Taking care

There’s nothing to say about today’s chemo session.  It was uneventful, exactly like two weeks ago.  After working a little and trying to read, I slept through most of it.  Before I dozed off, the nurse gave me some advice on skin care.

First of all, she said I was looking good.  Many patients have much more serious skin problems than I do.  They have pustules all over the face, down their necks, and sometimes on the rest of their bodies.  Some suffer from extreme dryness that can spread to the fingertips and the soles of their feet.  In the worst cases, the skin can break.  This is a gradual process.  Though progression is not necessarily linear, I might be in for worse as the therapy continues.

To help the skin and avoid the worst, the nurse gave me a set of care products provided by Amgen, the maker (or maybe not – production might be outsourced) of the anti-EGFR antibody that causes these symptoms.  I have to say thank you to Amgen a second time.  The set is really nice.  Once corona is defeated, I can use the bag on my travels.

Amgen wants me to take care of my skin.

The set contains a fancy skin cream, a body lotion, a cleanser that can only be purchased in a pharmacy, and sunscreen.  I will most of them assiduously.  Normally, I’m not much of a skin care person, but with the limited action I’ve taken over the last few days, I can already see benefits.  There is no reason to suffer unduly or run around with a face like a juicy pizza.

The second topic I discussed today was influenza.  In Switzerland, there’s a big push to get more people vaccinated than in normal years. The country’s health authority has ordered twice as many vaccine doses as last year.  In Germany, the picture is similar.  The aim is to vaccinate significantly more people than usually.  The rationale behind this is twofold.  First, for corona patients, whose numbers are expected to rise in the cold season, to get the best care, the health system needs to be protected from flu patients.  Second, testing capacity should be reserved for patients likely to be infected with corona.  A ton of flu patients with similar symptoms might overwhelm testing.

To me, this doesn’t make much sense.  People are acutely aware of the presence and possible danger of corona.  Most take good protective measures to avoid infections.  These precautions are equally effective against influenza.  Add to this that influenza is much less infectious than corona, and I’m convinced that we won’t be seeing much of a flu season this winter.  Seeing this way, corona will thus save lives – though fewer than it has already claimed.  I will not get vaccinated.  My doctor didn’t disagree.  He didn’t see a pressing need either.

The only difference between today’s chemo session and all previous ones was the starting time.  I’ve never begun therapy after lunch.  While fasting, lunch is a bit of a hypothetical concept, but it still nicely divides the day.  There are good and bad aspects to starting late.  One good thing is that I could work for half a day – and work is fun.  Another good thing is that my period of dead-tiredness after therapy is shorter.  I go to bed a few hours after returning from the hospital.  The bad thing is that I’ll have to wait until tomorrow night to break my fast.  I fear a rather long and unpleasant day.

First impression

Ten days after the beginning of yet another therapy, the third one now, I can draw a first conclusion.  Things are happening.  The drugs are doing something.  I can’t say anything about their action against the tumor, but the side effects are clear and as expected.

My nose looks like Boris Yeltzin’s after a particularly boozy day.  It’s big, ruddy and doesn’t seem to fit my face.  The skin on either side of the nose is irritated.  It has grown a lawn of tiny pimples.  Squeezing them out – a laborious and painful procedure that’s probably not what the doctor would recommend – leaves behind the scarred surface of a battlefield.

On the upside, my blood vessels are much pleased that the anti-VEGF antibody is gone.  Each morning over the last few months, I used to blow huge chunks of bloody mucus from my nose.  It looked a bit like the Texan Chainsaw Massacre.  Not exactly painful, but quite unpleasant.  This seems to be improving now, while everything around my nose is getting worse.

My face is extremely dry, from the lips to the forehead.  I’ve started applying lip balm throughout the day.  When I rub my forehead, skin comes off in a shower of tiny flakes.  Flucha’s rejuvenating night cream – a gift of mine a few years back that’s been largely ignored – has found a more appreciative new home in my bathroom.  It helps me get some moisture back into my skin.

