Tiemo Katzenberger

University of Wuerzburg, Würzburg, Bavaria, Germany

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Publications (67)283.18 Total impact

  • T Katzenberger · O Al-Taie · W Fischbach · M Eck
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    ABSTRACT: The detection of a diffuse infiltrate of heterogeneous small B-cells in the lamina propria mucosae invading the epithelium and destroying the glandular tissue by discrete aggregates of three or more marginal zone B-cells above the basal membrane (so-called lymphoepithelial lesions) is suspicious of a mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach. The demonstration of a monoclonal B-cell population by immunohistochemistry, in situ hybridization or PCR excludes a benign lymphatic lesion. In the differential diagnosis with other small B-cell lymphomas in the stomach, a panel of five different immunohistochemical markers is useful to diagnose a small lymphocytic lymphoma (CD5 and CD23 positive), a mantle cell lymphoma (CD5 and cyclin D1 positive) or a follicular lymphoma (BCL2 and CD10 positive). The presence of the translocation t(11;18)(q21;q21) or the API2/MALT1 rearrangement could give further information about the clinical course and the prognosis of a gastric MALT lymphoma.
    Der Pathologe 12/2014; 36(2). DOI:10.1007/s00292-014-2055-3 · 0.64 Impact Factor
  • Gastroenterologie up2date 12/2013; 9(04):232-236. DOI:10.1055/s-0033-1359105
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    ABSTRACT: Background: Patients undergoing radical cystectomy (RC) for urothelial carcinoma of the bladder (UCB) are at risk for upper urinary tract recurrence (UUTR), especially in case of carcinoma in situ (CIS). Data on the impact of CIS in the urinary bladder on ureteral tumour involvement or UUTR are conflicting. We presently evaluate the accuracy of intraoperative frozen section analysis (FSA) of the ureteral margin, the incidence of ureteral tumour involvement and their impact on UUTR in patients undergoing RC for UCB with versus without CIS of the bladder. Material and Methods: Between 2003 and 2007, 243 patients underwent RC in our department. 176 of these for UCB, either without CIS (n = 117, group I) or solitary/concomitant CIS (n = 59, group II). FSA was performed. Patients were followed up for UUTR. Results: Overall, 403 ureteral margins - including re-resections - were analysed (group I, n = 232; group II, n = 171). One patient (0.85%) in group I and 21 patients (35.6%) in group II had tumour involvement of the ureter (p < 0.0001) at the time of RC. The false-negative rate of FSA compared to final histopathology was 0.4% (1/232) for group I and 2.9% (5/171) for group II, respectively. Mean duration of follow-up was 26 months (1-72). In group II, 2 patients (1.1%) had UUTR in the follow-up; both had initially positive and subsequently false-negative FSA. Conclusions: Tumour involvement of the ureter is found significantly more often in solitary or concomitant CIS of the bladder. Intraoperative ureteral FSA is accurate and should be recommended in these patients. Ureteral tumour involvement predisposes to UUTR especially with initial positive margins mandating careful follow-up. © 2013 S. Karger AG, Basel.
    Urologia Internationalis 10/2013; 92(1). DOI:10.1159/000353230 · 1.15 Impact Factor
  • O Al-Taie · C G Dietrich · D Flieger · T Katzenberger · W Fischbach
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    ABSTRACT: Introduction: In earlier studies, involvement of the small intestine was reported in patients with gastrointestinal lymphoma. Prospective data on the involvement of the small intestine in patients suffering from gastric extranodal MZBCL of MALT do not exist so far. In this study, we investigated the frequency of the involvement of the small intestine and the role of capsule endoscopy in patients with gastrointestinal extranodal MZBCL of MALT and of follicular lymphoma.Patients and Methods: 40 consecutive patients with gastrointestinal extranodal MZBCL of MALT (26 men, 14 women, aged 27 - 80 years), and 7 patients with known follicular lymphoma of the small intestine (5 men, 2 women, aged 34 - 63 years) underwent capsule endoscopy.Results: Involvement of the small intestine was identified by capsule endoscopy in all 7 patients with known follicular lymphoma of the small intestine. In 6 of 40 patients with gastric extranodal MZBCL of MALT abnormal findings could be observed, three of these findings indicative for lymphoma involvement of the small intestine. However, in each of these 3 cases, intestinal involvement had been already diagnosed by conventional GI endoscopy before capsule endoscopy.Conclusions: Capsule endoscopy is able to detect involvement of the small intestine in patients with gastrointestinal lymphoma. However, involvement of the small intestine seems to be rare in patients with gastric extranodal MZBCL of MALT. In summary, routine diagnostic work-up of the small intestine, e. g. by capsule endoscopy seems unnecessary because of the rare involvement of the small intestine and an excellent long-term outcome irrespective of a possible intestinal manifestation.
