Tag Archives: PSA

June 13, 2020 · 10:47 am

CAR-T and related immunotherapies


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One of your co-subscribers to this blog contacted me and asked if I would write a blog about CAR-T cells, and I have decided to include the closely related bi-specific antibody therapies. I am very intimidated by even attempting this, because the complexities of this field are daunting, so please do NOT show this post to your PhD immunologist cousin.

As most readers probably know, the immune system consists broadly of the “humoral” and “cellular” arms. When you get corona virus, (or any other virus) both arms are activated. Broadly speaking, your B-cells (lymphocytes that live in the lymph nodes and also circulate in your blood stream) make antibodies that attach to targets (“antigens” – in the case of corona virus, the spike protein you are tired of looking at on TV is the target antigen we hope a vaccine can be made from) and can inhibit the virus or can clear the antigen from your circulation. Antibodies consist of proteins (chains) that combine with each other and this is where things start getting VERY complex, but a single B-cell can make only one type of antibody (called a monoclonal antibody). Whether you know it or not, if you have an interest in prostate cancer, monoclonal antibody technology is “why you are here” – PSA detection was made possible by isolating a monoclonal antibody that would bind to Prostate Specific Antigen. But with modern recombinant DNA techniques, the chains that make up these antibodies can be combined in highly variable ways never found in nature. The history and complexity of the antibody story is illustrated here from this article. Screen Shot 2020-06-13 at 10.31.25 AM

The Y-shaped figure above is “an antibody” and the colored chains are the proteins in the antibody that can be extremely variable and give the antibody its ability to bind to any target. Note that the two arms of the antibody could be designed so that one arm would bind to one target and the other arm could bind to a different target. Voila! You could design one arm to bind to PSMA and another to a killer T-cell that would link a killer cell to your cancer cell.

Screen Shot 2020-06-13 at 10.42.33 AM

 This is the general idea behind an innovative cancer approach you may hear about called BiTE. In this figure, the working part of the tips of two “Y” antibodies have been linked and when injected into a patient, in theory the “killer” T-cell is forced to bind to the tumor cell via its “TAA” or tumor antigen. If you are a dedicated reader of this blog, you already are thinking about a great target antigen I previously introduced you to, PSMA. 

Now on to my VERY oversimplified description of CAR-T cells. The terminology refers to Chimeric Antigen Receptor – T cells. The science of these is related to the above description of antibodies in the following way: On the surface of the T-cells in your lymphocyte library is a completely different group of proteins that allow the T-cells to bind to and recognize antigens, much like the antibody system we discussed above. These proteins combine in chains on the surface of the cells to form “T-cell receptors”. Unlike the antibody system, their interactions with antigens are further modified by requiring recognition of “self”. Non “self” is why people who receive a kidney or heart transplant must receive drugs to suppress the immune system that will reject the transplant. Unfortunately cancer cells are mostly recognized as “self” so we don’t reject them. BUT… again using recombinant DNA technology, the T-cell receptors (TCR) can be re-designed so they DO recognize a tumor target, even though it is “self”. You can start with lazy, somewhat unresponsive T-cells that might be in the blood or even infiltrating a tumor, take them out, modify the receptor (dramatically as shown in the following figure), and force them to recognize a cancer, then re-infuse them into the patient like any blood transfusion.

Screen Shot 2020-06-13 at 11.02.34 AM

In the figure (taken from this article), the “antibody like” part of the receptor that controls “self” is CD3 and the “antibody like” part of the TCR receptor that binds to a tumor antigen or virus infected cell are the green proteins marked alpha and beta. The recombinant magic that is WAY beyond this blog is everything on the right. If you have the time and interest in really delving into CAR-T therapy for cancer, you really do have to read this article. But, for those who wonder “so why aren’t we doing this?”, the Cliff’s Notes answer is that (1) it is VERY expensive – each patient has to have his/her T-cells taken out and modified, expanded, then re-infused; (2) it has only worked well for blood cancers like leukemias so far; and (3) even though PSMA or some similar tumor target might be thought to be “tumor specific”, it turns out these targets are often expressed in low levels in places like your brain or lung. When the CAR-T cells begin attacking your normal tissues, you are in a world of hurt. If you have followed the COVID-19 story, you may have heard about the “cytokine storm” that is killing people by destroying their lungs. As you might imagine, combining these approaches with the other “hot” area of immunotherapy, the PD-1 inhibitors I have previously written about could make CAR-T treatment more effective but the toxicities even worse.

