Supplemental Figure Legends
Supplemental Figure 1- Myc levels in FVB and transgenic mammary glands
Western blot analysis of total Myc protein (A) and exogenous HA-tagged Myc (B) for the mammary glands from the various strains of MMTV-Myc mice demonstrates Myc levels. Quantification of total
Myc (C) and exogenous HA-tagged Myc (D) protein levels in relation to the Grb2 standard is shown.
Western blot analysis of lysates from non-transgenic FVB mammary glands and mammary glands from the transgenic T58A lines demonstrates the increase in expression relative to wild type controls (E).
Quantification of Myc protein levels in the T58A transgenic lines is also shown(F). FVB Myc levels were standardized to 1.0 in order to reveal the degree of Myc overexpression in the transgenic lines.
Supplemental Figure 2 –The Relationship between Myc Expression and KRas Mutations
Quantitative RT-PCR reveals relative levels of Myc expression in virgin and lactating mammary glands of
WT13, Leder Myc, and TA14 strains. Leder Myc refers to the original line of MMTV-Myc mice (16).
Expression levels were standardized to the virgin WT13 strain and error bars represent the standard deviation between the three experimental replicates (A). The percentage of tumors with KRas mutations in Leder Myc, WT13, and TA14 strains (B).
Supplemental Figure 3 – Types of Activating Mutations in KRas in Myc Induced Tumors and Human
Breast Cancer
The percentage and type of KRas mutations in tumors as reported by the COSMIC database (9056 total tumors) for human cancers as compared with wild type MMTV-Myc (33 tumors) and MMTV-Myc T58A
(24 tumors).

Supplemental Figure 4- KRas mutations occur most frequently in the TA39 strain of EMT tumors
The percentage of tumors featuring KRas mutations for each histological type is shown for the individual strains of MMTV-Myc tumor prone mice.
Supplemental Figure 5 - Principle Components Analysis of Gene Expression Data from Myc Induced
Tumors.
Batch effects between separate array experiments are illustrated with a principle components analysis(A) . Using Bayesian factor regression methods, batch effects were removed as illustrated in the principle components analysis (B).
Supplemental Figure 6- Statistical Analysis of Pathway Probabilities in EMT and Squamous Tumors.
A statistical comparison between EMT and squamous tumors for AKT (p<0.001) (A), E2F1 (p<0.001)(B), p63(p=0.0047)(C), and RhoA (p=0.0437)(D) signal pathway activation probability (A-D respectively).
Supplemental Figure 7- The stabilization of Myc in T58A mammary glands and the decrease of Myc protein levels in EMT-type tumors
A Western blot analysis of total Myc protein and exogenous HA-tagged Myc for tumors from the various strains of MMTV-Myc mice is shown (A-J). Total Myc is shown on the left and HA-Myc on the right for
EMT, microacinar and papillary tumors (when available) for each strain.

Supplemental Figure 8- Quantification of western blot analysis reveals stabilization of Myc in T58A mammary glands and loss of Myc in EMT-type tumors.
Quantification of protein levels from Supplemental Figure 7 for total Myc and HA-Myc are shown for tumors from the various strains of MMTV-Myc mice, in the same order as the previous figure (A-J).
Supplemental Figure 9- Protein levels of total and exogenous Myc correlate with gene signatures of
Myc pathway activation.
Protein levels of total Myc significantly correlate (p=.005, R=.5344) with predicted Myc signaling pathway activation by application of gene signatures (A). Similarly, protein levels of HA-Myc also significantly correlate (p<.0001, R=.7381) with predicted Myc signal pathway activation by application of gene signatures(B).
Supplemental Figure 10- Principle Components Analysis of Gene Expression Data from Myc Induced
Tumors and Human Breast Cancer.
Batch and platform effects between mouse tumor and human breast cancer gene expression data is illustrated with a principle components analysis (A). Using Bayesian factor regression methods, batch and platform effects were removed as illustrated in the principle components analysis (B).

Supplemental 11- Various strains of MMTV-Myc mice develop EMT-type tumors that are similar to
Myc-low human claudin low breast cancer.
MMTV-Myc tumors that are EMT-type and are similar to the Myc-low claudin low human breast cancer subtype contain a demographic of 21% of tumors from the WT21 strain, 29% of tumors from the WT13 strain, 14% of tumors from the TA41 strain, 22% of tumors from the TA39 strain, and 14% of tumors from the TA14 strain.
Supplemental Figure 12- Expression of Human Claudin Low Tumor Markers in Myc Induced EMT-type
Tumors and claudin low tumors.
A comparison of various tumor types of mouse mammary tumors for RMA normalized gene expression levels of markers of human claudin low tumors (A). Similarly a comparison between intrinsic subtypes of human breast tumors for expression levels of markers for human claudin low tumors(B).
Supplemental Figure 13- MMTV-Myc tumors of the EMT-type feature stem cell-like properties
Gene set enrichment analysis comparing EMT-types of MMTV-Myc tumors with other histological types of Myc induced using a signature for genes that are upregulated in mammary stem cells (A). Likewise,
MMTV-Myc tumors of the EMT-type compared to other histological types of Myc induced tumors using a signature for genes that are downregulated in mammary stem cells(B).
Supplemental Figure 14- Statistical Analysis of Pathway Probabilities in Myc-Low Claudin Low Tumors and Myc-High Claudin Low Tumors.
A comparison between the Myc-low and Myc-High human claudin low tumors statistical differences in predicted pathway activation for Akt, β-catenin, E2F1, Myc, p110, and TNFα (A-F respectively) probabilities.

Supplemental Figure 15- Statistical Analysis of Pathway Probabilities in Microacinar-like Luminal B
Tumors and other Luminal B Tumors.
A comparison of β-catenin (p<0.001) and Stat3 (p=0.009) pathway activation between a cluster of predominantly human Luminal B breast cancers that are similar to Myc induced microacinar tumors and another cluster of mainly human luminal B breast cancer (A,B respectively).
Supplemental Figure 16- Human claudin low breast cancers have a high probability of Ras signaling pathway activation.
Ras pathway activation probabilities are shown for human claudin low breast cancer and reveal that nearly 80% of human claudin low tumors have greater than a 0.50 probability of Ras signaling pathway activation.
Supplemental Figure 17- Human claudin low breast cancer and KRas mutant MMTV-Myc tumors of the
EMT-type are not KRas addicted.
Gene set enrichment analysis with a KRas addiction signature compares MMTV-Myc KRas mutant tumors and MMTV-Myc EMT-type KRas mutant tumors by GSEA using a KRas addiction signature(A). A comparison between human claudin low tumors and basal breast cancer (B).