Ugh! but thank you for posting this.

For what it's worth, below is my assessment of genetic therapy with regard to breast (not necessarily to other) cancer:

1. In PALOMA-1, patients with targeted mutations fared no better than patients without them."PALOMA-1 was split into two parts, wherein the first part included 66 patients with ER-positive, HER2-negative advanced breast cancer.The second part examined 99 patients with ER-positive, HER2-negative disease and specific biomarkers, including cyclin D1 amplification, p16 loss, or both. Although preclinical data had suggested that ER-positive patients with cyclin D1 amplification and p16 loss might be best responders, this didn't bear out in in the clinical trial."From: https://www.genomeweb.com/clinical-genomics/pfizers-palbociclib-doubles-pfs-her2-negative-breast-cancer-falls-short-overall
2. Focusing solely on mutations ignores the tumor's microenvironment (surrounding tissue) that influences the tumor's behavior.A research team found that the progression of different types of breast cancer in mice was influenced differently by the tissue – the so-called tumor microenvironment - in which the tumor is embedded. In this study, the MMP9 gene (which has been linked to cancer progression) was deleted in two mouse models.The absence of the MMP9 protein delayed tumor onset only in one mouse model, and had no effect in the other model.The reason for this inconsistency appears to be IGFBP-1, another molecule (which, if present,resides in the tumor microenvironment) that MMP9 is known to act upon.If IGFBP-1 was not there, MMP9 didn't have an effect, but if IGFBP-1 is there, then MMP9 is active. This suggests that IGFBP-1 interacts with MMP9 to promote tumor formation.The study's results suggest that trials of MMP inhibitors could focus on patients whose tumor microenvironment contains IGFBPs. From: http://www.cshl.edu/news-and-features/tumor-surrou...
3. Researchers are beginning to learn that, at least in some cases, targeting genetic mutations through drugs can occasionally backfire.In one study that targeted the PI3K mutation, it was determined that monotherapy (single drug) treatment may actually worsen a patient's cancer by causing more aggressive tumor cell behavior and increasing the likelihood of metastases to other organs. In the study, PI3K inhibition caused mitochondria (the portion of the cell responsible for energy production) to migrate to the peripheral cytoskeleton of the tumor cells, whereas the mitochondria of untreated cells were seen clustered around the cell nucleus.The net result of this was that PI3K inhibition diverted the mitochondria to specialized regions of the cell membrane that are implicated in cell motility, and the cells could move spontaneously, which permitted invasion. From: http://www.targetedonc.com/articles/pi3k-inhibitio...

General Considerations Regarding Targeted Therapy:

1. In order to be a candidate for targeted therapy, the cancer must express a mutation(s) and there must be a drug targeting that mutation(s).
2. Simply having a mutation does not mean that the mutation is dangerous.For example, a person may be albino but that doesn't mean that being an albino is deadly.
3. The mutation may not be dominant over other mutations in the same tumor.
4. Breast cancer is exceedingly complex because a single tumor may express a specific mutation in one "slice" of the tumor but not in another slice of the same tumor. In addition, a mutation that's found in one tumor within a patient may not be present in another tumor within that patient.
5. Tumors are greater than the sum of their mutations.They secrete proteins and enzymes, are able to influence their microenvironment (and vice versa,) and communicate via cellular pathways. Much of this is independent of genetic mutations.

Note: The only time I've ever seen targeted therapy to be effective against bc is when a mutation causes overexpression of a receptor on the cell's surface, such as HER2-neu.

Stephanie, that is indeed an interesting quote! I believe that until Complementary and Integrative therapies are studied and leveraged along with the tumor microenvironment, co-morbidities, germline mutations and other factors, we will not make true headway against bc.

Just today, while researching clinical trials for Complementary and Integrative therapies (including but not limited to Iscador and Diet), I ascertained that the vast majority are located in countries other than the US. Companies here simply do not stand to gain from these types of therapies.

Additionally, oncologists receive kickbacks for the Pharma drugs they prescribe: "Doctors typically buy the drugs from the companies, get reimbursed for much of the cost by Medicare and private insurers, and on top of that get these rebates based on the amount they have purchased." From: http://www.nytimes.com/2007/05/14/opinion/14mon1.h...

Until this terribly broken schematic is changed, true headway against mbc will likely remain elusive.