Non-Neoplastic Epithelial Proliferative Lesions	Major Neoplastic Lesion(s) in the Clinical/Pathological Differential Diagnosis
• Polypoid-Papillary Cystitis • Nests of von Brunn, Cystitis Cystica, and Cystitis Glandularis • Nephrogenic "Adenoma" (Metaplasia) • Squamous Metaplasia and Related Lesions	• Papillary Neoplasm • Deceptively Benign-appearing Transitional Cell Carcinoma (TCC) (tubular/nested, microcystic, inverted) • Clear Cell Carcinoma • Signet Ring Cell Carcinoma • Squamous Cell Carcinoma
Treatment Effect and Unusual Forms of Cystitis
• Treatment Effect: Radiation Injury & Chemotherapy • Unusual Forms of Cystitis • Amyloidosis	• Transitional Cell Carcinoma • Lymphoma
Reactive Mesenchymal Spindle Cell Lesions
• Inflammatory Pseudotumor Post-operative Spindle Cell Nodule	• Myosarcoma (& other Sarcoma types) • Sarcomatoid Carcinoma • Carcinoma with atypical stromal cells
Ectopic or Misplaced Tissue Within the Urinary Bladder
• Mullerian Lesions: - Endometriosis - Endocervicosis - Mullerianosis • Fallopian Tube Prolapse • Ectopic Prostatic Tissue	• Adenocarcinoma primary versus secondary
Developmental and Related Abnormalities
• Fibroepithelial polyp • Urothelial, Urachal and mullerian duct cysts	• Carcinoma & Sarcoma
Normal Anatomical Structures
• Paraganglia	• Paraganglioma, • Nested TCC • (Sarcoma & Melanoma)

Nests of von Brunn, Cystitis Cystica, and Cystitis Glandularis
Nests of von Brunn and cystitis cystica are two of the most common lesions encountered, and there are several metaplastic lesions that may occur, including glandular differentiation in cystitis cystica, the latter being referred to as cystitis glandularis. Nests of von Brunn are usually an incidental microscopic finding, often present in the trigone region. They may be found in association with mucosal inflammation or with no apparent underlying abnormality. In several autopsy studies, nests of von Brunn were present in 86 to 94 percent of cases, occurring over a wide age range, commonly without inflammation of the bladder mucosa [7, 49, 127] . These nests are not considered to be a risk factor for the development of carcinoma.

Usually nests of von Brunn are not a diagnostic challenge. The nests are just beneath, and typically separate from, the urothelium, with an orderly non-invasive arrangement of smoothly contoured, round, islands of cytologically bland transitional cell epithelial cells surrounded by a basal lamina. Prominent aggregates of nests of von Brunn may resemble an inverted papilloma [103]. When these nests are very numerous with deeper than usual placement in the lamina propria they may have a worrisome microscopic appearance. Florid, hyperplastic collections of nests of von Brunn must be distinguished from the "deceptively bland" or "nested" variant of transitional cell carcinoma [110, 120, 133] . Hyperplastic nests of von Brunn have a non-infiltrative base with the nests extending to the same horizontal level [120]. Typically, transitional cell carcinoma has infiltrative, irregularly distributed, variably sized and shaped nests with angular, pointed contours, set within a reactive stroma, often associated with infiltration by single cells or 2 to 3 cell clusters [133]. It is important to note that nests of von Brunn may have reactive epithelial atypia. In addition they may be secondarily involved by in-situ neoplasia and this must not be mistaken for invasive disease. Carcinomatous nests have a higher proliferation rate, as indicated by MIB-1 immunostaining, and may more often be positive for p53, but the variability of staining precludes relying solely on these markers for a definitive diagnosis in this circumstance [120].

Nests of von Brunn may develop central degenerative changes with microcystic lumina, referred to as cystitis cystica. This is a less common finding, but some have found it in up to 60 percent of bladders upon close inspection [127]. Cystitis cystica may be evident grossly as discrete nodular mucosal elevations ranging in size from 2 to 5 mm. Florid examples may produce a worrisome polypoid fleshy lesion [24]. The cysts typically contain clear or yellowish fluid that appears pink in hematoxylin and eosin stained tissue. The epithelium lining the cysts is cuboidal to flattened, cytologically bland, and often mixed with inflammatory cells. Cystitis glandularis occurs when this epithelium undergoes glandular differentiation with an inner lining of cuboidal to columnar cells that contain abundant mucin. It is readily recognized when there are tall columnar mucinous cells with interspersed goblet cells, closely resembling intestinal epithelium [16, 131] . The intestinal-type epithelium may be extensive, especially in patients with non-functional bladders, and the metaplasia may be complete with Paneth cells and argyrophil-positive endocrine cells [16]. Mucinous metaplasia of the overlying urothelial surface epithelium may be present.

