advanced prostate cancer research

//advanced prostate cancer research
advanced prostate cancer research 2017-10-19T10:43:23+00:00
Joel Nowak
Hello, I’d like to welcome you to another Malecare telephone conference. My name is Joel Nowak, and I am Malecare’s director of advocacy and advanced prostate cancer programs. I am given the honor of moderating our teleconference programs.
Today’s teleconference is going to be a little different than some of our prior ones. Today, we have the great fortune to have a personal friend of mine in a real live and absolutely brilliant prostate cancer researcher to talk with us about an investigation drug that she has invented, or I should say developed, to treat prostate cancer. My guest, Dr. Mary Sadar is the distinguished scientist at the British Columbia Cancer Agency having received her Ph.D. from the University of Bradford in the United Kingdom in biochemistry. She also has done post doctoral work at AstraZeneca in molecular biology and at the British Columbia Cancer Agency, the department of endocrinology with her post doctoral works specifically in prostate cancer.
She has served on over 50 grant panels including five years at the NIH study session for drug discovery and molecular pharmacology and has been and is still the chief scientific officer of a biotechnology company which she has founded called ESSA. Dr. Sadar discovered a novel drug target for prostate cancer. She screened drugs against this target and brought a clinical candidate of this drug into clinical trials that are currently ongoing in both the United States and in Canada. This is the first drug in clinical trials targeting an intrinsically disordered protein region in a first in class drug of the end terminus of the androgen receptor. We’re going to come back to what that all means in a few seconds. Her work is a first in type to the entire field of steroid hormone receptors with no other small molecule inhibitor reported to bind to the end terminus. During this teleconference, Dr. Sadar will hopefully help us understand what it is she has done.
Dr. Sadar is also the 2017 chair of the United States Department of Defense programmatic review panel for prostate cancer. She is the first Canadian to serve as chair of this conference. That’s a heck of an introduction because you are a heck of a researcher and heck of a person. I’d like to welcome you, Dr. Sadar. It’s really good to talk with you.
Dr. Sadar:
Thank you very much.
Joel Nowak:
Dr. Sadar, I was wondering if you could tell us a little about your research, specifically maybe translate what it is that I said so that we can understand it.
Dr. Sadar:
My research is focused on advanced prostate cancer. It’s focused on the protein in the human body that causes most prostate cancer to grow and rapidly proliferate, to increase in number. The treatment for advanced prostate cancer is unfortunately castration which is to reduce the male sex hormone and that male sex hormone works on this protein called the androgen receptor that I have been studying for 20 years.
What I’ve been doing is trying to figure out how this androgen receptor continues to fuel advanced prostate cancer even though these men are castrated. That’s really what I’ve been doing for the past 21 years and trying to find therapeutics, trying to find drugs that will benefit these men for a longer life, hopefully, improve their quality of life.
Joel Nowak:
Are there are other drugs that target this particular protein, the androgen receptor?
Dr. Sadar:
Yes. When men with advanced prostate cancer are treated for advanced disease, they receive LHRH analogs which reduce their testosterone levels, and that really targets androgen receptor because it reduces testosterone levels, male sex hormones that binds to the androgen receptor. There is also abiraterone which is used which reduces the amount of androgens, steroids, in men that are receiving it, and that has beneficial effect, and it works again on reducing testosterone or these steroids that bind androgen receptor.
There’s also anti-androgens. There’re a number of anti-androgens. Probably the most well known one now is enzalutamide, but there’s also the whole family which is the bicalutamides, flutamide, nilutamide. There’re a lot of these anti-androgens. They work on the opposite end of where my drug works. They work in the same spot that testosterone and other steroids will bind to androgen receptor. It’s like a competition. They’ll fill the spot that testosterone normally would fit on androgen receptor to prevent the testosterone from working on the androgen receptor.
It is a well known target. What’s unique about my research is that’s not the important part of the androgen receptor because in advanced disease that part of the androgen receptor where testosterone interacts with the androgen receptor it might not be made anymore and it might be a truncated androgen receptor. That would mean all of these therapies, all the anti-androgens, abiraterone, castration, wouldn’t have any effect on these truncated androgen receptors. Where my research fits in this is we are targeting the part of the androgen receptor that isn’t lost in the disease, and that’s called the end terminal domain. It’s present on all forms of androgen receptor that cause the disease to keep proliferating and growing.
Joel Nowak:
The time that this drug would probably be used would be at the time that a man becomes castrate, and these other drugs stop working.
