In whom does BAT work? Some new clues - Advanced Prostate...

Advanced Prostate Cancer

16,121 members19,677 posts

In whom does BAT work? Some new clues

Tall_Allen profile image

Bipolar androgen therapy (BAT) has intrigued me since 2015 when I first wrote about it. But the nagging question has always been, and still is, what are the biomarkers that determine if BAT helps, hurts, or does nothing other than provides a nice vacation from ADT? A small trial suggests that there may be genomic predictors. They found that some mCRPC patients got a better PSA response from BAT if they had germline (inherited) or somatic (tumor biopsy) genomic mutations of the tp53 gene and one of either RBI gene or PTEN gene loss. It did not guarantee success - in fact 7 of the 17 men with tp53+PTEN loss had increases in PSA on BAT, and in 3 of the 7 men with increases, PSA more than doubled, indicating that BAT may have made them much worse off.

They also pointed out that in the recent trial of cabazitaxel+carboplatin at MD Anderson, the same genomic predictors of success were found. They propose a comparative trial of the 2 therapies in men who have mutations in tp53 and one of the two (either rb1 or pten).

ncbi.nlm.nih.gov/pmc/articl...

74 Replies

Thanks for staying on top of everything.I think I recently read where a majority of CRPC develop the PTEN loss and tp53.

I don’t key on CRPC as i am not there yet.

Tall_Allen profile image
Tall_Allen in reply to KocoPr

It may be true as gene mutations increasingly mount. For men with PTEN loss at the beginning, there's a really interesting clinical trial:

clinicaltrials.gov/ct2/show...

Thanks for this interesting post!

Thank you very much TA

Very interesting. Thank you for this.

The other indicator is BRCA2. The evidence is patchy and not reliable. The most reliable way to determine is do it. (conditions apply). Basically you know after 3 months whether it worked. At worst, should be about where you would have been if no action taken.

Seasid profile image
Seasid in reply to kaptank

What if you have mets in your spine? Would be the BAT too risky to do? I am thinking here about nerve compression. I had sciatica, very intense nerve pain before starting my Degarelix injections. The pain disappeared 7 days after starting Degarelix ADT.

EdBar profile image
EdBar in reply to Seasid

My onco is Dr. Sartor who has a lot of experience treating patients with BAT. One of his criteria is that patients be asymptomatic.

Ed

Seasid profile image
Seasid in reply to EdBar

Thanks. i don't have much symptoms now thanks to early chemotherapy and Degarelix. I am afraid of my mets in my spine. I think it would be better for me not to do BAT. It is too risky, but that is only my opinion.

Tall_Allen profile image
Tall_Allen in reply to Seasid

My understanding is they will not take patients who ever have been symptomatic. I agree with you that the risk is much greater than any potential gain. The benefit is mostly in QOL and if it increases pain, that negates that benefit.

Seasid profile image
Seasid in reply to Tall_Allen

I think early after my diagnosis I searched the internet in 2018/19 and the only person who was ever cured from advanced prostate cancer received BAT. I believe you have to have certain genetics for that. That could be the ground why the reasearchers ask you to do genetic testing on your biopsy sample. Unfortunately my biopsy sample didn't pass the stringent quality requirements of Peter Mac in Melbourne, so they didn't perform it as the biopsy sample physical size was too small. At least that was given to me as a reason by my oncologist registra for Peter Mac not doing the genetic testing on my biopsy sample. Looks that I need to provide a better sample for the analysis. Bone mets samples are not easy to get and process, so we are thinking about liquid biopsy but it would take 2 months to get back the results of the liquid biopsy from the USA? I am not sure in all of that as I was told about it in one minute. I have only 10 minutes every 2 months with my medical oncologist registra.

mtnwife profile image
mtnwife in reply to Seasid

My husband has mets to lymph, bone/spine and possible lung and is starting his second BAT treatment (He had his first 10 month BAT treatment in 2020 followed by an enzalutamide rechallenge that lasted 8 months) in a couple of weeks. Unless you are on opiates for pain, you'll want to ask a doctor who is a believer in BAT if you are a candidate. Some doctors and laypeople do not encourage the use of high dose T.

