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Invasive Urothelial Carcinoma

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  • Progression to invasive urothelial cancer is believed to occur via 2 molecular pathways: hyperplasia/papillary (70-80%) and flat/dysplasia (20-30%) pathways, both are associated with chr. 9 losses at initiation.
    • Majority in flat pathway progress to invasive carcinoma (image A), and is associated with abnormalities in p53 and Rb genes.
    • Hyperplasia pathway is associated with HRAS and EGFR mutations, and although has high recurrence (~70%), only few (~15%) progress to invasive cancer.

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  • Histology:
    • Invading urothelium shows irregular nests, single cell infiltration or tentacular finger-like projections (image B), (image C), & (image D).
    • Invasive component may show with higher grade or more cytoplasm (squamoid) than overlying non-invasive component ("paradoxical differentiation").
    • Stromal response such as desmoplasia, retraction or inflammation.
  • Assess level of invasion for staging.
    • Presence and status of involvement of muscularis propria (pT2) should be reported in TURBT for adequate staging.
  • May undergo spindle cell change that resemble sarcoma* (sarcomatoid carcinoma) and may have malignant heterologous components (termed carcinosarcoma, such as component of malignant skeletal muscle – rhabdomyosarcoma, bone – osteosarcoma or cartilage – chondrosarcoma).
    • Has poorer prognosis than usual urothelial carcinoma.

* Vast majority of sarcomas are composed of spindle cells and that this cell type almost characterizes sarcoma entity; carcinomas are mostly of polygonal cell morphology.