These side effects are in line with what EGFR antibodies are known to cause.  They aren’t grave.  I need to look after my face to avoid turning into a freak, but I’m not suffering acutely.  If the symptoms don't get much worse, I can handle them.  With corona still keeping tight restrictions on the number of international destinations available to travelers not inclined to quarantine for two weeks, I’m not seeing any customers.  As long as I’m not scaring my colleagues, I’m fine.  I’ll take the second session on Wednesday without any apprehension.

Perambulations

Our journeys through life are strange ones.  Decisions we take or events that occur around us often have only a small effect on what happens to us.  We might not notice the subtle changes in our lives or only realize their significance later when looking back from a very different place.  Daily developments are often like the slow heating of water that the frog – to his eventual detriment – does not perceive.

It was six years ago to the day that Flucha and I rode bicycles along a river in the southwest of Germany whose name I had never heard of before setting out.  Flucha was on the heavy and unambitious bicycle she had bought used to get her around town.  I had rented something that revived my joy of bike touring.  If I had had a similar set of wheels years earlier, my tours down to Hungary and to the end of Brittany would have been much less painful.

I don’t remember whose idea our bike trip was nor how it came about.  Flucha and I had never done such a thing together.  I was doubtful until halfway through the first day whether she’d collapse by the side of the road because the bike had worn her out.  In the end, she arrived at our goal for the day, a forlorn town near another river that we’d ride along the next day back to the railway station where we’d started, in almost the same shape as me: sweaty, covered in dust and exhausted but happy about the achievement.  We had an unexpectedly delicious dinner that we paid for by bank transfer a couple of days later because we had no cash and they didn’t accept our cards, and made a baby.

At that moment, it wasn’t clear that anything was happening or that anything had changed, but everything was different afterwards.  Before the baby was born, I had quit my comfortable but dead-end academic job in London and moved to Switzerland to work for a company whose prospects I couldn’t judge well.  Flucha hung out at her temporary post in Germany a bit longer.  She made the move to Switzerland a year and a half later, a little girl in tow.  Another year and a bit later, the boy was born.  He knows nothing of our ambulatory past yet.  Switzerland is his home.

Late this afternoon, we were sitting on the terrace of one of the cafés in town.  The sun was blocked by low clouds.  It was still pleasant but summer is definitely over.  A hill half a mile ahead blocked my view of the distance.  A similar hill rose to my right.  It was easy to see Baden as a protective bubble, the world far removed, beyond the hills, with little to no impact on the goings-on in town.

This feeling can be hard to shake off.  Corona is still raging around the world, coming back to Europe with a vengeance after ravaging the Americas, but our little lives continue undisturbed.  It’s hard to see the connection.  We go to work every morning.  Our children are intimately familiar with the term coronavirus and the small changes the virus has made to their habits – the more frequent washing of hands and the sneezing into armpits – but blissfully unaware of any peril.  They spend their days in childcare and kindergarten as always.  At night, we all return home to the center of our happiness.  It’s an absurd situation, if one stops to think about it.

In her second year of kindergarten, the girl has started extracurricular activities to an extent that may seem a bit excessive.  She takes a rhythm class on Mondays, does an hour of entropic physical exercise on Thursdays and attends an atelier on Fridays, a course that’s revealed to us an impressive range of her artistic talents.  She knows half of the town and is nobody’s fool.  Earlier today, we dropped her off at a bus stop for a teaser afternoon with the Scouts.  She returned two hours later, exhausted, happy and eager for more.

I know that we live privileged lives and that we’re extremely lucky.  I get happy whenever I sit down, zoom out and think about this.  We’ve been blessed in almost everything that has happened to us over the last few years.  I’m ready to extend this statement to my early years.  Not that there was a sense of destiny or that one step followed the previous one with convincing logic.  More often, things happened by change, out of a burst of initial enthusiasm that somehow took hold and was reinterpreted as a rational decision, or for convenience.  But together, all these little steps shaped my life, and I’m extremely happy with where I am.

Fountain of youth

Today I started the third chemotherapy program.  It’s very similar to the first two.  The main ingredient is still 5-fluorouracil, which damages dividing cells by messing with DNA replication in a way that’s not fully understood.  Fasting convinces healthy cells to go into a deep sleep.  5-FU should thus only harm cancer cells, which can’t keep from growing.  So far, this hasn’t worked as well as I had hoped and, naively, expected.

