Example of using 23andme to get a rough estimate of BAT effectiveness EDIT: Germline so most of these do not apply.

[PCaWarrior]

EDIT: I thought the DTC tests were somatic. That was lame. They are germline. The process I went through can help me if a somatic test finds mutations. But this particular snapshot was a waste of time, except for the AR variant. I probably have it, but to low to be picked up by my germline test.

Took a couple of hours but I searched 23andme for all possible DNA variants that predict BAT efficacy. Main ones are BRCA1/2, TP53, AR, PTEN, and in my case ATM. Then I ran them through Gemini, Perplexity, and ChatGPT. I did this multiple times and asked in various ways and in modes other than just research. For the final analysis and the beginning ones I used deep research modes. I need to follow up with some ctDNA and RNA testing. If I take the clinical accuracy as 100% (it isn't close but I can't estimate it), then the average prediction of synergy with a PARPi is about 99% and for SPA sensitivity, it is also about 99%.

I am going to follow up with FoundationOne tests if my insurance will cover.

If anyone is interested and has 23andme data (or likely data from other DTC services - DNA SNPs) it's straightforward to calculate something similar - but tedious.

Goto you.23andme.com/tools/data/ and search for a gene. Copy and paste into an AI. Ask the question: how does this predict bipolar androgen therapy efficacy?

You could also get your raw data (you.23andme.com/tools/data/.... You need to request it and I'm not sure how to process it.

Genetic Variants (SNPs)

Disclaimer

This information is for informational purposes only and is NOT medical advice. Interpretations based on Direct-to-Consumer (DTC) genetic data (e.g., specific rsIDs) for clinical decision-making—especially regarding cancer treatment—are unreliable and potentially misleading. Follow-up testing with prostate cancer–specific, FDA-approved assays is essential (e.g., FoundationOne Liquid CDx for BRCA2/TP53/AR status via ctDNA and FoundationOne RNA for AR mutations including the AR-V7 splice variant).

The clinical significance of these variants has not been clinically verified.

________________________________________

DNA Variant Table (all of these variants were on the chip)

Gene/Marker Variant/rsID Genotype/Status Estimated Detection Accuracy Clinical Significance BAT Relevance

BRCA1 rs189382442 & rs552911643 T/T (biallelic) 25-50% Loss-of-function mutations lead to homologous recombination deficiency (HRD), rendering tumors more vulnerable to DNA damage. High sensitivity to BAT-induced DNA damage; enhances synergy with PARP inhibitors.

BRCA2 rs276174802 Loss-of-function 30-60% Biallelic inactivation results in HRD, increasing replication stress and double-strand breaks (DSBs) upon treatment. HRD tumors are highly sensitive to BAT, and this state synergizes with PARP inhibitors (e.g., olaparib).

TP53 rs78378222 (and others, e.g., rs1800372) T/T (pathogenic) 80%-95%(multiple variants detected) Impaired DNA repair that may amplify BAT-induced DNA damage, though associated with a more aggressive cancer phenotype. Enhances the therapeutic window for BAT—especially when combined with PARP inhibitors—by further compromising DNA repair.

AR rs201097725 C/C 95%-98% Variants may enhance AR signaling under supraphysiologic androgen (SPA) pulses, potentially increasing susceptibility to growth arrest induced by BAT. High AR dependency generally predicts a good BAT response, though resistance may emerge through AR downregulation.

ATM rs1800056 T/T (homozygous) 40%-60% A truncating mutation (p.Arg35Ter) leading to ATM loss-of-function, classified as pathogenic per ClinVar. A strong predictor of synergy when combining BAT with PARP inhibitors due to impaired double-strand break repair.

ATM rs587779826 T/T (homozygous) 40%-60% Likely pathogenic missense variant disrupting ATM kinase activity, also compromising the DNA repair process. Enhances synthetic lethality when BAT-induced DNA damage is paired with PARP inhibition.

Additional Note: Intact MSH2 status (suggesting microsatellite stability and no evidence of Lynch syndrome) is also relevant, though not included in the table.

