal microscopy. TLR4, TLR5 and TLR9 were expressed by gastric epithelium in antrum and corpus of all patients with H. pylori gastritis (n = 14) and with noninflamed gastric mucosa (n = 5). TLR4 was expressed at the apical and the basolateral pole of the gastric epithelium as well in noninflamed gastric mucosa as in H. pylori gastritis. TLR5 and TLR9 expression in the noninflamed gastric mucosa was identical to that of TLR4 with localization at the apical and the basolateral epithelial pole. However, in H. pylori gastritis TLR5 and TLR9 expression on the gastric epithelium changed to an exclusive basolateral localization without detectable expression at the apical pole. In the human stomach, the gastric epithelium expressed TLR4, TLR5 and TLR9, which gives it the possibility to interact with H. pylori. Furthermore, gastric epithelial TLR4 expression is highly polarized in an apical and a basolateral compartment, whereas TLR5 and TLR9 polarization seems to be a process dynamically influenced by H. pylori infection. This polarized and dynamically regulated gastric epithelial expression of TLRs supports a sentinel role for these receptors in the mucosal immunity to H. pylori.

DNA-Binding Proteins↗
PubMed2003

[Immunochemical demonstration of human herpes virus 8 in conjunctival Kaposi's sarcoma].

BACKGROUND: Angiomatous lesions of the conjunctiva and chronic conjunctivitis are frequently difficult to differentiate. CASE: A 28 year old white male sought help because of a conjunctival swelling. A biopsy made elsewhere had revealed a capillary haemangioma of the conjunctiva. Recently striking alterations of the skin led to the suspicion of a Kaposi's sarcoma. Immunohistochemical and dermatological examinations confirmed the diagnosis of a Kaposi's sarcoma and viral testing of serum revealed an HIV-infection. Besides intensive antiviral therapy, our patient underwent local irradiation of the right eye, the nose and of the left shoulder with an external beam. CONCLUSIONS: Kaposi's sarcoma is the most frequent Aids-associated malignant tumor. In about 30% of all patients with Aids, a Kaposi's sarcoma is diagnosed. The angiomatous character may lead to the histopathological diagnosis of a haemangioma. Human herpes virus 8 is known to be the transforming element.

AIDS-Related Complex↗
PubMed2003

Pleiotropic effects of CXC chemokines in gastric carcinoma: differences in CXCL8 and CXCL1 expression between diffuse and intestinal types of gastric carcinoma.

CXC chemokines modulate host immunity, neovascularization, growth and invasive behaviour of tumours. Despite their relevance in tumour biology, chemokine expression in intestinal- and diffuse-type gastric carcinoma, which exhibit a completely different growth pattern, has not been investigated in detail. In this study, expression of the CXC chemokines CXCL8 [interleukin (IL)-8], CXCL1 [growth-related oncogene alpha (Gro alpha)], CXCL9 [monokine induced by interferon (IFN)-gamma] and CXCL10 [IFN-gamma-inducible protein-10 (IP-10)] and the corresponding chemokine receptors CXCR1-3 was investigated by immunohistochemistry in intestinal- and diffuse-type gastric carcinoma. Tumour cells of all patients expressed CXCL8. CXCL8 expression was significantly stronger in tumour cells of diffuse- rather than intestinal-type gastric carcinoma (P < 0.01) as determined by a semiquantitative score. CXCL1 was expressed almost exclusively by diffuse- but not intestinal-type carcinoma cells. The corresponding chemokine receptors, CXCR1 and CXCR2, were found on carcinoma cells. Furthermore, CXCL8 expression correlated with number of tumour vessels (P < 0.01), suggesting an angiogenetic function in gastric carcinoma not only in vitro but also in vivo. CXCL10 and CXCL9, attractants for T cells, were expressed by peritumorous macrophages in close proximity to IFN-gamma-producing CXCR3-positive T cells in both tumour types. These chemokines may attract gastric carcinoma-infiltrating T cells via an IFN-gamma-mediated pathway and enhance host immunity against the tumour. In gastric carcinoma a complex interplay between CXC-chemokine signals derived from both tumour cells and tumour-infiltrating immune cells may exhibit pleiotropic effects in tumour biology that go far beyond their originally described functions as leucocyte chemoattractants. Because CXCL8 and CXCL1, which are known to increase growth and invasive behaviour of malignant tumours, are significantly stronger expressed in diffuse- than intestinal-type gastric carcinoma, one may speculate that these chemokines influence the different growth pattern of gastric carcinoma types.

