It really is remarkable how far cancer treatment has progressed, even in the last few years. I'm one of the unfortunate people who, through a close family encounter with cancer, knows more about this stuff than anyone should have to. The oncologist told my relative that if they had presented with this particular cancer just a decade ago, his recommendation would have been to start hospice care.
However, in recent years, a very effective checkpoint inhibitor immunotherapy has been developed for the cancer in question. ~2x the success rates of traditional chemo, greatly increased overall survival statistics, and with massively reduced side effects. The results speak for themselves: this drug has granted my relative years of extra life in the worst case, and a path to a deep, long remission in the best case.
I think that as the technology develops, by 2040 we'll be looking back at the present state of the art with the same incredulity that we currently have for, like, bloodletting with leeches in the Middle Ages. I think they've been saying this for a long time now, but it's truer than ever that a real cure for cancer is right around the corner.
As a person who currently has stage IV NSCLC, I can add some context to this:
YMMV.
One thing to remember is that "Lung Cancer" is not just one thing. There are mutations of different genes, there are overexpressions of different genes. Each one has its own new medicines. Also, some peoples' cancers are more aggressive than others, and while for many they can find the right drug, for some nothing works.
Keytruda works wonders for some. It did not for me. I had 4 treatments of the CPP (carboplatin, pemetrexed, and pembrolizumab) triad, which had some success. They then put you on "maintenance," which is the PP without the carboplatin (which is the really old school platinum-based chemo). Maintenance did nothing for me. My main tumor grew more than 50% in 2 months.
Last summer I started 9 months on a chemo/immuno that was geared towards my specific mutation. It actually did wonders. It resulted in a 98% shrinkage of my main tumor before I ended up with pneumonitis from it and had to stop. But I've been able to be off treatment for the entire summer. I know there are others who have tried this, and it didn't work.
So yeah, I'm really, really glad your relative was able to get some relief from the Keytruda. But I also wish it were the wonder cure for everyone that it was for them.
I was diagnosed with stage III NSCLC February '21. Radiation, chemo, and a bilobectomy. I had the ALK+ morphology which meant I wasn't a candidate for immunotherapy but I've been on alectinib since my surgery in June '21 with no signs of recurrence so far.
The process is grueling in hindsight, but I'm glad to hear you're getting results. At first I would have said "if this is going to kill me, make it sooner rather than later" to avoid a drawn-out painful experience, but I'm starting to appreciate what the buying time really means. It's hard with all that's going on but get your head straight and make sure you enjoy it.
Thanks for sharing your story and treatment details. I should add that my relative's cancer has no particularly interesting mutations, but does have a high PD-L1 expression, which from what I can tell is the reason Keytruda was more likely to work for their situation.
> that was geared towards my specific mutation
This is actually one of the things that gives me hope for the future: genetic testing on a tissue sample of the patient's cancer is standard, and for many of the specific oncogenes that we know about, there exist therapies targeted to those specific mutations: https://www.cancer.org/cancer/lung-cancer/treating-non-small...
One thing I've learned is that even in the face of good news, cancer is a horrible time, and I wouldn't wish it on anyone. But I'm likewise glad to hear about your results from the latest treatment, and hope things stay as positive as they can for you.
I am hopeful we can move metastatic cancer (which is the true evil of cancer) to a controlled chronic condition.
BTW-- our oncology doctor believes in synergies between chemo and pembro, but I sometimes wonder if it's truly the chemo. Also, Pembro is not without its side-effects.
> in recent years, a very effective checkpoint inhibitor immunotherapy has been developed for the cancer in question. ~2x the success rates of traditional chemo
> I think they've been saying this for a long time now, but it's truer than ever that a real cure for cancer is right around the corner.
I think thats quite a leap. For prostate cancer( most common cancer among men), top line therapies are still androgen blockage that was discover 70 yrs ago, chemo and radiation. Keytruda failed to deliver any significant survival benefits[1].
Yes we've gotten better at slash, burn , poison methods. Radiation is more trageted and sophisticated. Diagnostics are more precise. Chemo drugs have better safety profiles.
But these are all marginal improvements. None of which indicate anything that we are close to a cure.
Only hope we still have is to catch it earlier and go ham on it. Most of the slash,burn, poison methods are being FDA approved for earlier use.
