Introduction

The "Partin tables" were originally developed by urologists Alan W. Partin, M.D., Ph.D., and Patrick C. Walsh, M.D. based on accumulated data from hundreds of patients who had been treated for prostate cancer.

Ingeniously correlating the three things that were known about a man's disease -- PSA level, Gleason score, and estimated clinical stage -- the tables were designed to help men and their doctors predict the definitive pathological stage (determined after surgery, when a pathologist examines the removed prostate for the presence of cancer) and best course of treatment.

Now the tables have been updated to reflect the trends in presentation and pathologic stage for men newly diagnosed with clinically localized prostate cancer at James Buchanan Brady Urological Institute. Clinicians can use these nomograms to counsel individual patients and help them make important decisions regarding their disease.

Nomograms

Tables I to IV demonstrate the probability of presenting with the various pathologic stages when the preoperative serum PSA, biopsy Gleason histologic grade, and clinical stage (AJCC 1992) are known. The updated nomograms have modified PSA groups and Gleason sum groups. The PSA groups are divided into five categories: 0 to 2.5, 2.6 to 4.0, 4.1 to 6.0, 6.1 to 10, and more than 10.0 ng/mL to further substratify men with respect to their PSA level. Additionally, we substratified the Gleason scores into modified groups based on the risk of recurrence. In previous work from our institution, Kaplan-Meier actuarial survival curves (data not shown) for men with follow-up of more than 8 years demonstrated that biochemical progression free survival for tumors with Gleason score 2 to 4 were similar, as were those with a within-the-groups Gleason score of 5 to 6 and 8 to 10. ⁷

Thus, these Gleason scores were subgrouped as 2 to 4, 5 to 6, or 8 to 10. Likewise, previous data have also demonstrated that Gleason sums of 3 +4=7 and 4 +3 =7 behave differently and warrant substratification.⁸

Like our previous nomograms, PSA, Gleason score (biopsy), and clinical stage contributed significantly to the prediction of pathologic stage in the multinomial log-linear progression (P < 0.001). Also, as seen in our previous nomograms, similar results were seen when PSA was used as a continuous variable and all two-way and three-way interactions were tested and added little to the statistical significance of the final model (P > 0.05). The final model contained only the main effects, and the combination of the three variables predicted better than any single variable. The medians (95% confidence intervals [CIs]) of the predicted probabilities from the multinomial log-linear regression analysis of 1000 bootstrap samples from the original study group are presented in the nomograms (Tables I to IV). The numbers within each cell of the nomogram represent the percentage of likelihood of a given pathologic stage based on the regression of all three variables combined. For example, a man with a preoperative serum PSA level of 2.7 ng/mL and a biopsy Gleason score of levels less than 10.0 ng/mL, and nonpalpable (Stage T1c) disease. This dramatic change in presentation, which may be due to PSA and better screening strategies, has nonetheless caused a major stage migration for prostate cancer, with nearly 60% of newly diagnosed cases presenting with localized or regional disease.¹ Our methods for predicting the pathologic stage, which were primarily developed from data collected from men treated before this stage migration,2-4 must also evolve to allow us to make accurate predictions for men newly diagnosed with prostate cancer. For this reason, we have updated our nomograms ("Partin Tables") to better represent the demographic, clinical, and biochemical data of men presenting with prostate cancer in 2001. Like our previous tables, simple, easily obtainable variables were used (se-rum PSA, biopsy Gleason score, and clinical stage [AJCC TNM-1992]) and combined into simple-to-use tables.

Several patients and physicians who used the previous nomograms ² suggested that an individual with a serum PSA level of 4.1 ng/mL must have a higher probability of organ-confined disease than an individual with a PSA of 10.1 ng/mL with the same stage and Gleason score (eg, T2c and 3 +4 = 7). Intuitively, this seemed obvious; however, the previous tables "lumped" these men into the same group and provided limited differentiation with respect to the likelihood of the various pathologic stages. In the previous (1997) nomograms, both men would have had a likelihood of organ-confined disease of 25%; the new (2001) nomograms provide the first man with a likelihood of organ-confined disease of 31% (95% CI 23% to 41%). The second would have only an 11% (95% CI 7% to 17%) chance of organ-confined disease and no overlap in the confidence intervals. Additionally, two men with similar PSA levels (eg, 5.2 ng/mL) and similar digital rectal examination results (eg, T2a) might have a biopsy Gleason score of 3 +4 = 7 (44% chance of organ-confined disease, 95% CI 39% to 50%) compared with a man with a biopsy Gleason score of 4 + 3 = 7 who has only a 33% chance of organ-confined disease, 95% CI 25% to 41% (little overlap in confidence intervals). The further stratification of the Gleason groups and the PSA groups are provided to better capture the actual probabilities of the various pathologic stages for the individual patient.

The primary value of these updated "Partin Tables" will be for counseling patients regarding the probability of their tumor being a specific pathologic stage, rather than a strict decision-making tool. The nomograms may help patients and their treating physicians make informed decisions based on the probability of a pathologic stage, the individual patient's risk tolerance, and the values they place on the various potential outcomes. In addition, the use of these nomograms may aid in the rational selection of patients to undergo definitive therapy for prostate cancer with the hope of further improving the numbers and percentage of cancers that receive effective therapy that will cure the disease.

Conclusion
We have updated our nomograms for predicting pathologic stage for prostate cancer with a more contemporary cohort of men treated between 1994 and 2000. The new nomograms combine PSA, biopsy Gleason score, and clinical stage with improved substratification of both Gleason and PSA groups. The new "Partin Tables" may help us counsel our patients regarding their likelihood of having various pathologic stages and aid in important decision making.

References

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