Dr. Sadar:
That’s where we’re starting. We’re starting our clinical trial that’s ongoing right now. It’s a dose escalation study. It’s a phase I that we’re doing right now. It is in men that have become resistant to abiraterone or to enzalutamide or some men received both of these therapies, so both treatments. That’s where we’re looking now. We’re looking at quite late in the disease, so after men have received a lot of treatments and those treatments no longer work, that’s where our drug has been slotted in to see if we can help those men.
In the event that our drug works, well hurrah, but then we’ll try to move the drug earlier. We’ll try to move it into earlier disease because theoretically if it is having the effect that we see in the laboratory it should help men with earlier disease as well.
Joel Nowak:
How do you see this effect in the lab?
Dr. Sadar:
We have a lot of different models. You can never truly mimic human disease like treating a patient, so we have cell lines. We have many different cell lines. These cell lines were made from men that had metastatic disease, and that metastatic disease was removed and their cells were then grown in a culture dish, and then we try our drugs on these cells that are growing in culture dishes. We have a lot of molecularly engineered cells that have readout systems on them, so if we know if our drug is working.
For example, we engineered our human prostate cancer cells. These were cells that were originally from a man with a prostate cancer metastases to his lymph node and his clavicle region. We engineered those cells so that when the androgen receptor, which is the target, when the androgen receptor was pushing proliferation and causing cells to grow and dive, that the cells would emit light. How we screened for drugs was let’s see which drugs can turn off the light.
There is specific equipment for that. There’s assays for that, but that was really one of our assays. We screened I think about 36,000 drugs. That’s actually relatively low, but we got lucky. Always with a bit of luck helps. The drug that we found was this EPI-506 is the drug that’s in the clinic. It turned off the light of these cells that we engineered. Then there was a whole battery of tests. Then we test how specific the drug is. Does it kill other cells which wouldn’t be good because we only want to kill prostate cancer cells. We don’t want to kill bladder cells or epithelial cells in the intestine and all those things. You start to check how specific the drug for prostate cancer.
Then, of course, we do our animal studies which most closely mimics human disease, and that’s where you take these human prostate cancer cells and you grow tumors in animals, unfortunately, you have to do this because that’s the closest to human. These tumors will grow in these castrated animals just like what happens in human disease, and then we give the animals our drugs, our EPI-506, and we would see this wonderful effect on the tumor stop growing, reduced tumor growth. It’s sort of the full line from in the bench to animal testing, and then of course, in order to get into the clinic we had to do the FDA protocols for safety and toxicity.
Joel Nowak:
What’s involved in that?
Dr. Sadar:
Oh boy. It’s very expensive. I couldn’t do that in my lab. Now the biggest hurdle first was money because I can do the molecular biology as an academic, so I received grants, a lot of grants, lots from the US Army, from NIH, to the biochemistry molecular biology. Now in order to get the dollars to create a drug that goes in the clinic and to pay for all of the tests that the FDA required, all the safety, toxicity, chemistry. It’s all chemistry. You have to have a chemical compound that’s safe going into humans. We had to spin out a company just to get private money, so from angel investors, from venture capitalists, from investment banks, et cetera. That was the point of where we had to now look at other places for money to look at commercialization of this technology. That was the first step.
It cost a lot of money to do all these tests. Then once we had the company in place, many very qualified people in areas that I have no expertise were hired. They started to do the chemistry. They started to look at the toxicology of the compound. How long does the drug last in animals? Does it stay in the blood long enough to potentially effect the tumor, or does it just go through the body immediately and never really get absorbed? All of these factors have to be considered before creating a drug.
It’s extremely expensive. Like I said, you can’t do this with academic dollars. It’s very difficult. The company was formed. People were hired to interact with the regulatory people at the FDA. A chief medical officer was hired, Frank Perabo, who is the superstar in the field. He did many of enzalutamide clinical trials. It now became a little bit of a monster that in order to get in the clinic you have to now have so many different areas of expertise well beyond my lab, my little teeny lab. It bloomed.
Joel Nowak:
You’ve created or certainly were the impetus to start this thing. It’s kind of your baby. What’s it like to, I guess, to somewhere lose some control of your baby? I’m making an assumption. I don’t know if that’s correct, but do you feel that way?