Seasid profile image
Seasid in reply to mtnwife

I can understand that. Thanks. I don't have pain now but I had sciatica pain related to the cancer just before starting my ADT Degarelix. 7 days after starting Degarelix my sciatica disappeared. My ex wife thought that I could have BAT, but she is also not a doctor either.

mtnwife profile image
mtnwife in reply to Seasid

The only way to find out if you are a candidate is to talk to your doctors! Since BAT is new and involves a lot of testosterone which freaks out people in the prostate cancer world, you may have to talk to more than one. Doctors are human and also want to stay employed, so using a non-SOC treatment is taboo for many. It's that whole fear of going outside the box and you having a heart attack and suing and they are responsible. I completely understand why more don't offer it.

NickJoy profile image
NickJoy in reply to mtnwife

Do you have a Dr you would recommend? Thank you.

mtnwife profile image
mtnwife in reply to NickJoy

Hi NickJoy, I'd start with your current oncologist and if they aren't willing, see if they would consult with one of the docs like Denmeade, Antonarakis, or Markowski. You might have to do the initial leg work to make the connection, but it would give your doctor confidence (and take away liability) having someone more experienced involved.

NickJoy profile image
NickJoy in reply to mtnwife

Thank you

Tall_Allen profile image
Tall_Allen in reply to NickJoy

I'd recommend sticking to clinical trials or doing it with an oncologist who has a IRB-approved protocol. It scares me that some guys try it on their own. They are taking their lives into their hands.

NickJoy profile image
NickJoy in reply to Tall_Allen

Thank you.

kaptank profile image
kaptank in reply to Seasid

I think if you have mets, particulary in the spine, be aware of high likelihood of pain due to inflammation. So far the only trials have been on asymptomatics. What little evidence there is seems to indicate that pain will fluctuate according to T (ie go down as T declines). We just don't know and caution is advised.

Seasid profile image
Seasid in reply to kaptank

I could always stop BAT.

kaptank profile image
kaptank in reply to Seasid

Anecdotal reports seem to indicate that the pain declines about a week after T injection. But you might have trouble finding an MO willing to try on the basis that not much is known about BAT and symptomatic men. There was a report long ago about a man whose existing pain reduced with supra T but most reports (not many) advise increased pain. These were from the very early small trials at Johns Hopkins.

Note that after the first injection, everyone reports a flare in PSA which subsides in about 2 months. PSA in the first month is unreliable (I advise against a test in the 1st month - not worth the anguish) But in the 2nd and 3rd months you should get an idea whether it is working. Even if not working, its a good idea to rechallenge with the anti androgen such as Enza (not Abi which doesn't seem to work as well with BAT)

kaptank profile image
kaptank in reply to kaptank

One other titbit from those early trials is that men who did suffer pain but decided to continue found that pain was much reduced on subsequent doses. Denmeade has said that there is no evidence that supra T causes a rapid growth in PCa. The initial flare in PSA may be due to dead cells. The flare phenomenon is observed in most treatments that kill PCa cells.

Seasid profile image
Seasid in reply to kaptank

I agree 👍

kaptank profile image
kaptank in reply to Seasid

Yikes! DO NOT USE T PROPIONATE! It causes pain in most folks. Some are OK, but the majority it hurts like hell. Ask me how I know! Body builders use it to get a quick bulk up and say, hey, just man up. That is not good for PCa sufferers.

Seasid profile image
Seasid in reply to kaptank

I was offered a following BAT clinical trial as I live there: clinicaltrials.gov/ct2/show...

Tall_Allen profile image
Tall_Allen in reply to kaptank

That is not what they've subsequently learned- about 20% deteriorate rapidly using supra T.

smurtaw profile image
smurtaw in reply to Seasid

Check out testosterone propionate. Similar to cypionate but about twice as fast. So, if you got pain it would clear faster. Or you could even do Androgel or a fast-acting oral.

kaptank profile image
kaptank in reply to smurtaw

Yikes! DO NOT USE T PROPIONATE! It causes pain in most folks.

smurtaw profile image
smurtaw in reply to kaptank

It's a short ester so causes more pain than cypionate. Neither of them hurt me. Guess I'm lucky or maybe my glute nerves are dead.

I self-inject. I go slow and use a high gauge needle for the injection. Probably has more to do with it than luck or dead nerves.

Seasid profile image
Seasid in reply to smurtaw

I was offered a following BAT clinical trial as I live there: clinicaltrials.gov/ct2/show...