The other two things(one of which you've mentioned) are immune checkpoint blockade if you have MSI-hi/dMMR or PARP inhibition if you have BRCA2+. Even if you are lucky to have these mutations these drugs are a hit or miss[1].
I agree that my original comment is very optimistic--for what it's worth, Keytruda has thus far been very effective in the case I'm talking about, so I have some bias here. I concede that even in my "double the effectiveness" example, we're talking about doubling something like a 20% 5-year OS.
By "around the corner" I'm really talking about, like, 20-30 years out, which I think is fairly soon in terms of cancer treatment progress. You're right that it reads like a leap in the context of my comment.
Part of this is because prostate cancer has such a high success rate. With treatment, the 5 year survival rate for early prostate cancer is over 99%, and is was close to 98% 20 years ago.
The current approach of regular prostate exams + treatment isn’t perfect but it’s extremely effective.
Prostate cancer is, from what I understand, one of the cancers with the least amount of genetic differences from normal tissue. That makes it harder to target. It also explains the general failure of checkpoint inhibitors.
As others have mentioned it depends. For instance the initial trials with pembrolizumab weren't the silver bullet the media makes them out to be today, until they identified what features might common among patients that did see a response, e.g. mismatch repair deficient cancers, because the tumor needs to be spitting out enough of these tumor-specific neoantigens to be targted by the immune system. That generally happens with highly mutated tumors such as those found in mismatch repair deficient tumors. The reason why the immune system was not targeting the tumors like it should have given the neoantigens until you take the drug is because the tumor cells presents the correct receptors that the immune system expects from healthy cells, which prevents the immune response. When you block that receptor as these drugs do, and also have many of these tumor specific neoantigens being expressed, then the immune system is able to target the tumor cells for death and the drug works well.
It's moving so fast even doctors(sans oncologists, perhaps?) can't keep up.
Brother's been a doctor about 15 years. Huge extended family is aging, and of course cancer creeps in. Of course family members call to get his opinion, and he's been wrong every single time(thankfully). Usually saying something like 'oh, she'll be dead within 2 years' and them living 6, or 8. And in one case calling something a death sentence that was actually, seemingly at least, cured.
It's entirely possible he's just a shit doctor, but I like to think it's that progress has moved a ton since he's studied up on it last.
Would you be willing to share the type of cancer? Also, was the person you're referring to (can't tell if it was a relative) able to bypass traditional chemotherapy and go straight to the immunotherapy given the prognosis? Or did the oncologists require chemo first and only then your contact was able to receive the immunotherapy?
Thanks for sharing anything you can. If more comfortable sharing in private, I can be reached at asuela1 at yahoo's email service (it's my spam account, but I'll check it if you tell me you wrote back there).
Stage IIIC NSCLC, specifically a superior sulcus tumor, advanced enough to be considered inoperable. Standard of care in this case was induction radiotherapy, followed by a single course of combination chemotherapy consisting of carboplatin, pemetrexed, and pembrolizumab (the last of which is the cutting-edge immunotherapy I'm talking about; brand name Keytruda.) After that, patients are prescribed the pemetrexed and immunotherapy alone for a long 2-year "maintenance" course, at which point treatment options will be reassessed.
Surgery was not an option here because of the size and location of the mass, but after the initial course of chemo a PET-CT showed an 80% reduction in size. After some time on pembrolizumab, symptoms continue to improve and surgery may be back on the table soon.
(edited for a more accurate picture of maintenance treatment; thanks to borbulon for refreshing my memory)
This. A close friend of mine was diagnosed with stage III stomach cancer. He lost massive amounts of weight and I almost thought he was not going to make it. And a year later he is back at work and doing pretty well.
It is not a single disease, but rather a result of several errant biological outcomes. The mortality rates have improved a lot with better treatments, and around 60% of the population will develop some form of the disease in their lifespan.
The most disturbing part is most people are unaware they are ill until relatively late stages of the disease.
If you live long enough, one will know many good people that go this way. It is a worthy area of research, as it improves the lives of many families. =)
Yes, my cancer was discovered pretty early by pure chance in a CT for an unrelated issue. I had zero symptoms, was really fit and pretty much never sick.
Who knows how long it would have had time to mutate and grow otherwise. Early detection is a really important issue for cancer treatments.
Looks as promising as any other promising cancer therapy in phase I trials!
