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Profiles of different subtypes of breast cancer

Sign
Subtypes *
Luminal A
Luminal B
HER2
Basaloid
Quantity ER+/HER2 cells
87 %
82 %
20 %
10 %
Quantity HER2+ cells
7 %
15 %
68 %
2 %
Quantity TNBC cells
2 %
1 %
9 %
80 %
p53 path
TP53 mutation (12 %)
MDM2 increase (14 %)
TP53 mutation (32 %)
MDM2 increase (31 %)
TP53 mutation (75 %)
MDM2 increase (30 %)
TP53 mutation (84 %)
MDM2 increase (14 %)
PIK3CA/PTEN path
PIK3CA mutation (49 %)
PTEN mutation/loss (13 %)
INPP4B loss (9 %)
PIK3CA mutation (32 %)
PTEN mutation/loss (24 %)
INPP4B loss (16 %)
PIK3CA mutation (42 %)
PTEN mutation/loss(19 %)
INPP4B loss (30 %)
PIK3CA mutation (7 %)
PTEN mutation/loss(35 %)
INPP4B loss (30 %)
RB1 path
High expression of RB1
Gain Cyclin D1 (29 %)
Increase CDK4 (14 %)
Low expression ofCDKN2C

Gain Cyclin D1 (58 %)
Increase CDK4 (25 %)

Gain Cyclin D1 (38 %)
Increase CDK4 (24 %)
RB1 mutation/loss (20 %)
Gain Cyclin E1 (9 %)

High expression ofCDKN2A
mRNA expression
High ER cluster
Low proliferation
Low ER cluster
High proliferation
HER2-signature
High proliferation
Basal signature
High proliferation
Number of copies
Increase diploids
Many with quiet genomes
Increase aneuploids
Many with focal amplification
Increase aneuploids
High genomic instability
Increase aneuploids
High genomic instability
DNA mutations
PIK3CA (49 %)
TP53 (12 %)
GATA3 (14 %)
MAP3K1 (14 %)
TP53 (32 %)
PIK3CA (32 %)
MAP3K1 (5 %)
TP53 (75 %)
PIK3CA (42 %)
PIK3R1 (8 %)
TP53 (84 %)
PIK3CA (7 %)
DNA metilation
Hyper-methylation
Hypo-methylation
Protein expression
High estrogen signaling
High cMYB
Subtype responsive to RPPA
Less estrogen signaling
High FOXM1 and cMYC
Subtype responsive to RPPA
High expression of HER1 and HER2
High expression of DNA repair proteins,
PTEN and loss of p-AKT signature