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Bladder Carcinoma

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Bladder Carcinoma 30 Bladder Carcinoma 1. GROSS DESCRIPTION Specimen — urine cytology/bladder washings/cystoscopic biopsy/transurethral resection bladder (TURB)/ cystectomy/cystourethrectomy/cysto- prostatectomy (including seminal vesicles)/cystoprostatourethrec- tomy/anterior or total exenteration (including uterus and adnexae ± rectum). — weight (g) and size (cm). ⎯ length (cm) of ureters and urethra. ⎯ bladder cancer commonly presents with symptoms of painless haema- turia and investigation is by urinary cytology, cystoscopy and biopsy. Cytology is good at designating high-grade papillary, in-situ and inva- sive urothelial neoplasia but poor at separating low-grade papillary lesions from reactive atypia and cellular changes associated with calculi, in-dwelling catheters, recent instrumentation and post- therapy changes. Biopsy is with “cold” cup forceps or a small diathermy loop, the advantage of the former being good preservation of histological detail. Flexible cystoscopy is easier for the patient and allows a wide field of vision but rigid cystoscopy with a larger lumen allows instrument access for transurethral resection of superficial bladder tumours with diathermy to the base (TURBT). Deep biopsy of the muscularis propria is important staging information in inva- sive tumours and may be submitted separately by the urologist. Further staging is by a combination of endoluminal ultrasound, CT and MRI scan. Carcinoma in situ is usually treated by topical chemotherapy (mitomycin) or immunotherapy (bacille Calmette– Guérin (BCG) therapy) or resected by TURB if localized. Widespread disease may necessitate radical surgery. Superficial urothelial cancer confined to the mucous membrane is resected transurethrally with submission of multiple fragments and follow-up by cystoscopy. Adjuvant intravesical therapy is used for high-grade or recurrent disease. Muscle-invasive tumours require radical surgery with cystec- tomy ± in continuity prostatectomy/urethrectomy and regional lym- phadenectomy, and in the female cystourethrectomy or an anterior exenteration. 314 HISTOPATHOLOGY REPORTING Tumour Site — fundus/body/trigone/neck/ureteric orifices. — anterior/posterior/lateral (right or left). — single/multifocal. — diverticulum. Size — length × width × depth (cm) or maximum dimension (cm). Appearance — papillary/sessile/ulcerated/mucoid/keratotic/calcification. — bladder mucosa: erythematous/oedematous (carcinoma in situ). Edge — circumscribed/irregular. 2. HISTOLOGICAL TYPE Transitional cell (urothelial) carcinoma — 90% of cases. ⎯ usual type: papillary or sessile. variants with deceptively benign features: — microcystic type: intraurothelial microcysts containing protein secre- tions mimicking cystitis cystica. — nested type: uniform cell nests in the lamina propria mimicking florid Von Brunn’s nests but with an irregular margin and look for muscle invasion. Potentially aggressive. — micropapillary type: resembles ovarian serous papillary carcinoma. Associated with stromal retraction artefact mimicking lymphovascu- lar invasion. Also shows true LVI and is a high-grade tumour. — inverted type: architecturally similar to inverted papilloma but has WHO II/III cytology. Look for muscle invasion. — also clear cell, plasmacytoid, lipid cell, with pseudosarcomatous stroma (see below), trophoblastic cells (HCG positive) or prominent lymphoid infiltrate (lymphoepithelioma) variants. Squamous cell carcinoma — 5% of cases. — classical/verrucous/basaloid/sarcomatoid, i.e. the same range of tumours as encountered in the upper aerodigestive tract. — old age and associated with calculi, schistosomiasis or diverticulum and chronic infection. Prognosis is poor with a 13–35% 5-year survival and two-thirds are pT3/pT4 at presentation. 30. BLADDER CARCINOMA 315 Adenocarcinoma — the common cloacal embryological origin of bladder and rectum high- lights the range of glandular differentiation that can be seen in the bladder mucosa. — 2% of bladder malignancy. — enteric, mucinous (colloid), signet ring cell, clear cell (mesonephroid), ex villous adenoma, or adenocarcinoma not otherwise specified (NOS). — can arise either from intestinal metaplasia/cystitis glandularis (60%), extrophy, diverticulum or bladder dome wall urachal remnants (30%). Usually muscle invasive and of poor prognosis (particularly signet ring cell carcinoma). Transitional cell (urothelial) carcinoma with mixed differentiation — squamous cell carcinoma/adenocarcinoma components are seen in 20–30% of high-grade invasive transitional cell carcinomas empha- sizing a capacity for divergent differentiation. Spindle cell carcinoma — “sarcomatoid carcinoma” or carcinosarcoma. — old age. Large and polypoid with a poor prognosis (50% dead within 1 year). There may be