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. Author manuscript; available in PMC: 2011 Feb 14.
Published in final edited form as: Clin Cancer Res. 2009 Jan 15;15(2):485–491. doi: 10.1158/1078-0432.CCR-08-0933

Fig. 1.

Fig. 1

Detection of RET/PTC rearrangements and BRAF mutation in recurrent PTC. A, RET/PTC1 rearrangement from patient #39 was detected in total RNA. The positive control (+control) was cDNA made from TPC-1 cells (positive for RET/PTC1 rearrangement), and negative control (−control) was cDNA made from NPA87 cells (BRAF mutated and no RET/PTC rearrangements). B, total RNA was prepared from paraffin-embedded tissues (from patients #10, #18, #25, #28, #42, #47, #48, and #57) and RT-PCR was done to detect RET/PTC 2 or RET/PTC3 rearrangement (arrow). The PCR product was visualized on a 2% agarose gel stained with ethidium bromide. Actin was used as a control. The positive controls for RET/PTC2 and RET/PTC3 were plasmids containing the cDNAs of each gene and negative controls were buffer only without any cDNA added. C, PCR product of exon 15 of BRAF from patients with dual mutations (#18, #25, #28, #42, and #57) was sequenced with forward primer (left) and reverse primer (right). Arrows, the transition from T to A by forward primer and A to T by reverse primer.