Cystitis glandularis may have a worrisome gross appearance, particularly when it produces a polypoid mass [131]. In most cases, the microscopic distinction of cystitis glandularis from adenocarcinoma is easily achieved as the epithelial structures are mucosal based and arranged just beneath the urothelial surface in an orderly fashion, and the glandular epithelium lacks significant cytological atypia. Occasionally, it may have an appearance that makes this distinction more difficult [110, 131] . Cystitis glandularis can be an extensive lesion, and mucous extravasation into the stroma can occur, but this should not be taken as presumptive evidence of a malignant tumor [51, 131] . Rarely, cystitis glandularis extends to involve the superficial muscularis propria, potentially leading to misinterpretation as an invasive carcinoma [51]. Of course, any degree of atypia, particularly in the intestinal-type of cystitis glandularis, should lead to a thorough evaluation for the possibility of an adenocarcinoma. In the vast majority of cases, the degree of atypicality found in adenocarcinoma of the bladder is far greater than what might be encountered in cystitis glandularis [51].

It appears that, in some cases, there may be a progression of cystitis glandularis to carcinoma. There are reports of close juxtaposition or merging between areas of glandular metaplasia with intestinal-type adenocarcinoma [62] and with the rarely encountered villous adenoma of the bladder [2, 21, 93, 111] . Several cases of prolonged cystitis glandularis of intestinal type with subsequent development of adenocarcinoma have been described [32, 62, 134] , and this has been associated with chronic indwelling catheterization [27]. Similarities of mucin types of secretions found in intestinal-type cystitis glandularis, villous adenoma of the bladder, and adenocarcinoma of the bladder support the concept of a metaplasia to dysplasia to carcinoma progressive sequence or continuum [21, 75] . This concept has been reinforced with the finding of nuclear localization of beta-catenin in intestinal type cystitis glandularis, in association with increased levels of TNFalpha expression, similar to that found in Barrett's esophagus where these molecular events have been shown to be part of the signalling pathway in the progression to adenocarcinoma [14].

Nephrogenic "Adenoma" (Metaplasia)
Nephrogenic adenoma is a distinctive benign lesion typically found in areas of urothelial mucosal trauma, irritation, or inflammation [37, 81, 136] . Most patients will have a history of previous urinary tract instrumentation [83, 84] . It may be an incidental finding or the patient may present with hematuria, dysuria or frequency [83]. The lesion usually occurs in the urinary bladder of adults, more often in men than in women [37, 81, 136] . Uncommonly, it is found in children [47]. It typically involves a single site, but may occur at multiple sites. Most lesions are less than 1 cm in size, but sizes of 1 to 4 cm and greater have been reported [81, 136] . The cystoscopic appearance of nephrogenic adenoma may simulate a papillary, sessile or in-situ carcinoma, or have the appearance of cystitis [83, 84] . In one study, 17/31 (55%) cases were polypoid at endoscopy [83]. The diagnosis is rarely suspected clinically and histopathological examination is required for the diagnosis [83]. One or more recurrences of the lesion can occur. In two recent studies, the lesion recurred in 7 of 31(23%) patients [83] and 5 of 8(63%) patients [84].

Microscopically, nephrogenic adenoma is confined to the urothelial mucosa, at times with a band-like growth. The lesion usually exhibits a range of patterns with variable proportions of each, including tubular, microcystic, solid nested, and papillary patterns [37, 81, 136] . The tubular pattern often predominates and it may be the only pattern present. The tubules are generally small and round, at times closely packed, but often loosely distributed within an inflamed edematous stroma. Branched and elongated tubules may be present. There may be a prominent peri-tubular basement membrane. Gradual transition of the tubules, with progressive tubular dilatation, into microcysts often occurs; and the cysts may be a prominent feature. When present, the papillae are small slender papillary structures found on the mucosal surface. Solid nests of cells are almost always a focal finding, although a limited area may have a diffusely solid pattern [81, 136] . The cells lining the tubules, cysts, and papillae are predominantly cuboidal to low columnar with a small amount of cytoplasm; flattened cells are found in the larger cysts. Hobnail cells are also found in up to 70% of cases [81] and cells with clear cytoplasm may be present. Transitional cell epithelium is absent. The cells are bland with nuclei that are small and dark with a degenerative appearance, or open and vesicular with occasional nucleoli. Mitoses are rare to absent. The lumina may contain eosinophilic material, but overt mucinous differentiation is typically not present.

