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André N Vis

Publications and source records attributed to André N Vis.

7 recordsLinked to original sources
PubMed2006

Metastatic disease of screen-detected prostate cancer : characteristics at diagnosis.

BACKGROUND: Screening for prostate cancer has not only led to a stage migration, but also to a higher incidence of the disease. A decrease in mortality has occurred in several countries during the same time period. Risk stratification of screen-detected cancers at diagnosis has become more important for the anticipation and interpretation of changing incidence/mortality ratios. METHODS: From 1993 to 1998, 633 men were diagnosed with nonmetastatic prostate cancer in the prevalence screen of the Rotterdam section of the European Randomized study of Screening for Prostate Cancer (ERSPC). The characteristics at diagnosis of men who developed metastatic disease were compared with men without evidence of metastases during follow-up. RESULTS: During the median follow-up of 7.5 years, 41 men developed metastatic disease. After 10 years the metastasis-free survival rate was 89.6%, the overall survival 64.7%. In a Cox-model 2logPSA (prostate-specific antigen), biopsy Gleason score and the number of biopsy cores with prostate cancer were independent predictors for the development of metastases; the latter only predicted metastases that presented within 60 months of follow-up. CONCLUSIONS: The metastasis-free survival of men with prostate cancer detected in a prevalence screening was very high. Whether this was related to the beneficial effects of screening or to overdiagnosis due to screening (or both) remains unclear. The prognostic factors known for clinically diagnosed disease also hold for screen-detected disease.

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PubMed2006

Should we replace the Gleason score with the amount of high-grade prostate cancer?

OBJECTIVES: The stage and grade shift of currently diagnosed prostate cancer has led to a diminished prognostic power of the Gleason score system. We investigated the predictive value of the amount of high-grade cancer (Gleason growth patterns 4/5) in the biopsy for prostate-specific antigen (PSA) and clinical relapse after radical prostatectomy. METHODS: PSA-tested participants (N=281) of the European Randomized Study of Screening for Prostate Cancer (ERSPC) who underwent radical prostatectomy were analyzed. Besides clinical features, and serum-PSA, histopathologic features as determined in the diagnostic biopsy and matching radical prostatectomy specimen were related to patient outcome. RESULTS: At a median follow-up of 7 yr, 39 (13.9%), 24 (8.5%), and 12 (4.3%) patients had PSA >/=0.1 ng/ml, PSA >/=1.0 ng/ml, and clinical relapse after radical prostatectomy, respectively. Using Cox proportional hazards, PSA level (p=0.002), length of tumour (p=0.040), and length of high-grade cancer (p=0.006) in the biopsy, but not Gleason score, were independent prognostic factors for biochemical relapse (PSA >/=0.1 ng/ml) when assessed as continuous variables. In radical prostatectomies, the proportion of high-grade cancer (p<0.001) was most predictive of relapse (PSA >/=0.1 ng/ml). For PSA >/=1.0 ng/ml and clinical relapse, the amount of high-grade cancer, both in the biopsy specimen (p=0.016 and p=0.004, respectively) and radical prostatectomy specimen (p=0.002 and p=0.005, respectively), but not Gleason score, was an independent predictor. CONCLUSIONS: In biopsy and radical prostatectomy specimens of surgically treated prostate cancer, the amount of high-grade cancer is superior to the Gleason grading system in predicting patient outcome. We propose that, in addition to the Gleason score, the amount of Gleason growth patterns 4/5 in the biopsy (whether absolute length or proportion) should be mentioned in the pathology report.

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PubMed2006

The actual value of the surgical margin status as a predictor of disease progression in men with early prostate cancer.

OBJECTIVES: The surgical margin status after radical prostatectomy for prostate cancer has long been considered a powerful prognostic factor, as well as an important risk factor for local recurrent disease after radical prostatectomy. In this study, a critical analysis of the predictive value of the surgical margin status was performed. METHODS: A well-described cohort of 281 participants of a population-based randomized screening trial who underwent radical prostatectomy between 1994 and 2000 was analyzed. Besides pathologic tumor stage, Gleason score, percentage of high-grade cancer, and tumor volume, the prognostic value of the surgical margin status for disease outcome (prostate-specific antigen [PSA] relapse, local recurrence) was statistically evaluated. Specifically, site ('apical' or 'circumferential') and extent of surgical margin negativity ('negative', or 'close') or positivity ('focal' or 'extensive') was assessed. RESULTS: At a median follow-up of 7 yr (range, 5-120 mo), 39 (13.9%) and 7 (2.5%) men had biochemical failure (PSA >/=0.1ng/ml), and local relapse, respectively. The surgical margin status was positive in 66 (23.5%), with 26 (9.3%) at the prostatic apex. The margin status was an independent statistically significant risk factor for biochemical relapse, though not for local relapse. Of those with positive margins, 22 (33.3%) had PSA relapse and 4 (6.1%) had local recurrence, whereas these figures were 17 (7.9%) and 3 (1.4%) for those with a negative surgical margin, respectively. The extent of margin positivity was not predictive of PSA relapse nor was the site of the surgical margin. CONCLUSIONS: In surgically treated prostate cancer, the surgical margin status has, although being a statistically significant prognostic factor, only limited predictive value for PSA relapse and local recurrent disease. The majority of men with (extensive) positive surgical margins will not experience PSA relapse nor local disease progression, even in absence of adjuvant radiotherapy. So, cases with a positive margin of resection may still be cured, although the procedure in itself was not 'radical'.