________________________________________

Summary of Clinical Implications & Recommendations

• Impact on BAT Efficacy:

o BRCA1/BRCA2 Loss-of-Function: High likelihood of deep and prolonged responses (PSA50 rates of ~67% for BRCA1 and ~47% for BRCA2; median PFS of ~11 and ~5.5 months, respectively).

o TP53 Mutations: Enhance sensitivity to BAT-induced DNA damage while indicating a potential for aggressive disease—requiring careful monitoring.

o AR Alterations: High AR dependency generally predicts a favorable BAT response.

o ATM Loss-of-Function: Predicted to synergize strongly with PARP inhibitors when used with BAT.

• Therapeutic Strategies:

1. BAT + PARP Inhibitors: Even in the absence of pathogenic BRCA2 mutations, BAT may downregulate BRCA2, creating an HRD-like state that is exploitable by PARP inhibitors (e.g., olaparib).

2. Biomarker Testing: Confirm HRD status via ctDNA testing (FoundationOne Liquid CDx) or tumor sequencing; consider additional functional assays (e.g., RAD51 foci assay).

3. Alternating Therapy: Cycling BAT with AR inhibitors (such as darolutamide) may exploit AR resensitization, as seen in the WOMBAT trial.

4. Combination with Immunotherapy: For patients with TP53/AR alterations, combining BAT with immunotherapy (e.g., nivolumab) may provide additional benefit (supported by COMBAT trial data).

• Overall Conclusion:

Your genetic profile—particularly the inactivation of BRCA1, the presence of TP53 mutations, and ATM loss-of-function—suggests potential benefit from combination therapies involving BAT with PARP inhibitors or immunotherapy. Ongoing monitoring of AR, TP53, and ATM status using liquid biopsies and approved genomic assays is recommended to guide treatment decisions.

[PCaWarrior]

Variant table

variant table BAT prediction

[Maxone73 in reply to PCaWarrior]

ATR inhibitors seem to work better than PARPi when you are ATM

[PCaWarrior in reply to Maxone73]

PARPi has been trialed with BAT but not ATR inhibitors.

Theoretically PARPi, ATRi and BAT might work together. But no trials and the side effects might add up. What do you think? ATRi side effects less than or more than PARPi? If the same or less maybe I'll work some SPA phases with ATRi instead of PARPi or even try one with both (pulsed and with SPA the side effects of PARPi are not noticeable).

[PCaWarrior in reply to Maxone73]

The drugs are in development. I take the effective dose of curcumin, sulforaphane, and EGCG. If FoundationOne confirms ATM maybe I'll double up around the start of SPA.

I went through the usual 3 AI redundancy check. They all substantially agreed for a change. And no arguments needed on my part. AIs are a great help but more often than not I need a drink after dealing with them.

Natural ATR Inhibitors: Efficacy, Dosing, and Synergy with BAT/Olaparib

Key: Evidence Grade (A-F)

• A: Clinical trial evidence

• B: Strong preclinical data

• C: Mechanistic/indirect evidence

• D: Hypothetical/limited data

Natural ATR Inhibitors

Compound Strength (A-F) Effective Dose Mechanistic Theory Notes

Oridonin B- 20–40 mg/day Direct ATR kinase inhibition (IC50: ~3 μM). Preclinical tumor regression in ATM-null models. Rabdosia rubescens (3–5g dried herb). Moderate bioavailability and good half-life

Expensive

Curcumin D+ 500–1,000 mg Downregulates ATR/Chk1 via NF-κB suppression. Synergizes with DNA-damaging agents. Turmeric (10–20g powder).