Although often referred to as a nephrogenic adenoma, this lesion is generally considered a metaplastic epithelial lesion that has been misnamed. There has been some ongoing discussion of the derivation and pathogenesis of this lesion. The immunohistochemical profile provides some support for the urothelial origin of this lesion. The lesional cells are immunoreactive for cytokeratin 7 and 20, and they show a membranous pattern of positivity with uroplakin immunostains [80, 114] . However, one recent study on nephrogenic adenoma of the urinary bladder in renal transplant recipients found chromosomal evidence for derivation of the bladder lesion from renal tubular cells [65]. Of interest, a small number of cases are positive for CD10 and renal cell carcinoma antigen [80], and free PNA lectin receptor sites are found in the epithelial lining of the tubular luminal surface in nephrogenic adenoma and embryonic kidney [28].

One must be aware of the range of appearances of nephrogenic adenoma to avoid its misinterpretation. Of note, the papillary growths are not lined with transitional cell epithelium, and usually characteristic tubules are found in the stroma just beneath the papillae. At times nephrogenic adenoma may have numerous tiny tubules with inspissated eosinophilic luminal contents surrounded by compressed cells, giving an overall appearance that mimics a signet ring cell carcinoma [136]. Uncommonly, low-grade transitional cell carcinoma may form small nests and tubules [110, 133] , requiring careful scrutiny to avoid confusion with nephrogenic adenoma. The neoplastic tubules have a discernable rim of transitional cells, in contrast to the cuboidal or low-columnar cells found in nephrogenic adenoma, and a subtle but appreciable degree of atypia is present in the lining cells. This variant of transitional cell carcinoma will not have a prominent peri-tubular basement membrane, and the mixture of patterns seen in nephrogenic adenoma will not be present. The presence of hobnail cells and clear cells in nephrogenic adenoma may suggest the possibility of clear cell carcinoma, a tumor that very rarely occurs in the bladder [135]. In contrast to nephrogenic adenoma, clear cell carcinoma occurs most frequently in middle-aged to elderly females without a history of injury or inflammation [135]. It typically forms a sizeable destructive mass with a diffusely infiltrating pattern, and there is malignant cytological atypia with increased mitotic activity [9, 79, 135] . There may be associated Mullerian remnant tissue or foci of transitional cell carcinoma may be admixed with the clear cell carcinoma [79].

Squamous Metaplasia and Related Lesions
Squamous metaplasia of the urothelium develops in response to injury and frequently is found next to other metaplastic and reactive lesions such as polypoid cystitis or cystitis glandularis. It is reported to be more common in women than men [126] and is commonly found in chronic cystitis, non-functional bladders, and chronic schistosomiasis of the bladder [139]. Typically a white or grey-white patch is visualized at the time of cystoscopy [128], and dramatic examples of squamous metaplasia with marked keratinization diffusely involving the bladder have been reported [113]. Microscopic examination reveals stratified squamous epithelium, with or without keratinization, that is cytologically bland with orderly maturation. The mucosa often has an undulating or "corrugated" appearance; the metaplastic epithelium may be thickened or thinned. Tangential sectioning with oblique orientation of the mucosal surface may produce squamous epithelial islands and squamous metaplasia may involve nests of von Brunn , but the lack of an infiltrative pattern and the bland cytology will indicate the benign nature of the process. Invasive squamous cell carcinoma, including the extremely rare verrucous carcinoma of the bladder, are usually large destructive masses unlikely to be confused with a metaplastic process [34, 92] . It is important to note that vaginal-type glycogenated non-keratinizing stratified squamous epithelium is present in the trigone and bladder neck region in many women [63]. Similar epithelium has been reported involving the bladder trigone in men who have received estrogen therapy for prostatic carcinoma [44].

Difficulties in interpretation may arise when varying degrees of atypia, including squamous cell carcinoma-in-situ, are encountered. Any degree of atypia should be viewed with suspicion because it may indicate the presence of squamous cell carcinoma elsewhere in the specimen or in adjacent unsampled mucosa. The presence of squamous metaplasia itself may be an indicator of an increased risk for the development of squamous cell carcinoma. With long-term follow-up of up to 30 years, up to 25% of patients with squamous metaplasia subsequently develop squamous cell carcinoma of the urinary bladder [11, 25] . When it occurs, the mean elapsed time from initial diagnosis of squamous metaplasia to the development of carcinoma is 11 years [11]. Rarely, an exophytic papillary squamous cell carcinoma occurs. There is diffuse co-expression of epidermal growth factor receptor and transforming growth factor alpha in hyperplastic keratinizing squamous metaplasia, similar to that found in verrucous carcinoma and well differentiated squamous carcinoma [115]. The presence of metaplastic urothelium in association with superficial bladder carcinoma, be it squamous or glandular metaplasia, may be associated with resistance to intravesical BCG therapy [10].