    Zeitschrift für Gastroenterologie 08/2013; 51(8):727-732. DOI:10.1055/s-0033-1335077 · 1.67 Impact Factor
  • Zeitschrift für Gastroenterologie 08/2012; 50(08). DOI:10.1055/s-0032-1323877 · 1.67 Impact Factor
  • Cancer Research 07/2011; 71(8 Supplement):2248-2248. DOI:10.1158/1538-7445.AM2011-2248 · 9.28 Impact Factor
  • C. Platz-Baudin · T. Katzenberger · M. Eck
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    ABSTRACT: Die mikroskopische Kolitis ist eine klinisch-pathologische Entität, die neben der typischen Klinik mit wässrigen Diarrhöen eine charakteristische Histologie aufweist. Da die Koloskopie einen endoskopischen Normalbefund zeigt, ist die mikroskopische Kolitis eine Domäne der Histopathologie. Morphologisch werden lymphozytäre und kollagene Kolitis unterschieden. Die lymphozytäre Kolitis zeigt eine Vermehrung der intraepithelialen Lymphozyten auf >20Lymphozyten pro 100Deckepithelien, die kollagene Kolitis eine Verbreiterung des subepithelialen Kollagenbands auf mehr als 10µm. Zur genauen Quantifizierung sind entsprechende Zusatzfärbungen hilfreich. Bei entsprechender Klinik ist die Entnahme von Stufenbiopsien – möglichst mit Lokalisationszuordnung – zu empfehlen, da die mikroskopische Kolitis Darmabschnitte aussparen kann und physiologisch die Lymphozytenanzahl in den verschiedenen Darmabschnitten variiert. Während die Verbreiterung des Kollagenbands als relativ spezifisch für die Diagnose einer kollagenen Kolitis gilt, findet sich eine Lymphozytose der Kolonschleimhaut auch im Rahmen anderer Erkrankungen. Für die korrekte Diagnosestellung ist hier die Korrelation des histomorphologischen Befunds mit der klinischen Symptomatik und dem Leitsymptom der wässrigen Diarrhö entscheidend. Microscopic colitis is a clinicopathological entity which, in addition to typical symptoms such as watery diarrhea, is characterized by its specific histopathology. Since colonoscopy yields normal findings, microscopic colitis belongs in a histological domain. The term encompasses two forms: lymphocytic and collagenous colitis. Histologically, lymphocytic colitis shows an increase in intraepithelial lymphocytes of more than 20 lymphocytes per 100 surface colonocytes, while collagenous colitis is characterized by a thickened subepithelial collagen layer of more than 10µm. Specific stains help in the quantification of both. Since microscopic colitis does not always affect the entire colon and the number of intraepithelial lymphocytes varies physiologically, obtaining stepwise biopsies of the colon (with information on location where possible) is recommended. A thickened collagen layer is relatively specific for collagenous colitis, whereas intraepithelial lymphocytosis is also found in other diseases. Therefore, to make a correct diagnosis, it is important to correlate histological findings with clinical symptoms, including the main symptom of watery diarrhea. SchlüsselwörterMikroskopische Kolitis–Klinisch-pathologische Entität–Lymphozytäre Kolitis–Kollagene Kolitis–Wässrige Diarrhö KeywordsMicroscopic colitis–Clinicopathological entity–Lymphocytic colitis–Collagenous colitis–Watery diarrhea
    Der Pathologe 07/2011; 32(4):275-281. DOI:10.1007/s00292-011-1432-4 · 0.64 Impact Factor
  • S. Warich-Eitel · T. Katzenberger · M. Eck
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    ABSTRACT: Zusammenfassung Polypoide Dysplasien bei chronisch-entzündlicher Darmerkrankung (CED) werden klassischerweise in DALM („dysplasia associated lesion or mass“) und ALM („adenoma-like mass“) unterteilt. DALMs entstehen auf dem Boden der chronischen Entzündung, haben ein hohes Karzinomrisiko und bedürfen der Kolektomie. Sporadische Adenome entstehen koinzidentell im Rahmen der Adenom-Karzinom-Sequenz und sind mit einer lokalen Abtragung ausreichend therapiert. In letzter Zeit wurden „adenoma-like-DALMs“ abgegrenzt, die trotz Entstehung auf dem Boden einer CED eine überlappende Morphologie zu den sporadischen Adenomen zeigen. Adenomähnliche DALMs scheinen ein deutlich geringeres Entartungsrisiko als klassische DALMs zu haben und können deswegen ähnlich den sporadischen Adenomen durch eine lokale Abtragung mit nachfolgender Überwachung adäquat therapiert werden. Voraussetzung hierfür ist die Abtragung in toto sowie das Fehlen dysplastischer Veränderungen im Restkolon.
