Bob’s Journey – June 2004 to Summer 2014

This graph shows the variations in my PSA from July 2002, when it still measured 1.0, to early Spring 2010, when the cancer really began to take hold. Note that during these first six years my PSA did not rise above 8 before we intervened

The graph above shows my PSA from July 2002, the last date my PSA consistently measured 1.0 on the screening test then recommended each year for males in their 50s and 60s, to May 1, 2010. Please note that all PSA measurement results are less than 8 ng/ml. For all our concern, disappointments and tears over the apparent failure of these first treatments, we “hadn’t seen nothing yet!” I devote the first part of this comprehensive post to describing the treatments and results of the first six years because, for many men with cancer too advanced for surgery, one or more of these has been sufficient to drive prostate cancer into dormancy. Then, I’ll pick up my story in the Summer of 2010 and describe my more recent experience with Provenge, Taxotere chemotherapy, Zytiga, Sprycel, and Xtandi. To put things in context the next chart shows my entire PSA from July 2002 to late Summer 2012.

This chart shows my entire PSA history. It starts in July 2002, just as I was retiring from full-time work, through the summer of 2012. While the first six years were characterized by many cutting edge treatments and disappointments, the roller coaster rides of the recent years keep us constantly in shell-shock.

It frightens me to realize that those “huge peaks” on the first chart above are but tiny blips when my entire PSA history is plotted on one chart. Truly, we had “not seen nothing yet.” And, now that we HAVE seen it, I have lopped off the first six years of data. In the chart shown further down, at the beginning of the discussion titled, “Summer 2010,” the plot will start from just before the Provenge experience. Fall 2003 to Spring 2010 I count five distinct phases of treatment and response during the first six years: Phase 1 – PSA rise, biopsy, initial diagnosis, first hormone blockade and radiation therapy This phase began in Fall 2003 and ended in mid-2006. (I have always wondered why this happened during the first year after I stopped working full-time.) In May 2004 my HMO physician found my PSA had risen above 4.0, the magic number, and appeared to be rising rapidly. A biopsy in early June, a CT scan, and a bone scan showed: (1) full involvement of my prostate gland with Gleason (4+5=9) cancer and, (2) a possible lesion in my right hip. In early July I started on hormone blockade (Lupron-only) to shrink the prostate gland and arrest further growth, as well as monthly Zometa infusions to forestall osteoporosis. In late November we accepted a “long-shot” recommendation from our Palo Alto VA Hospital physicians to go for intensity-modulated radiation therapy (IMRT). The rationale – my prostate gland is small (~20 cc) and the apparent lesion in the hip lies in about the same plane as my prostate gland. The radiation therapy was completed early in March 2005; at the end of March I started the full hormone blockade, also known as full androgen deprivation therapy, ADT-3 (Lupron, Casodex, and Proscar). By mid-October 2005 my PSA had dropped below 0.01 ng/ml. This is another magic number. When a cancer patient’s PSA drops below 0.01 ng/ml, it is said to be “undetectable”.  During all of 2006, I took no drugs, except for the usual maintenance dose of Proscar. We continued to pay close attention to the diet recommendations for prostate cancer patients. Phase 2 – Testosterone recovery, cancer “awakening”, second round of hormone blockade This phase began in about Fall 2006. As my testosterone slowly recovered to about 500 ng/dl. In late October 2006, my PSA began doubling every three weeks. This is extremely rapid. Since my blood tests were then done only quarterly, we were unaware of this rapid rise until mid-April 2007. My PSA reached a zenith of about 8 ng/ml in early May; I went back on ADT-3 immediately. It dropped even faster than it had risen, and we enjoyed a feeling of control through the summer of 2007. Phase 3 – “Hormone refractory” stage, second-line hormonal therapy, including estrogen patches Beginning in August 2007, my PSA began to rise again. Initial PSA measurements, now monthly, indicated a return to the three week doubling time. When the cancer cells, as measured by increasing PSA, appear to begin growing again, in spite of the hormone blockade therapy, the cancer is said to have become “hormone refractory”. In a 2007 book entitled, “Beating Prostate Cancer”, Dr. Charles Myers, Jr., describes a “second-line” hormonal therapy utilizing ketoconazole in place of one of the hormone blockade drugs, as well as transdermal estrogen to go after prostate cancer that has metastasized in the skeleton. In early November 2007, we upped the daily dose of transdermal estrogen. By early January 2008 my PSA had declined smoothly to about 0.06 ng/ml. Phase 4 – Second-line therapy, plus immune system boost, antiangiogenesis & resveratrol This phase began in early 2008 and continued until mid-summer 2009. In January 2008 we started daily injections of the immune system booster, Leukine, and a 14 days on / 14 days off regimen of an antiangiogenetic, an agent known to inhibit blood supply formation for new cells. That program was stopped after just one month because the Leukine was temporarily taken off the market. In May 2008 we added daily doses of resveratrol, an agent known to “soften up” the prostate cancer cell population for destruction by the immune system. In January 2009, we began again daily injections of Leukine and resumed the 14 days on / 14 days off regimen of the antiangiogenetic. You can see from the first chart above that my PSA stayed very low during that entire period. But, we had yet to find a “knockout punch”. Phase 5 – Using differentiation agents for “growth arrest” Starting in late November 2009, I began adding to my daily regimen a modest daily dose of curcumin, the active ingredient in turmeric. Use of this differentiation agent, along with the resveratrol, continued through Spring 2010. Both curcumin and resveratrol have been shown effective as differentiation (or growth arrest) agents for prostate cancer, i.e., agents that “soften up” the cell population for the immune system. By early January 2010, I had worked my way up to 3600 mg/day of the curcumin. The chart below shows my PSA response to the curcumin dose, as well as the impact of both low-dose nitroglycerin and Sandostatin that I started in late March and late May 2010, respectively.