Condyloma accuminatum has rarely been encountered in the urinary bladder, most often in the trigone and bladder neck in a patient with ano-genital condylomata [26, 56] . The lesion is identified by its characteristic papillomatous thickened squamous epithelium with koilocytotic cells. As at other body sites, condyloma of the urinary bladder may show varying degrees of atypia and transformation to squamous cell carcinoma has been reported [123]. Verrucous carcinoma of the bladder, a very rare tumor found almost exclusively in regions where schistosomiasis of the bladder is endemic [34], is differentiated from a condyloma by its larger downward expansion of invasive bulbous fronds of very well-differentiated squamous epithelium.

Unusual Forms of Cystitis
Many forms of cystitis have been categorized in terms of their predominant pathological appearance. The descriptive categories include eosinophilic [38], follicular [95], emphysematous [90], hemorrhagic [105], encrusted [42], gangrenous [107], and granulomatous [43] cystitis: any of these forms of cystitis may be associated with variable degrees of reactive urothelial atypia that can mimic dysplastic or neoplastic epithelium, and they may have an appearance of a mass. Eosinophilic cystitis has been reported to mimic invasive carcinoma, at times with a palpable mass, especially in children [38]. Of note, the reverse situation can occur: neoplasia may be associated with inflammation. For example, transitional cell carcinoma-in-situ can mimic interstitial cystitis [117]. Rarely, low-grade lymphoma of the urinary bladder occurs and inflammatory infiltrates must always be evaluated with this possibility in mind [5, 58] . A very unusual case of bladder involvement by a myeloproliferative disorder with dysplastic megakaryocytes has been described [50].

Xanthogranulomatous cystitis [122] and malakoplakia [66, 101] are two very rare diseases of the urinary bladder that may cause diagnostic problems because of the infiltrative appearance of large aggregates of histiocytes. Both malakoplakia of the bladder and xanthogranulomatous cystitis typically occur in a middle-aged adult, associated with gram negative urinary tract infection [66, 101, 122] . Malakoplakia of the urinary tract is more common in women than men [101]. Both diseases typically produce multiple yellowish-brown, at times umbilicated, mucosal plaques that are usually less than 2 cm in size. Occasionally, larger polypoid protrusions occur and there may be necrosis, giving a cystoscopic appearance that suggests a neoplasm. Histological examination reveals an accumulation of cytologically bland histiocytes with abundant, vacuolated, variably eosinophilic cytoplasm (von Hansemann cells), typically within the lamina propria just beneath an intact urothelium. In addition to the sheets of histiocytes, malakoplakia has cytoplasmic and extra-cellular targetoid eosinophilic bodies (Michaelis-Gutmann bodies): these microscopic structures are a necessary feature for the diagnosis of malakoplakia. Michaelis-Gutmann bodies are the result of an acquired macrophage defect that gives rise to the accumulation of phagolysosomes containing fragments of bacterial wall that are inadequately and incompletely digested [66, 101, 104] . Michaelis-Gutmann bodies typically contain calcium and iron salts and can be highlighted with special histochemical stains for these substances [104].

Amyloidosis
Amyloidosis of the urinary bladder may occur as a primary disease or be the result of secondary bladder involvement by systemic disease. The more common primary amyloidosis often presents with hematuria and typically produces a nodular or polypoid tumor-like lesion that is potentially mistaken for carcinoma at the time of cystoscopy [3, 17] . Secondary involvement of the bladder by systemic amyloidosis occurs less often, may cause massive hematuria and usually has more of a diffuse erythematous appearance [78]. Primary amyloidosis predominantly involves the stroma of the lamina propria, although vascular involvement may also occur. There may be a foreign body giant cell reaction to the amyloid deposits. Secondary amyloidosis of the bladder predominantly involves the blood vessel walls. Amyloid deposition can be recognized microscopically by its amorphous pink colour and its presence can be confirmed with a Congo red histochemical stain. Electron microscopic examination will reveal a characteristic feltwork of non-branching amyloid fibres [3].

