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  • 1
    Electronic Resource
    Electronic Resource
    Metastatic RCC arising in a transplant kidney (1998)
    Springer
    European radiology 8 (1998), S. 1441-1443 
    Details
    ISSN: 1432-1084
    Keywords: Key words: Renal cell carcinoma ; Transplantation ; Immunosuppression ; Kidney ; Neoplasms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We report a case of metastatic renal cell carcinoma arising in a cadaver transplant kidney 6 years after transplantation. Due to molecular analysis of the tumor tissue we could prove that the carcinoma originated from the male donor. After tumor resection and interruption of immunotherapy, the concomitant bone and lymph node metastases resolved with alpha-interferon and interleukin-2-based immunotherapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003300050570
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  • 2
    Electronic Resource
    Electronic Resource
    The Gap Junctional Protein Connexin(Cx)43 in Testicular Cancer: its Loss Marks Progession from Carcinoma In Situ to Invasive Germ Cell Tumour (2005)
    Berlin, Germany : Blackwell Verlag GmbH
    Anatomia, histologia, embryologia 34 (2005), S. 0 
    Details
    ISSN: 1439-0264
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Carcinoma-in-situ (CIS) of the testis is known to be the pre-invasive stage of most human germ cell tumours (seminoma and non-seminoma), but the mechanisms leading to an increased pubertal proliferation of CIS cells after a long latency and to progression of CIS to an invasive malignancy are still not known. Additionally, CIS and seminoma have also been reported in equine testis (Veeramachaneni and Sawyer, 1998). The gap junctional protein and tumour suppressor gene connexin(cx)43 represents the predominant cx in human, canine and rodent testis so far and it is expected to play a key role for the regulation of both proliferation and differentiation of germ cells (spermatogonia and spermatocytes), and its gene- and protein-expression pattern is typical for the pubertal terminal differentiation of somatic Sertoli cells. Using cDNA-microarray analysis, in-situ hybridization (ISH), RT-PCR from tissue homogenate and semi-quantitative RT-PCR from well defined microdissected tubules with normal spermatogenesis, CIS, intratubular seminoma (ISe) and from seminoma cells from invasive seminoma we found a downregulation of cx43 starting in intratubular CIS, leading to a complete loss in most invasive seminoma cells. This indicates that regulation of cx43 expression takes place at transcriptional level confirming and expanding earlier studies of protein expression (Brehm et al., 2002). This reduction of cx43-expression suggests that an early intratubular derangement in cx43-gene expression and disruption of inter-cellular communication between Sertoli cells and/or Sertoli cells and pre-invasive tumour cells via cx43-gap junctions may play a role in the proliferation of CIS cells and seminoma cells and in the progression phase of testicular seminoma development.References  Veeramachaneni, D. N., and H. R.Sawyer, 1998: Carcinoma in situ and seminoma in equine testis. APMIS 106, 183–185.Brehm R., A. Marks, R. Rey, S. Kliesch, M. Bergmann and K. Steger, 2002: Altered expression of connexins 26 and 43 in Sertoli cells in seminiferous tubules infiltrated with carcinoma-in-situ or seminoma. J. Pathol. 197, 647–653.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1439-0264.2005.00669_16.x
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  • 3
    Electronic Resource
    Electronic Resource
    The T-type calcium channel blocker mibefradil reduced interstitial and perivascular fibrosis and improved hemodynamic parameters in myocardial infarction-induced cardiac failure in rats (2000)
    Springer
    Virchows Archiv 436 (2000), S. 147-157 
    Details
    ISSN: 1432-2307
    Keywords: Key words T-type calcium channel blockade ; Mibefradil ; Myocardial infarction ; Cardiac remodeling ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Fibrillar collagen accumulates within the interstitium and around coronary arteries following cardiac failure and is responsible for abnormal myocardial stiffness and reduced coronary performance associated with impaired cardiac function. The aim of the study was to determine the effects of long-term treatment with the T-type calcium channel antagonist mibefradil on myocardial remodeling and cardiac function after chronic myocardial infarction (MI). MI was induced by permanent ligation of the left coronary artery in male Wistar rats. Animals were assigned to sham-operated, placebo-treated or mibefradil-treated (10 mg/kg per day p.o.) MI groups. Treatment with mibefradil was started either 7 days before, 24 h after, or 7 days after ligation and continued for 6 weeks after MI. At this time point, mean arterial blood pressure (MAP), heart rate (HR), left ventricular end-diastolic pressure (LVEDP) and cardiac contractility (dP/dtmax) were measured in conscious rats. Morphometric parameters were determined in picrosirius red-stained hearts: total heart weight (THW), interstitial and perivascular collagen volume fraction (ICVF, PCVF), myocardial infarct size (IS), vascular perimeter (VP), inner vascular diameter (IVD) and media thickness (MT). Six weeks after MI, MAP and dP/dtmax were decreased, and LVEDP was increased in placebo-treated animals. In mibefradil-treated animals whose treatment started 7 days before or 24 h after MI, MAP and dP/dtmax were higher, and LVEDP was lower than in placebo-treated controls. THW, ICVF, PCVF and MT were higher in placebo-treated animals. Mibefradil treatment resulted in higher ICVF and IS, higher VP and IVD (when started 7 days before MI) and lower PCVF and MT (when started 7 days before or 24 h after MI) than were observed in placebo-treated controls. Chronic treatment with mibefradil reduced interstitial and perivascular fibrosis and improved cardiac function in MI-induced heart failure in rats. Cardiac remodeling was best prevented when treatment was begun before the ischemic event.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00008215
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  • 4
    Electronic Resource
    Electronic Resource
    Das lokalisierte benigne Pleuramesotheliom (1994)
    Springer
    Langenbeck's archives of surgery 379 (1994), S. 307-309 
    Details
    ISSN: 1435-2451
    Keywords: Benign pleural mesothelioma ; Localized ; Diagnosis ; Surgical management ; Prognosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das benigne Pleuramesotheliom ist ein sehr seltener Tumor, für deren Ursprung die Mesothelien, aber auch das submesotheliale Bindegewebe diskutiert wird. Daher werden these Tumoren in der Literatur u. a. auch als Pleurafibrom, submesotheliales Fibrom, lokalisiertes fibröses Mesotheliom und monophasischer Spindelzelltumor beschrieben. Das Wachstum dieser Tumoren ist sehr langsam und geht über Jahre his Jahrzehnte. Im Gegensatz zum häufiger auftretenden malignen Pleuramesotheliom ist ein gehäuftes Auftreten nach Asbestex-position nicht zu beobachten. Wir berichten über eine 47jährige Patientin mit einem großen benignen Pleuramesotheliom im Bereich des rechten Thorax.