Antigens, CD↗
PubMed2001

Mapping of epitopes in discoidin domain receptor 1 critical for collagen binding.

The binding and activation of the discoidin domain receptor 1 by collagen has led to the conclusion that proteins from the extracellular matrix can directly induce receptor tyrosine kinase-mediated signaling cascades. A region in the extracellular domain of DDR1 homologous to the Dictyostelium discoideum protein discoidin-I is also present in the secreted human protein RS1. Mutations in RS1 cause retinoschisis, a genetic disorder characterized by ablation of the retina. By introducing point mutations into the discoidin domain of DDR1 at positions homologous to the retinoschisis mutations, ligand binding epitopes in the discoidin domain of DDR1 were mapped. Surprisingly, some residues only affected receptor phosphorylation, whereas others influenced both collagen-binding and receptor activation. Furthermore, two truncated DDR1 variants, lacking either the discoidin domain or the stalk region between the discoidin and transmembrane domain, were generated. We showed that (i) the discoidin domain was necessary and sufficient for collagen binding, (ii) only the region between discoidin and transmembrane domain was glycosylated, and (iii) the entire extracellular domain was essential for transmembrane signaling. Using these results, we were able to predict key sites in the collagen-binding epitope of DDR1 and to suggest a potential mechanism of signaling.

Amino Acid Sequence↗
PubMed2001

A novel proliferation-associated variant of CFR-1 defined by a human monoclonal antibody.

The germline coded human monoclonal IgM antibody 103/51 was isolated from a gastric carcinoma patient. This antibody binds to a 130-kd membrane molecule and has a mitotic effect on tumor cells in vitro. To characterize the target, we sequenced the protein and showed that the antibody binds to the cysteine-rich fibroblast growth factor receptor (CFR)-1, which is highly homologous to MG-160 and the E-selectin-ligand (ESL)-1. The epitope was determined by glycosidase-digestion experiments to be an N-linked carbohydrate side chain. Immunohistochemistry was used to investigate the tissue distribution of CFR-1. Different healthy tissues were tested and only the collecting tubes of the kidney, the Golgi apparatus, and the glomerular and fascicular zones of the adrenal gland stained positive. However, on malignant tissue the receptor is overexpressed in nearly all tested stomach cancers (12 of 15) and other tested carcinomas (13 of 15). Most interestingly, the receptor is also present in Helicobacter pylori gastritis and gastric dysplasia, but absent on uninflamed stomach mucosa. This restricted tissue pattern indicates that antibody 103/51 reacts with a membrane-bound variant of CFR-1, which is mainly expressed on transformed cells and precursor lesions and is essential for proliferation processes. The possible activity of antibody 103/51 as an activating ligand in these proliferative changes of gastric epithelial mucosa is discussed.

Adenocarcinoma↗
PubMed2001

[Tumor cell embolism to pulmonary arteries].

A 69-year-old male presented with symptoms of fulminant lung embolism and, despite immediate therapy with plasminogen activator, died of acute right heart failure. At autopsy multiple tumor cell emboli were detected in small pulmonary vessels in addition to widespread liver metastases from an urothelial carcinoma. - In a 23-year-old female a malignant gastric ulcer and multiple liver metastases were diagnosed at initial presentation. She too died from pulmonary hypertension due to a series of lung embolisms which occurred despite heparin therapy. At autopsy, many small pulmonary arteries were filled with adenocarcinoma cells; the primary gastric tumor and liver metastases were confirmed. These cases demonstrate that the shedding of tumor cells from hepatic metastases can obstruct the pulmonary vessels and lead to acute cor pulmonale. Tumor cell emboli should be considered in the differential diagnosis of acute pulmonary hypertension, especially in patients with a known tumor. They may, however, also represent the first clinical signs of previously unrecognized malignancy.