There is a renaissance in cancer drug delivery at present, exemplified by antibody drug conjugates. The tech in the article is very interesting, and a superb bioengineering effort. A caveat is that complex multi-unit therapies don’t have a great track record. They are hard to manufacture reliably, and have a very large optimisation volume, so it’s difficult to increment the development as you only have finite resources for human trials. Contrast this with small molecules where there is a well defined process over various chemical and pharmacokinetic factors, prior to testing in humans. We also lack a good system for developing and trialing ‘platform’ tech like this - the current system is set up for single drugs/combos to be tested and eventually reimbursed in each cancer type separately. If you have a platform for delivering tailored therapies agnostic of cancer type, you will run into many barriers. There is currently only one drug I know of simultaneously approved across multiple cancer types (pembrolizumab in mismatch repair deficient tumours, a rare population). So many challenges ahead of the hype here.
I may be missing something but the article does not explain how the bacteria target is actually targeting the cancer cells. Of course, if you can design an ideal universal cancer targeting mechanism, the active ingredient itself is beside the point. Did anyone else catch this?
Stopping DNA replication across the body will be fatal. This is what eventually kills with radiation toxicity.
The article is missing lots of detail. They use antibodies to target receptors which are highly expressed by tumors, such as Epidermal growth factor receptor (EGFR).
"Given that the EDV surface is coated with lipopolysaccharide (LPS), single-chain bispecific antibodies were attached to the EDV surface where one arm of the antibody is directed to the O-polysaccharide epitopes and the other arm is directed to a tumour cell surface receptor for example Epidermal growth factor receptor (EGFR) which is found on the surface of over 70% of solid tumours"
and
"The EDVs being 400 nm rapidly fall out of these fenestrations and enter into the tumour microenvironment and since they carry the bispecific antibody on the EDV surface, the anti-EGFR component binds to EGFR on the tumour cell surface. This provokes macropinocytosis and the EDVs are taken into the early endosomes, followed by lysosomes and broken down in these organelles releasing the drug PNU-159682. The drug enters into the tumour cell cytoplasm and the nucleus and intercalates with the chromosomal DNA resulting in tumour cell apoptosis. In the event that a tumour type does not express EGFR for example liver cancer, which expresses asialoglycoprotein, then the bispecific antibody can be changed to anti-asialoglycoprotein while the anti-O-polysaccharide component remains constant. Similarly, HER-2 positive breast cancers can be targeted via anti-HER2/anti-O-polysaccharide bispecific antibody"
It does, from the article: "“Normally, our blood vessel walls are all sealed pipes,” Brahmbhatt says. “But around wherever the cancer is growing, the blood vessels are known to be very defective. They have got a lot of holes in them.”
Brahmbhatt and his collaborator Jennifer MacDiarmid devised a clever ploy. They would send a Trojan horse into malignant cells and turn cancer’s own trickery against it.
The Trojan horse, in this case, is a product of a harmless bacteria that’s been genetically engineered to have specific qualities. When this genetically engineered bacteria divides, it yields a tiny non-living cell of 400 nanometers in diameter—the right size to slip through the damaged vessels and mingle with the tumors."
I see. I do wonder how specific that is though. Potentially it could be toxic to other areas where vasculature could be "leaky". Like in the filtration mechanisms in the kidney.
Targeting the cancer's vascular supply is also a known anti-cancer mechanism of action (anti-angiogenics). How will this method not have the same toxicity as that one?
I loved Michael Levin's thoughts on solving cancer. Kind of similar to immunotherapy but on a level of reprogramming the cells back that got 'lost' from their big purpose in their organ.
I can't help but mention that there are two dominant schools of thought regarding cancer treatments:
1. The Somatic theory of cancer ('bad genes/out-of-control cellular replication')
2. The metabolic theory of cancer ('cancer cells ferment blood sugar for energy via an ancient emergency metabolic pathway')
Both have merit, but a complete occlusion of one would be bad.
I wrote an open letter, long ago, to a wealthy person who was on the board of a cancer research center, suggesting they read a book and fund the key research scientist:
I thought of the metabolic theory of cancer as I opened this page, because all cancers have a similar reliance upon certain energy generation pathways, which implies a corresponding vulnerability for treatment.
Some people find it interesting enough to click through, read the article, and to read the book.
Oncologist here.
You can think of drug development as an extremely wide funnel with a minuscule exit hole.
At any given time a medium sized pharmaceutical company has 300-500 drug candidates.