I hope this has been helpful and that your immunologist cousin or highly informed oncologist will forgive the effort to simplify a very promising but challenging field. I’m also grateful to the myriad of incredible researchers who have put this all together for us “cancer fighters” and their dedication is equally as worthy of honor as other warriors on front lines.

 

 

 

 

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January 22, 2020 · 3:59 am

Dear Abby, my PSA…


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If you are a reader of this blog, it is likely that you or a close friend/relative has dealt with or are dealing with prostate cancer. Hence, you have become the “expert” in your family or book club or similar for people who know your story. One of the most frequent questions I encounter in such circumstances is a question about someone’s recent PSA. As an example, an 86 year old otherwise healthy cardiologist recently called me asking what to do about his  PSA that had gone from 4-ish to 6-ish during the last 2 years.

There are a few generalizations that seem to apply to most of these queries. First, the PSA increases at a fairly predictable rate with age. As a crude rule of thumb, I tell patients/friends that it should be less than 2 when you are 50, less than 3 when you are 60, and less than 4 when you are 70. A recent article in JAMA illustrates this point nicely. In the PLCO cancer screening trial, 10,968 men aged 55-60 had a baseline PSA drawn and were then followed with various screening strategies for prostate, colon, or lung cancer. Among the men with baseline PSA of <0.99, the incidence of developing clinically significant prostate cancer in the next 13 years was only 1.5%, whereas if their baseline PSA was 2-2.99, the chances increased to 10.6%. The authors concluded that ” These findings suggest that repeated screening can be less frequent among men aged 55 to 60 years with a low baseline PSA level (ie, <2.00 ng/mL) and possibly discontinued among those with baseline PSA levels of less than 1.00 ng/mL.” What to do for my octogenarian cardiologist friend is more complicated, of course.

A second generalization is that if someone has chosen to follow his PSA more closely, say on an annual basis, because they have read enough about screening to feel that regardless of the controversy, they wish to do so, they should plot their data. A column of numbers is much harder to interpret than a visual graph. There is an easy way to do this by entering the data on a website like this one: Doubling-Time.  It is also important to realize that different labs may give slightly different values on the same patient – particularly challenging if one is trying to torture the data in the lowest ranges of detectability (<0.2).

Thirdly, and related to the plotting approach, for any given patient with known metastatic prostate cancer, the absolute value of PSA may be less important than the rate of change (doubling time). A rising PSA that goes from 3 to 6 in 6 months is of greater concern than someone with a PSA going from 150 to 160. Of course having a lower value generally means a lower cancer burden, but I once had a patient enjoy elk hunting during the later stages of his disease with a PSA over 2000. He had relatively few symptoms in spite of his advanced disease.

Lastly, and related to my aging cardiologist friend, there’s a lot more to know than the PSA in most cases. When I asked him what his urinary habits were (unchanged) and what his rectal exam revealed (he hadn’t had one), I suggested he should visit a urologist for a more complete picture. If you biopsied his prostate, there is probably >50% chance of finding cancer at his age, but the key question is whether it would be a “clinically significant” cancer (Gleason score >3+3=6, or multiple cores positive etc.) In addition, one now has the opportunity to do pre-biopsy tests such as Select MDx, PHI, or ExoDx with newer tests being developed all the time to try and NOT find patients with low risk disease who might never need any sort of treatment.

So, at your next cocktail party when a friend asks about PSA, you can gently explain the complexities you are all too familiar with, and hopefully guide them in the right direction. And if you are interested in more blogs, I recently discovered Snuffy Myers’ blog site, Prostapedia, that has numerous blogs from highly respected prostate experts with great ongoing updates. Happy New Year and most importantly EXERCISE!

 

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April 9, 2019 · 9:38 pm

What we see and what YOU get.


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Will Rogers is said to have stated, “When the Oakies left Oklahoma and moved to California, it raised the IQ of both states.” This story has given rise to the concept of the “Will Rogers phenomenon” in medicine that is very well explained in this essay. Basically, it provides a cautionary message when evaluating new therapies in cancer medicine, because if a new study has taken advantage of newer diagnostic techniques to eliminate some of the patients with higher risk (say those with metastases), then it could easily be that an improved result is not from the new therapy, but from the ability to throw out the higher risk patients from a study cohort.

