Holger Moch
University of California, San Francisco
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Featured researches published by Holger Moch.
Human Pathology | 1995
Urs Wagner; Guido Sauter; Holger Moch; Hedvika Novotna; Rita Epper; Michael J Mihatsch; Frederic M. Waldman
Frequent recurrences and multicentricity of bladder cancer suggest that alterations of the urothelium distant from the tumor may be relevant to prognosis. In this study immunohistochemistry and fluorescence in situ hybridization (FISH) were used to examine expression of p53, erbB-2, and epidermal growth factor receptor (EGF-r), genomic aberrations, and tumor cell proliferation (Ki67 LI) in normal and dysplastic urothelium. Biopsy specimens examined included normal urothelium (n = 40), mild dysplasia (n = 34), moderate dysplasia (n = 18) and carcinoma in situ (CIS; n = 20). Several different oncogene expression patterns were found, only some of which were associated with dysplasia. EGF-r expression was equally frequent in normal and dysplastic urothelium and showed a strong association with Ki67 LI (P < .0001). A purely superficial erbB-2 positivity was present in both normal and dysplastic biopsies. However, diffuse erbB-2 positivity and p53 overexpression were both associated with advanced dysplasia (P < .0001 each). FISH analysis showed erbB-2 gene amplification and p53 deletions in selected CIS, as well as a marked chromosome 17 copy number heterogeneity in all six CIS examined. These findings indicate a considerable genomic instability in bladder CIS. They show that both erbB-2 and p53 are altered during malignant transformation. Detectable oncogene expression alone, however, is not diagnostic of malignancy in bladder urothelium.
Genes, Chromosomes and Cancer | 1996
Joseph C. Presti; Holger Moch; Victor E. Reuter; Danh Huynh; Frederic M. Waldman
Renal oncocytomas are uncommon tumors of the kidney that are considered to be of low malignant potential. Neither conventional cytogenetic nor restriction fragment length polymorphism analyses have identified consistent genetic alterations in their genomic DNA. The purpose of the present study was to identify the genetic alterations associated with the development of renal oncocytomas. We studied 13 renal oncocytomas by using comparative genomic hybridization, and we identified loss of genetic material from chromosomes 1 and/or 14 in six of these tumors. These alterations may represent early genetic events in the development of these tumors. Genes Chromosom Cancer 17:199–204 (1996).
Acta Cytologica | 1996
Guido Sauter; Georg E. Feichter; Joachim Torhorst; Holger Moch; Hedvika Novotna; Urs Wagner; Ursula Dürmüller; Frederic M. Waldman
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.
Human Pathology | 1994
Holger Moch; Guido Sauter; Michael J Mihatsch; F. Gudat; R. Epper; F. Waldman
Tumor proliferation in bladder cancer is associated with tumor behavior. To assess the association between Ki-67 labeling index (LI), p53, and c-erbB-2 overexpression, formalin-fixed tissue samples of 160 patients with transitional cell carcinoma (TCC) of the urinary bladder were studied by immunohistochemistry. Ki-67 LI was strongly associated with tumor stage (P < .0001), tumor grade (P < .0001), and p53 status (P = .0014) but not with erbB-2 overexpression (P > .2). Ki-67 LI was higher in p53-positive tumors (19%) than in p53-negative tumors (14%) when all stages were compared. Ki-67 LI was independent of p53 expression in pTa tumors (p53-positive, 9%; p53-negative, 11%), showing that p53 overexpression alone is not sufficient to induce rapid tumor cell proliferation in pTa tumors. Ki-67 LI also was independent of p53 expression in pT2 to pT4 tumors (p53-positive, 20%; p53-negative, 23%), indicating that p53 expression is not necessary for rapid tumor cell proliferation in advanced stages. However, there was a striking difference in Ki-67 LI between p53-positive pT1 tumors (22.0% +/- 8.8 standard deviation [SD]; n = 20) and p53-negative pT1 tumors (9.7 +/- 8.3 SD; n = 22; P = .0001). These results suggest that increased proliferation in p53-positive pT1 tumors is caused by additional alterations that occur during tumor progression.