From this group 50 make it to phase 1 trials. 40 get slashed due to toxicity, company abandons them, gets bought by third party and sits in sleepy storage.
10 advance to phase 2 trials where 5-8 may not end up having enough efficacy/too toxic, does not improve survival.
The remaining 3-5 advance to phase 3 where they can suffer the above as well.
Tl:dr: Things usually work in the lab where all ideas start. Until a compound goes through thorough human experimentation believe little.
Phase 1 trials are used to determine drug toxicity. All that reault really says is that the new drug won't itself kill the patients. It still needs to be compared relative to the standard of care in larger phase 2 and 3 trials.
Thanks, that's an interesting insight into the dropoff rate for these ideas. Do you have an opinion on what the bottleneck is? Volume of ideas, length of testing, or perhaps flawed approach in general?
This is the bottleneck for one company. We have many companies this size doing the same thing.
The issue is large companies (novartis/BMS) sometimes sit on compounds and refuse to develop because they think it may not be worth it, may think a certain disease (read market) is saturated, or they may be waiting for the 'right time'. It can be frustrating.
Smaller companies have 2-3 compounds which they actively work to develop but most of them end up getting acquired by the big fish.
The extreme complexity of biology. There's no substitute to just trying things and seeing if they work, because you will never understand what's going on beforehand.
Thanks. I had read of success infecting tumors with virus, that the immune system will control only outside the tumor. But I didn't hear any more about it. What happened with that?
The universal cancer treatment will be full body transplant.
As long as the cancer isn't in the patient's brain, the patient's head could be removed and transplanted onto a donor (brain dead) body. This would render the patient a quadriplegic, but with repeated study over decades we might be able to repair the nervous system.
There isn't a large set of brain dead bodies to draw from, so if this process proves successful, perhaps we could one day start growing human bodies in labs from a monoclonal source. If we remove their ABO and MHC antigens, we might be able to lessen the need for an ongoing life-altering immunosuppressant regimen. These lab grown bodies would be headless/brainless from the outset via gene and surgical deactivation during development to remove any ethical issues. The bodies could be artificially innervated and pumped with the hormonal signals they need to grow until it's time to harvest them.
Cancer is thousands and thousands of different disease states, and it will remain a difficult landscape for the foreseeable future. A non-molecular approach of wholesale cancer tissue removal (via body replacement) seems like an out of the box solution that could work.
Readit News
However, in recent years, a very effective checkpoint inhibitor immunotherapy has been developed for the cancer in question. ~2x the success rates of traditional chemo, greatly increased overall survival statistics, and with massively reduced side effects. The results speak for themselves: this drug has granted my relative years of extra life in the worst case, and a path to a deep, long remission in the best case.
I think that as the technology develops, by 2040 we'll be looking back at the present state of the art with the same incredulity that we currently have for, like, bloodletting with leeches in the Middle Ages. I think they've been saying this for a long time now, but it's truer than ever that a real cure for cancer is right around the corner.
YMMV.
One thing to remember is that "Lung Cancer" is not just one thing. There are mutations of different genes, there are overexpressions of different genes. Each one has its own new medicines. Also, some peoples' cancers are more aggressive than others, and while for many they can find the right drug, for some nothing works.
Keytruda works wonders for some. It did not for me. I had 4 treatments of the CPP (carboplatin, pemetrexed, and pembrolizumab) triad, which had some success. They then put you on "maintenance," which is the PP without the carboplatin (which is the really old school platinum-based chemo). Maintenance did nothing for me. My main tumor grew more than 50% in 2 months.
Last summer I started 9 months on a chemo/immuno that was geared towards my specific mutation. It actually did wonders. It resulted in a 98% shrinkage of my main tumor before I ended up with pneumonitis from it and had to stop. But I've been able to be off treatment for the entire summer. I know there are others who have tried this, and it didn't work.
So yeah, I'm really, really glad your relative was able to get some relief from the Keytruda. But I also wish it were the wonder cure for everyone that it was for them.
The process is grueling in hindsight, but I'm glad to hear you're getting results. At first I would have said "if this is going to kill me, make it sooner rather than later" to avoid a drawn-out painful experience, but I'm starting to appreciate what the buying time really means. It's hard with all that's going on but get your head straight and make sure you enjoy it.
Keep on keeping on.