    Der Pathologe 07/2011; 32(4):282-288. DOI:10.1007/s00292-011-1433-3 · 0.64 Impact Factor
  • S Warich-Eitel · T Katzenberger · M Eck
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    ABSTRACT: Polypoid dysplasia in inflammatory bowel disease (IBD) is categorized as DALM (dysplasia associated lesion or mass) or ALM (adenoma-like mass). DALMs are etiologically related to the underlying inflammatory disease, have a high risk of cancer and remain an indication for colectomy. Sporadic adenomas occur coincidentally according to the adenoma-carcinoma sequence. They are adequately treated by polypectomy. More recently, a special group of lesions has been termed as "adenoma-like DALM" which shows a morphological overlap with sporadic adenomas in spite of arising against the background of chronic IBD. Adenoma-like DALMs may possess a lower risk of malignancy in contrast to non-adenoma-like DALMs. They may be treated adequately by polypectomy and continued monitoring if the lesion has been excised completely and there is no evidence of flat dysplasia elsewhere in the colon.
    Der Pathologe 06/2011; 32(4):282-8. · 0.64 Impact Factor
  • C Platz-Baudin · T Katzenberger · M Eck
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    ABSTRACT: Microscopic colitis is a clinicopathological entity which, in addition to typical symptoms such as watery diarrhea, is characterized by its specific histopathology. Since colonoscopy yields normal findings, microscopic colitis belongs in a histological domain. The term encompasses two forms: lymphocytic and collagenous colitis. Histologically, lymphocytic colitis shows an increase in intraepithelial lymphocytes of more than 20 lymphocytes per 100 surface colonocytes, while collagenous colitis is characterized by a thickened subepithelial collagen layer of more than 10 µm. Specific stains help in the quantification of both. Since microscopic colitis does not always affect the entire colon and the number of intraepithelial lymphocytes varies physiologically, obtaining stepwise biopsies of the colon (with information on location where possible) is recommended. A thickened collagen layer is relatively specific for collagenous colitis, whereas intraepithelial lymphocytosis is also found in other diseases. Therefore, to make a correct diagnosis, it is important to correlate histological findings with clinical symptoms, including the main symptom of watery diarrhea.
