The C2 carcinomas, characterized by an immune signature, are evenly divided over the two morphological tumour clusters which could be due to presence of immune cells in these tumours that are not present in cell lines. However, we did observe a gene cluster associated with immune response overexpressed in the C2 tumours as well as the Spindle cell lines suggesting that there may also be a cell autonomous effect, and it is not only the microenvironment that contributes to the immune signature. Closer examination of the clustering showed that the Spindle cell lines have a very similar gene expression pattern as seen for the C1 tumours, the Round cell lines resembled the C5mesenchymal subtype and the Epithelial cell lines the C4 subtype. This could imply that the in vitro morphological phenotypes resemble the clinical molecular subtypes and could be used to select relevant cell lines for tumour subtype specific studies. Interestingly,Ginsenoside-Re 61/152 genes overexpressed in the Spindle-like cluster overlap with the 292 genes up regulated in the C1 subtype explaining the association we see between the C1 subtype tumours and the Spindle cell lines. Furthermore, we see a small overlap between our in vitro morphology genes with the CLOVAR subtype signature of 100 genes which is enriched for genes that are up in the CLOVAR Mesenchymal subtype that are also high in the Spindle subtype. Both the C1 and the Mesenchymal subtype show a worse prognosis and an increase in stromal gene expression that for the C1 subtype correlates with Ginsenoside-Rc extensive desmoplasia and low tumour cell percentage. This suggests a greater contribution of the stromal compared to the epithelial tumour cells in these subtypes. Indeed, stromal fibroblasts play an important role in tumourigenesis and prognosis in several cancer types. However, with our analyses of 39 cell lines we show that the spindle-shaped epithelial tumour cells also strongly contribute to the stromal signature underlining the importance of an epithelial tumour cell autonomous effect additive to the stromal cells. The tumour microenvironment is also involved in multidrug resistance through a range of putative mechanisms, e.g. by decreasing drug concentrations through increased interstitial fluid pressure, 3D structure or by activating cellular pathways through ECM-Integrin binding, the so-called cell adhesion-mediated drug resistance.