Figure 3.
Distinct patterns of copy-number alterations are observed in different TP53-mutated malignancies. The y-axis indicates the proportion of samples with a copy gain (blue, positive direction) or loss (red, negative direction) overlapping each gene, genome wide. Only mostly diploid samples without evidence of whole-genome doubling and with at least 50% of autosomes copy neutral are included. For the PCAWG data, all tumor types with at least 20 mostly diploid, TP53-mutated samples are included. Data sets included (top to bottom): TP53-mutated AML/MDS (n = 41), wild-type TP53 CBF AML (n = 18), and TP53-mutated lymphoid (B-NHL, n = 20; CLL, n = 6), esophageal (n = 24), hepatic (n = 56), ovarian (n = 23), pancreatic (n = 96), and prostate (n = 43) malignancies. B-NHL, B-cell non-Hodgkin lymphoma; CLL, chronic lymphocytic leukemia.

Distinct patterns of copy-number alterations are observed in different TP53-mutated malignancies. The y-axis indicates the proportion of samples with a copy gain (blue, positive direction) or loss (red, negative direction) overlapping each gene, genome wide. Only mostly diploid samples without evidence of whole-genome doubling and with at least 50% of autosomes copy neutral are included. For the PCAWG data, all tumor types with at least 20 mostly diploid, TP53-mutated samples are included. Data sets included (top to bottom): TP53-mutated AML/MDS (n = 41), wild-type TP53 CBF AML (n = 18), and TP53-mutated lymphoid (B-NHL, n = 20; CLL, n = 6), esophageal (n = 24), hepatic (n = 56), ovarian (n = 23), pancreatic (n = 96), and prostate (n = 43) malignancies. B-NHL, B-cell non-Hodgkin lymphoma; CLL, chronic lymphocytic leukemia.

Close Modal

or Create an Account

Close Modal
Close Modal