We are certainly at risk of this now in prostate cancer. In the last 5-10 years, a number of more sensitive scans have been introduced that can reveal metastatic deposits previously missed by standard technetium-99m bone scans or CT scans. Most of these rely on the technology known as PET (positron emission tomography) scanning. The first clinical PET scans mostly utilized glucose to which a positron emitter, Fluorine-18, was attached. For bone metastases, it is easy to see how much more sensitive F-18 scans are as shown in this image: (Same patient – A. “Regular” Tc-99m bone scan  B. NaF-18 PET scan)

Screen Shot 2019-04-08 at 5.01.55 PM

Suppose you have a new treatment that is for patients “with 10 or fewer” bone metastases. If you are comparing the new treatment with one that was used in the past, and you now use the PET scan (on the right), this patient would not be eligible, whereas in the past (old scanning technique) he would have been. He clearly has a higher tumor burden than 10 metastases. Hence, he is now eliminated from the new study, and therefore the new study will automatically look better in terms of outcome than previous treatments. This is called “stage migration” or the “Will Rogers phenomenon”.

For “soft tissue” metastases (lymph nodes, liver, lung, etc.) the regular Fluorodeoxyglucose FDG-PET scans were approved decades ago for lung cancer, colon cancer, lymphomas and breast cancer but they never worked well for prostate cancer. A simplistic explanation may have to do with the different metabolism of prostate cancer which tends to utilize lipid rather than glucose for energy. (see our study here). Therefore researchers looked for other metabolites that would light up prostate cancer. Acetate and choline could be labelled with Carbon-11 and worked well. However, C-11 has a half life of only 20 minutes, so making the label in a cyclotron had to be done essentially in the room next door to the scanner and injected immediately into the patient. Another metabolite taken up by prostate cancer, an artificial amino acid (fluciclovine), could be labeled with F-18, worked well and has now been approved, called the Axumin scan.  Potentially even better will be the PSMA scan, now in research mode.

The net result of these new scans is to allow physicians to answer the frequent question patients ask, “Where is the PSA coming from?” The problem then becomes the title of this essay – What we see and what You get. There are numerous scenarios. For example, a patient who comes in with a very aggressive Gleason 9 cancer and a PSA of 12.3. Should we go immediately to a routine bone and CT scan, or just order an Axumin scan? And if we find 2 positive spots, one in a rib and the other in a lymph node, does that mean the patient can’t be cured?? Five years ago, we would have never known about the metastases and we would have operated or used radiation therapy in a curative attempt. Screen Shot 2019-04-09 at 9.56.43 PMWhat about the patient with a rising PSA 5 years after he had surgery. We do a PSMA scan and find a solitary node near the left iliac artery. Should we irradiate the node? What about operating and removing it – remember, it may not look any different from all the other nodes to the surgeon. Which one should he/she take out? And what is accomplished by these efforts? Should the PSA go down (yes if that’s the only metastasis) and what to do if it doesn’t go down. Are we playing “whack a node”? How many times do we go after spots that keep showing up, versus starting some sort of hormone therapy?

There is an excellent article addressing some of these questions written by my good friend Chris Sweeney and colleagues that you can read here. A summary quote from their article states, “Given the current limited understanding of how reliable these scans are in predicting the need for appropriate management change, data-driven guidelines and standardized consensus approaches are more critical than ever.” A review of some of the early attempts to treat a small number of metastases (called oligometastatic disease) has just appeared here. One example of a paper reporting interesting results is summarized as follows: “Of the retrospective reports, the largest includes 119 treatment‐naive patients who had ≤3 sites of oligorecurrence and received SBRT to all involved sites, with 92 of 119 (77%) undergoing pretreatment choline PET. The 3‐year distant PFS [progression free survival] rate of 31% and the 3‐year OS rate of 95% are favorable and suggest a subset of patients likely benefitted from aggressive local therapy; however, conclusions from these data are limited in the absence of a comparative control arm.”

