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K Remberger

Publications and source records attributed to K Remberger.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Interferon alpha-2a in the treatment of diffuse thoracic angiomatosis in adulthood--a ase report].

A diffuse angiomatosis affecting thoracal organs is a rare, frequently fatal disorder occurring mainly in childhood. The definite diagnosis is usually made by autopsy. A specific treatment does not exist. In the case report presented here we describe the course of an 37-year old patient presenting initially with dyspnea and hemoptysis. Radiological investigations showed a mass lesion in the anterior superior mediastinum, bihilar masses and a periesophageal mass with soft tissue density and a pericardial effusion. Bilateral interstitial infiltrations were also present. CT-guided mediastinal biopsies and bronchial mucosal biopsies were nonspecific. Open-lung biopsy revealed the diagnosis of an extensive diffuse angiomatosis affecting mediastinum, pericardium and pleura. During the 18-month monotherapy with interferon-alpha 2a the patient showed significant improvements of clinical as well as laboratory and radiological parameters. The presented case confirms the experience of several authors, that the diagnosis of a diffuse thoracal authors can only be made by open lung biopsy or autopsy. The presented case also underlines the possibility of a palliative therapy of aggressive angiomatous diseases with interferon-alpha 2a.

Adult↗
PubMed2000

Malignant odontogenic myxoma of the maxilla: case with cytogenetic confirmation.

An odontogenic myxoma of the maxilla with an aggressive clinical course is presented. The tumour arose in a 53-year-old patient, recurred two times after extended maxillectomy and ultimately caused the patient's death by uncontrollable local disease with infiltration of the cranial cavity. Microscopically, the tumour showed histological features of a low grade malignant myxosarcoma with cellular areas, enhanced mitotic activity and nuclear pleomorphism. Cytogenetic analysis revealed an unexpectedly aberrant hypertetraploid chromosome complement, that was considered as incompatible with the usual karyotypic patterns of benign tumours.

Humans↗
PubMed2000

Gene amplification at chromosome 1pter-p33 including the genes PAX7 and ENO1 in squamous cell lung carcinoma.

Gene amplification is a frequent event in lung cancer, specifically in squamous cell lung carcinoma. Recently, we reported amplifications on chromosomal bands 3q26.1-q26.3 with the genes BCHE and SLC2A2 amplified in 40% of squamous cell lung carcinomas. Here, we identified an amplified domain within chromosomal bands 1pter-p33 in squamous cell lung carcinoma using reverse chromosome painting. A panel of nine genes which have previously been assigned to region 1pter-p33 was tested for amplification using comparative PCR. The ENO1 gene that encodes enolase and the PAX7 gene that encodes a transcription factor were most frequently amplified. Specifically, the gene ENO1 was amplified in six and the gene PAX7 in five out of 37 cases which included both biopsies and paraffin-embedded tissues of squamous cell lung carcinomas. In total, we identified amplifications of at least one gene at bands 1pter-p33 in 10 out of 37 tumors (27%). Together, our data indicate that a novel and frequent amplification unit is present in squamous cell lung carcinoma with the center of the amplified domain in the vicinity of the genes PAX7 and ENO1.

Carcinoma, Squamous Cell↗
PubMed1999

Simultaneous detection of DNA fragmentation (apoptosis), cell proliferation (MIB-1), and phenotype markers in routinely processed tissue sections.

In situ DNA fragmentation assays have proved to be particularly useful in the detection of apoptosis in routinely processed, paraffin-embedded tissue sections. In the present study, a triple-antigen labelling technique was performed to demonstrate DNA fragmentation (apoptosis), cell proliferation (MIB-1), and phenotypic markers in the same tissue section. The in situ apoptosis assay was conducted with the TUNEL method developed by a avidin-biotin alkaline phosphatase complex (ABcomplex/AP). The proliferation-associated MIB-1 antigen was demonstrated in the second staining sequence by the avidin-biotin peroxidase method (ABC). The phenotypic markers chromogranin A or prostate-specific antigen (PSA) were visualized by the alkaline phosphatase anti-alkaline phosphatase method (APAAP) in the third staining sequence. The feasibility of this triple-labelling technique was tested in formalin-fixed, paraffin-embedded tissue of prostatic adenocarcinomas from 8 patients with recurrent, hormone-refractory disease. Although these tumours revealed marked neuroendocrine differentiation, cell proliferation and apoptosis were detected exclusively in non-endocrine (chromogranin A-negative) tumour cells that expressed PSA variably. The triple-labelling protocol described here allows the phenotypic characterization of proliferating and apoptotic cell populations in the same tissue section. It may be useful in studies of tissue kinetics in physiological and pathological processes.

