The broad variety and rapid change in mechanisms within cancerous cells is one of the reasons that cancer is hard to tackle - every cancer is different and evolving. Circumventing this to find truly effective cancer therapies will require the discovery of some mechanistic commonality that can be targeted, some biological process that all cancers depend on and which distinguishes their cells from non-cancerous cells. The proposed SENS approach, for example, is to go right to the root and remove all ability to lengthen telomeres in the body, as all cancers depend on that. The mainstream research community aims to find markers for cancer stem cells, or low-level mechanisms shared between cancers to some degree and which can be sabotaged to slow down or reverse progression of the disease. Not all shared mechanisms are sufficient to build a true cure, unfortunately.
Here is an example of one such lesser mechanism in the early stages of research and development:
Epithelial to mesenchymal transition is important to embryonic development, turning stationary epithelial cells into mobile mesenchymal cells to move them within the embryo. For example, a cell might be converted and then gather with other cells forming, for example, the kidney. Once there, it transitions back to an epithelial cell again and stays put. Research has shown that carcinomas, tumors that form in the epithelium (lining) of organs are able to reactivate EMT. About 85 percent of all solid tumors are carcinomas.
"We found that FOXC2 lies at the crossroads of the cellular properties of cancer stem cells and cells that have undergone epithelial to mesenchymal transition (EMT), a process of cellular change associated with generating cancer stem cells. There are multiple molecular pathways that activate EMT. We found many of these pathways also activate FOXC2 expression to launch this transition, making FOXC2 a potentially efficient check point to block EMT from occurring."
[Researchers believe] that targeting FOXC2 pathway [will] be an effective therapeutic strategy for inhibiting EMT and consequently reducing EMT/cancer stem cell-associated metastasis, relapse and therapy resistance.