This chart from the Winter-Spring 2010 shows our attempts to differentiate better the progeny of the most poorly differentiated cancer cells so that my immune system might destroy them. It didn’t work for me.

The steady upward march of the PSA (orange dots) shows that none of these differentiators was having much impact at all. More aggressive measures were called for. When I wrote the first version of this post two years ago in May 2010, we were profoundly disappointed. After six years of androgen deprivation therapy (ADT-3), intensity-modulated radiation therapy (IMRT), second-line hormonal therapy, antiangiogenesis drugs and doses of cancer cell differentiation agents, all had failed to control PSA for more than a few months. And, we had just been crushed to find both a rapidly rising PSA and a bone scan report that showed an increase in the number of metastases in my spine, ribs and pelvis. What in the hell to do next? Two years later, the paragraph below is still valid. Looking back (in May 2010)……….what have I learned from this experience so far? I am certainly glad that I had monitored my PSA in the years prior to 2003. Just the sudden jump in November 2003 (from 1.0 in July ’02 to 3.6 in Nov. ’03) should have been a clue. Few physicians were that smart back in 2004; it is fortuitous that my HMO internist checked it again in May 2004. Think about whether I would be here today without the warning provided by the routine PSA screening test now dismissed by the US Preventive Services Task Force! As PCa patients, we are similar in some and different in other ways. Cancer research of the last two decades has identified many common patterns. Still, the treatment procedure that works well for one patient may be much less effective for another. Many of the treatments that have worked well for so many others haven’t done diddlysquat for me and others with advanced disease. Consequently, it is important to take charge of one’s own disease. My goal is to learn what works in my body, to get control of my PCa tumor population, drive those cells into dormancy and keep them there. My medical team and my support team (family, friends, and UsTOO support group members) have helped enormously. As a “high-risk” patient on all three counts – Gleason score >8 at diagnosis, distant metastasis at diagnosis, and extremely rapid PSA doubling time after initial treatment failure – I take as my responsibility the life-long task of achieving this goal. PCa patients are not alone. Medical, emotional and spiritual support is nearby. I’m glad I tapped into that in the beginning. There are many helpful references both in print and on the web. In addition to Dr. Myers’ book cited above, another by Stephen Strum and Donna Pogliano entitled, “ A Primer on Prostate Cancer: The Empowered Patient’s Guide,” should be read by patients wanting to understand their disease and all the treatment options available. PSA June 2010 - June 2013.005

Summer 2010 – Provenge

From the chart above you can see that my PSA started climbing again by mid-year 2010. At that time FDA approval of the PCa “therapeutic vaccine” Provenge was barely a month old, and many of us advanced patients were scrambling to gain access. The chief’s staff found a clinic near us in the WDC-metro area that had participated in the clinical trials. I passed the interview for these first “on-market” administrations of the vaccine and began my first leukapherisis on June 25th. The chief was sufficiently concerned that, absent the Provenge opportunity, he wanted me to start Taxotere chemotherapy ASAP. Thus began the series of four “roller coaster rides” we have experienced since then. For more details of the Provenge experience in Summer 2010 please go to one or more these posts: Provenge Immunotherapy; Provenge Immunotherapy Cycles – 2 done, 1 to go!; and Eighty Days Post-Treatment.

