• We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Logo of amjpatholAmerican Journal of Pathology For AuthorsAmerican Journal of Pathology SubscribeAmerican Journal of Pathology SearchAmerican Journal of Pathology Current IssueAmerican Journal of Pathology About the JournalAmerican Journal of Pathology
PMC full text:

Figure 1.

An external file that holds a picture, illustration, etc.
Object name is jh0812750001.jpg

A: ALK-11 immunostaining performed on case 1 shows granular cytoplasmic staining confined to the myofibroblastic cells. B: Representative karyotype of case 1 (arrows indicate breakpoints). C: FISH performed on a destained preparation of the metaphase cell in B with a 2p23 breakpoint spanning probe shows a signal split [der(2), arrow, der(17), arrowhead]. Bicolor FISH studies performed on cytological touch preparations of cases 1 (D, left) and 2 (D, right) with probes flanking the 2p23 breakpoint show a split of the Spectrum Orange and Spectrum Green signals in two cells each, indicating disruption of ALK. Normal FISH signals are present in the remaining morphologically smaller and rounder cells (inflammatory cells). E: Portion of agarose gel showing products of second step hemi-nested RT-PCR for CLTC-ALK for case 2. The first step used the CLTC-FWD primer with ALK-REV; the second step used the CLTC-FWD primer with the ALK-3′ primer (see Materials and Methods for primer sequences). No RNA and no R.T. controls refer to lack of RNA or lack of reverse transcriptase, respectively, in the first step. M: portion of size marker PhiX174/HaeIII. F: CLTC-ALK fusion junction sequence from case 1. The identity of all transcripts was confirmed by sequencing.