Ur raw and normalized microarray data is publically available in the Gene Expression Omnibus database

increase in CDH2 in both DT22 and DT28 cells is a classic example of BC cells undergoing epithelial to mesenchymal transition (EMT). Unique expression of cadherin 19 by DT22 cells and protocadherin FAT2 by MCF-10A cells was observed, but little is known about these cadherins or their potential roles in cancer. Altered expression of catenins, both lower (MDA-MB-231, SK-BR-3, and MCF-7 cells) and higher (DT22 and DT28 cells) when compared to MCF-10A cells was also observed. Offering methodological information that can expose the weaknesses of the study's data collection in representing the community as a complete could lead to paper rejections Changes in catenin levels have also been correlated with cancer progression. Decreased levels of a-catenin have been associated with poor BC prognosis [37], and MDA-MB-231, SK-BR-3, and MCF-7 cells had fewer spectral IDs for this protein than MCF-10A cells. In contrast, abnormally higher levels of b-catenin are associated with metastasis and poor prognosis [38] due to activation of Wnt signaling and altered expression of multiple genes implicated in cancer progression and metastasis [41]. These actions are thought to be the result of the translocation of b-catenin from the inner PM to the nucleus. MDA-MB-231, SK-BR-3, and MCF-7 cells had a fewer spectral IDs of membrane-associated b-catenin compared to MCF-10A cells, and this fact may reflect this classic situation of a specimens to define the frequency of KIT expression in TNBC are variable, ranging from 30% to 90% of TNBCs examined [26,27]. The higher representation of the ephrin receptor EPHA2 in MDA-MB-231 cells, ErbB3 in DT22 cells, and PTK7 in DT28 cells indicates that BC cells might exploit multiple signal transduction pathways to fuel growth. The insulin receptor exists in two isoforms, with isoform B being involved with glucose metabolism and isoform A, in concert with insulin-like growth factor 1 receptor (IGF1R), being involved with cell proliferation [28]. The interplay of isoform A and IGF1R, and the insulin receptor switch in expression from isoform B to isoform A in certain cancer cells, are subjects of great interest in the development of new targeted therapy protocols [29]. Interestingly, DT22 cells had higher spectral IDs for IGF1R and 23 of the 28 spectral IDs for the insulin receptor were unique to isoform A, indicating a proliferative program resulting from the interaction of these two receptors. When examining the targeted therapies that are currently available for cancer treatment, more than half of them are directed at PM-based tyrosine kinases (Table S1). Interestingly, many of these tyrosine kinase targets were initially described in unrelated types of cancer, including leukemia, non-small cell lung cancer and gastro-intestinal stromal tumors [302]. This sharing of oncogenic proteins by many diverse cancers lends support to the more recent notion that cancers should be classified by their molecular signatures rather than by their tissue of origin, a concept that could currently expand the number of targeted therapies available for BC treatment.Figure 4. RT-PCR demonstrates the quantitative nature of the MS data. RNA was isolated from each of the cell lines, cDNA was made, and RT-PCR was performed to determine whether the spectral ID numbers were correlated to transcript levels of selected genes. Spectral ID numbers are displayed above each graph and the gene symbol is below those numbers cancer cell losing b-catenin at the PM.