Conceptually speaking, a broad-spectrum combination chemotherapy that can simultaneously target many of the key anti-cancer receptors, pathways and mechanisms with little-to-no toxicity makes a lot of sense. Instead of using one, two or three targeted therapies (which can't possibly act on the great number of subpopulations of mutated cells that often exist in many cancers), and hoping that the death of the bulk of the cancerous cells will be enough to avoid a relapse, this approach would also attack the minority subpopulations of mutated cells as well (as shown below).
In practical terms, however, isn't entirely clear just how many cellular targets will be needed to optimize this approach. A depiction of the surface of a cell is shown below (Image credit :Cancer.gov) with just small sampling of cellular receptors listed on the right which have been shown to play a role in cancer. Note that aberrant signalling in many receptors can actually instigate multiple hallmark characteristics of the disease, and many receptors are capable of instigating the same hallmarks of other receptors. Indeed it is this high level of redundancy that makes cancer so difficult to stop. Because if cells with a tumor are mutating regularly, using a targeted therapy that acts on only one receptor can quickly become ineffective if another form of mutated emerges which is acting to instigate the same hallmarks of the same disease using different pathways.
In fact, there are well over a hundred receptor types and many internal mechanisms that would serve as attractive targets in the design of a broad-spectrum combination chemotherapy. Yet there is no shortage of research on food and plant-based compounds that can act on these targets. A short list of natural compounds that are known to act on these same pathways is shown below.
Many of these plant based compounds are being tested and trialed in isolation, or in combination with existing therapies with limited success. But the real challenge lies ahead. A much longer list of molecular targets needs to be assembled, and the literature needs to be scoured to identify and map natural compounds that can act on those targets if we hope to develop the basis for a broad-spectrum combination chemotherapy that can be advanced experimentally and tested for safety and efficacy.
Ultimately, if an oncologist/physician has biomarker or biopsy information that pinpoints the most prominent forms of cellular mutation in any given instance of cancer, a specific and narrowly targeted therapy that is highly effective may still be the most desirable path to achieve the fastest possible remission. But in any event, having a non-toxic, broad-spectrum therapeutic option that can be initiated rapidly after diagnosis, and used in concert with a narrowly targeted therapy would still be the best way to reach small and/or unidentified subpopulations of other types of mutant immortalized cells and reduce the chances of a relapse.