Natural history of prostate cancer

Although the natural history of prostate cancer (PCa) has not been fully elucidated, it is thought to arise from damaged prostate epithelium and progressively develop over many decades [27]. Prostate disease is heterogeneous and multifocal, further complicating the understanding of its progression. Based on autopsy studies, about one-third of men over the age of 50 years display histological evidence of PCa. However, a majority of these cases remain clinically insignificant, underscoring the variability in PCa and the protracted nature of this disease [3, 28].

The likelihood of disease progression of PCa is difficult to predict. Detection of cancer from a biopsy can result in a localised diagnosis; however, upon a prostatectomy, it may be revealed that the disease had grown outside the margins of the gland or even had metastas-ised. Conversely, certain men diagnosed with PCa may live out their natural lives without suffering any morbidity or mortality from the disease.Therefore, it becomes imperative to determine whether or not a particular lesion will stay localised or spread beyond the confines of the gland [3]. The usually slow progression of prostate cancer allows delaying or avoiding definitive treatment (active surveillance) in selected patients if some prerequisites are fulfilled. The younger a candidate is for active surveillance, the more strict the tumour-related criteria that should be used [29].

Research has revealed insights into the likely progression of prostate tumours. It has been shown that certain high-grade tumours proceed on a more aggressive course than low-grade, well-differentiated tumours and therefore should be managed accordingly [30]. The Gleason score is one of the most powerful prognostic factors in prostate cancer [31]. In elderly patients with clinically localised, conservatively managed prostate cancer, the probability to survive the disease for at least 10 years ranges from 77% to 98% when the Gleason score is 7 or less, whereas this rate is only 33-75% in patients with a Gleason score of 8-10 [32]. The prolonged nature of PCa progression highlights the opportunities for clinical therapeutic interventions that could reduce the risk of disease development and slow it or treat the existing disease. Through the Cancer and Leukimia Group B (CALGB) cooperative study group, Halabi and colleagues performed a polled analysis combining data from 6 trials and more than 1100 patients with CRPC accured from 1991 to 2001 [33], and created a prognostic model for risk stratification of metastatic CRPC patients. The observed median survival durations (in months) were 7.5 (95% confidence interval [CI] 6.2-10.9], 13.4 (95% CI 9.7-26.3],

18.9 (95% CI 16.2-26.3], and 27.2 (95% CI 21.9-42.8] for the first, second, third, and fourth risk groups, respectively. The factors involved in this model can be broadly divided into clinical variables that reflect the condition of the host (eg, performance status, anemia, fatigue), the tumor burden (eg, sites of metastatic disease, PSA level, alkaline phosphatase level), or the biologic aggressiveness of the cancer itself (eg, lactate dehydrogenase [LDH] levels, Gleason sum).

The clinical course of metastatic castration-resistant prostate cancer has changed considerably, primarily because of factors such as earlier diagnosis, stage migration and changes in clinical practice patterns. Earlier initiation of androgen-deprivation therapy and the increased use of diagnostic imaging have contributed to earlier detection of metastatic disease in androgen-deprived patients. Furthermore, new treatments have further extended the time to the terminal phase of the disease, extimating the duration of the course of metastatic castration-resistant prostate cancer measured from the first documented metastasis (in the castrate state) until death may now extend beyond 5 years.

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