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World Health Organization Classification of Tumours Pathology and ...

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ABCFig. 1.47 A t(X:1) RCC. Note tubular <strong>and</strong> papillary architecture. B t(X:17) renal carcinoma. Note alveolar growth pattern <strong>and</strong> clear cells. C t(X:1) RCC. Note compactnested architecture. D t(X:1) RCC. Note papillary architecture with foam cells.DFig. 1.48 Xp 11.2-translocation renal carcinoma.Note strong nuclear labeling <strong>of</strong> the tumour cells.TFE3 protein expression.Fig. 1.49 Xp11 translocation carcinomas. Partialkaryotypes showing t(X;1)(p11.2;q21) in a renaltumour from a male (courtesy <strong>of</strong> Dr. Suresh C.Jhanwar) <strong>and</strong> a t(X;17)(p11.2;q25.3) in a renaltumour from a female. The positions <strong>of</strong> the breakpointsare indicated by arrows (st<strong>and</strong>ard G-b<strong>and</strong>ing).Reprinted <strong>and</strong> adapted with permission fromP. Argani et al. {109}.carcinomas <strong>and</strong> the s<strong>of</strong>t tissue ASPScontain identical ASPL-TFE3 fusion transcripts,the t(X;17) translocation is consistentlybalanced (reciprocal) in the formerbut usually unbalanced in the latter(i.e. the derivative X chromosome is notseen in ASPS) {109}.Prognosis <strong>and</strong> predictive factorsVery little is known about the clinicalbehaviour <strong>of</strong> these carcinomas. While theASPL-TFE3 renal carcinomas usuallypresent at advanced stage, their clinicalcourse thus far appears to be indolent.38 <strong>Tumours</strong> <strong>of</strong> the kidney

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