Maybe we simply have to refer back to another quote from Will Rogers, “America is a nation that conceives many odd inventions for getting somewhere but it can think of nothing to do once it gets there.” Stay tuned…

 

 

 

 

 

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April 28, 2018 · 9:53 am

Improving our focus


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I have had two life changing experiences in focusing. The first was when my wife discovered the Myers-Briggs personality classification system and found I am a “strong P”. This meant I couldn’t help it when I was on my way to take out the garbage, noticed a light had burned out, put the garbage down and went to get a light bulb, but found that there was a spot on the carpet that needed cleaning and finally found the carpet cleaner but an hour later wondered why there was a garbage sack in the hall. Prior to her discovery, she just thought I was an idiot, but she became [somewhat] more tolerant of the foibles when she could “classify” me. The second was when I had my congenital cataracts removed and new lenses inserted in my eyes. It was a whole new world of color. I had been living in a fish tank with scum on the glass and “wow, the world is really pretty!” was my response when I took the patches off the next morning. “Trees have LEAVES!”

Focus in understanding prostate cancer is becoming clearer as well. For several decades we have known that the Gleason scoring system is pretty darn good at predicting the cancer’s behavior, adding a lot to what we knew when there was only the digital rectal exam… “Oh, oh, that feels like a really big tumor” or “Maybe I’m feeling something but I can’t be sure”.  Then came the number of biopsies positive, the percentage of each core, differentiating 3+4 vs 4+3, and now an avalanche of new molecular markers, briefly reviewed here. Combining the old standby risk categories with the newer methodologies has been challenging.

A recent paper in the JCO provides us with one way of integrating the old risk categories with the newer molecular classifications. Using the widely adopted risk categories of the NCCN, the authors added to this, one of the more mature molecular classifiers, the 22 gene Decipher™ scoring system to reclassify (focus) a new model to predict outcomes. As I explained previously, these genetic tests are typically developed looking at the level of gene expression in biopsies or in removed prostates in a group of patients for whom an outcome is known (examples include prostate cancer free survival at 10 years or freedom from metastases at 5 years). The investigators (or companies) then go to a different institution or collection of biopsy material and see if their gene expression model developed from the first group accurately predicts the outcome in the second group. This is called “validation” of the test. Decipher has done all of this. The question is how it might change the risk classification of the “old” system.

This figure illustrates how it plays out when a large number of institutions collaborate to study the information gained and develop a new model.Screen Shot 2018-04-28 at 10.16.05 AM

As an example of how this can be used in the “real life” clinic, we are often faced with a patient who has a “favorable intermediate” prostate cancer. Let’s say this is a 75 year old man with excellent health. Should we advise that he adopt a “watchful waiting” strategy, given his age and the relatively low risk? By adding the genomic test, you can see that 27% of the time, this might be a bad recommendation. Similarly, in the unfavorable intermediate group, 40% of patients are moved into a high risk category. Such a patient might be well advised to “do more” (example: more prolonged ADT with radiation, or use of brachytherapy in addition to external beam radiation if they had chosen radiation therapy as their preferred treatment modality).

These kinds of improved focus will allow investigators to do better studies prospectively as well. In breast cancer it is already a standard of care to do molecular classification of certain stages and types of tumors, allowing women to make far better decisions on whether (for example) to take chemotherapy in addition to surgery/radiation. In prostate cancer, where I have been concerned that we aren’t “racing for the cure“, rather we are “crawling for the cure”, it looks like we may be catching up. Research is the answer – sign up and contribute!

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February 25, 2016 · 11:28 am

No pain, no gain?


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One of my patients last week had a heartfelt discussion regarding the survival benefit of ADT vs his quality of life. He enjoys body building and showed me some pretty dramatic pictures of himself during his last ADT cycle (on intermittent therapy) versus now, when he had been off treatment for ~6-9 months. Added to his concern was his decline in libido and sexual function during ADT, a common complaint especially among younger patients. The question of quality vs quantity of life was,of course, utmost on his mind.