Adenocarcinoma↗
PubMed2000

Identification of immunogenic antigens of Helicobacter pylori via the Escherichia coli hemolysin secretion system(1).

We describe a new procedure allowing the generation and detection of immunogenic antigens from Helicobacter pylori via the hemolysin secretion apparatus of Escherichia coli. The gene (or gene fragment) encoding the H. pylori protein (or protein domain) is inserted in-frame into a residual portion of the hemolysin gene (hlyA), encoding the HlyA secretion signal (HlyA(s)). These fusion proteins are secreted efficiently by E. coli. This new approach allows the identification of immunodominant antigens by using sera derived from H. pylori-infected patients suffering from different gastroduodenal pathologies. Three immunodominant antigens bearing the ureB (urease B-subunit), flaA (flagellin A-subunit), and an unknown ORF (HP0888) encoding an E. coli FecE analogous protein fused to hlyA(s) were identified and characterized.

Antigens, Bacterial↗
PubMed2000

Helicobacter pylori induces DNA damage in vitro.

A close association between Helicobacter pylori infection and the development of gastric adenocarcinoma in humans has been demonstrated. Therefore, the direct induction of DNA damage by H. pylori was investigated here using the in vitro micronucleus assay. After 5 days of incubation with bacterial lysate a dose-dependent formation of micronuclei was found, which was not limited to cytotoxic protein concentrations and was not observed after treatment with Escherichia coli lysate (control). This induction of DNA damage may be a link between chronic H. pylori infection and development of adenocarcinoma of the stomach.

Animals↗
PubMed2000

Helicobacter pylori in gastric mucosa-associated lymphoid tissue type lymphoma.

Infection with Helicobacter pylori triggers the acquisition of gastric mucosa-associated lymphoid tissue (MALT) and provides the background for MALT-type lymphoma development. This concept has been supported by a high association of H. pylori infection and MALT-type lymphoma and by the regression of most lymphomas after eradication therapy. In almost all patients with MALT-type lymphoma, serum antibodies to H. pylori were detectable. However, H. pylori was found only in 78% of the patients on histological examination. In addition to other effects, changes in the gastric micro-milieu caused by tumor infiltration of the gastric mucosa may be responsible for the loss of the bacterium. The discrepancy of high seroprevalence and lower histological yield has been already described in other gastric diseases, e.g. atrophic gastritis or gastric carcinoma with extensive destruction of the gastric mucosa. H. pylori strains expressing the CagA protein have been associated with duodenal ulceration and gastric carcinoma. A very high percentage of patients with MALT-type lymphoma is also infected by CagA+ strains of H. pylori as tested by immunoblotting. Antibodies directed to CagA were detectable in the serum as well as in micro-cultured gastric mucosa. Infection with H. pylori may be a precondition for the development of gastric MALT-type lymphoma. In particular, CagA+ strains of H. pylori may, together with additional up to now unknown factors, play a role in the development of gastric MALT-type lymphoma.

Gastric Mucosa↗
PubMed2000

Mucosal humoral immune response to CagA shows a high prevalence in patients with gastric MALT-type lymphoma.

In the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT)-type lymphoma, CagA-positive Helicobacter pylori strains have been suspected of making a significant contribution. To investigate this hypothesis in more detail, the mucosal humoral immune response of 15 patients with gastric MALT-type lymphoma was examined in the tumor and in the tumor-free gastritis of the same patient. Mononuclear cells from different sites (antrum, corpus, lymphoma) were cultured. Culture supernatant and serum of the same patient were used for immunodetection of CagA. All patients displayed an immune response to CagA in the tissue-culture supernatants. Although the humoral immune response in the tumor was restricted to a very few H. pylori antigens, antibodies directed against CagA protein were found in most patients. The immune response to CagA in nearly all lymphoma patients--not only in the serum, but also in the mucosa, including the tumor site--support the hypothesis that CagA is involved in the pathogenesis of gastric MALT-type lymphoma.

Antibody Formation↗
PubMed2000

CXC chemokines Gro(alpha)/IL-8 and IP-10/MIG in Helicobacter pylori gastritis.