Antigens, Nuclear↗
PubMed1999

Estrogen receptor expression in prostate cancer and premalignant prostatic lesions.

Estrogens have been implicated in prostatic cancerogenesis and tumor progression. The mechanisms underlying estrogen signaling in human prostate tissue, however, remain poorly understood. Using immunohistochemical and in situ hybridization (ISH) techniques, the present study demonstrates the classical estrogen receptor (ERalpha) in premalignant lesions and prostatic adenocarcinoma through the various stages of the disease. Conversely, the novel characterized ERbeta subtype was undetectable in human prostate tissue. High-grade prostatic intraepithelial neoplasia revealed ERalpha mRNA and protein expression in 28% and 11% of cases evaluated. Focal ER immunoreactivity was detected in a minority of low- to intermediate-grade adenocarcinoma. High-grade (primary Gleason grade 4 and 5) tumors revealed ER protein expression in 43% (62% respectively) of cases. The most significant ERalpha gene expression on mRNA and protein levels was observed in hormone refractory tumors and metastatic lesions, including lymph node and bone metastases. Results of the current study suggest that estrogens can affect prostatic cancerogenesis and neoplastic progression through an ER-mediated process in human prostate tissue.

Adenocarcinoma↗
PubMed1999

Expression analysis of genes at 3q26-q27 involved in frequent amplification in squamous cell lung carcinoma.

Gene amplifications are known to occur frequently in lung cancer. Recently, we identified gene amplifications at 3q26 in squamous cell lung carcinoma (SCC) using reverse chromosome painting. Here, our aim was to analyse the expression of genes which map within the amplified chromosomal region. The genes which were selected for their known function and their potential involvement in tumour development included the genes for ribosomal protein L22 (RPL22), butyrylcholinesterase (BCHE), glucose transporter 2 (SLC2A2), transferrin receptor (TFRC), thrombopoietin (THPO) and the phosphatidylinositol-3 kinase catalytic alpha polypeptide (PIK3CA). While five genes were expressed in the majority of the 17 samples of SCC, the gene for the glucose transporter 2 (SLC2A2) was expressed in only three cases, excluding SLC2A2 as the target gene of the amplification unit. For a subset of tumours, we determined the amplification status of the six genes. The TFRC, PIK3CA, BCHE, THPO and SLC2A2 genes were amplified in several cases, whereas the RPL22 gene was amplified in only one case. The combined amplification and expression data of this and our previous studies indicate that the amplified region at 3q26 contains several genes that are transcribed in SCC, providing the possibility that several amplified and functionally important genes at 3q26 may be involved in the pathogenesis of SCC.

Blotting, Southern↗
PubMed1999

[Placenta morphology and Doppler ultrasound of umbilical cord vessels in premature infants].

OBJECTIVE: There is a raised morbidity and mortality in fetuses with pathological waveforms in the umbilical arteries. Less differentiation of the placental villi could (partly) explain this finding. MATERIALS AND METHODS: We examined a total of 51 placentas (28th to 35th week of gestation) as to a correlation between dopplersonographical findings in the umbilical arteries and placenta morphometry. RESULTS: In the groups with pathological waveforms there was not only a reduction in the weight of the placenta and child, but also less differentiation of the placental villi. The occurrence of so-called sprouts did not correlate with the dopplersonographical findings. CONCLUSIONS: The raised fetal morbidity and mortality in premature infants with pathological waveforms in the umbilical arteries can at least partly be explained less differentiation of the placental villi. We found no correlation with the occurrence of sprouts.

Adult↗
PubMed1999

Conservative surgery for chondrosarcoma of the first metacarpal bone.

A rare case of a chondrosarcoma of the first metacarpal bone is presented. The lesion was radiographically interpreted initially as an enchondroma and treated conventionally by curettage and cancellous autologous bone grafting. After final histology, a low-grade chondrosarcoma was reported. A resection of the entire first metacarpal bone was performed, followed by reconstruction using an autologous corticocancellous bone graft and plate fixation, creating arthrodeses of the adjacent joints. Although isolated enchondromas are considered to have no malignant potential, histological examination is essential to rule out malignancy. A preoperative biopsy should be recommended in lesions suspected to be chondromas. Chondrosarcomas are rarely located in bones of the hand, where they are usually treated by amputation. With the case presented we wish to advocate that cases of low-grade, intraosseous chondrosarcoma (stage IA) can be treated by conservative surgery, especially when it is located in the thumb.

Adult↗
PubMed1998

In situ hybridization analysis of genes coding collagen IV alpha1 chain, laminin beta1 chain, and S-laminin in prostate tissue and prostate cancer: increased basement membrane gene expression in high-grade and metastatic lesions.

