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. 2020 May 8;21(9):3323. doi: 10.3390/ijms21093323

Figure 5.

Figure 5

Computational Models of Non-Del(5q) MDS Patients with Genetic Mutations and Uninformative Karyotype. MDS patient-specific gene copy number variations, gain-of-function gene mutations, and loss-of-function gene mutations were computationally modeled and lenalidomide treatment digitally simulated. Two-dimensional maps showing intracellular pathways show the mechanisms of lenalidomide sensitivity in (A) RUNX1 mutant MDS. (B) Lenalidomide resistance was observed in non-del(5q) MDS cases harboring mutations in SF3B1 and TET2. Arrowed lines indicate agonistic relationship. Barred lines indicate antagnostic relationship. Line colorations are to assist the human eye in discriminating among the pathways. Somatic genes in dark blue boxes indicate copy number variation (CNV) deletions (DEL) derived from cytogenetic abnormalities. Somatic genes in light green indicate CNV amplifications (AMP) derived from cytogenetic abnormalities. Somatic genes with mutations resulting in loss of function (LOF) are indicated in light blue boxes. Somatic genes with mutations resulting in gain of function (GOF) are indicated in dark green boxes.