The difference today is the antibody.  Going by the trade name of Vectibix, it binds to the epidermal growth factor receptor and prevents it from receiving growth signals, such as EGF, and reacting to them by stimulating cellular growth. Without growth signals, cells don’t grow, or much less so.  Tumor will be held in check.  That, anyway, is the idea.

Some of the mutations in the signaling protein KRAS stimulate growth without requiring activation by EGFR.  This is why these mutations are linked to cancers.  My mutation is apparently different.  I really have to make an effort to understand what’s going on at a biochemical and structural level.  There’s a fair number of nice papers out there on this topic, waiting to be read.

The major side effect of the previous antibody was diarrhea.  That’s what the doctor and the patient information sheet said.  But might have been right, but my case was different.  As I received the antibody after three days of fasting, with my gut cleaned out already, diarrhea wasn’t an issue for me.  It became an issue a day later during the transition from fasting to eating.  What I ate didn’t always find my digestive tract a hospitable place and frequently didn’t linger.  I take a drug that helps with this like a charm.

At the beginning of each treatment session, I always get a pile of drugs to swallow.  By now I don’t know what they’re all good for.  One pill is against nausea, two are steroids of obscure purpose, the fourth I have no idea about.  This morning, I got a fifth, against possible allergic reactions against the antibody.  During the therapy, I get an injection that’s supposed to keep the excessive sweating that irinotecan might cause in check.  By now, I get more drugs to be able to endure chemotherapy than make up the therapy.

The antibody I got today for the first time can trigger an acne-like reaction with severe pustules on the skin, my doctor said.  Most patients suffer from this.  I read that this can be seen as the antibody doing its job.  A bit of acne will make me feel 30 year younger, I told the doctor.  Nothing to worry about.  I might have to show my ID the next time I buy a beer, but that’s ok with me.

As I wander down the ladder of therapy options, from first-line therapy to second-line and now third-line therapy, I wonder what places individual therapies in this ranking.  Is it that the first therapy is the one that’s proven most successful in clinical trials and with patients and that the others will work less well?  Or are they comparable in their efficacy but the first therapy given is the one patients tend to accept most happily because of the fewest side effects overall?  This is hard to tell for me.  I don’t get many side effects, but today was probably the worst day of all.

Maybe it was in my head.  I’ve started almost every therapy session so far with a mind full of optimism.  Nothing concrete, just a feeling that things are going well and that I’m on the right track.  This morning was different.  After too many scans that didn’t show any progress (to put it mildly), it’s hard to keep up a positive façade.  The question of why I’m doing this kept popping up in my head.  I didn’t help that I found fasting almost unbearable this time.  There is no point, my mind wailed.  This is not the answer I would give, but I felt too weak to give any answer.

Chemotherapy went as usual, without any problems.  I started reading and writing a bit but dozed off pretty quickly.  When I rode my bicycle home, I didn’t feel much better.  I had a couple of hours on the sofa before picking up the boy from childcare.  Back home, Flucha told me I looked like a ghost.  I felt like a ghost too, or a least like someone not part of the living anymore.  I went to bed before 7, utterly destroyed.  At this rate, it will take more than the new antibody’s side effects to make me feel young again.

Restart

It is quite easy to get used to fasting.  It is equally easy to get unused, if there is such a word.  I last ate 24 hours ago, and I’m not liking it one bit.  As always, I’m not hungry, but I’m already irritable, and I can’t wait for this to end.  Before my three-week break, I breezed through the first day of fasting without any discomfort.  Now I have two and a half days without food ahead of me, and I’m questioning the wisdom of it.  Eating is good.  Enjoying food is good.  Depriving myself of it might have some speculative and unsubstantiated value for me, which is why I will follow through with it, but it doesn’t make me happy.