Inflammatory Pseudotumor
Inflammatory pseudotumor of the urinary bladder is a recently described but now well documented benign proliferative mesenchymal spindle cell lesion that may be mistaken for a sarcoma [41, 46, 48, 53, 55, 64, 88, 89] . It has also been referred to as a pseudosarcomatous fibromyxoid tumor [88, 89] . It is a rare lesion that has a non-specific presentation, with painless gross hematuria being the usual symptom. Typically, it arises in a patient with no recent history of urinary tract trauma or infection. The majority of cases have occurred in children and young adults, with only a few cases reported in patients over the age of 50 years [53, 64, 88, 89] . The female:male ratio is about 2:1. Over 85 cases have now been reported and, to date, clinical follow-up of up to 180 months has been uneventful, even in those patients who have been treated with curettage alone [41, 48, 53, 55, 64, 88, 89] . There is a recent report of spontaneous regression of inflammatory pseudotumor of the urinary bladder [68].

Cystoscopy usually reveals an exophytic or polypoid mass. On gross examination the mass is frequently soft and gelatinous [53, 88, 89] . Less commonly, it is a firm white submucosal or intramural nodule [53]. The lesions range in size from a few centimeters up to a reported size of 13 cm [41, 48, 53, 55, 64, 88, 89] .

On microscopic examination, the spindle cells are typically widely separated and haphazardly arranged in a myxoid stroma [53, 55, 64, 88, 89] . There is a prominent network of fine blood vessels with scattered lymphocytic and histiocytic inflammatory cells, giving a granulation tissue-like appearance. Neutrophils and eosinophils may be present. Often there are extravasated red blood cells, and conspicuous large aggregates of red blood cells may form. The cellularity is variable and areas with a vague fascicular arrangement of the spindle cells may be found. In some lesions, areas with a more compact cellularity, at times with a more fascicular arrangement and greater amounts of intercellular collagen, may predominate [53]. This second pattern often has a prominent lymphocytic and plasmacytic inflammatory infiltrate. In both patterns, infiltration into the muscularis propria is common and the lesion may extend through the bladder wall [53, 55, 64, 88, 89] .

The lesional spindle cells have the distinctive morphology of reactive myofibroblasts: bipolar cells with eosinophilic, elongated, tapering cytoplasmic processes that lack striations, and central oval nuclei with smooth nuclear contours, open chromatin pattern, and occasional nucleoli. Rounded and stellate cells may be present. Anaplastic or pleomorphic features are absent. Occasional mitoses may be found but the mitotic activity is typically low and there are no abnormal mitotic figures [53, 55, 64, 88, 89] .

Special studies may be needed to be confident of the diagnosis and to exclude other lesions considered in the differential diagnosis. Procurement of additional tissue may be necessary for this purpose. The spindle cells of an inflammatory pseudotumor are typically immunoreactive for vimentin and muscle-specific actin and negative for epithelial markers. Of note, an occasional case has demonstrated cytokeratin immunoreactivity in the spindle cells [45, 53, 64, 94, 100] , presumably due to cross-reactivity of actin filaments with the cytokeratin antibodies. Cytokeratin positivity is not absolute evidence of an epithelial tumor.

Recently, expression of anaplastic lymphoma kinase (ALK-1) has been detected in inflammatory pseudotumor using immunohistochemical techniques [45, 94] . One study found 5/6 inflammatory pseudotumors immunoreactive for ALK-1 [94] and another found ALK-1 positivity in 6/16 cases [45]. However, fluorescent in-situ hybridization did not detect chromosomal translocation involving the ALK gene in 4 cases that were positive for the ALK-1 immunostain [45]. Sarcomatoid carcinoma and myosarcoma are negative for ALK-1 [94].

Ultrastructural examination reveals myofibroblastic differentiation with abundant rough endoplasmic reticulum and sub-plasmalemmal bundles of thin filaments with focal densities [53]. There is no evidence of fully developed smooth muscle or skeletal muscle differentiation. Flow cytometric analysis of DNA content has generally demonstrated a lack of aneuploidy [53, 64, 89] , although there is one report of an aneuploid cell population in 1 of 2 cases studied [46]. This same study found an abnormality in chromosome 2 (2del(2)p23) in a karyotypic analysis of one case [46]. An inflammatory pseudotumor of the bladder with a chromosomal abnormality involving chromosome 12 has been recently reported [36].