> that was geared towards my specific mutation
This is actually one of the things that gives me hope for the future: genetic testing on a tissue sample of the patient's cancer is standard, and for many of the specific oncogenes that we know about, there exist therapies targeted to those specific mutations: https://www.cancer.org/cancer/lung-cancer/treating-non-small...
One thing I've learned is that even in the face of good news, cancer is a horrible time, and I wouldn't wish it on anyone. But I'm likewise glad to hear about your results from the latest treatment, and hope things stay as positive as they can for you.
I am hopeful we can move metastatic cancer (which is the true evil of cancer) to a controlled chronic condition.
BTW-- our oncology doctor believes in synergies between chemo and pembro, but I sometimes wonder if it's truly the chemo. Also, Pembro is not without its side-effects.
> I think they've been saying this for a long time now, but it's truer than ever that a real cure for cancer is right around the corner.
I think thats quite a leap. For prostate cancer( most common cancer among men), top line therapies are still androgen blockage that was discover 70 yrs ago, chemo and radiation. Keytruda failed to deliver any significant survival benefits[1].
Yes we've gotten better at slash, burn , poison methods. Radiation is more trageted and sophisticated. Diagnostics are more precise. Chemo drugs have better safety profiles.
But these are all marginal improvements. None of which indicate anything that we are close to a cure.
Only hope we still have is to catch it earlier and go ham on it. Most of the slash,burn, poison methods are being FDA approved for earlier use.
The other two things(one of which you've mentioned) are immune checkpoint blockade if you have MSI-hi/dMMR or PARP inhibition if you have BRCA2+. Even if you are lucky to have these mutations these drugs are a hit or miss[1].
I don't feel optimistic about a cure at all.
1. https://www.businesswire.com/news/home/20220803005334/en/Mer...
By "around the corner" I'm really talking about, like, 20-30 years out, which I think is fairly soon in terms of cancer treatment progress. You're right that it reads like a leap in the context of my comment.
The current approach of regular prostate exams + treatment isn’t perfect but it’s extremely effective.
Brother's been a doctor about 15 years. Huge extended family is aging, and of course cancer creeps in. Of course family members call to get his opinion, and he's been wrong every single time(thankfully). Usually saying something like 'oh, she'll be dead within 2 years' and them living 6, or 8. And in one case calling something a death sentence that was actually, seemingly at least, cured.
It's entirely possible he's just a shit doctor, but I like to think it's that progress has moved a ton since he's studied up on it last.
A programmer who would ignore the developments since 2007 would be unusable.
Thanks for sharing anything you can. If more comfortable sharing in private, I can be reached at asuela1 at yahoo's email service (it's my spam account, but I'll check it if you tell me you wrote back there).
Surgery was not an option here because of the size and location of the mass, but after the initial course of chemo a PET-CT showed an 80% reduction in size. After some time on pembrolizumab, symptoms continue to improve and surgery may be back on the table soon.
(edited for a more accurate picture of maintenance treatment; thanks to borbulon for refreshing my memory)
It is now standard of care for melanoma, for one, but it isn't successful for all cancers, (or even all melanoma mutations).
The most disturbing part is most people are unaware they are ill until relatively late stages of the disease.
If you live long enough, one will know many good people that go this way. It is a worthy area of research, as it improves the lives of many families. =)
Who knows how long it would have had time to mutate and grow otherwise. Early detection is a really important issue for cancer treatments.
Looks as promising as any other promising cancer therapy in phase I trials!
There is a renaissance in cancer drug delivery at present, exemplified by antibody drug conjugates. The tech in the article is very interesting, and a superb bioengineering effort. A caveat is that complex multi-unit therapies don’t have a great track record. They are hard to manufacture reliably, and have a very large optimisation volume, so it’s difficult to increment the development as you only have finite resources for human trials. Contrast this with small molecules where there is a well defined process over various chemical and pharmacokinetic factors, prior to testing in humans. We also lack a good system for developing and trialing ‘platform’ tech like this - the current system is set up for single drugs/combos to be tested and eventually reimbursed in each cancer type separately. If you have a platform for delivering tailored therapies agnostic of cancer type, you will run into many barriers. There is currently only one drug I know of simultaneously approved across multiple cancer types (pembrolizumab in mismatch repair deficient tumours, a rare population). So many challenges ahead of the hype here.
Stopping DNA replication across the body will be fatal. This is what eventually kills with radiation toxicity.