    Notes: Abstract Benign mesothelioma of the pleura is a very rare tumor. The cells responsible originate from either the mesothelium or the submesothelium. This is why such tumors are described in the literature as fibroma of the pleura, mesothelial fibroma, localized fibrous mesothelioma and monophasic spindle cell tumor. Their growth, is very slow taking several years or even decades. In contrast to the more common malignant mesothelioma of the pleura, it is not related to asbestos exposure. This report deals with a 47-year-old woman patient with a giant benign mesothelioma of the pleura in the region of the right thorax, which was completely removed by thoracotomy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00186398
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  • 5
    Electronic Resource
    Electronic Resource
    Secondary acute myeloid leukemia with translocation (4;11) and MLL/AF4 rearrangement in a 15-year-old boy treated for common acute lymphoblastic leukemia 11 years earlier (1995)
    Springer
    Annals of hematology 70 (1995), S. 31-35 
    Details
    ISSN: 1432-0584
    Keywords: Secondary leukemia ; Translocation t(4,11) MLL/AF4 rearrangement ; PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Secondary acute myeloid leukemia occurring in a 15-year-old boy 11 years after initial treatment of a common lymphoblastic leukemia (c-ALL) is described. Initial complete remission was terminated after 4 years by an isolated testicular relapse, followed by first bone marrow relapse within 18 months. After he achieved remission again, an allogeneic bone marrow transplantation from his HLA-identical brother was performed. Five years and 9 months later, the patient developed thrombocytopenia, leukopenia, and anemia, but bone marrow biopsies at this time demonstrated only myelofibrosis, with no blast cell population present. A polymerase chain reaction assay of a peripheral blood sample recognized the mRNA fusion region for the MLL/AF4 rearrangement, i.e., the molecular equivalent of the translocation (4;11)(q21,q23). Four weeks later, a blast cell population with AML-M1 morphology according to the FAB classification appeared in the bone marrow, and translocation (4;11) was detected by cytogenetics. Thus, secondary leukemias with chromosomal 11q23 rearrangement can develop after a long latency period and can be diagnosed earlier with the PCR technique.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01715379
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  • 6
    Electronic Resource
    Electronic Resource
    Secondary acute myeloid leukemia with translocation (4;11) and MLL/AF4 rearrangement in a 15-year-old boy treated for common acute lymphoblastic leukemia 11 years earlier (1995)
    Springer
    Annals of hematology 70 (1995), S. 31-35 
    Details
    ISSN: 1432-0584
    Keywords: Key words Secondary leukemia ; Translocation t(4;11) ; MLL/AF4 rearrangement ; PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary  Secondary acute myeloid leukemia occurring in a 15-year-old boy 11 years after initial treatment of a common lymphoblastic leukemia (c-ALL) is described. Initial complete remission was terminated after 4 years by an isolated testicular relapse, followed by first bone marrow relapse within 18 months. After he achieved remission again, an allogeneic bone marrow transplantation from his HLA-identical brother was performed. Five years and 9 months later, the patient developed thrombocytopenia, leukopenia, and anemia, but bone marrow biopsies at this time demonstrated only myelofibrosis, with no blast cell population present. A polymerase chain reaction assay of a peripheral blood sample recognized the mRNA fusion region for the MLL/AF4 rearrangement, i.e., the molecular equivalent of the translocation (4;11)(q21,q23). Four weeks later, a blast cell population with AML-M1 morphology according to the FAB classification appeared in the bone marrow, and translocation (4;11) was detected by cytogenetics. Thus, secondary leukemias with chromosomal 11q23 rearrangement can develop after a long latency period and can be diagnosed earlier with the PCR technique.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01715379
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    Paper (German National Licenses)
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