Dr. Sadar:
Absolutely, I feel that way. It’s having to build trust. This is my baby. I’ve worked for 20 years on this. To then pass it over into hands that aren’t my hands I have to have trust that those are good hands that it’s going into, that they’re going to do everything they can to make sure it was the best shot possible of succeeding in the clinical trials. I’ve done everything that I could here in my lab. Over 20 years, I’ve had at least 10-13 people working on it every single day for those 20 years. It’s a lot of time and effort.
There is the trust. There is the learning to let go a little bit. I can’t run the clinical trials. I can’t do the chemistry, so I have to believe that it’s in good hands, and it is. The people that ESSA have hired are absolutely outstanding. They’re superstars. I’ve only mentioned one, but there’s a whole number of superstars that were hired into this company. I can breathe easy. I can realize it’s in good hands.
Joel Nowak:
Great. Actually, I want to go back a little bit to something you’ve said when you described the trial which is, as you said, a phase I trial. If you would for those people who may not know what phase I trial is, if you give a brief description of that. You also mentioned the words dose escalation. If you could describe what that means I would appreciate it.
Dr. Sadar:
Yes. When you go on to patients, this is the first in human clinical trial meaning this drug that we’ve made has never ever been put into humans before. What you have to do is you have to make this enormous leap. Everything we’ve done has been in animals. Animals have much faster metabolism. They handle drugs differently than humans. How do you decide what dose should be the first dose in humans that will be safe?
That’s really what a phase I is. It’s figuring out what dose is safe in humans, what is the highest dose you can put into humans that are still safe meaning you’re not getting a lot of really horrible toxic effects that would compromise the patient’s health or compromise the patient from continuing on the drug. That’s what a phase I is. The FDA actually tells the company which dose they can start with, and that’s based on their animal studies, their toxicity studies that they had to give the FDA so the FDA can decide what dose is the first dose that you give patients.
In our clinical trial, they’re all prostate cancer patients. None of them are healthy. There’s not a placebo arm. There’s nothing like that. All of them are patients. All of them receive the drug. You start with three patients per cohort. The first three patients have been dosed at the lowest dose, and for us that was 80 mg in a patient. Once they go through 30 days, I believe it was 30 days, and there’s no adverse, there is adverse event, then another group of patients can then start on a dose that’s higher. You keep doing this. You keep testing three patients moving up the amount of drugs that they’re receiving until you start to see some toxicity.
It’s cancer, so you want to get as much drug as you possibly can into patients because you want every chance possible of affecting the tumor. You really want to have what’s called a maximum dose, maximum tolerated dose. That’s what a phase I is. It’s finding the dose.
It’s not really about seeing whether the drug works or not. The dose that we’re starting at it with right now that we’ve finished the first three patients was a very low dose. It’s not predicted to be efficacious because it’s so low, but you may get some clinical data because we are monitoring blood levels, we’re monitoring PSA. We’re doing all these things. Once we get to an efficacious dose, which keep your fingers crossed that we do, and that we can put a lot of this drug into patients we should get some sort of read out about whether we’re having any effect on PSA levels. Plus patients they will tell you if they’re feeling well or not. You get a lot of feedback from patients.
Once you ….
Joel
Nowak:

Do you have the opportunity … I’m sorry, go ahead.
Dr. Sadar:
I was going to say, so once you find that dose then you start the phase II studies. The phase II is really to give an indication of whether the drug has any effect on the tumor, and you increase the numbers of the patients.
Joel Nowak:
How do you evaluate in the phase II whether or not it’s had an effect on the tumor?
Dr. Sadar:
In our trial, of course, there’s always PSA. That’s one of the major readouts. It’s usually a 50% drop in PSA. PSA, of course, is measured in the blood of patients, prostate specific antigen is what that stands for. We also look, I believe, we’re looking at tumor volume. I think we are doing some analysis of how much tumor burden these patients have. I’m not sure what else actually, probably the quality of life as well and maybe morphine use. I’m blurry here on our on all the aspects of the clinical trials because I’m not the clinician. Our chief medical officer, Frank Perabo, designed all those clinical trials.
Joel Nowak:
Right. Are you still working on this drug in the lab, or is that something that is not happening anymore?
Dr. Sadar:
We are working on this drug in the lab. What my academic research is looking at is we know that prostate cancer forms resistance to drugs. That’s been the problem. You treat men with these therapies and eventually they develop resistance, so you switch to another drug and eventually develop resistance. Of course, we’re thinking what if our drug develops resistance? What resistance would that be? What mechanism would that involve?