PSA and Bone-specific alkaline phosphatase (ALP) through period of the three Provenge cycles in June and July 2010, as well as the five months following. This period is the time of “Provenge-training” of my immune system. The steady increase in ALP – green curve – shows bone repair activity as a response to tumor progression more consistently than the “wandering” PSA.

I think the idea behind Provenge is the wave of the future. What could be better than training my own immune system to ride herd on these bad guys and keep them dormant. Unfortunately, the evidence so far is sparse, and the treatment far too expensive. And, the manufacturer makes nearly no effort to gather information from those of us who have received the vaccine. From the chart above, clinical evidence (blood tests, declining PSA, better bone scans – routine indications of growth arrest) seems altogether lacking at this point. The best thing I’ve heard an oncologist say about Provenge is that her patients who have received the vaccine tend to be surviving still. I sometimes wonder if this drug might be more effective for men whose cancer is less advanced.

  2011 – Taxotere Chemotherapy and Zytiga

The chart below shows my PSA and Alkaline Phosphatase S ( an indicator of bone reconstruction) at the presumed end of the “Provenge training session”. In November 2010 the chief and his colleagues took a tumor sample from one of my vertebrae and sent it to the lab of Caris DX for genetic analysis. The results came back in early January 2011; the data showed vulnerability of my tumors to many drugs, some familiar and some nearing FDA approval. One of these was Taxotere – a long-standing workhorse for PCa chemotherapy.

This chart begins at a point several months after completion of my three cycles of leukapheresis, Provenge activation of my dendritic cells for PAP, and re-infusion. It shows a continuing rise of my PSA through the end of 2010. It also shows the wonderful PSA response we achieved from the Taxotere infusions in the first five months of 2011. (The initial jump and then decline of the two alkaline phosphatase markers during that period is consistent with expectations.)

On January 10, 2011, with my PSA approaching 60 (the highest yet), we gave up waiting for any clinical evidence that Provenge was having any beneficial impact, stopped daily Leukine injections and ketoconazole doses that were designed to augment the “Provenge-training” of my immune system, and scheduled pre-chemo baseline bone and CT scans. I was a sick puppy. I couldn’t eat adequately because of 20+ pounds of retained fluids that filled my right leg, lower abdomen and stomach areas. I had trouble getting sleep because of sciatica pain that bothered me when I lay prone in bed. (At the time I thought the sciatica was aggravated by the edema [fluid retention]. Now, I’m not so sure.) I received my first chemotherapy dose of 135 mg Taxotere on January 24, 2011. Five days later, before my white blood cell count reached its nadir for that cycle, we climbed on a plane for California to escape the bitter mid-Atlantic winter cold. Through friends we had already arranged to continue the chemotherapy at a cancer clinic near our home in San Jose. Thus began a very successful series of treatments that helped us regain control of the cancer. The chart above shows the PSA response to 135 mg infusions of Taxotere every three weeks for eighteen weeks. By all accounts the response is remarkable.

Zytiga

Zytiga, previously known as abiraterone acetate, was approved by the FDA for prostate cancer patients in the Spring of 2011. The link above provides an illustrated description of this drug and how it is supposed to work. Since my PSA was under control (1.2 – 1.3 ng/ml) at the end of the six cycles of chemotherapy (Round 1), the chief suggested I try this new drug over the summer. For me it turned out to be an unmitigated disaster. I took it as directed for more than 75 days beginning in June 2011. By mid-August my stomach could no longer deal with the constant digestive system upset from the peculiar dosing scheme. Moreover, my PSA had climbed steadily all summer, frequently doubling in as few as 13 days, a ridiculously rapid rate. By mid-September my PSA had risen to around 125 (a new high). I needed pain killers for the first time in order to sleep at night. I was too weak to sit up in the waiting room at our northern Virginia (NoVA) clinic. Within 10 days of our return NoVA I was back on full dose chemo. (I had not yet learned that low dose chemo would work as well.)

This chart shows the rise of PSA during the summer while taking Zytiga. (The companion rise of the ALP and BALP are NOT good signs.) Round 2 of Taxotere chemotherapy, which began Sept. 16, 2011, was as effective as Round 1 earlier in the year.