Starting from the initial diagnosis, every (maybe that should be every !!) prostate cancer patient will experience a decrement in quality of life. Those who elect “watchful waiting” will nevertheless experience anxiety regarding the shadow of CANCER following their footsteps. Sure, you can put it out of your mind, but turn around and there it is, like the neighbor’s unwanted cat stalking you. Then there is the anxiety over what the next PSA will be. And if on active surveillance, what will that next biopsy show?? These issues are both real, disturbing, and often under-appreciated in the discussions surrounding screening…”we should still be screening, but not treat the men who don’t need it…” Really? What about the 80% of men who die at age 90 with prostate cancer at autopsy who never had to deal with the shadow? (The inevitable counter-argument is, “yes, and what about those who had early detection of a high grade cancer whose life was saved?”)

We also tend to ignore the impact of competing mortality in our discussions. “Sure you had a stent placed last year, and you already survived that small colon cancer, so why wouldn’t we be aggressive in treating this new problem?” Dr. Sartor provided an elegant discussion of this in an editorial on the PIVOT trial you can read here. Whatever the flaws in that study, it remains clear that we are not very good at predicting the non-prostate cancer “future” for our patients, and the older you are, the thinner the ice gets regardless of how many marathons you run.

When patients choose one form of primary treatment vs another, they are weighing the different side effect profiles of surgery or radiation as much as which is “most effective”. I often give patients a copy of this article from NEJM and encourage them to spend some time looking at the graphics in Figure 1 to get some idea of what they will face in the way of side effects from treatment. As any honest physician would tell them, treatment will involve side effects, some permanent, in the best of circumstances.

In the setting of more advanced disease, for example a patient who presents with metastases outside the pelvis, the recent CHAARTED and STAMPEDE trials both suggest an advantage to the earlier use of docetaxel chemotherapy in combination with ADT as opposed to ADT alone. These data suggest that “pay me now or pay me later” analysis favors the “pay me now” approach in terms of overall survival. But at what price for quality of life? Fortunately most chemotherapy side effects are reversible, but distinctly unpleasant, potentially making the equation something like “4 months of misery to provide 14 months of longer life….not all of which will be great anyway”.

Even in the very advanced setting, there is some evidence that greater toxicity results in improved survival. A recent analysis of the TROPIC trial of cabazitaxel suggested that the patients who had the most “toxic response” in terms of dropping their neutrophil count benefited the most in terms of overall survival.

While all of this seems incredibly negative (for which I apologize), the history of oncology as a field has been the incremental improvement in survival AND the development of newer treatments that provide such advances with diminishing toxicity. Pediatric leukemia, as discussed extensively in “The Emperor of All Maladies” is a great example of how pioneering patients and physicians worked together to find cures and reduce side effects. We may only be at the beginning of such achievement in prostate cancer, but with the advent of the newer hormonal and imaging agents, increasingly sophisticated surgery and radiation, vaccines and immunotherapy, and even the chemotherapies now available, we have  no doubt reached the end of the beginning. Onward!

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October 30, 2014 · 10:39 am

Yay…Movember is here. Let’s kick Pca


Hi friends and relatives (those who will admit it…),

This Movember, I’ve committed my upper lip to help change the face of men’s health by growing a moustache, now I need your support at http://mobro.co/michaelglode.The Movember Foundation is the leading global organization committed to changing the face of men’s health. I’m passionate about this cause because too many men are dying unnecessarily from prostate cancer. In 2014, more than 233,000 men will be diagnosed with prostate cancer. Even better, join our team and donate to yourself and invite your friends/family to the cause! Our team is here: http://us.movember.com/mospace/index/search/?q=university%20colorado

 The Movember Foundation is working tirelessly with an urgent goal in mind: accelerating breakthroughs in prostate cancer research that will benefit patients and their families. Movember is achieving this with the formation of the largest, global alliance of prostate cancer researchers and clinical specialists, who are tackling the toughest prostate cancer challenges. I had the privilege of hearing the updates on the research they have been sponsoring last week at the PCF retreat. More progress in the last 5 years than in the previous 25. Take a look there for updates/posts yourself!

I need your support to fund this important work. Together, we can create a world where no man dies of prostate cancer.

You can donate by:

– Donating online at http://mobro.co/michaelglode (and follow the pathetic growth of my not-so-manly moustache…)

– Writing a check to ‘Movember’, referencing my registration ID: 5798901 and mailing it to:  Movember, P.O. Box 1595, Culver City, CA 90232

You can learn more about the important work and impact Movember is having at: http://us.movember.com/programs. There’s a lot riding on this moustache, thank you for your support!