    Der Pathologe 06/2011; 32(4):275-81. · 0.64 Impact Factor
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    ABSTRACT: According to the current World Health Organization Classification of Lymphoid Tumours, follicular lymphoma is subclassified into three grades according to the number of centroblasts. Follicular lymphoma grade 3 can be further divided into types A and B. Almost all available genetic data on grade 3B follicular lymphomas have been generated from tumors with an additional diffuse large B-cell lymphoma component. The purely follicular type of follicular lymphoma grade 3B is a rare neoplasm. We performed a detailed immunohistochemical (CD10, IRF4/MUM1, BCL2, Ig light chains) and genetic (translocations of BCL2, BCL6, MYC, IRF4) characterization of the largest series of purely follicular cases of grade 3B follicular lymphoma available to date, comprising 23 tumor samples. We also included 25 typical grade 1 or 2 follicular lymphomas, 9 follicular lymphomas with large centrocytes and/or high proliferation indices (FL/LCC), 12 cases of follicular lymphoma grade 3A, 16 cases of diffuse large B-cell lymphoma/follicular lymphoma grade 3B and 15 follicular lymphomas in which a straightforward distinction between grades 3A and 3B was not possible. Translocations affecting BCL2 and BCL6 genes are rare in grade 3B follicular lymphomas (2/23, 9% and 4/23, 17%) when compared with grade 1 or 2 follicular lymphomas (22/25, 88%, P<0.001 and 0/25, P<0.05), FL/LCC (7/9, 78%, P<0.001 and 2/9, 22%), grade 3A follicular lymphomas (7/12, 58%, P<0.01 and 2/12, 17%), unclassified grade 3 follicular lymphomas (6/15, 40% and 2/15, 13%) and diffuse large B-cell lymphoma/follicular lymphoma grade 3B (2/16, 13% and 8/16, 50%, P<0.05). MYC translocations were detected occasionally in FL/LCC, follicular lymphoma grade 3B, and diffuse large B-cell lymphoma/follicular lymphoma grade 3B (13%-22%), but not in grade 1, 2 or 3A follicular lymphomas (P<0.05 when compared with follicular lymphoma grade 3B). Both follicular lymphoma grade 3B and diffuse large B-cell lymphoma/follicular lymphoma grade 3B were enriched in samples with a CD10(-)IRF4/MUM1(+) immunophenotype (8/19, 42% and 7/16, 44%), with the vast majority of them lacking BCL2 translocations. In contrast, 42/46 grade 1 or 2 follicular lymphomas, FL/LCC and grade 3A follicular lymphomas were CD10(+) (91%) while 0/46 expressed IRF4/MUM1. None of the tumor samples tested with increased IRF4/MUM1-expression harbored a translocation of the IRF4 gene locus. Our results show that grade 3B follicular lymphomas form a distinct category of follicular lymphomas with infrequent BCL2 and BCL6 translocations, while grades 1, 2 and 3A follicular lymphomas and FL/LCC display homogeneous features with frequent BCL2 translocations and a CD10(+)IRF4/MUM1(-) immunophenotype.
    Haematologica 06/2011; 96(9):1327-34. DOI:10.3324/haematol.2011.042531 · 5.87 Impact Factor
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    ABSTRACT: Tumor suppressor genes are often located in frequently deleted chromosomal regions of colorectal cancers (CRCs). In contrast to microsatellite stable (MSS) tumors, only few loss of heterozygosity (LOH) studies were performed in microsatellite instable (MSI) tumors, because MSI carcinomas are generally considered to be chromosomally stable and classical LOH studies are not feasible due to MSI. The single nucleotide polymorphism (SNP) array technique enables LOH studies also in MSI CRC. The aim of our study was to analyse tissue from MSI and MSS CRC for the existence of (frequently) deleted chromosomal regions and tumor suppressor genes located therein. We analyzed tissues from 32 sporadic CRCs and their corresponding normal mucosa (16 MSS and 16 MSI tumors) by means of 50K SNP array analysis. MSS tumors displayed chromosomal instability that resulted in multiple deleted (LOH) and amplified regions and led to the identification of MTUS1 (8p22) as a candidate tumor suppressor gene in this region. Although the MSI tumors were chromosomally stable, we found several copy neutral LOHs (cnLOH) in the MSI tumors; these appear to be instrumental in the inactivation of the tumor suppressor gene hMLH1 and a gene located in chromosomal region 6pter-p22. Our results suggest that in addition to classical LOH, cnLOH is an important mutational event in relation to the carcinogenesis of MSS and MSI tumors, causing the inactivation of a tumor suppressor gene without copy number alteration of the respective region; this is crucial for the development of MSI tumors and for some chromosomal regions in MSS tumors.