Seasid profile image
Seasid in reply to kaptank

What do you think about this BAT clinical trial?: clinicaltrials.gov/ct2/show... It could be available for me as I live there, but maybe it is to risky for me as I have lots of mets in my spine?

Tall_Allen profile image
Tall_Allen in reply to Seasid

Chemo works better when cells are actively dividing, and maybe periodic high doses of T can accomplish that:

nature.com/articles/bjc2014189

The first BAT trial included one kind of chemo (etoposide), but 3 patients had severe toxicity, so it wasn't included in subsequent BAT trials:

ncbi.nlm.nih.gov/pmc/articl...

Carboplatin usually isn't given without a taxane for prostate cancer, but maybe it will work with BAT.

Seasid profile image
Seasid in reply to Tall_Allen

Good question about carboplatin chemotherapy treatment working alone with BAT only. What would be a ground for that?

Tall_Allen profile image
Tall_Allen in reply to Seasid

IDK- good question, ask them.

Seasid profile image
Seasid in reply to Tall_Allen

I wish, and I will try, but we never have enough time. We have only 10 minutes every 2 months.

mtnwife profile image
mtnwife in reply to Tall_Allen

Tall Allen, the trial you wrote the post about specifically says about BAT: "Patients who received prior taxane chemotherapy had a shorter median PFS in comparison to chemotherapy-naïve patients (8.4 vs 3.6 mo; log-rank p = 0.04; Fig. 2B). The median OS estimate for the whole cohort was 34 mo (95% CI 15–not reached; Fig. 2C). Similarly, patients without prior chemotherapy had a longer median OS in comparison to taxane-treated patients (38 vs 15.1 mo; log-rank p = 0.04; Fig. 2D)." Testosterone (at least in this study) works best WITHOUT chemo. The authors report that "chemotherapy-naïve patients experienc[ed] the most favorable outcomes" and that their "data suggest that BAT may induce clinically meaningful responses in aggressive-variant prostate cancers with a more favorable safety profile in comparison to a taxane/platinum doublet".

I'm really surprised you glossed over--or didn't mention at all--the relevance of not having done chemo with superior outcomes of BAT. (At least for this subset of men who had TP53 and one other mutation (PTEN or RB1).)

Tall_Allen profile image
Tall_Allen in reply to mtnwife

When patients have not done chemo, it just means that their cancer is less progressed. Less progressed patients do better with every therapy. It is a commentary on the patient's starting point, not the influence of chemo on BAT. That's why the authors propose randomizing patients to chemo or BAT.

Seasid profile image
Seasid in reply to Tall_Allen

I was thinking the same way like you. Otherwise what could be a reason that BAT is inferior with prior chemotherapy? I myself jumped into very early chemotherapy because I was very scared that the intense sciatica nerve pain will otherwise return soon. Plus I had multiple spine mets. One of them as high as my neck. I was really afraid that I may end up disabled from my neck down. Thanks God I am fine now.

mtnwife profile image
mtnwife in reply to Tall_Allen

That is just not true. Since docetaxel was approved in 2004, it hasn't had a great response rate (3 mo survival gains over mitoxantrone) but it was/is the best they have. There still aren't huge benefits with any chemo for late stage prostate cancer.

Only in the last few years has prostate cancer treatment taken the route of breast cancer treatment with early use of chemo at diagnosis. Used early, docetaxel definitely has survival benefits as shown in the STAMPEDE trial.

Chemo during late stage mCRPC use still has very little benefit for longevity but is a good treatment for pain.

Plus, the approval of enzalutamide, abiraterone and radium-223 gave doctors options that are so much more effective than docetaxel. They are the "go to" drugs now, but before 2012, docetaxel was the only option.

It will be interesting to see how many years it will take for BAT to go mainstream.

Tall_Allen profile image
Tall_Allen in reply to mtnwife

Perhaps I wasn't clear. Most men, unfortunately, do not use docetaxel until it has little chance to do any good. Therefore, docetaxel use is a frequent indicator used in research studies, to show that patients are near the end of their rope and have exhausted all other possibilities.

Docetaxel, used early enough, has equal survival improvement compared to Zytiga. In the US, more patients use Zytiga; but in the UK and Europe, docetaxel was the first drug used in newly diagnosed men with metastases.

Now, with triplet therapy, it will be used in combination with an advanced hormonal.

Used at the end, all the drugs you named, and Pluvicto, increase survival by 3-5 months. The real opportunity is in using them earlier.

