Katja Schuster

Technische Universität Dresden, Dresden, Saxony, Germany

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Publications (4)14.56 Total impact

  • Pathology - Research and Practice 12/2004; 200(4):259-259. DOI:10.1016/S0344-0338(04)80419-9 · 1.40 Impact Factor
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    ABSTRACT: Renal cancer consists of a heterogeneous tumor group which is characterized by complex cytogenetic and molecular genetic abnormalities. In this study, three different techniques were applied to screen renal cancers for genetic alterations. We studied 99 primary, sporadic renal cancers (96 renal cell carcinomas and three other renal cancers) by a comparative evaluation of different microsatellite markers, comparative genomic hybridization (CGH) and AP-PCR. The AP-PCR produces a genomic fingerprint after an AluEI DNA restriction digest of tumor DNA samples. Microsatellite alterations were investigated using nine microsatellite markers spanning well-known regions of FhiT and VHL (3p14.2, 3p26) but also of oncogenes and tumor suppressor genes like Myc-L1 and TP53Alu (1p32, 17p13.1). To receive a genomic fingerprint, AP-PCR was carried out for all patient samples. Performing AP-PCR, only one case out of 99 displayed genomic imbalance. Seven of 99 investigated primary renal cancers showed alterations in up to four microsatellite loci (TP53Alu, Myc-L1, D3S1300, D3S1560, D3S1317, D3S4260). Three markers (Bat25, Bat26, REN) did not reveal any aberrations within the tested tumor samples. Six cases with microsatellite alterations and four without were examined by CGH. Five samples yielded aberrations, four of them were positive for microsatellite alterations. Only one tumor sample displayed microsatellite alterations, shift patterns in AP-PCR and alterations analyzed by CGH. Our data suggest that genomic aberrations found by microsatellite analysis are also detectable by CGH with the restriction of a minimum of alterated DNA of >10 Mb. Based on this study of RCC and in contrast to other reports for solid tumors, we conclude that AP-PCR is far less informative in investigation of renal cancers.
    International Journal of Molecular Medicine 07/2004; 13(6):835-42. DOI:10.3892/ijmm.13.6.835 · 2.09 Impact Factor
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    ABSTRACT: Few studies have investigated the loss of heterozygosity and microsatellite instability in soft tissue sarcomas. Therefore, we analyzed samples of human soft tissue sarcomas to determine the status of the chromosomal region 12q14-15, which contains the MDM2 gene encoding the well-known counterpart of the tumor suppressor p53. In addition, we determined whether an amplified MDM2 gene was present in the samples. Of the 88 soft tissue sarcoma samples, 24 (27%) showed evidence of loss of heterozygosity of markers representing 12q14-15, and 12 (14%) showed evidence of microsatellite instability. Of the 72 samples analyzed by semiquantitative polymerase chain reaction, 15 (21%) possessed an amplified MDM2 gene. Loss of heterozygosity (P =.008) and microsatellite instability (P =.035) were significantly more common in Stage I tumors than in higher stage tumors. This result indicated that these alterations occur early in soft tissue sarcoma progression and possibly define a subgroup of soft tissue sarcoma. Surprisingly, MDM2 amplification in soft tissue sarcoma patients was associated with a prognosis better than that of patients without the amplification; however, this difference was not statistically significant (P =.6). Furthermore, of the tumors with an MDM2 amplification, 40% (6/15) also experienced loss of heterozygosity at 12q14-15; in contrast, only 16% of tumors without an MDM2 amplification (9/57) underwent a loss of heterozygosity. A concomitant occurrence of deletions and amplifications resulting from deficiencies in the nonhomologous end-joining pathway could in part explain this finding.
    Modern Pathology 12/2003; 16(11):1109-16. DOI:10.1097/01.MP.0000096045.51700.66 · 6.19 Impact Factor
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    ABSTRACT: Deregulation of DNA mismatch repair is a common mechanism for the development of hereditary nonpolyposis colon carcinoma and related familiar cancers, but it also plays a role in the tumorigenesis of sporadic cancers. Although the protein expression of the two main components of DNA mismatch repair, hMSH2 and hMLH1, has been described in soft tissue sarcoma (STS) patients, its prognostic impact is yet to be determined. The authors investigated the expression of the DNA repair proteins hMSH2 and hMLH1 by Western blot analysis in tumor samples of 57 STS patients. The correlation between the expression of hMSH2/hMLH1 and survival was studied in a Cox proportional hazards regression model, which was adjusted for the prognostic effects of staging, tumor entity, and radicality of tumor resection. Nine of 57 STS (16%) showed reduced expression of hMSH2 and reduced expression of hMLH1 was detected in seven STS patients (12%). In a Kaplan-Meier analysis, the median survival for patients with reduced expression of the hMSH2 protein was 18 months, whereas the patients with a normal expression of hMSH2 survived for an average of 68 months. A multivariate Cox proportional hazards regression model revealed a significant correlation between the reduced expression of the hMSH2 protein and poor survival (relative risk = 4.7; 95% confidence interval [CI]: 1.3-17.2; P = 0.019). Reduced expression of the hMSH2 protein is an independent negative prognostic factor for STS patients.
    Cancer 05/2003; 97(9):2273-8. DOI:10.1002/cncr.11326 · 4.89 Impact Factor

Publication Stats

35 Citations
14.56 Total Impact Points


  • 2004
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2003
    • Martin Luther University of Halle-Wittenberg
      • Institute for Pathology
      Halle-on-the-Saale, Saxony-Anhalt, Germany
    • St. Jude Children's Research Hospital
      Memphis, Tennessee, United States