Fig. 4

crb adult heterozygotes have an increased susceptibility to cancer. (A) Percentage of wild-type or crb heterozygous fish that developed tumors after MNNG treatment. (B–E) The most common tumors seen in crb heterozygotes after MNNG treatment (C and E) and the corresponding wild-type structures (B and D). (Scale bars: Left, 200 μm; Right,50 μm.) (B) Sagittal section through normal zebrafish eye. Lens (L), retina (R), and normal choroidal vascular plexus (VP) are shown. (C) Vascular neoplasm arising in the retinal vascular plexus and pushing the retina to the center of the eye. The tumor is composed of plump, atypical endothelial cells forming vascular channels. (D) Sagittal section through normal zebrafish testis containing spermatogonia located at the tubule periphery (white arrowhead), spermatocytes with more condensed nuclei (white asterisk), and fully differentiated spermatozoa (white arrow). (E) Testicular germ cell tumor where the lobular architecture of the testis is completely effaced by a massive proliferation of undifferentiated spermatogonia. Spermatocytes and spermatozoa have been replaced by the tumor. (F) Enrichment plot of the B-myb signature genes in the human lung adenocarcinoma data set. The plot shows the location of the B-myb signature genes (blue bars) in the gene list ranked by the p53 phenotype. The running enrichment score as a function of position in the gene list is shown in red. The signal-to-noise scores of all 7,129 genes in the gene list are shown in gray, with positive scores representing markers for the p53 mutant class and negative scores representing markers for the p53 wild-type class. The signature genes are clearly overrepresented at the left side of the gene list, representing their enrichment in the p53 mutant class.