The systems (each system consists of a segmentation method, a featureset, and a classifier) were compared with each other in terms of their performance on the diagnosis of the set of breast masses.
In addition, CACNA1D protein expression could be detected in all major breast cancer subtypes (cancer type, positive expression; luminal, 3/6; triple-negative, 7/8; Her2-positive, 4/4; healthy breast, 0/1) from a set of breast carcinoma patient samples (Fig. 3e).
To provide a better definition of the subtypes of epithelial cells comprising the breast epithelium, we performed a systematic analysis of a large set of breast epithelial markers in more than 15,000 normal breast cells, which identified 11 differentiation states for normal luminal cells.
The resulting experimental signatures of responses to lactic acidosis and hypoxia are evaluated in a heterogeneous set of breast cancer datasets.
The pathway signatures, combined with the validation set of breast tumor samples, were standardized using MatLab (version 7.1).
Evidence for a CIMP phenotype among breast cancer only recently emerged from a methylation profiling study analyzing a set of breast cancer cell lines [42].
In the present study, we used this approach to assess the methylation profiles in a set of breast tumors and normal breast tissues.
For the analysis of more than one independent data set of breast cancer patients (e.g., NKI data sets and the Duke University data set) each data set was normalized separately and then combined together.
In the same set of breast cancer samples, we quantified the level of MYC mRNA.
Figure 1 shows a representative example of a set of breast images used in the analysis.
Lastly, FHLBC is only a proxy measure for a complex set of breast cancer-relevant exposures shared among families.