Poor bioavailability and short half-life

EGCG C- 400–800 mg PI3K/AKT/mTOR inhibition → reduces ATR-mediated replication stress. Matcha powder (10 g/day) provides 600-700 mg of EGCG. Moderate bioavailability and moderate half-life

Sulforaphane C 10–40 mg NRF2-mediated antioxidant response → ATR depletion. Broccoli sprouts (100–200g). Good bioavailability and short half-life

Genistein C- 50–100 mg Phytoestrogen blocks ATR recruitment to DSBs. Synergizes with radiation. Soy (500g tofu/day). Moderate bioavailability and moderate half-life

Berberine C- 500–1,000 mg AMPK activation → ATR inhibition. Synergy with olaparib in TNBC models. Barberry (1–2g root extract). Poor bioavailability and short half-life

Quercetin D- 500–1,000 mg Indirect ATR suppression via ROS/PI3K-AKT. Weak standalone efficacy. Onions (500g raw), capers (200g). Poor bioavailability and moderate half-life

Resveratrol D- 100–200 mg SIRT1 activation → indirect ATR suppression. Limited bioavailability. Poor bioavailability and short half-life

Apigenin D- 50–100 mg CDK inhibition → weak ATR/Chk1 modulation. Parsley (50g fresh). Poor bioavailability and short half-life

Ursolic Acid D- 150–300 mg ER stress induction → ATR/Chk1 suppression. Low bioavailability

Synergy with Bipolar Androgen Therapy (BAT)

1. Mechanistic Theory:

• BAT induces supraphysiologic testosterone → replication stress → DSBs.

• ATR inhibitors (e.g., oridonin, curcumin) block replication stress repair → mitotic catastrophe.

• Example: Oridonin + BAT caused 60% tumor regression in ATM-null models.

2. Key Compounds:

• Oridonin/Curcumin: Enhance BAT-induced DNA damage in HRD tumors (BRCA1/2/ATM LOF).

• Berberine/EGCG: Amplify AR-driven MYC suppression under SPA pulses.

Synergy with Olaparib (PARP Inhibitor)

1. Mechanistic Theory:

• Olaparib blocks PARP → SSB repair failure → replication forks collapse.

• ATR inhibitors (e.g., berberine, sulforaphane) prevent fork restart → synthetic lethality.

2. Key Compounds:

• Berberine: Reduces olaparib resistance in BRCA1/2-WT tumors via ATR/ATM crosstalk.

• Genistein: Enhances olaparib efficacy in AR-V7+ tumors (preclinical PSA50: 40%).

Triple Synergy (BAT + Olaparib + Natural ATRi)

1. Theoretical Framework:

• BAT: Causes replication stress via SPA-induced DNA damage.

• Olaparib: Blocks PARP-mediated SSB repair.

• ATR Inhibitors: Prevent replication stress recovery → synthetic lethality.

2. Optimal Stack:

• Oridonin (20mg) + Curcumin (500mg): Direct ATR inhibition + NF-κB suppression.

• EGCG (400mg) + Berberine (500mg): PI3K/AMPK dual pathway blockade.

Practical Considerations

1. Bioavailability Issues:

• Curcumin/berberine require piperine (black pepper) for absorption.

• Oridonin is fat-soluble; take with dietary fats.

2. Drug Interactions:

• Berberine inhibits CYP3A4 → may increase olaparib toxicity.

• Resveratrol may antagonize AR under BAT (avoid high doses).

Supporting Evidence:

• Oridonin showed 60% tumor regression in ATM-null models with BAT.

[KocoPr]

Russ here is a way to make all your poor bioavailable phytonutrients much more bioavailable.

This is my master TP53 Kill blend procedure and dosing. It will require some experience making tinctures the correct way plus the correct equipment. Perculation setup for temp sensitive herbs, soxhlet extractor for making tinctures on 1 day, ultrasonic homogenizer for encapsulating all phyto chemicals in liposomals.

If anyone is interested in learning this let me know i can put up a post on FPC group.

TP53 + Senolytic Kill Window Master Blend – v2 (with Apigenin) – Full Protocol

Purpose

This updated liposomal blend is designed for use during the Darolutamide/Orgovyx phase plus daro washout week of the BAT protocol. It combines TP53-targeting and senolytic actions by incorporating apigenin (from parsley tincture) alongside other synergistic polyphenols. This version replaces the need for a separate senolytic formula.

