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June 26, 2020, marked the 20th anniversary of the publication of the first working draft from the Human Genome Project. At a special White House event to commemorate the results of this 10-year public effort (it was really more like 50 years since the discovery of DNA, but I digress), then-President Bill Clinton called the project “the most wondrous map ever created by humankind”, and touted its promise to detect, prevent, and treat disease.  Obtaining that first sequence from one human cost about $2B and resulted from a massive global public/private partnership.

Another advance in hormonal approaches to controlling prostate cancer is available for our consideration. The results of the HERO trial demonstrate efficacy and safety advantages of oral relugolix when compared to standard of care leuprolide, given via intramuscular injection every three months. The results open up two areas for discussion: 1) is an oral ADT feasible, effective and necessary and 2) do LHRH antagonists confer cardiovascular and disease control benefits compared to LHRH agonists? It provides us with choice and a lot to ponder in terms of how this treatment may alter patient outcomes, practice patterns, and the future of our approaches to many stages of prostate cancer. 

In the summary slide of one of my 'go-to' talks I pose the question “Have we reached the limits of androgen receptor (AR) targeting?”. Of course, I don’t know the answer, which is precisely why it is framed in the form of a question on a summary slide. But I think about it a lot. So, let’s ponder this question a little.

As a medical oncologist, I may rely a little less than my radiation or urology colleagues on the Gleason score for prognosis and treatment decision making. Most of our decisions are based on the pace of disease and extent, and of course whether it is castration-resistant or castration sensitive. However,  I do look at it and in particular, it factors into the data ‘stew’ that one creates within an individual case and how we approach it.

Chemotherapy improves survival when given to patients prior to radical prostatectomy.

It is the latest, and potentially the last, piece of data in the decades-long march of this important and interesting (but much-maligned) therapy. Will this news change practice?

The clinical development of therapies targeting DNA repair pathways in prostate cancer is now well underway. It is a hopeful on-ramp for prostate cancer into the world of molecular oncology. We are beginning to see the emergence of consistent data and some surprises. There is a significant reason for hope, for example, that the poly ADP ribose polymerase (PARP) inhibitors will become a standard of care for patients with BRCA1 or BRCA2 alterations.

A highly practical and interesting study, CARD, was recently presented at ESMO and published in the NEJM. It’s a study that answers a lot of questions, creates a few others, and can be translated into the clinic relatively quickly.

The CARD study randomized patients with castration-resistant prostate cancer (CRPC) to either treatment with cabazitaxel  ( taxane chemotherapy) or a second ‘sequence’ of androgen receptor (AR) targeted therapy (ARTT) – enzalutamide in patients with prior abiraterone exposure, or vice versa.

Treating cancer is hard. Its even hard when you have years of experience and are considered an expert. 

Communication with patients is always a challenge, as is gathering all the information you need to make an informed decision. Then there’s the energy and time that are required to keep up with the clinical literature in your space, and the scientific/basic literature of it if you are so inclined. 
I continue to be surprised by the biology of prostate cancer, and how much guessing we are still doing. The good news is the number of tools in the tool chest is increasing. Also, even in situations where they don’t direct our actions, our ability to gain an understanding of the molecular underpinnings of the disease may inform our discussions with patients.
I recently followed a minor twitter based jousting match between various cancer treating specialists about how we present the goals of care to patients. The conversation went something like this (on Twitter):

1. Dear Surgeons - stop telling patients “We got it all” signed, Medical Oncologists.
2. Dear Medical Oncologists – please inform your patients that your treatments for metastatic disease are palliative, not curative. Signed, Surgeons and Radiation Oncologists.
I have been thinking a lot about the outliers, the exceptional responders, those rare patients for whom we have cracked the code and end up with a PSA of zero after we treat them with abiraterone, immunotherapy or other treatments - and what to do about them.
I have stated many times in this forum before that treating castration-resistant prostate cancer (CRPC) is analogous to trying to hit a moving target. The better we get at treating it, the more the disease is able to evolve and adapt and acquire new mechanisms of drug resistance and lethality.
I love the year-end lists and the person of the year articles that always come out at this time. whether it is TIME magazine or Sports Illustrated or even People magazine (…not that I follow the worlds sexiest man and woman contest that closely), they help us give a perspective of the shifts in our world that occur within a year.
I just returned from a tremendously insightful meeting at the National Cancer Institute on the lineage plasticity of prostate cancer. The focus of the meeting was the myriad changes that systemic treatment induces in prostate cancer over time – most notably the emergence of neuroendocrine/small cell prostate cancer. I’ll address this entity in a subsequent entry. Before that, though, the striking focal point of discussion at the meeting was a single molecule -RB  ( or, the retinoblastoma gene)
Earlier this year I wrote a piece on the need to learn from the ERA-223 experience and pitched it in the context of the Apollo 13 moon mission, dubbed a “successful failure’ because it revealed a variety of problems in the space mission and created the opportunity to revise process based on continued close scrutiny of the data*. At ESMO 2018, the closer scrutiny of ERA-223 has indeed delivered some new information about our best practices in mCRPC.
Here’s some interesting science to follow and think about in the context of mCRPC treatment. – how cancer and cancer treatment will influence and even accelerate aging – and what we can do about it.

My institution, the University of Minnesota, recently launched a “Medical Discovery Team on the Biology of Aging” a program that brings together clinicians,
If things were different, I might be writing this blog about using Selinexor in prostate cancer.

Or, I might be working on the design of the phase III study of BEZ235 in mCRPC, or the use of AMG-102 plus mitoxantrone in patients following docetaxel for mCRPC.
A new diagnosis of metastatic prostate cancer is life-altering.  Deciding on the treatment used to be straightforward but it’s not anymore. After addressing this issue with patients for many years, and staying abreast of the latest developments, I describe an approach to starting treatment in five questions for both the patient
Ever since they were introduced, the question of the efficacy of a combined approach with abiraterone and enzalutamide has been questioned.  We are now getting to the point of seeing the results of these approaches and a window into how similar, or distinct, these two therapies are.
I quip sometimes when lecturing that a clinician will make their first decision to use a new therapy based on the data - but the second time they make the decision to use that therapy it will be based on their experience. Although obviously a gross oversimplification,  I think it does reflect the fact that we obtain biases as we treat patients. 

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