Characterization of alternative pathways and possible CNAs associated with the deletion 17p in progenitor clones with t(4;14). Key cytogenetic translocations resulting in CNAs for risk are indicated inside of clones. Note: FISH probes depicted in cartoon are 1q12 (red) and 1q21 (green) and chromosome arm colors are 1 (yellow), 17 (blue), 18 (auburn). Subclone A depicts clones of patient 12, B of patient 36, and C of patient 46. Arrows indicate probable derivation of subclones. The JT1q12 instability originates from a triradial of 1q (second from left), which results in an extra copy of the JT1q12 translocating to different RCs (subclones A-C). Subclone A shows that the JT1q12 can translocate directly to chromosome 17 resulting in a der(1;17) with a whole-arm loss of 17p and gain of 1q21 and a high-risk subclone. Subsequent subclones are also high risk, although JT1q12s can be lost as micronuclei (A₁) and/or reconfigure on the same or different RC and 1q21 CN and remain stable (A₂). In subclones B and C, different sequential translocations of JT1q12 result in high-risk subclones as well. Subclone B demonstrates the JT1q12 translocation first to18p in an intermediate risk clone and second to 17p, resulting in a high-risk subclone (B₁). The detection of the high-risk clone (B₁) 5 months before the detection of the intermediate-risk progenitor clone (B) in this patient suggests that alternating dominance or clonal tiding had occurred. In subclone C, the JT1q12 first translocates to the 18q23 telomere, resulting in a der(1;18) chromosome aberration and an intermediate-risk subclone. The second JT1q12 translocation from 18q23 to17 results in a high-risk clone with a focal amplification of 18q23, gain of 1q21, and deletion of 17p (C₁).