Figure 2.
The molecular classification of MM. Data from the COMMpass study (clinical trial identifier: NCT0145297) are summarized, showing the 5 nonoverlapping subgroups and their associated gene expression, CNVs, SVs, and SNVs. The pinwheels show the expression of CCND, MAF, NSD2, and FGFR3 for individual patients in each group. Gains of chromosomes (or arms) are shown in blue (1 copy) or purple (>1 copy). For illustration, the hyperdiploid subgroup is further subdivided into those with (HRD11-positive) and without (HRD11-negative) trisomy 11, and the patients without translocations or hyperdiploidy are labeled nHRD2 (MM, NOS). Mutations of FGFR3 (black) and PRKD2 (gray) are common in NSD2, whereas mutations of CCND1 (black) and IRF4 (gray) are common in CCND. A variety of different mutations can activate NF-κB (TRAF3, BIRC2/3, and others). Adverse secondary events include biallelic inactivation of CDKN2C, TP53, or RB1. MYC SVs are most common in hyperdiploid MM.

The molecular classification of MM. Data from the COMMpass study (clinical trial identifier: NCT0145297) are summarized, showing the 5 nonoverlapping subgroups and their associated gene expression, CNVs, SVs, and SNVs. The pinwheels show the expression of CCND, MAF, NSD2, and FGFR3 for individual patients in each group. Gains of chromosomes (or arms) are shown in blue (1 copy) or purple (>1 copy). For illustration, the hyperdiploid subgroup is further subdivided into those with (HRD11-positive) and without (HRD11-negative) trisomy 11, and the patients without translocations or hyperdiploidy are labeled nHRD2 (MM, NOS). Mutations of FGFR3 (black) and PRKD2 (gray) are common in NSD2, whereas mutations of CCND1 (black) and IRF4 (gray) are common in CCND. A variety of different mutations can activate NF-κB (TRAF3, BIRC2/3, and others). Adverse secondary events include biallelic inactivation of CDKN2C, TP53, or RB1. MYC SVs are most common in hyperdiploid MM.

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