    Carcinogenesis 02/2011; 32(4):636-42. DOI:10.1093/carcin/bgr011 · 5.27 Impact Factor
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    ABSTRACT: Haematologica 2011 [Epub ahead of print] Citation: Horn H, Schmelter C, Leich E, Salaverria I, Katzenberger T, Ott MM, Kalla J, Romero M, Siebert R, Rosenwald A, and Ott G. Follicular lymphoma grade 3b is a distinct neoplasm according to cytogenetic and immunohistochemical profiles. Haematologica. 2011; 96:xxx doi:10.3324/haematol.2011.042531 Publisher's Disclaimer. E-publishing ahead of print is increasingly important for the rapid dissemination of science. Haematologica is, therefore, E-publishing PDF files of an early version of manuscripts that have completed a regular peer review and have been accepted for publication. E-publishing of this PDF file has been approved by the authors. After having E-published Ahead of Print, manuscripts will then undergo technical and English editing, typesetting, proof correction and be presented for the authors' final approval; the final version of the manuscript will then appear in print on a regular issue of the journal. All legal disclaimers that apply to the journal also pertain to this production process. Haematologica (pISSN: 0390-6078, eISSN: 1592-8721, NLM ID: 0417435, www.haemato-logica.org) publishes peer-reviewed papers across all areas of experimental and clinical hematology. The journal is owned by the Ferrata Storti Foundation, a non-profit organiza-tion, and serves the scientific community with strict adherence to the principles of open access publishing (www.doaj.org). In addition, the journal makes every paper published immediately available in PubMed Central (PMC), the US National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature.
  • Gastroenterologie up2date 12/2010; 6(04):238-242. DOI:10.1055/s-0030-1255962
  • Zeitschrift für Gastroenterologie 10/2010; 48(10). DOI:10.1055/s-0030-1267713 · 1.67 Impact Factor
  • T Kudlich · M Wilk · H Lührs · T Menzel · T Katzenberger · W Scheppach · M Scheurlen · R Melcher
    Zeitschrift für Gastroenterologie 10/2010; 48(10). DOI:10.1055/s-0030-1267714 · 1.67 Impact Factor
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    ABSTRACT: We analyzed morphological and immunohistochemical features in 174 aggressive B-cell lymphomas of nodal and extranodal origin. Morphological features included presence or absence of a follicular component and cytologic criteria according to the Kiel classification, whereas immunohistochemical studies included expression of CD10, BCL-2, BCL-6, IRF4/MUM1, HLA-DR, p53, Ki-67 and the assessment of plasmacytoid differentiation. Patients were treated with a CHOP-like regimen. While the presence or absence of either CD10, BCL-6 and IRF4/MUM1 reactivity or plasmacytoid differentiation did not identify particular cytomorphologic or site-specific subtypes, we found that expression of CD10 and BCL-6, and a low reactivity for IRF4/MUM1 were favourable prognostic indicators. In contrast, BCL-2 expression and presence of a monotypic cytoplasmic immunoglobulin expression was associated with an unfavourable prognosis in univariate analyses. Meta-analysis of these data resulted in the development of a cumulative immunohistochemical outcome predictor score (CIOPS) enabling the recognition of four distinct prognostic groups. Multivariate analysis proved this score to be independent of the international prognostic index. Such a cumulative immunohistochemical scoring approach might provide a valuable alternative in the recognition of defined risk types of aggressive B-cell lymphomas.
    Journal of Hematopathology 11/2009; 2(4):187-94. DOI:10.1007/s12308-009-0044-x
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    ABSTRACT: Very recently a gene marker panel that allows the mutational analysis of APC, CTNNB1, B-RAF and K-RAS was conceived. The aim of the present study was to use the 4-gene marker panel covering the Wnt and Ras-Raf-MEK-MAPK signalling pathways to determine the percentage of sporadic colorectal carcinomas (CRC) carrying at least one of the four above-mentioned genes in a mutated form alone and/or in combination with microsatellite instability (MSI) and to compare the sensitivity of the gene marker panel used in this study with that of gene marker panels previously reported in the scientific literature. CTNNB1 and B-RAF were screened by PCR-single-strand conformation polymorphism analysis and K-RAS gene mutations by restriction fragment length polymorphism analysis. For the mutational analysis of the APC gene mutation cluster region (codons 1243-1567) direct DNA sequencing was performed. The U.S. National Cancer Institute microsatellite panel (BAT25, BAT26, D2S123, D5S346 and D17S250) was used for MSI analysis. It could be shown that about 80% of early stage CRC (UICC stages I and II) and over 90% of CRC in the UICC stage IV carried at least one mutated gene and/or showed MSI. No significant increase in the gene mutation frequencies could be determined when comparing tumours in the UICC stage I with those in UICC stage IV. When compared with previously published gene marker panels the 4-gene marker panel used in the present study shows an excellent performance, allowing to detect genetic alterations in 80-90% of human sporadic CRC samples analyzed.