a recognizable in-situ or invasive epithelial (transitional, glandular, squamous or undifferentiated) component and cytokeratin/vimentin positive spindle cells with varying stromal differentiation, from non-specific fibrosarcoma-like to specific heterologous, mesenchymal differentiation, e.g. rhabdomyosarcoma, chondrosarcoma, osteosarcoma. Small cell carcinoma ⎯ primary or secondary from lung. CAM5.2/synaptophysin/CD56 posi- tive. Aggressive with early metastases to nodes, liver, bone and peri- toneum. May be pure or mixed with other in-situ or invasive bladder cancer subtypes and there is coexistent prostatic disease in 50% of cases. ⎯ large cell neuroendocrine carcinoma also occurs rarely. Undifferentiated carcinoma — no specific differentiation and a high-grade tumour. Malignant melanoma — primary or secondary (commoner). — note there can be spread to bladder from a primary urethral lesion. Metastatic carcinoma — metastases should be considered in any bladder tumour with unusual histology, e.g. adenocarcinoma or squamous cell carcinoma. Knowl- edge of a previous positive history and comparison of morphology are crucial. Metastatic disease in the bladder is usually solitary. 316 HISTOPATHOLOGY REPORTING — direct spread from adjacent pelvic organs (>70% of cases): prostate, cervix, uterus, anus, rectum, colon. To distinguish primary adenocar- cinoma from secondary colorectal carcinoma look for an origin at the dome from mural urachal remnants, or areas of adjacent mucosal intestinal metaplasia/cystitis glandularis in a primary lesion. A previ- ous positive history on cervical smear/biopsy or endometrial sampling raises the possibility of a primary gynaecological tract malignancy. Prostatic cancer is PSA/PSAP positive but CK7/CK20/34βE12 negative, which is the converse of bladder cancer. Note that some poorly differen- tiated or metastatic prostate cancers stain more strongly with polyclonal rather than monoclonal PSA with the potential for a false-negative result using only the latter. — distant spread: breast, malignant melanoma, lung, stomach. 3. DIFFERENTIATION/CYTOLOGICAL GRADE Flat, papillary and invasive urothelial neoplasia are graded separately. There are several classification options, although in the UK the WHO 1973 scheme remains in favour rather than the more recent WHO/ISUP 1998 consensus and WHO 1999 classifications due to concerns about their reproducibility. In general, they are based on the degree of cytoarchitec- tural abnormality characterized by increasing nuclear atypia, hyperchro- masia and crowding with up-regulated proliferative and mitotic activity. Flat urothelial neoplasia: comprises urothelial dysplasia (mild/moder- ate/severe) on a spectrum with, and severe dysplasia equating to, carci- noma in situ (CIS). Urologists will follow up a diagnosis of dysplasia but initiate treatment for CIS which may entail BCG immunotherapy, intrav- esical chemotherapy or surgery. Dysplasia and CIS (syn: low- and high- grade intraurothelial neoplasia, respectively) are to be distinguished from urothelial hyperplasia and regenerative atypia which can be encountered in a range of conditions, e.g. cystitis, calculi, an indwelling urinary catheter or post chemo-/radiotherapy. In addition to morphological clues, dysplasia/CIS overexpresses p53 and Ki-67 with strong, diffuse CK20 staining, whereas non-neoplastic urothelium tends to show only basal layer proliferative activity and CK20 staining of surface umbrella cells. Papillary urothelial neoplasia: papillary urothelial lesions with a spec- trum of minimal to marked cytoarchitectural abnormalities ranging from the very rare benign transitional cell papilloma covered by normal urothelium to the commonplace transitional cell carcinomas WHO I/II/III (G1/G2/G3). A WHO I/G1 carcinoma is the least disordered, being a low-grade lesion with <5% risk of progression to invasion. A WHO III/G3 tumour is the most anaplastic, being high-grade with a 15–40% risk of progression. Thus a papillary neoplasm is typed, graded and assessed for the presence of underlying invasion with comment on the absence or presence of dysplasia or CIS in the represented flat mucosa in the rest of the sample. A comparison of the classifications is given in Table 30.1. Table 30.1 Classification of papillary urothelial neoplasms WHO 1973 Transitional cell papilloma Transitional cell carcinoma WHO 0/G0 WHO I/G1* WHO II/G2† WHO III/G3† WHO/ISUP 1998 Urothelial papilloma Papillary urothelial neoplasm Low-grade urothelial High-grade urothelial carcinoma of low malignant potential carcinoma (PUNLMP) WHO 1999 Urothelial papilloma Papillary urothelial neoplasm Urothelial carcinoma of low malignant potential WHO I/G1 WHO II/G2 WHO III/G3 (PUNLMP) 30. BLADDERCARCINOMA ∗Low-grade disease. †High-grade disease. Note that the columns are not discrete categories
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