BACKGROUND: Recent immunohistochemical data have shown that invasive prostate cancer cells are separated from the host tissue by basement membranes (BM), and express associated adhesive molecules that bind to these de novo synthesized extracellular matrices. METHODS: In the present study, we used in situ hybridization techniques to determine steady-state levels of genes coding BM components (alpha1 chain of collagen IV, laminin beta1 chain, and S-laminin) in prostate tissue obtained from 15 radical prostatectomy specimens and 5 lymph node metastases of common prostatic adenocarcinomas. RESULTS: In benign prostate tissue, transcripts of these genes were detected predominantly in the basal cell layer, indicating that components of epithelial BMs are synthesized by basal cells and not by stromal cells. The cancerous lesions investigated revealed increasing collagen IV, laminin beta1 chain, and S-laminin mRNA levels when compared with benign prostate tissue. The highest steady-state levels were found in high grade (primary Gleason grade 4 and 5) carcinoma and lymph node metastases, and were predominantly localized in epithelial compartments of the cancerous tissue. CONCLUSIONS: These findings indicate that neoplastic BM in prostatic adenocarcinoma derive from tumor cells and not from the host tissue. Increasing transcriptional activities of genes coding BM components detected in poorly differentiated and metastatic lesions may accelerate the BM-forming process, which probably contributes to the ability of tumor cells to penetrate the extracellular matrix during the process of stromal invasion and metastasis.

Adenocarcinoma↗
PubMed1998

Relation between Bcl-2, cell proliferation, and the androgen receptor status in prostate tissue and precursors of prostate cancer.

BACKGROUND: Several recent studies have suggested an important role of the apoptosis suppressing Bcl-2 gene product in prostate cancer progression to an androgen-insensitive disease. METHODS: Using double-labeling techniques, we have investigated the nuclear androgen receptor (AR) status and the proliferation-associated MIB-1 antigen immunoprofile of Bcl-2 expressing cell types in benign prostate tissue, and high-grade prostatic intraepithelial neoplasia (HGPIN). RESULTS: In the peripheral and transition zone of the prostate gland, 77% of cycling (MIB-1 positive) epithelial cells coexpressed the Bcl-2 product and were phenotypically basal cells. Bcl-2 immunoreactive basal cells showed markedly reduced levels of the nuclear AR. In the central zone of the gland, increasing Bcl-2 immunoreactivity was detected in secretory luminal cell types that expressed the nuclear AR at low levels. 22% of HGPIN lesions (47 of 216 cases) overexpressed Bcl-2 in secretory luminal cell types, while most of HGPIN lesions (78%) showed the normal Bcl-2 phenotype restricted to the basal cell layer. No correlation was found between the Bcl-2 status and proliferative activity (P > 0.05). Conversely, markedly reduced levels of nuclear AR were detected in HGPIN overexpressing the Bcl-2 gene product. CONCLUSIONS: The present data suggest that Bcl-2 prevents the proliferation compartment from apoptotic cell death. The aberrant expression of the Bcl-2 gene product in subsets of HGPIN is associated with decreasing levels of the nuclear AR and may confer resistance to the androgen-dependent apoptotic cell death in the dysplastic epithelium.

Animals↗
PubMed1998

[Benign microglandular prostate lesions. Diagnostic criteria na differential diagnosis].

The scope of the present review is to define diagnostic criteria of benign prostatic lesions causing diagnostic difficulty in surgical pathology. The prostate harbors a variety of small acinar lesions that may mimic prostate cancer in biopsy specimens. Generally, the most important diagnostic clues are obtained on low-power magnification by assessing architectural features. Atypical adenomatous hyperplasia (AAH) is a small acinar proliferation closely related to hyperplastic glands. Diagnostic features of postatrophic hyperplasia include a lobular small acinar proliferation associated with atrophic and dilated acini. Basal cell hyperplasia and sclerosing adenosis show characteristic stromal changes that are uncommon in prostate cancer. Additional cytological features and intraluminal secretions are also important in the diagnostic evaluation of small acinar lesions in biopsy specimens. Negative immunohistochemical results obtained with basal-cell-specific cytokeratins should be evaluated in context with other diagnostic criteria. The unequivocal demonstration of basal cells in small acinar lesions excludes invasive cancer. Other rare small acinar lesions must be recognized when assessing biopsy specimens, including verumontanum-mucosa hyperplasia, Cowper's glands and mesonephroid hyperplasia. The various small acinar lesions discussed in the present review have no clinical significance, except atypical adenomatous hyperplasia (AAH), which may be a precursor of small acinar cancer of the transition zone. The biological and clinical significance of AAH, however, remains to be established.