Postoperative Spindle Cell Nodule
Unlike inflammatory pseudotumor, postoperative spindle cell nodule (PSCN) is associated with a recent history of urinary tract trauma, typically within three months of presentation [85, 118] . In one study, the mean age of a patient with PSCN was 65 years, presumably reflecting the greater likelihood of urinary tract instrumentation in the older male population [48]. PSCN, like inflammatory pseudotumor, may simulate a bladder neoplasm clinically and pathologically. Grossly, it may be friable or nodular and firm and it may involve the muscularis propria. PSCN also has a distinctive proliferative myofibroblastic spindle cell phenotype. It is often immunoreactive for vimentin, muscle-specific actin, and desmin. It may be immunoreactive for cytokeratin [125]. Ultrastructural examination reveals myofibroblastic and fibroblastic differentiation [85]. In contrast to inflammatory pseudotumor, PSCN is usually less myxoid, more cellular, and more mitotically active. PSCN and inflammatory pseudotumor may represent the same proliferative pseudosarcomatous spindle cell response at different stages of evolution.

Differential Diagnosis of Proliferative Reactive Mesenchymal Lesions
The major differential diagnosis of inflammatory pseudotumor and PSCN is with sarcoma, sarcomatoid transitional cell carcinoma, and transitional cell carcinoma with pseudosarcomatous stromal reaction. Myosarcomas, such as leiomyosarcoma in an adult or rhabdomyosarcoma in a child, are frequent diagnostic considerations that must be confidently excluded before rendering a diagnosis of inflammatory pseudotumor. Of note, up to 60% of leiomyosarcomas of the urinary bladder have myxoid areas [67]. Inflammatory pseudotumor differs from a leiomyosarcoma by having more variable cellularity, a greater inflammatory component, and a distinct vascularity resembling granulation tissue [53, 55, 64, 88, 89] . In addition, it has myofibroblastic differentiation rather than fully developed features of smooth muscle cells [53]. A rhabdomyosarcoma can be excluded by the lack of a uniform population of small hyperchromatic cells, an absence of a cambium cell layer and a lack of rhabdomyoblasts. Less often, other sarcomas that may involve the bladder such as a liposarcoma or malignant fibrous histiocytoma may be considered, but the diagnostic features of these tumors are not found. The presence of necrosis at the tumor-detrusor muscle interface, along with significant nuclear atypicality, are good indications of a malignant mesenchymal neoplasm [48]. Of note, sarcomas of the urinary bladder are ALK-1 negative, contrasting with the ALK-1 positivity that may be found in inflammatory pseudotumor [94]. Moderate p53 protein nuclear immunostaining may be found in sarcoma whereas there is rare to absent p53 immunostaing in inflammatory pseudotumor of the bladder [48].

Sarcomatoid carcinoma is much more common than sarcoma in the urinary bladder and, if a biopsy reveals an overtly malignant spindle cell lesion, sarcomatoid carcinoma is the most likely diagnosis [54, 138] . It usually occurs in an older patient, and anaplastic malignant cellular features with increased mitotic activity are commonly present [54, 138] . However, these tumors may have myxoid areas with less cytologic atypia, and this is occasionally a conspicuous feature, leading to possible confusion with inflammatory pseudotumor [54, 138] . A thorough examination of all available tissue will often reveal more typical areas of invasive or in-situ transitional cell carcinoma [54]. Immunohistochemical evidence of epithelial differentiation may be helpful in the context of overtly malignant cytological features, and the cytokeratin immunostain can be useful to highlight nests of epithelial tumor cells that may be otherwise overlooked on routine light microscopy [54]. As noted above, if the lesion is not obviously neoplastic, cytokeratin immunoreactivity should be interpreted cautiously. ALK-1 positivity would be supportive evidence for a diagnosis of inflammatory pseudotumor [45, 94] . Ultrastructural examination for evidence of epithelial differentiation may be helpful.

Pseudosarcomatous stroma may occur next to transitional cell carcinoma, and a superficial biopsy may only contain the reactive stromal component, possibly leading to a misdiagnosis of inflammatory pseudotumor [137]. Additional biopsy tissue may be needed, particularly if there is a history of bladder carcinoma. When atypical hyperchromatic stromal cells, sometimes with bizarrely shaped nuclei and a moderate amount of eosinophilic cytoplasm, are identified next to a carcinoma, the lesion may be misdiagnosed as a sarcomatoid carcinoma or carcinosarcoma: a potentially serious diagnostic error as either of these diagnoses indicates a very poor prognosis. A diagnosis of rhabdomyosarcoma may be suggested when these atypical stromal cells occur within a fibroepithelial polyp [129]. It is important to be aware of these atypical stromal cells that can also occur as individually distributed cells within the lamina propria of a bladder without tumor, sometimes but not invariably associated with inflammation or previous chemotherapy or radiation. These atypical stromal cells are vimentin positive and cytokeratin negative [55, 129] .

