Abstract
A broad spectrum of lesions, including hyperplastic, metaplastic, inflammatory, infectious, and reactive, may mimic cancer all along the urinary tract. This narrative collects most of them from a clinical and pathologic perspective, offering urologists and general pathologists their most salient definitory features. Together with classical, well-known, entities such as urothelial papillomas (conventional (UP) and inverted (IUP)), nephrogenic adenoma (NA), polypoid cystitis (PC), fibroepithelial polyp (FP), prostatic-type polyp (PP), verumontanum cyst (VC), xanthogranulomatous inflammation (XI), reactive changes secondary to BCG instillations (BCGitis), schistosomiasis (SC), keratinizing desquamative squamous metaplasia (KSM), post-radiation changes (PRC), vaginal-type metaplasia (VM), endocervicosis (EC)/endometriosis (EM) (müllerianosis), malakoplakia (MK), florid von Brunn nest proliferation (VB), cystitis/ureteritis cystica (CC), and glandularis (CG), among others, still other cellular proliferations with concerning histological features and poorly understood etiopathogenesis like IgG4-related disease (IGG4), PEComa (PEC), and pseudosarcomatous myofibroblastic proliferations (post-operative spindle cell nodule (POS), inflammatory myofibroblastic tumor (IMT)), are reviewed. Some of these diagnoses are problematic for urologists, other for pathologists, and still others for both. Interestingly, the right identification of their definitory features will allow their correct diagnoses, thus, avoiding overtreatment. The literature selected for this review also focuses on the immunohistochemical and/or molecular data useful to delineate prognosis.
Highlights
Simulators of malignancy are varied and frequently seen in the urinary tract
Some of them remain a challenge for the pathologist who must decide if the submitted material includes any lesion representing one of the many faces of bladder cancer [1], other non-urothelial malignant tumors, or a non-neoplastic lesion
The local immune response produced by Schistosoma hematobium seems to be mediated by IL-4 signaling, which is responsible for the urothelial hyper-diploid hyperplasia occurring in this infection, which seems to be a key precursor of bladder carcinogenesis in the form of squamous cell carcinoma [33]
Summary
Simulators of malignancy are varied and frequently seen in the urinary tract. Benign tumors, as well as infections, reactive inflammations, metaplastic and hyperplastic changes, and other conditions, may eventually mimic malignancy all along the urinary tract, from the renal pelvis to the urethra. Especially Proteus mirabilis and Escherichia coli, have been implicated in its genesis generally associated with infective phosphate lithiasis, especially [29] This condition mimics a tumor, its diagnosis does not preclude malignancy since cases of XI associated with cancer have been reported in the urinary tract [25,30]. The local immune response produced by Schistosoma hematobium seems to be mediated by IL-4 signaling, which is responsible for the urothelial hyper-diploid hyperplasia occurring in this infection, which seems to be a key precursor of bladder carcinogenesis in the form of squamous cell carcinoma [33] This disease is rare in non-endemic areas [32], but it is occasionally detected in non-endemic as a result of migratory movements from/to endemic countries. A faint melanocytic differentiation (HMB-45, Melan-A, etc.) (Figure 5), sometimes coupled with muscle markers expression (desmin, etc.), together with an absence of epithelial markers (cytokeratins, EMA, etc.), is the definitory immunohistochemical hallmark of this entity [64]
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