Atrophy↗
PubMed1998

[Morphogenesis of benign prostatic hyperplasia and prostatic carcinoma].

Enlargement of the prostate is an age-related, physiological process that is unique in human tissue. The prostate gland is the most common site of neoplastic disorders in men. Despite the growing impact of the various prostate diseases in terms of morbidity and mortality, the pathogenesis of benign prostate hyperplasia (BPH) and prostate cancer remains poorly understood. This reflects the complex composition of the gland with different anatomic, cellular and functional compartments that are differentially involved in benign and malignant disease processes. The present review summarizes new concepts on the morphogenesis of normal and abnormal growth in the human prostate. There is increasing evidence that prostatic stem cells are located in the basal cell layer that is basically involved in normal growth and the development of glandular hyperplasia and prostate cancer. High-grade prostatic intraepithelial neoplasia is considered the most likely precursor of clinically important cancer of the peripheral zone. Severe differentiation and proliferation abnormalities occur during malignant transformation of the prostatic epithelium. These premalignant changes are associated with abnormal expression of growth factor receptors, oncogene and suppressor gene products and genetic instability. During the process of stromal invasion the transformed cells lose their basal cell phenotype and produce basement membrane-like matrices. Common prostate cancer is mainly composed of exocrine cell types that remain androgen-responsive even in hormone-independent disease. The frequent occurrence of neuroendocrine differentiation in common prostate cancer reflects the differentiation potency of its stem cells. The endocrine phenotype derives from exocrine tumor cells via intermediate (amphicrine) cell types. Neuroendocrine tumor cells consistently lack the nuclear androgen receptor and represent an androgen-insensitive cell population in prostate cancer.

Cell Transformation, Neoplastic↗
PubMed1998

[Diagnostic criteria of prostatic carcinoma].

The histological diagnosis of prostate cancer relies on a combination of structural and cytological findings. Structural features are assessed at low power magnification. Malignant glands are recognised by their abnormal size, shape and location in relation to the surrounding benign glandular structures. The presence of pathological intraluminal secretions (pink amorphous secretions, crystalloids, blue-tinged mucinous secretions) is always suspicious, but not diagnostic for prostate cancer. Cytological criteria including nuclear and nucleolar enlargement, hyperchromasia and cytoplasmic changes have to be evaluated in comparison with the cytological features of surrounding benign glands. The presence of prominent nucleoli is neither diagnostic for malignancy nor represents an absolute requirement for the diagnosis of prostate cancer. The basal cell layer is absent in invasive adenocarcinoma, an important feature that has to be evaluated with care since benign glands may also lack detectable basal cells. The immunohistochemical demonstration of basal cells with high molecular weight cytokeratins excludes invasive cancer. This article reviews the histological criteria for the diagnosis of prostate cancer, including variants of common adenocarcinoma and therapy-induced changes.

Adenocarcinoma↗
PubMed1998

[Diagnostic criteria and differential diagnosis of prostatic intraepithelial neoplasia].

Prostatic intraepithelial neoplasia (HGPIN) is considered the most likely precursor of clinically significant prostate cancer. Biopsy remains the only definitive method for detecting these premalignant lesions. In this article we review the diagnostic criteria of HGPIN and discuss histological features that allow their distinction from other benign and malignant lesions. PIN is recognised at low power magnification as a thickened, basophilic and hyperchromatic epithelium in pre-existing acinar duct structures. This important histological feature is due to nuclear crowding and stratification. Distinction between HGPIN and low grade PIN (LGPIN), a lesion with little clinical significance, is made mainly on the presence or absence of prominent nucleoli. HGPIN lesions always retain an intact or fragmented basal cell layer. The different growth patterns of HGPIN (tufting, micropapillary, cribriform and flat) have no clinical significance but should be considered in the differential diagnosis together with normal structures, and both benign and malignant lesions. HGPIN has a high predictive value as a marker for prostate cancer but should not influence therapeutic decisions. Its identification in biopsy specimens warrants close surveillance with repeated biopsy.

Biopsy↗
PubMed1998

Morphogenetic concepts of normal and abnormal growth in the human prostate.

Benign prostatic hyperplasia (BPH) and prostate cancer are multifactorial disease processes, involving a growing number of biochemical, genetic and epigenetic factors. Their pathogenesis, however, remains poorly understood. The present review examines current morphogenetic concepts of normal and abnormal growth in the human prostate. This includes the role of basal cells in organogenesis and cancerogenesis, the impact of cell-matrix interactions, and the importance of cellular heterogeneity in tumour progression and hormone-insensitive growth. Knowledge of morphogenesis and morphology is required in any scientific approach to BPH and prostate cancer.

Cell Differentiation↗