Prostate carcinoma (PCa) is one of the most common cancers in men both in terms of incidence and mortality in Poland and worldwide (1).

Prostate cancer predominantly develops (70%) in the peripheral zone of the prostate gland. Approx. 10-15% of PCas are found in the transitional zone, and 15-20% in the central zone (2).

Carcinogenesis within the prostate gland is a biologically complex phenomenon. It typically begins with precancerous changes in the epithelium and progresses to invasive cancer. The processes commonly associated with precancerous changes or co-existing with cancer include prostatic intraepithelial neoplasia (PIN) and typical small acinar proliferation (ASAP). Originally, three PIN forms were recognized, differing by the degree of cellular abnormality and the percentage of abnormal epithelial cells: PIN 1 (benign), PIN 2 (moderate) and PIN 3 (severe) (3). Currently, just 2 PIN types are differentiated, namely low grade and high grade (4). Low grade prostatic intraepithelial neoplasia (LGPIN) has been determined to differ in nature from high grade prostatic intraepithelial neoplasia (HGPIN), as it is associated with cancer only in isolated cases (5, 6), and does not constitute a separate pathomorphological entity (7). PIN is diagnosed based on multiple clearly defined architectural and cytological criteria (8). Several features make PIN a precancerous change. It occurs in the prostate in the fourth and fifth decade of life, and its prevalence grows with age. PIN precedes PCa by a minimum of 5-10 years (9). It is found in approx. 60-90% of PCas and is frequently situated near (< 2 mm) invasive cancer site (5, 9-12). As opposed to PCa, PIN retains an intact or fragmented basal cell layer, hence its presence is not associated with elevated PSA level in blood serum. The percentage of HGPIN found in needle prostate biopsy without coexisting PCa ranges from 0.15-16% (5, 13-20). Prevalence of PCa identified in repeat biopsy of a gland where previously HGPIN was found ranges from 22-100% (5, 6, 18-23).

Atypical small acinar proliferation (ASAP) is a pathological change of the prostatic epithelium that may be indicative of PCa. ASAP consists in the presence of foci of small, atypical glands suspicious for cancer, yet not referred to as cancerous, since their basal membrane is preserved (24). The percentage of ASAP diagnosed in needle biopsy of the prostate gland, without coexistence of cancer, ranges from 1.5-6.3% (5, 13-20), whereas the prevalence of PCa identified in a follow-up biopsy of a prostate gland where ASAP was previously detected ranges from 22-100% (5, 6, 18-23).

Owing to the different morphology of the changes listed above, it should be remembered that when a follow-up prostatic biopsy is conducted, the location of cancerous tissue may differ from the location of previously identified HGPIN, whereas every repeat prostatic biopsy of a gland where ASAP was previously identified should heavily focus on the areas where it was found (21, 23, 25, 26). The process of carcinogenesis (fig. 1) involves mutation of cells in the afore mentioned precancerous changes, which, in turn, leads to dysplastic changes resulting with carcinoma in situ (CIS), and ultimately with invasive carcinoma. The majority of prostatic cancers are multifocal. The multiple foci typically arise in various prostatic zones and are characterized by varying histological grades (27-29).

A crucial element of tissue core examination is identifying their malignancy score. Malignancy is defined according to the rules developed by Donald Gleason (1920-2008) that he originally described in 1966 in the journal “Cancer Chemotherapy Report”, in his paper that had previously been rejected by two major urological journals (30-32). PCa grading according to Gleason scale is at present a universally used method of PCa evaluation.

As a young pathologist, Donald Gleason (fig. 2) worked on the histological interpretation of prostatic cancer at the Minneapolis Veterans Administration Medical Center from 1962. He based his study on the results of 280 prostatic biopsies performed between 1960-1964 (33). The scale he proposed has been in common use since 1978, when it was adopted by the American Cancer Society and approved by the WHO (33, 34).

Gleason scale recognizes 5 PCA malignancy patterns, ranging from 1 (least malignant) to 5 (most malignant) differing predominantly by the architectural features, and, to a lesser degree, by the appearance of the cancerous cells (fig. 3) (35).