Key Ingredients

- EGCG (from green tea extract, water-based)

- DIM

- Quercetin

- Apigenin (from parsley tincture, integrated)

- Tincture Concentrate: Berberine, Resveratrol, Fisetin, Skullcap, Piperine

- Sunflower lecithin

- Distilled water

Step 1 – Lecithin Hydration

1. Weigh 30g sunflower lecithin powder.

2. Add to 275 mL distilled water in a clean glass beaker or container.

3. Stir thoroughly and allow to hydrate for several hours or overnight.

4. Optional: Use magnetic stirrer to speed up hydration.

5. Once fully hydrated, this is your liposomal base.

Step 2 – EGCG Water Extraction

1. Weigh 6g green tea extract powder (≥50% polyphenols, ~30–40% EGCG).

2. Add to 30–40 mL distilled water

3. Add 300mg sodium ascorbate to improve EGCG solubility and stability.

4. Heat gently (40–45°C (104–113°F)) while stirring to fully dissolve.

5. Allow to cool before proceeding to next phase.

Step 3 – DIM and Quercetin Integration

1. Weigh your desired dose of DIM (e.g., 300–600mg) and quercetin (e.g., 500–1000mg) add 20ml 95% alc and make a slurry.

2. Once EGCG solution is cooled (below 45°C (113°F)), add DIM and quercetin slurry to the lecithin + EGCG blend.

3. Stir well. Do not overheat—both compounds are heat-sensitive.

4. Begin initial blending or mild homogenization (optional at this stage).

Step 4 – Tincture Phase Preparation (Including Apigenin)

1. Measure 15 mL of each tincture:

- Berberine

- Resveratrol

- Fisetin

- Skullcap (Scutellaria lateriflora)

- Piperine

- Parsley tincture (apigenin source)

Total volume: ~90 mL

2. Combine all tinctures into a single container.

3. Gently evaporate over low heat or magnetic stirrer (covered loosely) until final volume is 20–30 mL.

- Maintain temperature below 45°C (113°F) (113°F) (113°F) to preserve actives.

- Stir gently for uniform concentration.

4. Let the tincture concentrate cool to room temperature.

5. Add it slowly into the lecithin + EGCG + DIM + Quercetin blend.

6. Perform final ultrasonic homogenization for 10–15 minutes (start with short pulses).

Dosing and Timing

- Dose: 15–30 mL per day during Darolutamide/Orgovyx phase plus daro washout week

- Includes integrated apigenin (no need to co-dose parsley tincture separately)

- Avoid during High T phase

- Optional microdosing (5–10 mL) during ADT + darolutamide phase for TP53 maintenance

[PCaWarrior in reply to KocoPr]

I know that this is much better than what I do. I just add known synergists and bioavailability stuff like piperine or CYP3A4 inhibitors (grapefruit juice is an SOC inhibitor). And I look at half lives and try to time it.

Bottom line, I'm lazy.

[PCaWarrior in reply to KocoPr]

FDA "Grapefruit juice can block the action of intestinal CYP3A4, so instead of being metabolized, more of the drug enters the blood and stays in the body longer. The result: too much drug in your body. The amount of the CYP3A4 enzyme in the intestine varies from person to person."

Or characterize it. Take less of the drug to account for decreased elimination. Or of course we can take full dose and pay more money.

Typically if a drug is metabolized by CYP3A4, taking it with 8 oz of grapefruit juice increases serum levels 50%-80%. Usually it isn't difficult to find out the amounts from the FDA or the manufacturer.

I find this statement useless: "The amount of the CYP3A4 enzyme in the intestine varies from person to person.". Ok, and we're all different sizes too. I'm twice as big as many men but there are some who are even bigger than me. So, let me do the math, if my blood volume is 2x someone else's and we both take a "standard" dose of something, gee, will their levels be higher than mine?

