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Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

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A<br />

B<br />

C<br />

Fig. 1.47 A t(X:1) RCC. Note tubular and papillary architecture. B t(X:17) renal carcinoma. Note alveolar growth pattern and clear cells. C t(X:1) RCC. Note compact<br />

nested architecture. D t(X:1) RCC. Note papillary architecture with foam cells.<br />

D<br />

Fig. 1.48 Xp 11.2-translocation renal carcinoma.<br />

Note strong nuclear labeling of the tumour cells.<br />

TFE3 protein expression.<br />

Fig. 1.49 Xp11 translocation carcinomas. Partial<br />

karyotypes showing t(X;1)(p11.2;q21) in a renal<br />

tumour from a male (courtesy of Dr. Suresh C.<br />

Jhanwar) and a t(X;17)(p11.2;q25.3) in a renal<br />

tumour from a female. The positions of the breakpoints<br />

are indicated by arrows (standard G-banding).<br />

Reprinted and adapted with permission from<br />

P. Argani et al. {109}.<br />

carcinomas and the soft tissue ASPS<br />

contain identical ASPL-TFE3 fusion transcripts,<br />

the t(X;17) translocation is consistently<br />

balanced (reciprocal) in the former<br />

but usually unbalanced in the latter<br />

(i.e. the derivative X chromosome is not<br />

seen in ASPS) {109}.<br />

Prognosis and predictive factors<br />

Very little is known about the clinical<br />

behaviour of these carcinomas. While the<br />

ASPL-TFE3 renal carcinomas usually<br />

present at advanced stage, their clinical<br />

course thus far appears to be indolent.<br />

38 Tumours of the kidney

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