Original contributionIdentical clonal origin of synchronous and metachronous low-grade, noninvasive papillary transitional cell carcinomas of the urinary tract☆
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Cited by (37)
Neoplasms of the Urinary Bladder
2020, Urologic Surgical PathologyBladder cancer: Translating molecular genetic insights into clinical practice
2011, Human PathologyCitation Excerpt :However, there is currently no consensus concerning whether multifocal urothelial carcinoma is of monoclonal or oligoclonal origin. Many studies have suggested a monoclonal origin for multifocal TCC [229-240], but other studies have shown an independent origin for some multicentric urothelial tumors using similar methods [231,234,238,239,241-247]. A recent study suggests that both field cancerization and monoclonal tumor spread may coexist in the same patient [216].
p16<sup>ink4</sup> immunoreactivity is a reliable marker for urothelial carcinoma in situ
2008, Human PathologyCitation Excerpt :2) P16INK4 mutation may not play a role in the field effect of carcinogenic agents on urothelium. The field effect is speculated when urinary carcinogenic agents cause genetic alterations and carcinogenic progression in multiple urothelial cells, leading to multiple synchronous or metachronous tumors [36]. The current study showed the lack of immunohistochemical p16INK4 expression in the normal-appearing urothelium adjacent to the high-grade lesions.
Neoplasms of the urinary bladder
2008, Urologic Surgical Pathology: Second EditionBladder cancer, a two phased disease?
2007, Seminars in Cancer BiologyCitation Excerpt :In each case the tumors showed X-inactivating patterns consistent with a monoclonal origin. Li et al. [20] studied 10 patients with both synchronous and metachronous Ta/T1 tumors by X-chromosome inactivation analyses. Tumors from the same patient showed the same X-inactivation pattern indicating a monoclonal origin in all investigated cases.
On the Origin of Syn- and Metachronous Urothelial Carcinomas
2007, European UrologyCitation Excerpt :Thus if tumors A, B, and C in Fig. 1 show inactivation of the same X chromosome as indicated, they are likely to be clonal even though they do not share all late genetic changes. Sidransky et al [4] and Li et al [5] used X-inactivation studies to establish the clonal relationship among syn- and metachronous tumors from a total of 23 patients. In each case tumors from the same patient did show X-inactivating patterns consistent with a monoclonal origin.
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Presented in part at the 87th Annual Meeting of United States and Canadian Academy of Pathology, Boston, MA, February 28, 1998.