BAT is many years off from mainstream use. There has never been a Phase 3 trial. While it improves QOL and delays progression on enzalutamide, early results show no significant improvement in survival.

mtnwife profile image
mtnwife in reply to Tall_Allen

Agree with most of your reply, but disagree about BAT showing no significant improvement in survival. I'd still would like to see your data on that one--in my husband's case, starting BAT lead to a CLEAR improvement in his survival. Heck, the additional 8 months from the Xtandi rechallenge would be enough of a win but he got 10 more months of feeling great with BAT and is ready to start his second go around. This is the same guy who was given 18 months in Jan 2021, and ONLY if he did chemo. All other treatments had failed.Can you please link your info on survival? You've posted that tidbit a bunch of times but I haven't seen your data source and would like to read the original. Thanks in advance.

Tall_Allen profile image
Tall_Allen in reply to mtnwife

It was found on the largest BAT trial- the Transformer trial. It is easily seen in Figure 2D. The Hazard Ratio for overall survival was 0.95 (0.66-1.39) p=0.80 It showed that about a third of the patients had improved survival vs enzalutamide, but about a third had worse survival.

ascopubs.org/doi/10.1200/JC...

I certainly hope your husband has improved survival. But since you have no way of knowing how long he would have survived w/o BAT, no one can say if he had a "clear improvement in his survival." Let's hope that he is among the third that did.

mtnwife profile image
mtnwife in reply to Tall_Allen

Thanks for supplying the link. The 1/3 improve, 1/3 same, 1/3 worse is about what is seen in most PCA treatments. Some work, some don't, so if it works you stay on it and if it doesn't you pivot. If survival is the same, BAT would appear to be the clear winner. Low cost, good QOL vs enzalutamide $100,000+/year and lots of side effects.

Tall_Allen profile image
Tall_Allen in reply to mtnwife

The important takeaway of a non-significant HR is that there was no statistically significant effect on survival. And no, that is definitely not what we've "seen with most treatments." For example, the HR for early use of docetaxel in de novo metastatic men was 0.76 (95% CI: 0.62-0.92), so everyone who took it lived longer.

thelancet.com/journals/lanc...

Or, when docetaxel was tried in men with mCRPC, the HR was also 0.76 (95% CI: 0.62-0.94)

nejm.org/doi/full/10.1056/N...

In fact, when the 95% CI crosses 1.0, we rule out that therapy.

By "it works" for BAT, it extends time on Xtandi and provides very good breaks from ADT. It certainly does that - it doesn't extend survival. Other therapies that do extend survival should not be ignored.

Tall_Allen profile image
Tall_Allen in reply to mtnwife

I see you edited out some of your previous statements - glad you did. You also added:"Low cost, good QOL vs enzalutamide $100,000+/year and lots of side effects." The entire purpose of BAT in the TRANSFORMER trial was to extend the time during which enzalutamide was effective. So, in the trial, patients who went through BAT, were able to stay on enzalutamide 9 months longer if they did BAT before it. So the net cost is a great deal higher after BAT. The side effects of longer duration enzalutamide of course last longer too.

The benefit of BAT was to give the patients using it a break from castration for 3 months.

smurtaw profile image
smurtaw in reply to Tall_Allen

If you're going to use enzalutamide there are financial assistance options. It could be as cheap as $0-$10 a month.

Seasid profile image
Seasid in reply to mtnwife

Could you fill out your profile with data about when diagnosed and since are you on ADT? Thanks for your contribution to this post. Greatly appreciated. This is the way to make progress.

mtnwife profile image
mtnwife in reply to Seasid

Thanks for the reminder. Just updated bio with the basics of treatment since 2011.

smurtaw profile image
smurtaw in reply to mtnwife

He gave a summary description. I view summary descriptions as "data for dummies". This is another reason that we need the raw data (and profiles). TA said that BAT might hurt some men. That may or may not be true but this study does not show us this.

And, as seasid said, you could always stop. Danmeade is of the same opinion. "If you try, you might fail. But if you don't try, you'll never succeed."

Do you have the raw data for the subjects?

If PSADT was greater than the time they were on BAT, then a 100% gain isn't proof that BAT did them harm. And of course the same applies to post PSADT.

Without that data I don't know if we can state that BAT was harmful. It might have been helpful to 100% of the subjects. And we also need to think about what it provided (e.g. down-regulation of ARs). Perhaps the benefits are far greater than a simple PSADT change.