The chart above shows this rise of PSA during the time I took Zytiga in the summer of 2011 and the rapid drop after getting back on to chemo for Round 2. By late November my PSA was back in the 1.0 to 1.5 ng/ml range. Please note that we achieved the nadir in the PSA with just four cycles of chemo in this Round 2. With the Zytiga experience behind us we went to California for the winter expecting to enjoy being off the drugs and treatment regimens for at least a season.

2012 – Chemotherapy Round 3

At that point my system had absorbed ten full doses (135 mg per infusion) of Taxotere. That’s 1350 mg. I began to wonder what my limit would be. Arriving late December in California to a wonderful welcome from our hiking friends, our euphoria was short-lived. In January I began to take a small dose (20 mg/day) of Lasix to go to work on the edema in my right leg and abdomen. (At the same time the cancer was taking off again on what would become roller coaster ride number four – see chart below.) By late January the small dose of Lasix had done nothing for the edema, and the cancer was again close to out-of-control. The pressure from the fluid retention made eating more difficult by the day and pain from the sciatica made sleeping very difficult. Our California oncologist recommended getting back on chemotherapy ASAP. I didn’t feel strong enough to endure another blast of 135 mg of Taxotere and its after effects. He suggested an alternate regimen successfully used by a friend in our support group – take just 50 mg of Taxotere per week for three weeks in a row, then take a week off. This was my introduction to “low dose chemotherapy” (LDC) – a regimen I have been promoting enthusiastically ever since.

This chart shows

This chart shows my PSA and alkaline phosphatase (ALP) behavior during the winter/spring/summer of 2012. I received seven 50 mg infusions of Taxotere between February 3rd and April 2nd. I have prepared a chart comparing the effectiveness of these three chemotherapy rounds. It shows that low-dose chemotherapy (LDC) works just as well on my PSA as do the larger doses. The blue line in the chart above shows the impact of the 7 –  50 mg infusions of Round 3 alone – Feb 3 thru Apr 2. We returned to NoVA in mid-April and began a holiday from the chemotherapy. Surprisingly, my PSA stayed below 10 for nearly two months. What a delightful holiday that was! At our mid-May appointment, the chief suggested I try a combination of LDC-Taxotere and a drug named Sprycel because there was increasing evidence that the two worked synergistically against PCa. Sprycel turns out to be frightfully expensive stuff. How thankful we are for Medicare Part D! Nevertheless, I started taking 100 mg of Sprycel on June 1st, and we restarted LDC on June 15th, after PSA had climbed back over 20. Sprycel, also known as dasatinib, was developed for patients dealing with chronic myeloid leukemia. It inhibits the action of the SRC-family kinase. (In the article at this link, scroll down to the middle of page 4 and look for the paragraph titled “SRC inhibitors”.) References to this family of enzymes are found in several papers in the Journal of Clinical Oncology because of their involvement with leukemia, breast and prostate cancer.

Summer 2012 to Summer 2013

This past year has been similarly challenging. As noted in the section above, on June 1, 2012, I started taking 100 mg Sprycel daily, along with a 50 mg Taxotere infusion every two weeks. This seemed to go OK for about 6 months. Shown on the chart below is the rapid drop in Ntx ratio (orange curve) from 66 to 16. This is a several points lower than the upper end of the normal range. Since then, my Ntx ratio, a measure of osteoclast (bone destruction) activity has stayed comfortably in range (<24), even though I stopped taking Sprycel in mid-February 2013. Turning to PSA and bone ALP, notice that PSA steadily climbed throughout the summer and early fall while bone ALP wandered downward. (Bone ALP, or bone-specific alkaline phosphatase, is a measure of osteoblast (bone-repair) activity in the skeleton.)