"Given that the EDV surface is coated with lipopolysaccharide (LPS), single-chain bispecific antibodies were attached to the EDV surface where one arm of the antibody is directed to the O-polysaccharide epitopes and the other arm is directed to a tumour cell surface receptor for example Epidermal growth factor receptor (EGFR) which is found on the surface of over 70% of solid tumours"
and
"The EDVs being 400 nm rapidly fall out of these fenestrations and enter into the tumour microenvironment and since they carry the bispecific antibody on the EDV surface, the anti-EGFR component binds to EGFR on the tumour cell surface. This provokes macropinocytosis and the EDVs are taken into the early endosomes, followed by lysosomes and broken down in these organelles releasing the drug PNU-159682. The drug enters into the tumour cell cytoplasm and the nucleus and intercalates with the chromosomal DNA resulting in tumour cell apoptosis. In the event that a tumour type does not express EGFR for example liver cancer, which expresses asialoglycoprotein, then the bispecific antibody can be changed to anti-asialoglycoprotein while the anti-O-polysaccharide component remains constant. Similarly, HER-2 positive breast cancers can be targeted via anti-HER2/anti-O-polysaccharide bispecific antibody"
https://sfamjournals.onlinelibrary.wiley.com/doi/full/10.111...
I don't think this particular therapeutic automatically homes to all cancer cells. However, certain bacteria have been found to home to cancer cells, so maybe that helps too. https://wis-wander.weizmann.ac.il/life-sciences/cells-inside...
It is very exciting to see another tool in the toolbox to achieve higher cancer cell therapeutic specificity.
Brahmbhatt and his collaborator Jennifer MacDiarmid devised a clever ploy. They would send a Trojan horse into malignant cells and turn cancer’s own trickery against it.
The Trojan horse, in this case, is a product of a harmless bacteria that’s been genetically engineered to have specific qualities. When this genetically engineered bacteria divides, it yields a tiny non-living cell of 400 nanometers in diameter—the right size to slip through the damaged vessels and mingle with the tumors."
Targeting the cancer's vascular supply is also a known anti-cancer mechanism of action (anti-angiogenics). How will this method not have the same toxicity as that one?
https://www.youtube.com/watch?v=p3lsYlod5OU&t=8653s
1. The Somatic theory of cancer ('bad genes/out-of-control cellular replication')
2. The metabolic theory of cancer ('cancer cells ferment blood sugar for energy via an ancient emergency metabolic pathway')
Both have merit, but a complete occlusion of one would be bad.
I wrote an open letter, long ago, to a wealthy person who was on the board of a cancer research center, suggesting they read a book and fund the key research scientist:
https://josh.works/mike-clayville-can-have-a-huge-impact-on-...
I thought of the metabolic theory of cancer as I opened this page, because all cancers have a similar reliance upon certain energy generation pathways, which implies a corresponding vulnerability for treatment.
Some people find it interesting enough to click through, read the article, and to read the book.
oh boy
Eg https://www.cancer.gov/research/key-initiatives/ras/ras-cent...
Obviously not usually considered cause, but rather effect.
Deleted Comment
Tl:dr: Things usually work in the lab where all ideas start. Until a compound goes through thorough human experimentation believe little.
The issue is large companies (novartis/BMS) sometimes sit on compounds and refuse to develop because they think it may not be worth it, may think a certain disease (read market) is saturated, or they may be waiting for the 'right time'. It can be frustrating.
Smaller companies have 2-3 compounds which they actively work to develop but most of them end up getting acquired by the big fish.
As long as the cancer isn't in the patient's brain, the patient's head could be removed and transplanted onto a donor (brain dead) body. This would render the patient a quadriplegic, but with repeated study over decades we might be able to repair the nervous system.
There isn't a large set of brain dead bodies to draw from, so if this process proves successful, perhaps we could one day start growing human bodies in labs from a monoclonal source. If we remove their ABO and MHC antigens, we might be able to lessen the need for an ongoing life-altering immunosuppressant regimen. These lab grown bodies would be headless/brainless from the outset via gene and surgical deactivation during development to remove any ethical issues. The bodies could be artificially innervated and pumped with the hormonal signals they need to grow until it's time to harvest them.
Cancer is thousands and thousands of different disease states, and it will remain a difficult landscape for the foreseeable future. A non-molecular approach of wholesale cancer tissue removal (via body replacement) seems like an out of the box solution that could work.