    09/2009; 33(2):123-9. DOI:10.1016/j.canep.2009.05.001
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    ABSTRACT: To compare retrospectively the outcome of testis-sparing surgery (TSS) to radical orchiectomy (RO) in patients with Leydig cell tumor (LCT). Between 1992 and 2008, 16 patients with LCT of the testis were identified. All but 1 tumor could be detected by ultrasonography. Alpha-fetoprotein and beta-human chorionic gonadotropin levels were normal in all patients. Eight patients underwent RO (mean age at surgery 42 years [27-61]; median tumor size 12.9 mm [10-25]) and the remaining 8 underwent TSS (mean age at surgery 34 years [18-49]; median tumor size 8.6 mm [4-23]). Staging (abdominal computed tomography and chest x-ray or thoracic computed tomography) was negative in all patients. Median follow-up was 77 months (17-186) after RO and 42 months (1-86 months) after TSS. There was no local recurrence or metastasis in patients after RO. A metachronous LCT was removed from the spermatic cord 29 months after TSS of the ipsilateral testis in 1 patient. Another patient underwent surgical exploration of the testis 31 months after ipsilateral TSS because of a suspicious lesion identified in ultrasonography; a tumor was ruled out by histopathology. In the medium term, TSS is a safe procedure in patients with LCT <25 mm.
    Urology 08/2009; 74(2):370-2. DOI:10.1016/j.urology.2009.03.014 · 2.13 Impact Factor
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    ABSTRACT: The nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARgamma) is a key transcription factor regulating genes involved in adipogenesis, glucose homeostasis and cell differentiation. Moreover, PPARgamma has been demonstrated to control proliferation and apoptosis in various cancer cells. We investigated the biological effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's adenocarcinoma cells in vitro and in vivo. PPARgamma mRNA and protein were overexpressed in endoscopic biopsies of Barrett's epithelium and the human Barrett's adenocarcinoma cancer cell line OE33 as compared to normal esophagus and stomach and the esophageal squamous epithelium cancer cell line Kyse-180. PPARgamma activation by pioglitazone in OE33 cells in vitro led to reduced cell growth by induction of apoptosis. Effects of systemic PPARgamma activation by the thiazolidinedione pioglitazone on tumor cell proliferation and apoptosis were then assessed in vivo in nude mice bearing transplantable Barrett's adenocarcinomas derived from OE33 cells. Unexpectedly, enhanced growth of OE33 derived transplantable adenocarcinomas was observed in Balb/c nu/nu mice upon systemic pioglitazone treatment due to increased cell proliferation. These results indicate that PPARgamma is involved in the molecular pathogenesis of Barrett's adenocarcinoma formation and growth. However, activation of PPARgamma exerts differential effects on growth of Barrett's adenocarcinoma cells in vitro and in vivo emphasizing the importance of additional cell context specific factors and systemic metabolic status for the modulation of PPARgamma action in vivo.
    Journal of Gastroenterology 07/2009; 44(9):919-29. DOI:10.1007/s00535-009-0086-y · 4.02 Impact Factor

Publication Stats

2k Citations
283.18 Total Impact Points

Institutions

  • 1997–2009
    • University of Wuerzburg
      • • Department of Internal Medicine II
      • • Institute for Pathology
      • • Department of Pathology
      Würzburg, Bavaria, Germany
    • Pathologisches Institut Bremerhaven
      Bremerhaven, Bremen, Germany
  • 2003
    • Universität Ulm
      • Department of Internal Medicine
      Ulm, Baden-Württemberg, Germany