To try to address that what my lab did is we incubated these human prostate cancer cells with our drugs for very long period of time. It was about a year and a half. Eventually  we saw resistance, so eventually the prostate cancer cells started to grow in the presence of our drug. That’s resistance. The good thing is that it took a year and a half. If you put this into perspective, in tissue culture enzalutamide causes resistance with long-term culture in three months. Ours causes resistance in a year and a half, so six times longer. If that panned outs clinically that would be wonderful.
We still need to understand how the cancer cells are forming resistance to our drugs. We’re now analyzing these cells, and we have picked up one potential pathway that is manageable. I’m not going to describe more here because the work’s just not completed enough. I would like to make sure I’m standing on really firm ground, but in everything that we’ve looked at we have a resistance mechanism that we seem to be able to halt. That’s the whole theory behind us. If you can understand the resistance you could potentially do combination therapies in order to prolong the efficacy of the drug or maybe even potentially cure the patient if you do a cocktail.
Joel Nowak:
That’s an amazing word to use when we talk about prostate cancer, metastatic prostate cancer. It’s a word I don’t like to use, but it’s really optimistic and potentially so exciting sounding. It really is.
Dr. Sadar:
That’s my goal.
Joel Nowak:
Appreciate that. I’m sorry.
Dr. Sadar:
That’s always been the goal of my lab. We would really like to just get rid of the prostate cancer, just get rid of it out of these men.
Joel Nowak:
Which, of course …
Dr. Sadar:
We don’t want to lose sight of that.
Joel Nowak:
Which brings me to the question, how did you get into prostate cancer? Why prostate cancer? Why not breast  cancer, kidney cancer or arthritis?
Dr. Sadar:
I was very interested in cancer. My sister died of cancer when I was a child, so I was very aware of cancer. I knew that I just wanted to work in cancer. To me, there weren’t different types of cancer. Just cancer. That’s all you heard. You don’t hear it’s leukemia. You don’t hear it’s whatever.
As a child, I wanted to be a cancer researcher. When I went off to do my Ph.D. I did it on the dioxin transcription factor, dioxin receptor in fish, and had a wonderful Ph.D. experience. When I came back to Canada, I never thought I was smart enough to do human medical research, but I wanted to stay in Vancouver because that’s where I was living. My friends and family pushed me into applying for a position with Dr. Nicholas Petrovsky who Dr. Nicholas Petrovsky he was and M.D., Ph.D. He was the discoverer of dihydrotestosterone which is really what fuels prostate cancer and intermittent androgen suppression. He was the pioneer.
He was a real superstar in the prostate cancer field. I applied with him, and I was lucky enough that he hired me. What I did my Ph.D. on was the dioxin receptor which is the transcription factor, and actually there were things that I did with that transcription factor which was very similar to what I went on to do with the androgen receptor. Androgen receptor is also a transcription factor. What a transcription factor is is it’s something that binds to DNA to turn on lots of genes to turn on the production of making lots of  different things in the nucleus cells.
It wasn’t a big jump, but for me, I still remember when Dr. Petrovsky offered me the job and first day on the job. It was the best feeling ever. It was a gorgeous day in Vancouver. I walked down the road by the BC Cancer Agency happier than ever that I was in medical research, and I had a chance to make a difference.
Joel Nowak:
I think knowing you that you’ve already made a significant difference. If I understand correctly, the potential of what you’re doing could be such a breakthrough for men with metastatic prostate cancer. You may well make such a significant difference, and although I always, as I said, hesitate to use that word cure, if you can stretch the resistance and prevent the resistance that’s darn near close. Wow, that’s all I can say.
I get a little personal with you, if I might. You’re a woman and we know that men and women are not the same within science. They’re not treated the same, so I’m wondering would you be willing to share a little bit about your experience with being a woman in science?
Dr. Sadar:
Sure.
Joel Nowak:
You didn’t expect that. I’m sorry.
Dr. Sadar:
No, no. It’s a good question. As I’ve gotten older, I would say it’s changed, but when I was younger I would go to conferences and people would automatically assume that my students are post docs must be Dr. Sadar, not me. You get dismissed more easily I believe than a man would get dismissed. Credibility sometimes was the issue, being a young woman in the field. I still remember the very first conference I went to there was only one woman speaker at the conference. It was a conference all about urology. It was actually the Society of Basic Urologic Research, and there was only one speaker. That was Natasha Kyprianou. I think that was 1995 or 1996.