On Wednesday, if everything goes as I imagine it, I will start my third chemotherapy program.  It’s not much different from the first two.  The main ingredients, 5-fluorouracil and folinic acid, are the same.  The antibody is different.  It’s unlikely that a new antibody will make a striking difference to a failed therapy.  I will still submit to this therapy with eagerness and even joy.  It’s the only thing I have, it should, at the very least, slow the growth of the tumors, and it just might be more effective than what I’ve braved so far.  There’s no reason to start this with anything but unjustified optimism.

Instead of an anti-VEGF antibody, I will get one against EGFR.  Despite being a titled biochemist, I have only a vague understanding of the difference.  Antibodies themselves are relatively clear.  They are a class of proteins in the shape of a Y that specifically recognize short protein motifs for the purpose of eliminating intruders such as viruses and bacteria.  They can be raised against native proteins and, if they block interactions important in diseases, are candidates for development into drugs.

EGFR is the epidermal growth factor receptor.  I don’t know much more than the name tells me.  This receptor sits in the cell membrane and receives growth signals in the form of epidermal growth factor (EGF), a small protein.  VEGF is vascular epithelial growth factor.  I can’t say much beyond the fact that it is also a protein and has something to do with blood vessels.  Time to do some reading.

Growth factors, such as EGF and VEGF, regulate cellular metabolism, promote cellular growth and can stimulate tumor cell proliferation.  Tumor cells secrete VEGF to promote the growth of new blood vessels which will supply the tumor with the nutrients required for continued growth.  Anti-VEGF antibodies probably bind to VEGF and prevent its interaction with its receptor, thus breaking the signalling mechanism.  In theory, a lack of new blood vessels should prevent new metastases from taking hold.  This didn’t work for me.

EGFR is a bit different.  When activated, this receptor stimulates a signaling cascade that contains RAS proteins, of which KRAS is one.  KRAS in turn stimulates RAF kinase, which upregulates various metabolic activities.  The G13D mutation in KRAS – the amino acid glycine at position 13 in the protein sequence is changed into aspartate – goes a long way in explaining my cancer.  A paper I mentioned a long time ago claims that “protein synthesis and cell proliferation were significantly higher” in KRASG13D cells.  The paper also shows that KRASG13D cells were “highly transcriptionally responsive to EGFR activation”.  This might explain that EGFR inhibition is beneficial in KRASG13D cancers.  In three months we will know if this had an effect in my case.

Unfortunately, the connection between KRASG13D and EGFR inhibition is not as clear as I thought at first.  An intriguing paper explained why EGFR inhibition might work in cancers with the KRASG13D mutation when it doesn’t work in cancers with a mutation in residue 12 of KRAS.  This rationalized results from a retrospective analysis of phase 3 clinical trial data that showed a benefit of EGFR inhibition for patients with KRASG13D.  The problem here is that it compares the reaction of patients with wild-type KRAS and KRAS mutated in residue 12 with patients with KRASG13D cancers.  What should have been compared is KRASG13D cancers with EGFR inhibition versus KRASG13D cancers with VGEF inhibition.  On second thought (or a proper reading of the literature) there is no indication that EGFR inhibition is any better than VGEF inhibition.

A less than enthusiastic report in literature is no reason to drop a therapy.  I will try anything until it proves itself to be worthless.  Fasting, much hyped in certain quarters, has not made the difference for me.  Maybe the EGFR antibody will.

First anniversary

I almost missed an anniversary.  Yesterday a year ago, I headed to a doctor I didn’t know – chosen because his surgery is in the building next to where I work – to have my strange feebleness on the bicycle, the football pitch and the stairs up to my desk on the fourth floor explained.  There was also the strange issue of recurrent dull pain in my guts.  I expected nothing serious.

Exactly one year ago tonight, I underwent the world’s longest ultrasound, given without even a hint of what I’m sure the doctor suspected.  Later I prepared for the colonoscopy and endoscopy that were scheduled for the next morning.  The results have kept this blog busy ever since, but they didn’t throw my life in disarray.  The corona pandemic has been more effective in this regard.

