Atypical findings in prostatectomy specimen reports are rare, in our series less than 6%. DA is the most common tumor variant[1] and is part of the epithelial group neoplasms[2]. DA is often mixed with the acinar-type [1] (in our series all were mixed-type). Only one of our patients presented with obstructive symptoms, even though previous reports state they are common. The high percentage of biochemical recurrence in our study may be explained by the worse prognosis for ductal compared to acinar adenocarcinomas. 

Even though most prostate adenocarcinomas show few and dispersed NE cells, only 5-10% show accumulations of neoplastic NE cells, a category known as “focal NE differentiation in conventional prostatic adenocarcinoma”[3]. Our two cases fall into this category and both elevated PSA (contrary to literature)[3], which may be related to higher histological grades at diagnosis. 

In two cases reported the imaging findings of NE tumors were similar to the ones in other anatomic locations[4]. In our cases, the NE differentiation did not show a characteristic image behavior.

RS account for most of the sarcomas of the prostate[5]. Patients usually present obstructive urinary symptoms and a palpable mass[6] just like ours. RS appears in image as a large bulky heterogeneous pelvic mass that may infiltrate periprostatic/vesical tissues. Diffusion restriction and contrast enhancement may vary due to different cellular composition[6][7]. Our case has remarkably similar behavior to what is described in the literature, presenting as a large mass centered in the TZ, with bladder wall and seminal vesicle invasion (Fig. 2). 

The incidence of MA in our study does not differ from the literature (0.2 – 0.4 % of all prostate adenocarcinomas)[8][9]. Clinically, prostate MA is silent in early stages but eventually may present aggressively when invading the urethra and bladder[8]. Updated MA Gleason grading contradicts previous beliefs that all these tumors where always aggressive and this subtype of tumor does not implicate a poor prognosis[9]. 

Due to the extracellular proteinaceous fluid component, the MA usually presents with high T1 and T2 signal[6]. Nevertheless, the mucinous tumor in our study showed a mild-low signal on T2-WI, which may be explained by its location in the PZ[10]. In addition, MA does not show restricted diffusion, as in our case[8]. In our experience, this tumor showed a mild enhancement (Fig. 3). 

Most cases of GP are idiopathic but it may also develop as a consequence of previous intravesical BCG therapy (as one of our patients). GP may mimic prostate cancer both clinically (PSA elevation) and radiologically[11]. 

The most common radiological pattern of GP has a tumor-like appearance, showing a mass with T2-WI hypointense signal (when the granulomatous inflammation is located in the PZ). The non-necrotic granulomatous foci show restricted diffusion due to high cellularity and a moderate enhancement[12]. In addition, there may be associated infiltration of the periprostatic fat by inflammation, thus mimicking extraprostatic tumor extension[13]. Our three cases presented this MRI pattern. It is worth noting that all showed an atypical mild high T1-WI signal (Fig. 4). The second MRI pattern presentation of GP is a result of caseous necrosis[11][12] but apparently, none of our cases showed this appearance. 

Localized prostate amyloidosis is an extremely rare condition. The presence of amyloid deposits can change the texture of the gland and elevate PSA because of its inflammatory nature. The relation between aging and amyloid deposits could explain its association with adenocarcinoma of the prostate. Amyloid prostatitis may resemble acinar tumors at MRI[6]. Our case, however, did not show any features different from normal prostate tissue.