Tall_Allen profile image
Tall_Allen in reply to smurtaw

I don't understand what you are saying- their PSA shot up through the roof - what more do you need.

smurtaw profile image
smurtaw in reply to Tall_Allen

What was the time frame? What was the rate of increase before and after BAT?

Let's use a hypothetical example:

2018/01/01 PSA = .6

2019/01/01 PSA =1.8

PSA went up 200% in 1 year

Now we do BAT for 1 year

2019/01/01 PSA =1.8

2020/01/01 PSA = 3.6

PSA went up 100% in 1 year

Now we stop BAT

2020/01/01 PSA = 3.6

2021/01/01 PSA=10.8

PSA went up 200% in 1 year

If I have the raw data to look at it would be helpful. If we can't get it I don't think I am able to state that either BAT did or did not work.

Tall_Allen profile image
Tall_Allen in reply to smurtaw

The authors set PSA50 (PSA decreased by at least 50%) as their criterion as to whether BAT worked. They were not just hoping that PSADT slowed, they were hoping to decrease progression. Increases in PSA were deemed failures, as in all trials of this sort of thing (not just BAT). You can argue against PSA50 as a screener but slowing of doubling time has been found to be a poor indicator and is never used.

smurtaw profile image
smurtaw in reply to Tall_Allen

Ok. So we don't have the data and I can't state that BAT harmed anyone. It might have but that is a complete guess without a control group coupled with OS (or at least CSS).

Tall_Allen profile image
Tall_Allen in reply to smurtaw

This was just a small pilot trial looking at genomics. In larger trials of BAT, up to a third seem to be harmed on the basis of PSA changes. Even scarier is the finding that radiographic progression occurs even when there is no increase in PSA. There is little interest in conducting an RCT until there is more safety data.

smurtaw profile image
smurtaw in reply to Tall_Allen

Some RCTs are being done or are complete. Some of them are:clinicaltrials.gov/ct2/show...

clinicaltrials.gov/ct2/show...

clinicaltrials.gov/ct2/show...

clinicaltrials.gov/ct2/show...

clinicaltrials.gov/ct2/show...

mtnwife profile image
mtnwife in reply to Tall_Allen

For a guy who claims impartiality, I'm again surprised you single out BAT to say, "Even scarier is the finding that radiographic progression occurs even when there is no increase in PSA." You well know this occurs in LU-177, novel AR-targeted therapies, neuroendocrine subtypes and a host of other treatments. That's why people get scans and don't rely on PSA once they are mCRPC. It isn't the testosterone, it's the cancer.

Tall_Allen profile image
Tall_Allen in reply to mtnwife

You wrote: "For a guy who claims impartiality, I'm again surprised you single out BAT to say, "Even scarier is the finding that radiographic progression occurs even when there is no increase in PSA." You well know this occurs in LU-177, novel AR-targeted therapies, neuroendocrine subtypes and a host of other treatments. That's why people get scans and don't rely on PSA once they are mCRPC. It isn't the testosterone, it's the cancer."

Sorry, I missed this comment to me. I'm not singling out BAT- radiographic progression is an indication of failure of all therapies. The point is that one cannot just take comfort that PSA has been reduced - BAT apparently lowers PSA even when there is no effect on tumor number or size. The researchers at Johns Hopkins have investigated using Pylarify PET scans as a better indicator of progression. In a pilot test on 6 patients, 4 patients had reduced PSA (by at least 50%) after 3 months of BAT, but 2 of those 4 had radiographic progression on a Pylarify PET scan:

jnm.snmjournals.org/content...

Tall_Allen profile image
Tall_Allen in reply to smurtaw

BTW- do you understand that they truncate at 100% increase? Also the research discrediting PSADT without control as a progression marker was done at JH.

smurtaw profile image
smurtaw in reply to Tall_Allen

Thanks. I didn't know that but I did think it was perhaps clamped. Looked very suspicious to have a bunch of guys at exactly 100%. This is a reason why I like raw data. A lot can be hidden with summaries.

mtnwife profile image
mtnwife in reply to Tall_Allen

smurtaw is correct. Saying "their PSA shot up through the roof" is irrelevant without knowing why. The prior treatment of the study participants was all over the board from minimally treated to every treatment possible. At that point, many SOC treatments will cause PSA to double. It happens the further along you are. It isn't because of BAT, so there is no need to be so dramatic.