Mullerian Lesions
There is a spectrum of non-neoplastic lesions of mullerian differentiation that are known to involve the female urinary tract or pelvic peritoneum [61]. Catamenial urinary bladder symptoms indicates a significant likelihood of ectopic or misplaced mullerian tissue, such as endometrial-type or endocervical-type glands within the bladder [76, 119] . It appears that these lesions may either be misplaced tissues related to a previous surgical procedure or arise spontaneously as metaplastic tissue [22, 23, 30, 79] . The presence of 0C125 immunoreactivity in these lesions, along with co-expression of vimentin, cytokeratin, oestrogen and progesterone receptors, is consistent their mullerian derivation. [30, 79] . Rarely, Mullerian lesions such as endometriosis and endocervicosis may undergo malignant transformation to clear cell adenocarcinoma of the bladder [79].

Endometriosis
The most common and well recognized Mullerian lesion is endometriosis: a condition that involves the bladder in about 1 to 2 percent of women with pelvic endometriosis [4, 22, 98, 121] . The bladder is the most common site in the urinary tract to be involved by endometriosis and, although it may be the only apparent site of involvement, most often it is associated with endometriosis elsewhere in the pelvis [4, 22, 74, 98, 99] . It typically presents in a middle-aged woman and uncommonly occurs in post-menopausal women [121]. Vesical endometriosis has been described in men receiving estrogen therapy for prostatic carcinoma [96]. The bladder symptoms are often non-specific, but may be catamenial and associated with symptoms related to other sites of involvement in the female pelvis. Occasionally the condition may clinically mimic interstitial cystitis [98]. Laproscopic segmental bladder resection of endometriosis has been performed [76].

Cystoscopy typically reveals congested, edematous mucosa that may be intact or eroded, often with a dark blue or reddish brown color, although involvement of the deeper regions of the bladder wall by endometriosis may produce little or no mucosal abnormality. The lesions are usually 1 to 4 cm in size; lesions up to 8 cm in size have been reported [74, 98] . Most often endometriosis is found in the posterior wall or the trigone. Light microscopy reveals the typical appearance of endometriosis with scattered areas of mature endometrial glands, occasionally with focal mucinous metaplasia, surrounded by variable amounts of endometrial stroma [4, 22, 74, 98, 99] , often with hemosiderin deposition. Usually these lesions do not produce diagnostic difficulties. Some foci may have inflamed attenuated epithelium or may lack stroma, making their recognition more difficult, but they are unlikely to be confused with a neoplastic process [4, 22] .

Endocervicosis
Endocervicosis, the mucinous analogue of endometriosis, has only recently been reported in the urinary bladder [13, 23, 73, 82] . Diffuse mucinous glands are present, in contrast to endometriosis with mucinous metaplasia where the mucinous change is only a focal finding [74]. Endocervicosis predominantly occurs in the reproductive age group with a peak age frequency in the fourth decade [23, 82] , but it has been reported in women up to 65 years of age [13, 73] . To date, within the urinary tract, endocervicosis has only been identified in the bladder and all of the reported cases have occurred in isolation except for two associated with pelvic endometriosis [13, 23, 73, 82] . One case of a mucin-containing bladder sinus, lined by benign mucinous cells and occasional ciliated cells, has been reported in a 19-year-old woman, possibly representing ectopic cervical tissue [102]. A lesion in the posterior wall of the bladder, containing glands resembling endocervical, endometrial and "hobnail glands", referred to as a paramesonephric remnant with prominent mucinous secretion, has been reported in a 52-year-old woman [13]. Three women, aged 37, 44 and 46 years of age, have recently been reported with a mass in the posterior bladder wall that proved to be a benign mullerian lesion consisting predominantly of endosalpingiosis with minor components of endometriosis and endocervicosis: the term "mullerianosis" was proposed as a unifying term for these lesions [132]. A case of "mullerianosis" of the urinary bladder, associated with tubo-ovarian endometriosis, has been described in a 27-year-old woman who had no previous surgery [30].

Endocervicosis of the bladder may present with a variety of non-specific symptoms including pain, hematuria, frequency, dysuria, urgency and dyspareunia [13, 23, 73, 82] . The symptoms may be severe and persistent, and catamenial exacerbation has been reported [23]. In one report, three of the seven patients had a history of Caesarean section [23]. The lesion may be palpable on bimanual pelvic examination and, at cystoscopy, an intramural mass is seen with overlying intact urothelial mucosa. It lacks the red-blue color of endometriosis, and a mucous discharge may be appreciated at the time of curettage or biopsy. Like endometriosis, endocervicosis is usually found in the posterior bladder wall, and it also may be found in the trigone and posterior bladder dome [23, 73] . There is one reported case of vesical endocervicosis with involvement of the adjacent extravesical pelvic soft tissue [23]. Laproscopic segmental bladder resection of endocervicosis has been reported [72]. Clinical follow-up of up to 14 years in patients with endocervicosis of the bladder has been uneventful [23, 73] .