This chart shows

This chart shows changes in PSA, Bone ALP and Ntx ratio

In late November it seemed I spent more and more time “feeling wasted” after the infusions. I had started taking 160 mg/day of Xtandi (formerly MDV3100, newly FDA-approved, and renamed) per the plan with the chief. The drop in PSA and bone ALP in response to the Xtandi was prompt and encouraging. (See data points for December 3, 2012.) After that, the chart shows things “going to pot” again – bone ALP rocketing up and PSA meandering higher – what’s going on now? In response the chief suggested I ramp up on a dose of a steroid (prednisone) on the possibility my adrenal gland needed help; I started that in early December and worked my way up to 20 mg/day. Back in California in late December for the winter, we promptly made an appointment with our CA oncologist. The chief had already informed us that recent experience pointed to conflict between Taxotere and Sprycel – the latter tends to disable the pathway by which Taxotere is cleared from my system. This would keep more Taxotere in my system longer than “normal.” A lower dose of Taxotere – 40 mg – in mid-February appeared to have no impact, either on the cancer or my ability to tolerate the aftermath. So, we decided on another “big-boy” dose in mid-March to see if my cancer had become Taxotere-resistant. By early April we were back in VA; my VA oncologist concluded the PSA drop following the big-boy dose was sufficient to say that I am not yet Taxotere-resistant. And so began Chemo Round 4 –  three series (April, May, and June) of LDC infusions (three weeks on and a week off). In early May the chief told us he thought that the steroid might be interfering with Xtandi. So, I stopped both on May 6 and continued only on Taxotere for the two series of infusions in May and June. At the end of May my PSA had dropped to 31; bone ALP to 45. (see right side of the chart above) Looking ahead, I’m expecting to restart Xtandi in early July to see what it might do in the absence of any steroid. Xofigo (alpharadin) injections might come later in the summer.

Summer 2013 to Summer 2014

This past year was indeed the year of Xofigo. As suggested above, after completion of Chemo Round 4 in late June, I did start back on Xtandi on July 1st and continued it during the time we spent in northern Michigan. Xtandi cotinued to do me good things for me during those few weeks. And, it also caused substantial fatigue each day – an afternoon nap was not just a delightful option, it was mandatory. After we returned to NoVA in late August, local hospitals with facilities for handling radioactive materials used in nuclear medicine were ready. I stopped Xtandi at the end of August and received my first Xofigo infusion in early September. As shown on the chart below, the results were dramatic.

PSA&BALP Feb'14By the time we did PET/CT scans with both Na-F18 and Fluorodeoxylglucose (FDG) in mid-May, there appeared to be no viable cancer cells detectable in my skeleton. This gave rise to short-lived joy about my cancer being in remission. I felt OK in June and spent time preparing for some “minimally invasive back surgery to relieve the pain from the stenosis in my lower lumbar spine. Events began in July that we still don’t understand. That’s a story for the 2014-2015 installment.

Summer 2014 to Summer 2015
As June passed into July, I was indeed making a run at “minimally-invasive lower back surgery” to fix the stenosis in the lumbar spine. We had already spent a year trying epidural injections of steroids, taking various oral medications (Gabapentin and Lyrica) and going for physical therapy – all to no avail. At that time most chairs were uncomfortable, and we hauled around a “Healthy Back” cushion wherever we went. In June we made appointments with two orthopedic surgeons based on referrals from friends, chose one and scheduled the surgery for mid-July. That’s when things really went downhill. I had not had a Taxotere infusion for a year.

In early July I began having pain around my left rib cage. It felt like the shingles I had had in the summer of 2012 – but there was no rash. Since the location of the pain in my left rib cage raised red flags about heart issues, my trip through the pre-operational clearance maze ended up in the cardiologist’s office. These thorough folks wanted to do several additional tests. The weekend before the back surgery was scheduled, I felt I couldn’t manage to show up for the nuclear stress test the following Monday morning. So, the whole effort was postponed indefinitely.

In July things continued to slide downhill. In late July I was admitted to the local hospital for hyponatremia (dangerously low sodium in my blood). During that stay a CT scan was done on my abdomen where I was experiencing non-stop pain. Thus, we discovered large (1” by 1 ½“ in size) tumors in lymph nodes behind my peritoneum (retro-peritoneal nodes). Once I thought I had only bone lesions; here were some soft tissue tumors. “Not fair!”, I cried, “Make up your mind – soft tissue or bones – one or the other but not both”. And so it was a brand new ball-game. Help came in the form of Taxotere infusions which began in mid-August. I had trouble getting through the three sets of three low dose infusions through out September and October. I was down to 132 pounds and having trouble arresting the continual weight loss. I thought my time was about up.

Fortunately, the Taxotere rescued me again, the pain in my stomach slowly subsided, and I began to regain an appetite and some weight. Another CT scan showed progress on some shrinkage, but not enough. So, I began another round of Taxotere (Two sets of 3 infusions were planned) on November 19; these ended on December 29, 2014. It would be June 2015  before I went back on chemo again. Click on thumbnail at left.

PSA, BALP 2013,14,June15 During the first five months of 2015, I took an extended break from chemo – the accumulated impact of three infusions in a row followed by just a one week break, then to go again were clearly taking me down. During the winter months Xtandi (a relatively new oral drug) kept my PSA below 9. I continued that drug into the following summer.