The authors specifically point out "We did not identify any patients with neuroendocrine features on pathology. Pathology review was conducted on archived tissue and may not have detected neuroendocrine transformation in late-stage disease."

A mix of neuroendocrine and adenocarcinoma PCA could cause a lot of progression/psa increase issues unrelated to testosterone.

Tall_Allen profile image
Tall_Allen in reply to mtnwife

You wrote: "Saying "their PSA shot up through the roof" is irrelevant without knowing why. "

That was the entire point of their study - to find out why.

You wrote:"The authors specifically point out "We did not identify any patients with neuroendocrine features on pathology. Pathology review was conducted on archived tissue and may not have detected neuroendocrine transformation in late-stage disease." A mix of neuroendocrine and adenocarcinoma PCA could cause a lot of progression/psa increase issues unrelated to testosterone."

Treatment emergent NEPC occurs in 17% of heavily pretreated patients, and it does not cause PSA increase. It causes PSA to decrease because neuroendocrine tumors do not express PSA. PSA was the only measure used in this study.

Any chance they'll spark up crispr case 9 for PCa?

Well Written Tall Allen.I myself have wondered about biomarkers too. If you ever find any more specific information that would be great for all of us. Keep posting as you help us

LRV

Tall_Allen profile image
Tall_Allen in reply to Lrv44221

Biomarkers remain elusive, sadly, but they will keep looking.

You're up to Bat and we're in the Batter's Box...

Hit one for the Gipper...........

Good Luck, Good Health and Good Humor.

j-o-h-n Sunday 06/12/2022 3:35 PM DST

smurtaw profile image
smurtaw in reply to j-o-h-n

Ok Robin! The President will do his best.

j-o-h-n profile image
j-o-h-n in reply to smurtaw

Okie Dokie Batsy Baby....I read you 5 X 5. President will send fuel to aid the Akkadians as soon as he builds the oil pipeline through Delaware...

Good Luck, Good Health and Good Humor.

j-o-h-n Monday 06/13/2022 12:15 PM DST

After all my comments above, thought I'd update why my husband and I are proponents of BAT. In January 2020, my husband was failing Xtandi with his PSA doubling every 2 months. Instead of the chemo the doctors offered, he chose BAT outside of a clinical trial because he had been through most treatments including both Zytiga and Xtandi. Trials at the time did not allow prior treatment with multiple AR-targeted therapies. (Interestingly, in the study this post was written about, half the participants were prior treated with both.)He got 10 rounds of BAT approx. 28 days apart until his PSA spiked. He started his Xtandi rechallenge in October, 2021 with expectations that if it worked, it would work at best about six months. He responded to Xtandi for 10 months!! Just this week, after his PSA doubled to 10, he stopped Xtandi for a 3 week washout. (The washout can last from a minimum of 2 weeks to a max of 4. He is doing a three week washout due to the July 4th holiday schedule of his doctor.)

He is starting a second round of BAT which we hope does as well as the first go around, but we are realistic enough--and the data shows--that the second round doesn't last as long.

mtnwife profile image
mtnwife in reply to mtnwife

Forgot one more thing: my husband wouldn't qualify for the trial Tall Allen is writing about either. He has the TP53 mutation but not one of the others required.

Seasid profile image
Seasid in reply to mtnwife

Would your husband qualify for this trial?: clinicaltrials.gov/ct2/show...

mtnwife profile image
mtnwife in reply to Seasid

No, he has already done BAT so they wouldn't want him. My husband is one of the lucky super responders to BAT and has said all along he won't do chemo, so he wouldn't be interested in the carboplatin addition.

Seasid profile image
Seasid in reply to mtnwife

I am also not happy for the addition of carboplatin, but maybe they work synergistically? You have a contact details and you can ask them about the addition of carboplatin. I was told that if BAT works for me I could continue with it without carboplatin. They said that the depot testosteron injections into the buttocks which then work for about a week are very cheap. Maybe they could give it to you without carboplatin. I believe that you would need to organize for genetic testing of your metastasis or cancer or whatever they would request from you to qualify for the BAT. Do you understand? Just ask them. Maybe they are already doing it without carboplatin. Ask Professor Joshua. Ok? You have his contact details in that clinical trial link from me. I wish you luck.

You may also like...