I think there are several major differences between what you get from a doc like meyers and what you get from a more "by the book" doc.
1.) Timing: new prostate treatments are coming out a rapid clip. when a new drug comes out it is first tested on the sickest patients and approved for those cases. So that means a drug like abiraterone might be initially approved only for those who have failed HT and failed chemo. So let's say that approval happens; it is still an
open question whether the drug should be SAVED for those most severe cases or whether it is more effective if used earlier. it takes years of additional phase II and Phase III trials to answer the questions, but in the interim, a doctor has the legal right to prescribe the drug for an earlier stage patient. (However, that does not mean that the insurance will pay for it.) so there could be a period of, say five years,during which the official "by the book" treatment scheme holds a new drug for the latest stage, but in fact that new drug might have far greater effectiveness earlier on (as is the case with many prostate cancer treatments) but only a few docs might be willing to prescribe it earlier... and only a few patients might be able to pay for it earlier. It is a higher risk strategy for the patient because there is no assurance that the drug will perform better if given earlier, and in fact it is possible to generate drug resistance earlier than might otherwise occur. No easy answers in this.
2.) Genomics: Meyers talks about
doing genetic testing and using that info to tailor the treatment. Not all prostate oncologists agree on this at this point, as far as I can tell. Some think that the science is still too much in its infancy. It's clear that some genomic patterns are more indicative of a better or worse prognosis, but not yet clear that you can pick treatments based on genetic variants (the way it's done with breast cancer, treating ER+ cancer differently than ER- cancer.)
3.) Combinations: It's widely understood that combination therapy is better than monotherapy but to date the combinations have been limited by the piling up of toxicities of different therapies to unacceptable and life threatening levels. Meyers seems to do more experimenting than others combining therapies that rely on different biological mechanisms (or pathways) some of which have lower or at least different toxicity profiles.
For example, if I understand it correctly, zytiga and xtandi are basically both anti-androgen drugs and while one may be better than another, it's less likely that something synergistic (in a good way) will happen when they are combined.
However, looking more broadly, there is greater potential in combining drugs that affect very different pathways, for example (1) an immune system enhancer -- Yervoy, (2) curstirsen (which inhibits the clusterin protein),(3) Tasquinimod which inhibits the development blood vessels that feed metastatic tumors and allow them to flourish. (4) Sprycel - a tyrosine kinase inhibitor. All of these affect difference cancer mechanisms, so there is the potential that if drugs like these are given in combination that the cancer will be unable to mutate "out of the way" of the drug. At least that has worked with certain leukemias which are now completely and permanently curable.
There are many trials going on now that test different combinations of new and approved agents, e.g. sprycel with zytiga, custirsen with Docetaxel, For example this article
www.ncbi.nlm.nih.gov/pmc/articles/PMC3398601/pdf/10.1177_1756287212452196.pdf lists 9 different drugs being tested in combination with Zytiga. Since all of these are in the trial stage none of these combinations are going to be offered by a doctor who is simply going "by the book" of approved treatments.
Meyers' message as I understand it is that different patients have different kinds of prostate cancer, and that these cancers involve different kinds of genetic damage or differences at the cellular level, and therefore they will respond to different kinds of therapy. The goal is to have the right set of tests to perform (called biomarkers) which will tell the your doctor what is driving YOUR particular kind of cancer and therefore what particular type of therapeutic approach will work for it. But until we have a good set of biomarkers, we simply have to try a wide range of approaches with the aim of quickly figure out which ones work and which ones don't, for each individual patient.
I hope that helps.