In late November 2014 another biopsy was performed – this time on the retroperitoneal nodules. Like the previous bone and bone marrow biopsies, these samples were sent off to Caris Dx for genetic analysis. The results identified two drugs – one used for breast cancer, the other colorectal cancer – that would be active against my soft tissue mets. They also have strong side effects, possibly just too much for my now battered body. In addition, the genetic analyses showed I carry the TP53 gene. It seems to reliably prevent prostate cancer cells from becoming resistant to Taxotere. It’s not clear how much more “carpet-bombing” with chemo my body can handle. Until then, Taxotere is a reliable help.

In May 2015 we started another run at the back surgery. Why? Because I need to be able to walk without pain to get exercise and promote a better appetite. Little is known about the steady loss of strength, energy and stamina (SE&S) in cancer patients, but exercise is thought to be the best route up and out of this hole.

As we neared the end of June, PSA had risen above the magic number of 8. So, we tried the chief’s suggestion to go back on Taxotere (“It’s your drug,” he says.) That June infusion was administered on June 11. In the meantime appointments have been scheduled with both an orthopedic surgeon and neurologist to evaluate me for this minimally invasive back surgery.

Summer 2015 to Summer 2016

I seemed to tolerate the monthly low-dose Taxotere infusions OK. And, for a while, that regimen seemed to keep PSA in check. (Click on thumbnail below.) PSA & BALP Oct. '15 - July '16We also spent time working on the back surgery idea. That ended when a surgeon very popular in our old-folks community declared he couldn’t help. I was so stunned I never got around to asking him why. We did learn that accumulated neuropathy in my feet is the most likely cause of my poor balance. “Don’t think about getting rid of your walker any time soon,” he told us.

Then, both testosterone (T) and PSA start rising. In mid-September we started a holiday from Xtandi. I had been on that drug for more than eight months at that point. We had no reason to be suspicious of it but couldn’t think of anything else to try. You can see from the chart above that T declined back to undetectable and PSA dropped as well after we stopped the Xtandi.

In November the chief suggested I switch from Taxotere to Jevtana and to get another biopsy of the retroperitoneal nodules to see if I carried the genetic mutations that signaled good response to Lynparza and/or Opdivo. My NoVA oncologist had some reservations about my body’s ability to handle the side effects of Jevtana; he suggested two more rounds of low-dose Taxotere first. (See chart.) Next, the biopsy the day after Thanksgiving showed that the retroperitoneal nodules had shrunk too much to safely biopsy. Truly a mixed gift! On the brighter side the shrinkage of the retroperitoneal nodules may have taken some pressure off my stenosis issue. By late in our warm December I was pushing my walker for a mile round trip! Back muscle fatigue – yes, but pain – no!

Disappointed by the apparent  ineffectiveness of the two rounds of Taxotere in December and January we took off for California in mid-February to recuperate in the land of liquid sunshine. While El Niño was making Sierra snowpack and filling reservoirs, something else starting raining on my parade. First, edema came back – enough so that my NorCal oncologist suggested I get back on to some diuretics. Foolishly, I opted for the same dose of Zaroxlyn and Lasic that had worked so smoothly in early 2012. I forgot how far I had fallen in four years. Within a few days I became nauseous; a blood test showed I was again very hyponatremic – my blood level of sodium had dropped into the damage range. I began restraining my fluid intake to 34 ounces per day to combat the hyponatremia. This, on top of all the uncertainty about my next treatment, prompted us to go back to Virginia three weeks early.

In Virginia I raised my fluid intake to 60 ounces per day. I also started eating salty foods and drinking tomato juice. With this regimen my sodium is now back up in range. And, I seem to have suffered no ill effects from the period of hyponatremia. Since late March my PSA appears to have “stabilized” – a very unusual response when I am not being actively treated for the cancer. The chief still recommends I try starter doses of Jevtana to see how my body handles it, but I don’t feel strong enough to pursue it now. Jevtana is not without its side effects. He also thought that the cancer might gravitate to my adrenal glands because the adrenals are a source of androgens (cancer chow). I had another abdominal CT scan on June 2nd.

Sure enough, the scan does show growth of a nodule on my right adrenal gland. Local physicians judge that growth is not necessarily indicative of cancer. My July 1st blood test results were little changed from June. Going into this next year we will be watching and waiting.

Summer 2016 to Summer 2017

Extensions will be made to this post under the topic of Chronology approximately annually. In the interim please check periodic posts under Recent Progress.