Cancer‐specific and non‐cancer‐related mortality rates in European patients with T1a and T1b renal cell carcinoma

OBJECTIVE

To examine cancer‐specific and non‐cancer‐related mortality rates in 451 patients with T1a–bN0M0 renal cell carcinoma (RCC) treated with either radical or partial nephrectomy (RN or PN) in Europe.

PATIENTS AND METHODS

Between 1987 and 2007, 451 patients with T1a–bN0M0 RCC were treated for histologically confirmed RCC with RN or PN at one of seven participating European institutions. The preoperative American Society of Anesthesiology (ASA) score was available for all patients and was used to control for baseline comorbidities. The preoperative glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease study group equation. We used univariate and multivariate competing‐risks regression analyses to test the effect of the ASA score, GFR, T stage (T1a vs T1b) and nephrectomy type (RN or PN) on RCC‐specific mortality and non‐RCC‐related mortality.

RESULTS

In patients with T1a–b RCC cancer‐ specific mortality was unaffected by stage, nephrectomy type or GFR. Conversely, non‐RCC‐related mortality was strongly affected by the ASA score and GFR. Unlike in a previous report, nephrectomy type did not affect non‐RCC‐related mortality. This lack of significance relative to RN may stem from the relatively high rate of PN use in the present series.

CONCLUSION

PN or RN virtually eliminate the risk of cancer‐specific mortality in patients with T1a–b RCC. Poor preoperative ASA score and impaired renal function appear to represent relative contra‐indications to surgical management of T1a–b lesions.     

Detection and diagnosis of oral cancer by light-induced fluorescence

BACKGROUND AND OBJECTIVE: New techniques for non-invasive early detection and diagnosis of oral dysplasia and carcinoma are required. Our objective was to determine in the hamster cheek pouch model whether differentiation between the healthy tissue and the different stages of oral premalignancy and malignancy is possible using laser-induced fluorescence after tissue exposure to 5-Aminolevulinic acid (ALA). STUDY DESIGN/MATERIALS AND METHODS: DMBA carcinogenesis was applied to one cheek pouch in 18 hamsters for 0-20 weeks. Prior to sacrifice, 20% ALA was applied to the cheek tissues. Excised cheek tissues were cryosectioned and imaged using fluorescence microscopy with excitation at 405 nm, detection at 635 nm. After fluorescence measurement, H&E staining and histopathological evaluation were performed. RESULTS: Fluorescence intensity was significantly lower in healthy tissue than in pathological tissues. Significantly higher intensities and more "fluorescence hot spots" occurred in severe dysplasia and carcinoma than in healthy tissue, hyperkeratosis, mild and moderate dysplasia. CONCLUSIONS: Light-induced fluorescence after ALA exposure can differentiate between the different stages of premalignancy and malignancy. Its ability to differentiate between healthy tissue and early pathology is particularly interesting     

External validation of a nomogram predicting mortality in patients with adrenocortical carcinoma

OBJECTIVE

To develop nomograms predicting cancer‐specific and all‐cause mortality in patients managed with either surgery or no surgery for adrenocortical carcinoma (ACC).

PATIENTS AND METHODS

The models were developed in 205 patients with ACC and externally validated using 207 other patients with ACC, identified in the 1973–2004 Surveillance, Epidemiology and End Results database. The predictors comprised age, gender, race, stage and surgery status. Nomograms based on Cox regression model‐derived coefficients were used for predicting the cancer‐specific and all‐cause mortality, and were tested using area under the receiver operating characteristics (ROC) curve.

RESULTS

In cancer‐specific analyses, the median survival of patients within the development cohort was 26 months, vs 71 months in the external validation cohort (P < 0.001). In overall survival analyses, the median values were 21 vs 32 months for, respectively, the development and the external validation cohort (P < 0.001). Three variables (age, stage and surgical status) were included in the nomograms predicting cancer‐specific and all‐cause mortality. In the external validation cohort, the nomograms achieved between 72 and 80% accuracy for prediction of cancer‐specific or all‐cause mortality at 1–5 years after either surgery or diagnosis of ACC for non‐surgical patients.

CONCLUSION

Our models are the first standardized and individualized prognostic tools for patients with ACC. Their accuracy was confirmed within a large external population‐based cohort of patients with ACC.     

Factors contributing to the racial differences in prostate cancer mortality

OBJECTIVE: To analyse, in a retrospective cohort study, differences in rates of surgical treatment for prostate cancer between African-Americans and White Americans, and to evaluate the extent to which these differences are associated with disparities in survival rates between these groups. PATIENTS AND METHODS: Clinical, pathological, and demographic data from 4279 men diagnosed with clinically localized prostate cancer between 1980 and 1997 were used. The variables assessed included age, disease stage, tumour grade, comorbidities, treatment method, and socio-economic status (SES). Kaplan-Meier survival curves were generated and compared using log-rank tests. The Cox proportional hazards method was used for analyses involving adjustments for potential confounding factors. RESULTS: The surgical treatment rate was 17% for African-American and 28% for White patients (P < 0.001). In those patients treated conservatively or by radiation therapy, both crude and cancer-specific survival rates were lower for African-Americans than for Whites (P < 0.001). However, for patients undergoing surgery, differences in survival between African-Americans and Whites were not statistically significant. According to our models, SES explained 50% and surgical treatment rates approximately 34% of the differences in survival between African-Americans and Whites. CONCLUSIONS: This analysis suggests that the lower prostate cancer survival rates for the African-Americans in the present population can be largely explained by differences in SES and lower surgical treatment rates. Efforts to increase awareness of treatment options among African-American patients may be a way of improving survival in this group.     

Polymorphisms in the glutathione S-transferase M1, T1, and P1 genes and prostate cancer prognosis

BACKGROUND: Polymorphisms in glutathione S-transferase (GST) genes can increase oxidative stress, which may affect cancer prognosis. The aim of this study was to examine associations between GSTM1, T1, or P1 genetic variants and prostate cancer outcomes. METHODS: A population-based cohort of men (n = 752) from King County, Washington, diagnosed with prostate cancer in 1993-1996, and under long-term surveillance for mortality completed a follow-up survey about prostate cancer recurrence/progression. Cox PH models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for deaths from prostate cancer or other causes and prostate cancer recurrence/progression. RESULTS: There were 50 prostate cancer-specific deaths, 65 deaths from other causes, and 143 recurrence/progressions events during an average 9.6 years of follow-up. The adjusted HR for prostate cancer mortality was 3.8 (95% CI 1.6-8.9) among Caucasian men with the GSTM1-null genotype. There were no differences, however, in mortality from other causes or prostate cancer recurrence/progression between men with GSTM1-null versus not-null genotypes. The GSTT1 and GSTP1 genotypes were not associated with any of these outcomes. DISCUSSION: Results suggest that the GSTM1 genotype may be a useful biomarker to identify patients at higher risk for fatal prostate cancer.