 Mo Bro Michael Glode

http://mobro.co/michaelglode

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May 15, 2014 · 2:06 pm

Oh, no! My PSA is going up….do something….


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One of the most frustrating and frightening things that can happen to a prostate cancer patient is for there to be a recurrence of the PSA after he thought he had been cured by surgery, radiation therapy, or both. This is entirely understandable. It is no picnic to go through those treatments in the first place, and when the PSA is clearly going up, it can only mean (with very rare exception) that there are still cancer cells lurking somewhere in the body. The rate of the PSA rise can predict how long it will be until something shows up on a scan, and on average, this is about EIGHT years. The median time to death from prostate cancer after a PSA recurrence is 16 years.

For >95% of patients there is something that CAN be done to stem the rise in PSA. That is to go on hormonal therapy (androgen deprivation, ADT) which will drop the PSA, often all the way to undetectable levels, in over 95% of patients. Voila! Both patient and physician feel much better emotionally. But for the patient, there is a significant price to pay. Namely the hot flashes, loss of energy, weight gain, bone calcium loss, lack of libido and further decrease in sexual function to name a few. The question is whether this is “worth it”.

A study to be presented in the next few weeks at ASCO’s annual meeting, suggests it won’t make much difference if you start ADT early versus waiting until metastases, or perhaps even symptoms occur. Utilizing the CaPSURE database, the investigators evaluated over 2000 men who had PSA relapse. The estimated 5 year overall survival (87% vs 85%) and 10 year overall survival (72% vs 72%) were the same regardless of whether the men received immediate or delayed ADT. The same was true for death from prostate cancer…no significant difference. There are of course other considerations that may come into play like treating those patients who have highly aggressive disease earlier because one knows that there will be metastases within a year, or the patient simply can’t live with himself knowing his PSA is going up.

In my experience, it is the exceptional patient who is willing to go play golf or travel or enjoy his grandchildren and forgo PSA testing on a regular basis. I have trouble even convincing my patients to extend their PSA testing to 6 months from 3 months. The question is, does it make any sense to watch this “number”, any more than it would to have cardiac catheterization every 3 months to follow the slow but inexorable accumulation of calcium in your coronary artery? Or what about the 0.01 mm increase in your abdominal aortic aneurysm? Or the accumulation of two more tangles in the Alzheimer plaque in your brain. Just because we CAN measure PSA so easily certainly doesn’t mean we SHOULD, and I have seen far too many men let this number ruin their otherwise healthy lives.

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October 7, 2011 · 11:15 pm

The silent majority


Yesterday the US Preventive Services Task Force released information that it will recommend against routine PSA testing for prostate cancer. Predictably, there has been a firestorm of responses, mostly criticizing this finding. The most vocal critics are prostate cancer patients and advocates, including their physicians. As a physician who has cared for several thousand prostate cancer patients and a member of this community, I think it is appropriate to chime in. However, what I am about to say will not set well with many. Here is an inconvenient truth: If you live long enough, you will probably develop prostate cancer. 55% of men in their 50’s and 64% of men in their 70’s have prostate cancer when their prostates are carefully examined at autopsy. And the frequency goes up from there. These men are the silent majority – the ones who had no treatment, remained continent and potent in many cases, did not have the anxiety of knowing they had cancer, and lived a full life, dying from some other cause. In fact, prostate cancer accounts for only 4% of all deaths in men. The patients who have been diagnosed and successfully treated ALL feel that prostate cancer screening saved their lives. Most of us who treat prostate cancer or participate in screening for it would like to believe the same thing. Indeed there are some retrospective studies like the famed Tyrol, Austria study that would make us believe that prostate cancer screening is having a major effect. And yet, as I previously blogged on screening, randomized trials suggest that if we save lives at all, …1) It is only in men under 65 and 2) you have to screen and treat a very large number of men (with all those side effects), to save even one life. This controversy will not go away soon, and we all await the day when molecular testing can tell us which cancers we can safely ignore, even if we find them “by accident” on screening. Until then, I think it is perfectly reasonable to salute all of our men who have lived into their 70’s and 80’s, especially those 50% walking about who have prostate cancer and don’t know it and will never miss nor be harmed by NOT being treated or screened. They are the silent majority in this debate.

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