Infection with Helicobacter pylori causes chronic active gastritis, which is characterized by neutrophils infiltrating the gastric epithelial layer and the underlying lamina propria as well as by T, B lymphocytes and macrophages accumulating in the lamina propria. In this study, the chemokine profile responsible for the recruitment of these inflammatory cells is investigated. Using both RNA/RNA in situ hybridization and immunohistochemistry, the expression of the neutrophil and/or lymphocyte-attractant CXC chemokines growth-related oncogene alpha (Gro(alpha)), IL-8, interferon-gamma (IFN-gamma)-inducible protein-10 (IP-10), monokine induced by IFN-gamma (MIG) and the CC chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), -1beta, regulated on activation normal T cell expressed and secreted (RANTES) and monocyte chemoattractant protein-1 (MCP-1) is studied and microanatomically localized in the gastric mucosa. Macrophages in the lamina propria at sites with neutrophil infiltration and gastric epithelium infiltrated by neutrophils highly expressed the neutrophil-attractant chemokines Gro(alpha) and IL-8. Additionally, Gro(alpha) and IL-8 were expressed by neutrophils themselves localized within gastric epithelium, in the foveolar lumen and in the cellular debris overlying mucosal erosion. IP-10 and to a lower extent MIG, both selectively chemotactic for inflammatory T cells, were expressed by endothelial cells of gastric mucosal vessels and by mononuclear cells at sites with T cell infiltration. Expression of all other CC chemokines tested was significantly lower. These in vivo data indicate that a set of predominantly CXC chemokines modulates the inflammation in H. pylori gastritis. Gro(alpha) and IL-8 may play an important role in neutrophil trafficking from the mucosal vessel into the gastric epithelium, whereas IP-10 and MIG contribute to the recruitment of inflammatory T cells into the mucosa.

Chemokine CCL2↗
PubMed2000

Erdheim-Chester disease: evidence for a disease entity different from Langerhans cell histiocytosis? Three cases with detailed radiological and immunohistochemical analysis.

Erdheim-Chester (EC) disease is a rare pathological entity with a highly specific and characteristic pattern of radiographic bone changes. Histologically it resembles Langerhans cell histiocytosis (LCH), and it is still a matter of discussion whether EC disease is a distinct entity or a type of LCH. In this study, 3 cases of Erdheim-Chester disease were followed up over years and examined in detail both radiologically and immunohistochemically. All 3 cases showed the pathognomonic skeletal features for EC disease as well as an identical immunohistochemical phenotype quite different from LCH. Macrophages and Touton cells reacted strongly positive with the histiocytic marker CD 68, whereas staining with S100 and CD1a, markers for Langerhans cells, were negative. Both the immunohistochemical phenotype and the bone changes were clearly distinct from LCH.

Antigens, CD↗
PubMed2000

Comparative analysis of the Helicobacter pylori status in patients with gastric MALT-type lymphoma and their respective spouses.

UNLABELLED: Helicobacter pylori is of major importance for the development and progression of gastric MALT-type lymphoma. In case of localized low grade lymphoma successfully treated by Helicobacter pylori eradication reinfection by the bacterium may involve the risk of lymphoma reoccurrence. AIMS: To assess the frequency and type of Helicobacter pylori infection among patients with gastric MALT-type lymphoma and their respective spouses as potential sources of person to person spread of the infection. SUBJECTS: 35 patients with gastric MALT-type lymphoma and their cohabiting spouses. METHODS: We investigated serum IgG titers in response to the infection by Helicobacter pylori and to its virulence factors CagA and VacA by enzyme linked immunosorbent assay (ELISA) and by Western blot. RESULTS: Seropositivity of Helicobacter pylori, Cag A and Vac A was found to be 100/89/69% and 97/86/66% in patients and respective partners, respectively. The seroprevalence rates of the latter group by far exceed those of the German population. CONCLUSION: These data provide evidence for a high Helicobacter pylori infection rate in both patients with gastric MALT-type lymphoma and their respective spouses. Considering the latter as a potential source of reinfection with the risk of lymphoma reoccurrence for the successfully treated patient with gastric MALT-type lymphoma careful follow-up seems highly reasonable to decide on the necessity of a future test-and-treat strategy of this population.

Adult↗