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PubMed2005

Comparison of screen detected and clinically diagnosed prostate cancer in the European randomized study of screening for prostate cancer, section rotterdam.

PURPOSE: This report provides a comparison of characteristics detected in the screening and control arms of the European Randomized study of Screening for Prostate Cancer, section Rotterdam. MATERIALS AND METHODS: Between December 1993 and January 1999, 35,148 men 55 to 74 years old were randomized to European Randomized study of Screening for Prostate Cancer Rotterdam, including 17,635 in the screening arm and 17,513 in the control arm. Prostate specific antigen testing, digital rectal examination, transrectal ultrasound and sextant biopsies were offered to all participants in the screening arm according to 2 algorithms. All screening detected cancers and cancers found in the control arm were evaluated at the same cutoff point, that is January 1, 2003. To identify prostate cancer cases in the control arm yearly linkage was performed with the Rotterdam Cancer Registry database. Followup information was collected by chart review. RESULTS: By January 1, 2003, 1,269 cancers were detected in the screening arm and 336 were detected in the control arm. A shift to more favorable clinical stages and histological grades on biopsy was seen in the screening arm of the trial. T1C and T2 cancers were 5.8 and 6.2 times more often diagnosed, respectively, in the screening arm than in the control arm of the trial. Only 4.6% of control arm cancers were found through opportunistic screening. CONCLUSIONS: Although a favorable shift in prognostic factors was seen for the screening arm of the trial, these results do not provide evidence that prostate cancer screening has an effect on prostate cancer mortality.

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PubMed2004

FGFR3 and P53 characterize alternative genetic pathways in the pathogenesis of urothelial cell carcinoma.

Fibroblast growth factor receptor 3 (FGFR3) and P53 mutations are frequently observed in bladder cancer. We here describe the distribution of FGFR3 mutations and P53 overexpression in 260 primary urothelial cell carcinomas. FGFR3 mutations were observed in 59% and P53 overexpression in 25%. Interestingly, FGFR3 and P53 alterations were mutually exclusive, because they coincided in only 5.7% of tumors. Consequently, we propose that they characterize two alternative genetic pathways in urothelial cell carcinoma pathogenesis. The genetic alterations were reflected in the pathology and the clinical outcome, i.e., FGFR3 mutations were found in low-stage/-grade tumors and were associated with a favorable disease course, whereas P53 alterations were tied to adverse disease parameters.

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PubMed2003

Molecular grading of urothelial cell carcinoma with fibroblast growth factor receptor 3 and MIB-1 is superior to pathologic grade for the prediction of clinical outcome.

PURPOSE: Fibroblast growth factor receptor 3 (FGFR3) mutations were recently found at a high frequency in well-differentiated urothelial cell carcinoma (UCC). We investigated the relationship between FGFR3 status and three molecular markers (MIB-1, P53, and P27kip1) associated with worse prognosis and determined the reproducibility of pathologic grade and molecular variables. PATIENTS AND METHODS: In this multicenter study, we included 286 patients with primary (first diagnosis) UCC. The histologic slides were reviewed. FGFR3 status was examined by polymerase chain reaction-single strand conformation polymorphism and sequencing. Expression levels of MIB-1, P53, and P27kip1 were determined by immunohistochemistry. Mean follow-up was 5.5 years (range, 0.4 to 18.4 years). RESULTS: FGFR3 mutations were detected in 172 (60%) of 286 UCCs. Grade 1 tumors had an FGFR3 mutation in 88% of patient samples and grade 3 tumors in 16% of patient samples. Conversely, aberrant expression patterns of MIB-1, P53, and P27kip1 were seen in 5%, 2%, and 3% of grade 1 tumors and in 85%, 60%, and 56% of grade 3 tumors, respectively. In multivariate analysis with recurrence rate, progression, and disease-specific survival as end points, the combination of FGFR3 and MIB-1 proved independently significant in all three cases. By using these two molecular markers, three molecular grades (mGs) could be identified: mG1 (mutation; normal expression), favorable prognosis; mG2 (two remaining combinations), intermediate prognosis; and mG3 (no mutation; high expression), poor prognosis. The molecular variables were more reproducible than pathologic grade (85% to 100% v 47% to 61%). CONCLUSION: The FGFR3 mutation represents the favorable molecular pathway of UCC. Molecular grading provides a new, simple, and highly reproducible tool for clinical decision making in UCC patients.

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