The effect of race/ethnicity on prostate cancer treatment outcome is conditional: a review of Wayne State University data.

PURPOSE: The mortality rate for prostate cancer in black American men (AAMs) is 2 times greater than that in other ethnic groups. However, there is considerable controversy as to whether race/ethnicity is an independent predictor of survival outcome. We present conditions in which race/ethnicity is and is not an independent predictor of survival outcomes. MATERIALS AND METHODS: We examined the conditions of age, stage and year of diagnosis, and the role of race/ethnicity on disease-free survival in men who underwent consecutive radical prostatectomy as monotherapy from 1990 to 1999. Data were collected from 229 AAMs and 562 white American men prospectively in the Karmanos Cancer Institute Prostate cancer data bases. RESULTS: When the majority of the cohort had pathologically organ confined disease, race/ethnicity was not an independent predictor of disease-free survival. When the majority of the cohort had a mean age of 70 years or greater, race/ethnicity was not an independent predictor. In studies done in the late 1990s, when the stage of radical prostatectomy cases had shifted toward pathologically organ confined disease as the dominant stage, race/ethnicity was not an independent predictor. However, if the cohort was diagnosed at younger age and/or with more advanced prostate cancer, race/ethnicity became an independent predictor. In the early 1990s there was pathologically advanced disease in the majority of our cohort. CONCLUSIONS: Race/ethnicity as an independent predictor of prostate cancer is conditional and dependent on age, stage and year of diagnosis. Year of diagnosis is associated with a stage shift to earlier staged prostate cancer from the early to late 1990s. In general, study cohorts are often subranges of the entire spectrum of prostate cancer that are limited by these factors, especially stage at diagnosis and treatment. If diagnosed and treated early enough, although there is evidence suggesting that AAMs have more aggressive disease biologically, the role of race as a factor in outcome is significantly decreased. The age factor is more complex and must be discussed in more detail.

Prostate Cancer - Old Problems and New Approaches. (Part II. Diagnostic and Prognostic Markers, Pathology and Biological Aspects).

Diagnostic and prognostic markers for prostatic cancer (PCa) include conventional protein markers (e.g., PAP, PSA, PSMA, PIP, OA-519, Ki-67, PCNA, TF, collagenase, and TIMP 1), angiogenesis indicator (e.g., factor VIII), neuroendocrine differentiation status, adhesion molecules (E-cadherin, integrin), bone matrix degrading products (e.g., ICPT), as well as molecular markers (e.g., PSA, PSMA, p53, 12-LOX, and MSI). Currently, only PSA is used clinically for early diagnosis and monitoring of PCa. The histological differential diagnosis of prostatic adenocarcinoma includes normal tissues such as Cowper's gland, paraganglion tissue and seminal vesicle or ejaculatory duct as well as pathological conditions such as atypical adenomatous hyperplasia, atrophy, basal cell hyperplasia and sclerosing adenosis. A common PCa is characterized by a remarkable heterogeneity in terms of its differentiation, microscopic growth patterns and biological aggressiveness. Most PCa are multifocal with signi ficant variations in tumor grade between anatomically separated tumor foci. The Gleason grading system which recognizes five major grades defined by patterns of neoplastic growth has gained almost uniform acceptance. In predicting the biologic behavior of PCa clinical and pathological stages are used as the major prognostic indicators. Among the cell proliferation and death regulators androgens are critical survival factors for normal prostate epithelial cells as well as for the androgen-dependent human prostatic cancer cells. The androgen ablation has been shown to increase the apoptotic index in prostatic cancer patients and castration also promotes apoptotic death of human prostate carcinoma grown in mice. The progression of PCa, similarly to other malignancies, is a multistep process, accompanied by genetic and epigenetic changes, involving phenomenons as adhesion, invasion and angiogenesis (without prostate specific features).