I mention Japan to my boss.  He says, yes, definitely, we need to go.  Japan continues to say no.  I mention China.  We had planned to go there in early March, right when covid numbers became scary.  Now the country is closed.  I scheme to accompany one of our service engineers to Korea.  We don’t have much of a presence there.  My boss is all for it.  Korea says no.  I set my targets lower and start putting together a trip to the UK.  A week before that’s to take place, the UK put Switzerland on its risk list.  Rather than quarantining for two weeks, I stay in the office.  I have not traveled for work in nearly eight months, and I don’t see any opportunities on the horizon.

In the hospital on Tuesday, the doctor agreed to continue with chemotherapy but replace the antibody I was getting with one that is rather experimental.  This was contingent on the health insurance provider’s agreement to cover the cost.  My provider is the cheapest in the country.  Would they put up the money?

Today I received the confirmatory letter.  The treatment is covered for only three months (six sessions, I presume) and only thanks to the participation of the company that owns the patent on the drug.  Thank you, Amgen.  I’ll let you and the insurance company know how things are going.  Maybe we can continue beyond the initial three months.

I haven’t spoken with anyone at the hospital since getting the letter, but chemotherapy will probably resume next week.  I retained my appointment for Wednesday even though my therapy was suspended.  If the hospital confirms this tomorrow, I will start fasting again on Sunday night.  It’s not that I missed it but I’m happy to go back.  There is so much sense in this approach.

Besides the approval of the new therapy, I haven’t had any good news recently.  The disease has progressed.  That this was what the doctors had expected all along doesn’t make it any less upsetting.  Still, I rejoice in the fact that the progression has been slow.  I’ve survived the first year, and I feel good.  I’m looking forward to many more anniversaries.

No celebration

Today was another day of truth, in a way.  I had an appointment with the oncologist who will be looking after me after the trainee doctor who was responsible for me up to now left to continue her training in a different hospital.  The topic of conversation was the PET-CT scan from last Wednesday and the conclusion we can draw for the continuation of my therapy.

First off, the scan confirmed what the CT scan a week before had already indicated.  The tumors in my lung and liver have grown a bit.  Nothing dramatic, but clearly visible.  The tumor in one of the lymph nodes looked similar to before.  There were a few new tumors in the pulmonary pleurae, which are bags of cells that surround the lungs.  All of the tumors are metabolically active.

None of this is good news, but it’s not exactly unexpected and didn’t shock me.  The progression was to be expected, in particular after knowing the results of the CT scan.  I can even see positive aspects.  The progression is slow.  It’s not as if I’m going to die within the next half year.  The metastases in the peritoneum haven’t returned.  My condition is stable, even though stable means stably deteriorating.

When discussing the CT scan with my previous doctor, I got the feeling that she had given up.  She didn’t really talk about possible downstream therapies.  Instead, it was all about stopping chemo because it’s not doing anything.  This is not my approach.  The new doctor is more to my liking.

As others have done before, he ruled out anything but chemotherapy.  Radiation therapy makes no sense because the cancer is delocalized.  Surgery makes no sense for the same reason and because new metastases are still appearing.  I need to stop the growth of the cancer before anything else can be cut out of me.

So chemotherapy it is.  Here, the doctor is going with my suggestion of changing the antibody.  Instead of antibodies against VEGF (vascular endothelial growth factor), he will try to treat me with an antibody against EGFR (epidermal growth factor receptor).  Why do I write try?  EGFR antibodies are known to work against cancers without mutations in KRAS.  Recent results have shown that they might also work in cancers with my particular KRAS mutation.  These results are not clinical studies, and EGFR hasn’t been approved as a drug against my cancer.

The doctor will make the case to my insurance provider that the EGFR antibody should be covered but cautioned that they might say no because it’s experimental.  This sounds like something I would expect from the US health system, which is frequently represented as ruthless or even predatory – though I never experienced it as such.  I’m a bit surprised I experience this in Switzerland.  You might say an insurance company can simply not pay for all treatments a doctor might want to try.  On the other hand, why is the doctor (in this case supported by the joint opinion of the hospital cancer board) not the one who makes decisions on treatments?

If the insurance company says now, the doctor will ask the maker of the antibody to give us a few batches for free.  This sounded like the most normal thing to do.  Go figure.  The antibody would be used together with the chemotherapy I’ve just stopped.  This was not the doctor's idea, but Flucha and I convinced him.  He didn’t have an answer to our questions of what was wrong with continuing chemotherapy.