I hate say to it, but she in spite of giving the most amazing talk some of the men that I sat with all they talked about was how she looked. That just made me feel sick. There were very complimentary. Natasha’s a very beautiful woman, but it was just kind of disappointing that they weren’t listening to what she was saying. I have found that, but it’s gotten better. I would say it’s gotten enormously better in the 20 years, whether it’s just because I’ve become an older woman now, but I don’t think so. I think the world has changed in 20 years, I think. I think the medical field now views women with more, I sort of use the word respect, and we’re not easily dismissed with what we have to say. It still is tough being a woman, and I would especially tough in biotech.
Joel Nowak:
Right.
Dr. Sadar:
I’m the only board member.
Joel Nowak:
You’re certainly showing them up, aren’t you?
Dr. Sadar:
Women do bring different perspective. I would say that ESSA’s board has a woman on it, that’s me, but the rest are all, let’s say it lacks diversity. I bring the diversity card to the board. I don’t thinks this is really uncommon. I think it’s harder for women to become board members. Hopefully, that’s changing too.
Joel Nowak:
Right. I’m going to bring us back to the clinical trial, if I may. You’re currently in phase I which is a dose escalation trial. If I understand correctly, at some point you’ll come to a dosage that you decide or the FDA or you in consultation with the FDA decides that that’s your target dose. You’ve gotten the proper saturation and the toxicities are manageable I would assume is the way to look at it, and then the next step which you reflected on is to a phase II. Is kind of a reasonable summary?
Dr. Sadar:
Yes, that’s very accurate.
Joel Nowak:
You’re still in phase I. A man who may be interested in learning more about this phase I and perhaps how to get involved or even perhaps as you move into a phase II, because I am very optimistic that you will, how would they go about doing that?
Dr. Sadar:
On the website, clinicaltrials.gov, there is a description of the clinical trials if you put in a search of EPI-506 you’ll find the trial. There are only five sites for the phase I. There is a low number of patients because it’s pre dose, so the five sites are one in Canada which is at the BC Cancer Agency in Vancouver, Canada. There’s University of Washington in Seattle, Karmanos Cancer Center in Detroit. There’s Ann Arbor in Michigan, and there’s Scottsdale in Arizona. There are these five sites. It’s a very low number of patients right now in the phase I, but I definitely encourage men to look into it.
Joel Nowak:
If somebody, could they reach out directly to one of the centers, or they need to go through the clinicaltrials.gov website?
Dr. Sadar:
On the clinicaltrials.gov website it will say who the medical oncologist are each of these sites to contact. That’s probably one of the most efficient ways of inquiring. I get contacted a lot by patients that have read articles. Basically, it would be going to their own oncologist or urologist that they’re seeing and discussing with their oncologist or urologist the clinical trial, this EPI-506, with their oncologist, and then getting more information about entering the trial.
Joel Nowak:
Right, but they should go through their oncologist or the urologist, but they could also reach out directly I assume.
Dr. Sadar:
They could, they could. Just why mentioned maybe speaking to their own oncologist is there’s a lot of eligibility criteria, so it’s whether they fit into these eligibility criteria. Like for example, I’ll give you an example, we were a little bit late with some patients in our first dose and that was because patients can’t be on other treatments. If they’re on other treatments they have to be washed out, and they have to be washed out, it’s five half-lives of the drugs which can be up to a month. Things like enzalutamide have a very long half-life, looking at about a week half-life, so five half-lives is five weeks. That’s all. It might efficient to talk to their doctors about whether the fit the eligibility criteria.
Joel Nowak:
Um-hmm. Does someone have to life close to the trial site, or can someone come from a distance and still participate?
Dr. Sadar:
I believe that situation has already actually where a patient wasn’t right at the site for the center and was traveling to the center. I think it’s possible. The only one that I would say that gets more complicated is crossing borders. That’s beyond my expertise.
Joel Nowak:
Right. Just because one doesn’t not live, obviously, near one of the centers, if one is willing to travel they should still follow up with their physician and talk about eligibility, and then if they’re still interested to pursue it?
Dr. Sadar:
I think so.
Joel Nowak:
Right. The dosage or the drug as they take it is this something that’s in pill form? Is it an effusion? How does a man get it?
Dr. Sadar:
It’s in a kind of liquid gel capsule. I believe it’s kind of like a cod liver oil capsule, so it’s orally. You take it once a day.
Joel Nowak:
A man could take their pills and go home, and then check in whenever they’re supposed to check in again?
Dr. Sadar:
Yeah, I’m not completely sure of the protocol because it is a safety toxicity whether they have to have their blood levels measured and all these types of things, so I’m not sure how much time they need to be really close to the medical facility to monitor these things.