Gross examination of curettings or biopsy tissue may be unremarkable, but the partial cystectomy specimen usually reveals an ill-defined, intra-mural gray spongy soft tissue mass with mucoid areas and small cysts. The lesion is usually a few centimeters in size, but it may be up to 5 cm in greatest dimension [13, 23, 82] .Light microscopy reveals loosely distributed benign endocervical-type mucin-secreting glands, predominantly in the muscularis propria with, at times, focal extension into the deep lamina propria or the sub-serosal connective tissue [13, 23, 73, 82] . The glands vary in size with irregular shapes ranging from elongated to round and cystic. They lack a confluent growth pattern. There is abundant luminal mucous surrounded by a lining of simple cuboidal to columnar mucous cells with basally located nuclei and prominent apical eosinophilic and vacuolated cytoplasm. Occasional goblet cells may be present and cystic glands may be lined by flattened epithelium. The cells are generally bland; there may be occasional foci of mild to moderate cytological atypia. Mitotic figures are absent in most cases but rarely may be found in the glandular epithelium. The glands are surrounded by smooth muscle or fibrous, at times edematous, tissue. Peri-glandular elastotic stroma is found in some cases. Ruptured glands occur with extravasated stromal mucous that is surrounded by reactive fibroblasts and chronic inflammatory cells with mucin laden macrophages [23, 102] . There may be a prominent neutrophil infiltrate within the mucous. In about one-half of the cases, a careful search reveals a range of mullerian differentiation with focally ciliated tubal-type epithelium, and an occasional endometrial-type gland with a small amount of endometrial periglandular stroma [13, 23, 73] . The overlying urothelium is usually unremarkable, although focal replacement of the transitional epithelium by mucinous epithelium has been observed [23].

Endocervicosis has a pseudoinfiltrative growth pattern, at times with a reactive periglandular stroma, extravasated mucous and focal epithelial atypia, possibly leading to its misinterpretation as a well-differentiated adenocarcinoma [23]. Whenever an unusual bland or low-grade glandular proliferative lesion is encountered in the bladder of a woman, particularly in the reproductive age group, the possibility of a mullerian lesion such as endocervicosis should be considered. The recognition of a range of mullerian differentiation can be a helpful distinguishing feature. The major differential diagnosis includes either a deceptively bland primary adenocarcinoma, or secondary spread of adenoma malignum of the uterine cervix. A primary carcinoma of the bladder can have a very low-grade appearance with a small tubular pattern [110, 133] , but a pattern resembling adenoma malignum, with its distinctive array of irregular glands [39], would be extremely unusual. Secondary spread of adenoma malignum from the uterine cervix can usually be excluded by the absence of a mass in the uterine cervix or by obtaining a negative history in the patient who has had a previous hysterectomy. Usually adenoma malignum has some areas of greater atypia than that found in endocervicosis [39]. Most mucin-secreting adenocarcinomas that involve the urinary bladder, such as primary adenocarcinoma of signet-ring cell or intestinal type, urachal adenocarcinoma, or metastatic adenocarcinoma arising from the gastrointestinal tract, female genital tract, or elsewhere, are overtly infiltrative and cytologically malignant with significantly greater tissue destruction.

Fallopian Tube Prolapse
A case of fallopian tube prolapse into the base of the urinary bladder has been reported, producing a polypoid mass that was clinically interpreted to be carcinoma [6]. It occurred several months following a hysterectomy that was complicated by a vesicovaginal fistula.

Ectopic Prostatic Tissue
Ectopic glandular tissue also occurs in men, in the form of polypoid prostatic tissue. It may be an incidental finding or it may present with hematuria [59, 87] . It usually is found in the trigone, peri-ureteral orifice or interureteric ridge regions [59, 87] . Immunostaining reveals prostatic-specific antigen and prostatic acid phosphatase positivity in the glandular epithelium. Possibly such tissue is a type of metaplasia within altered urothelial mucosa. The prostatic tissue is usually never as extensive in its distribution as can occur with the various forms of mullerian lesions in the female bladder. Although spread of prostatic adenocarcinoma to the bladder may be a consideration, such tumors are usually overtly malignant, and often large, in contrast to the small and obviously bland appearance of ectopic prostate tissue. Benign prostatic hyperplasia can occasionally produce massive intravesical enlargement of the prostate [35].

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