If the antibody doesn’t become available, there are two alternative chemotherapies.  Both are oral, which means I’ve got to swallow pills throughout the day instead of going to the hospital for infusions.  One is trifluridine, which I had already discussed with the doctor in Zurich.  He wasn’t convinced this would be of much help.  The other is Regorafenib, a tyrosine kinase inhibitor that, according to Wikipedia, has achieved an average added survival of 1.5 months and isn’t even on the market in Germany because the agency that makes such decisions resolved that the potential benefit of the drug wasn’t high enough to justify the cost.  This is what my doctor wants to try first if we can’t get the EGFR antibody.

None of this sounds good.  To get my mind off these things, I asked the doctor a few questions related to the immune system that arose after my previous post.  What’s up with my T cells and why wouldn’t a PD-1 antibody that prevents tumor cells from inhibiting killer cells be a good idea?  There’s apparently nothing wrong with my immune system.  It’s just that tumor cells are difficult targets for immune cells.  Immunotherapy works best when tumor cells have mutations in certain DNA damage repair proteins.  In these cases, the tumor cells present bits of DNA on their surface that helps T cells recognize them.  I don’t have any of these mutations.  My cancer cells look as if coated with Teflon.  Immune cells with pass them by without stopping.

What we didn’t talk about were vitamin C and fasting and methadone.  To strengthen my arsenal in this increasingly difficult fight, I will contact the clinic by Lake Constance that accompanies patients during long periods of fasting.  Maybe they’re willing to infuse me with copious amounts of vitamin C.  I’d pay for that.  The other hope is the clinical study in Ulm that evaluates the use of methadone.  It started in March.  At some point they must have preliminary results.

The two most conventional chemotherapies have failed to rein in my cancer.  This is nothing to celebrate, but it’s also no cause for despair.  There are a lot of things to try before giving up becomes an option.  I can’t wait to continue the fight.

Immunotherapy

What triggered me yesterday to ponder my lack of scientific curiosity was a pair of papers published in the magazine Science two weeks ago.  I subscribe to Science and scan the contents every week.  Nevertheless, these two papers eluded me.  The only reason I noticed them is that they popped up in my regular search of recent high-profile publications containing protein structures solved with the detectors I sell.

Both Antitumor activity of a systemic STING-activating non-nucleotide cGAMP mimetic and An orally available non-nucleotide STING agonist with antitumor activity talk about orally available activators of a particular immune pathway that might help the body better fight cancer.  If this sounds like drugs, it's not, though one of the papers was authored by researchers at Merck, with a patent application mentioned.  The experiments were done in mice, and mice are not humans.  But the science behind the titles is quite intriguing.

Helping the immune system fight cancer is not a new idea, but it's one that's been gaining traction over the past ten years or so.  Immunotherapy should be the most normal thing in the world.  The immune system is designed to protect the body from all sorts of assaults – bacteria, viruses, liver transplants.  Cancer cells are just another aspect.  Since cancer cells are derived and don't differ much from endogenous cells, they are hard to recognize.  In addition, they've developed all sorts of mechanisms to evade or suppress the immune response.  The immune system is thus often struggling to contain cancers¹.

Still, immunotherapies exist.  Rather experimental at this point is adoptive T cell therapy.  The idea is to engineer a particular type of immune cells called T cells to kill cancer cells.  In CRISPR-engineered T cells in patients with refractory cancer, the authors extracted T cells from three patients.  They then genetically modified these cells to achieve two goals.  They blocked the production of a few proteins thought to inhibit the cells' ability to target tumours.  They also gave the cells the ability to recognize a protein produced by cancer cells.  Reintroduced into the original patients, the T cells remained detectable for nine months.  There were no side effects, but there didn't seem to be a beneficial effect either.  Research continues.