Joel Nowak:
Right.
Dr. Sadar:
I’m afraid I have no experience.
Joel Nowak:
Right. I would like to ask you the question as to how long you think the phase I will last, but if I understand correctly, you want it to last longer because it means you’re able to escalate the dose more and you really don’t know where that it. Timing wise is kind of unknown at this point. Is that correct?
Dr. Sadar:
Pretty much. There has been discussion that we’re probably looking at September, somewhere in that time, the end of the summer. The company is going to release some of the clinical data from the phase I around that time once the phase I is done. Exactly like you mentioned, you can’t be precise because you just don’t know how these things are going to pan out, but that’s the rough timeline that they’re looking at.
Joel Nowak:
Um-hmm.
Dr. Sadar:
We sure hope that it’s not shorter than that.
Joel Nowak:
If you have the data and you release it that’s obviously through a journal article or something of that sort, but you also have to communicate with the FDA. Correct?
Dr. Sadar:
Yes. I believe that the company has to keep communicating with the FDA all the time. Any adverse events have to be reported, all these types of things. I believe it becomes a very close relationship with the FDA.
Joel Nowak:
Um-hmm, and then if you want to move on from the phase I to a phase II, and I understand that you’re not a trialist, that you’re the creator so to speak, that you then need to go back to the FDA and get their approval to move from a phase I to a phase II.
Dr. Sadar:
Yes, I believe that’s correct. They have to make sure that the dose and everything is safe.
Joel Nowak:
Then obviously after that we move into a phase III where we will look for other things. Besides dosage, we look at survival benefits and perhaps quality of life. I’m hoping I’d like to see more often as part of end points of clinical trials. That’s something I know the advocacy world is trying to get the FDA to acknowledge. We could be talking about many years yet before we could actually see this in the clinic.
Dr. Sadar:
Yeah, I think one of the fastest from clinical trials to approval was for enzalutamide in this field. I think the period of time was about five years which is phenomenal. We would like to beat that if we could.
Joel Nowak:
Okay, good goal. A lot of us look for that.
Dr. Sadar:
I hope so. A lot of this comes down to recruiting patients, how efficient we are are recruiting patients. A lot of it comes down to also how good the drug is. When patients start hearing that the drug is working well recruitment tends to be faster
Joel Nowak:
Right. Obviously, your results and recruitment is what we need to stay focused on and hopefully see this in the clinic in about three to four years. How does that sound?
Dr. Sadar:
That sounds wonderful. That would be a dream come true.
Joel Nowak:
That’s great. I tell you, you have done some absolutely amazing, amazing work. Of course, this has potential to change lives of so many people, not only the men but of course their families and their friends and so forth. The potential impact here is just so significant. As a prostate cancer survivor myself I really want to thank you so much for your hard work and the frustrations that you must’ve gone through, and of course, for sharing this information with us.
I just want to say for all us thank you so much. I don’t know that you have anything you want to add that I’ve missed that you think people would want to hear. If not, that’s fine. What did I miss?
Dr. Sadar:
I’ll just add one thing. I give talks to patients quite frequently. The world has made massive improvements to cancer treatment over the years. As I said, my sister died of cancer when I was a child and that cancer is now very, very curable. I think the cure rates are about 95% or more. Things do improve. There are cures for cancer. They do develop. I hope the world stays very positive and conspiracy theories that there’s a cure in the drug companies stifling it that makes me feel very sad because I think the scientist in everyone is trying very hard to improve the quality of life and find cures for cancer and other diseases.
Joel Nowak:
Terrific. Thank you so much. We really do appreciate it. It is okay if we check in with you down the line to see how things are progressing?
Dr. Sadar:
Yes, yes, please.
Joel Nowak:
Terrific. Thank you so much. Dr. Marianne Sadar is an amazing woman, amazing prostate cancer researcher, and we’ve had the great opportunity to speak with her and learn a little bit about her work and some of the frustrations that she’s undergone. I am hoping in a number of years to be able to have another conversation with her where we’re talking about how we’re going to get this out into the clinical because we’re at that point. That’s what I look forward to, and I’m sure that’s what she looks forward to. Thank you so much for listening to this teleconference.

If you have any questions that you would like me to relay on to Dr. Sadar you can email them to me. My email is n the webpage, and I will send them on to her, and if she has the time we will ask that maybe she can makes some responses. Thank you again for listening.
Dr. Sadar:
Thank you.