The Journal of Urology | 1998
Joseph C. Presti; Holger Moch; Arnold B. Gelb; Danh Huynh; Frederic M. Waldman
PURPOSE To identify the genetic alterations associated with renal adenomas. MATERIALS AND METHODS We analyzed 37 renal adenomas obtained at autopsy (23 papillary and 14 non-papillary) by comparative genomic hybridization. RESULTS In papillary tumors, the median number of gains and losses of genetic material per tumor was 2.0 and 1.0, respectively. Papillary tumors were characterized predominantly by gains of genetic material on chromosomes 7 (57%), 17 (35%), 16 (26%), 12 (26%), 3 (22%), 20 (22%) and loss of a sex chromosome (83%). In 6 papillary tumors less than or equal to 5 mm. in diameter, gain of chromosome 7 occurred in 4 specimens. Initiating events for papillary renal adenomas include gain of chromosome 7 and loss of a sex chromosome. In non-papillary tumors, the median number of gains and losses of genetic material per tumor was 1.0 and 1.0, respectively. Non-papillary tumors were characterized by loss of genetic material on chromosome 3p (50%), loss of a sex chromosome (36%) and a gain of chromosome 5 (43%). The initiating event for non-papillary renal adenomas is the loss of chromosome 3p. CONCLUSIONS Renal adenomas demonstrate similar genetic alterations as clinically detected renal cell carcinomas. Their clinically indolent course may, in part, be a result of the lower number of genetic alterations per tumor than their clinically detected counterparts. Renal adenomas are thus small carcinomas which have not yet acquired the necessary genetic alterations leading to tumor progression.
Cytometry | 1995
Guido Sauter; Holger Moch; Thomas C. Gasser; Michael J. Mihatsch; Frederic M. Waldman
Eichelberg, Christian; Chun, Felix K; Bedke, Jens; Heuer, Roman; Adam, Meike; Moch, Holger; Terracciano, Luigi; Hinrichs, Kristin; Dahlem, Roland; Fisch, Margit; Schlomm, Thorsten; Sauter, Guido; Minner, Sarah (2013). Epithelial cell adhesion molecule (EPCAM) is an independent prognostic marker in clear cell renal carcinoma. International journal of cancer. Journal international du cancer, 132(12):2948-2955. | 2013
Christian Eichelberg; Felix K. Chun; Jens Bedke; Roman Heuer; Meike Adam; Holger Moch; Luigi Terracciano; Kristin Hinrichs; Roland Dahlem; Margit Fisch; Thorsten Schlomm; Guido Sauter; Sarah Minner
Swiss Medical Forum ‒ Schweizerisches Medizin-Forum | 2017
Kirsten D. Mertz; Bettina Bisig; Silvia Azzarello-Burri; Anita Rauch; Benno Röthlisberger; Laurence de Laval; Gieri Cathomas; Luigi Terracciano; Wolfram Jochum; Aurel Perren; Holger Moch; Peter J. Wild; Karel Heinimann
Senologie - Zeitschrift für Mammadiagnostik und -therapie | 2012
Manfred Dietel; Ralf Kronenwett; Werner Schlake; Kerstin Bohmann; Roland Penzel; Karsten Weber; Heinz Höfler; Ulrich Lehmann; Peter Schirmacher; Katja Specht; Margaretha Rudas; Hans-Heinrich Kreipe; Peter Schraml; Gudrun Schlake; Zsuzsanna Bago-Horvath; Frank Tiecke; Holger Moch; Markus Schmidt; Judith Prinzler; Dontscho Kerjaschki; Bruno V. Sinn; Martin Filipits; Christoph Petry; Carsten Denkert
Archive | 2011
Ferran Algaba; Hideyuki Akaza; Guido Martignoni; Holger Moch; Rodolfo Montironi; Victor R. Reuter