Already established are therapies based on antibodies that recognize and neutralize proteins that block the immune response.  Six antibodies with such function (nivolumab, pembrolizumab, cemiplimab, atezolizumab, avelumab, and durvalumab – the ab at the end of their names marking them as antibodies) have been approved for various cancers at various stages by the Food and Drug Administration in the US and possibly in Europe and Switzerland as well.  One of them, pembrolizumab, might apply in my case as a treatment of last resort when two or more lines of therapy based on fluorouracil and platinum-based drugs have failed.

The antibodies that I have received might technically also be considered immunotherapy.  Both of them were targeted against a growth factor that promotes the creation of new blood vessels (angiogenesis), which tumors need to sustain their growth.  This is not what I'm talking about here.  This post is about helping the immune system directly attack (and, optimally, beat) the cancer, not co-opting parts of it to make the cancer's life harder.

What is it about these STING activators mentioned at the very top?  STING is a protein at the heart of a complicated cellular pathway that leads to a T cell response.  It all starts with the recognition of the genetic material of cancer cells.  This recognition triggers a biochemical cascade that leads to the activation of STING.  The signalling cascade continues until T cells are recruited and primed to go after cancer cells.

The molecules identified in the two papers ensure that STING is active.  The details of these drug candidates are of little interest to me.  They're unlikely to become drugs within the next few years.  But the biology behind them is interesting.  I've learned that many cancer patients do not show sufficiently active T cells.  They would benefit from STING stimulation.  Am I among them?  Are my T cells not doing their job?  Has this ever been tested?  I'll certainly have something to talk about with my new oncologist on Tuesday.

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(1)  This statement might not be giving enough credit to the immune system.  It would probably be fairer to write that cancers form when the immune system fails to eliminate cells that turn cancerous.  These are rare, unfortunate events.  Most of the time, the immune system does its job.

Third PET-CT scan

I haven't written a scientific post in about two months.  With the resources I have and my training, I should do better.  I should read more, think about what I read, and post my conclusions. I will surely learn something and might pick up something unexpected.  Maybe I'll find something that gives my therapy a much needed boost or nudges it into previously unexplored territory.  On the other hand, it's always a long way from an exciting research paper to a proven therapy.  With this thought in mind, I got distracted, and now it's too late for anything substantial.  Instead, here's what happened today.

I had my third PET-CT scan, a follow-up on last week's somewhat inconclusive CT scan.  The technician was the same as last time.  I feel I should be getting loyalty benefits.  The procedure was also the same.  I arrived with an empty stomach, was hooked up to a drip and received a radioactively labeled sugar.  This sugar goes to where it's needed.  Cells of high metabolic activity turn it over and accumulate the radioactive label, which is then detected.

To distinguish cancer cells, which are always highly active, from healthy cells, one just has to remain immobile for an hour before the scan.  In a resting individual, most cells don't do much and consequently won't light up in the scan.  I lay in the same room as before, with the lights dimmed, a backlight photograph of a relaxing mountain scene on the wall and soothing music playing softly from a small stereo.

For the first time, I recognized the picture on the wall.  It showed Kleine Scheidegg, the saddle between Eiger and Lauberhorn, and Eiger, Mönch and Jungfrau in the background.  The Kleine Scheidegg station is the start of the Jungfrau railroad.  My mom and I had been there a month and a half ago.

After an hour of rest, the technician directed me to the scanner.  I lay down on the table and was driven through the big humming torus over the next twenty minutes or so.  By noon, the whole procedure was over.  I made it to work just on time for lunch.  A PET-CT scan has no detrimental effect on one's well-being.  The afternoon flew by.

The CT scan last week was much worse.  It had knocked me out.  The scan was obviously not directly responsible for this.  It's just radiation.  But it needs contrast agents for better images, and I once showed a minor allergic reaction to one of them.  Now I'm given the antihistamine tavegil before every scan.  It's most common side effects are sedation and somnolence.  I was warned not to drive a car for the rest of the day.  Riding my bicycle home didn't strike anyone as foolish.

According to the drug's information leaflet that I've just read, the peak of activity of tavegil is reached five to seven hours after injection.  I got my shot above five minutes before the contrast agent.  If I had got the injection a few hours earlier, I would probably have got away with a tenth of the dose and a tenth of the tiredness.  For this, I'd happily come to the hospital earlier.  Something to mention for next time.