Cytogenetic analysis and molecular anatomy of t(11;22)(q13;q11)/CCND1-IGL. (A) G-banding karyotype showing t(11;22)(q13;q11) (arrows). The karyotype was 47,XY,add(6)(q21),−9,t(11;22)(q13;q11),+2mar[12]/46,XY[8]. (B) FISH of chromosome preparations using the IGH/CCND1 DF probe, consisting of red-labeled CCND1 and green-labeled IGH. G-banding and FISH picture captured through the triple-bandpass filter are aligned. Hybridization signals are indicated by arrowheads of their respective colors. (C) FISH using the CCND1 BA probe, consisting of green-labeled centromeric 5′ CCND1 and red-labeled telomeric 3′ CCND1, followed by the IGL BA probe, consisting of red-labeled centromeric 5′ IGL and green-labeled telomeric 3′ IGL. G-banding and FISH captured through the rhodamine and FITC filters are aligned, and hybridization signals are indicated by arrowheads of their respective colors. (D) Top: Schematic diagram of 11q13/CCND1 and 22q11/IGL in the centromere (cen) to telomere (tel) orientation. Sequences of the primers for CCND1 (forward) and IGL (reverse) are described in supplemental Figure 5. Breakpoints are indicated by open arrows. The gray open arrows are the positions of the breakpoints determined by Komatsu et al (chr11:69 653,420/1 and chr22:22 905,055/6).⁷  Bottom: Nucleotide sequences of the CCND1-IGL junction (accession number LC582849) and deduced amino acids designated by the single-letter code. Twenty-two nontemplated nucleotides inserted at the junction are underlined. Vertical lines indicate nucleotide identity. Each breakpoint was chr11:69 651,255/6 and chr22:22 904,994/5 (open arrows). Amino acid residues reported to be mutated in MCL or non-hematologic cancers are underlined.¹⁹  FITC, fluorescein isothiocyanate.