Like my MO said one time "this isn't rocket science". She knew that I used to be a rocket scientist. Lol!

[Ichthus316 in reply to KocoPr]

Why should senolytics be avoided during the high T phase?

[PCaWarrior in reply to Ichthus316]

From my book: "Why Senolytics Should Be Avoided During Supraphysiological Androgen (SPA) Phase

The reasoning for avoiding senolytics during the high testosterone phase of Bipolar Androgen Therapy (BAT) is supported by emerging research on senescence in prostate cancer treatment.

Mechanistic Rationale

SPA-induced senescence appears to be an integral part of BAT's therapeutic mechanism rather than an unwanted side effect. Several key factors explain why clearing these senescent cells during the high androgen phase may be counterproductive:

1. SPA induces a specific type of senescence characterized by DNA double-strand breaks, G0/G1 cell cycle arrest, and cellular senescence that is AR-mediated and dose-dependent[1]. This differs from other therapy-induced senescence types.

2. MYC suppression dependency: A critical anti-tumor mechanism of BAT involves AR-mediated suppression of the MYC oncogene[2]. SPA-induced senescent cells contribute to this pathway, and premature elimination might interrupt this beneficial effect.

3. Metabolic vulnerability creation: SPA treatment drives polyamine synthesis in prostate cancer cells[3], creating metabolic conditions that enhance the effectiveness of subsequent treatments. Eliminating senescent cells could disrupt this metabolic priming.

Timing Considerations

The bipolar (cycling) nature of BAT therapy relies on the proper sequence and timing of high/low androgen phases:

• During high androgen (SPA) phase: Senescence induction serves as an initial tumor control mechanism

• During low androgen phase: Different pathways are activated that might make senescent cells more appropriate targets for elimination

As noted in research, resistance to SPA eventually occurs through decreased AR levels and activity with loss of MYC suppression[2]. The cycling between SPA and AR antagonists (like enzalutamide) appears critical for maintaining efficacy - eliminating senescent cells during SPA could disrupt this careful balance.

Clinical Implications

The available evidence suggests that rather than using senolytics during SPA phase, a more effective approach might be:

1. Allow SPA to induce senescence during high-testosterone phase

2. Consider senolytic strategies during the low-testosterone phase when they won't interfere with SPA's mechanisms

3. Focus on maintaining the oscillations in AR activity that appear crucial for BAT efficacy[2]

Although therapy-induced senescence may eventually promote tumor growth through SASP in some cases, eliminating SPA-induced senescent cells too early could weaken BAT’s effectiveness. The timing of senolytic treatments relative to the BAT cycle must therefore be managed with care. There is currently no clinical evidence supporting the use of senolytic interventions during either the SPA or ADT phases of BAT. However, it seems both safe and potentially beneficial to apply them during the ADT phases, while their use during the SPA phases remains uncertain. To remain cautious, I limit their use to the ADT phases.

1. A “Bipolar Androgen Therapy: Mechanisms and Clinical Implications” – pubmed.ncbi.nlm.nih.gov/313...

2. B– “Cellular Senescence Induced by Supraphysiological Androgen Levels in Prostate Cancer” –pmc.ncbi.nlm.nih.gov/articl...

3. C+ “Preliminary Findings on Androgen Therapy Effects in Prostate Cancer Patients” – medrxiv.org/content/10.1101...

4. A- “The Dual Role of Androgen Receptor Signaling in Cancer: Oncogenic and Tumor Suppressive Functions” – frontiersin.org/journals/on...

5. B- “Advances in Selective Androgen Receptor Modulators for Cancer Treatment” – explorationpub.com/Journals...

"

KokoPr might have different or the same reasons.

[Ichthus316 in reply to PCaWarrior]

Thanks for the info. Is this from a different book than "Adaptive Bipolar Androgen Therapy for Prostate Cancer"? I browsed the onedrive version but didn't find much on senolytics. All of your page numbers say "2" ...or am I doing something wrong? KokoPr appears to take his concoction of senolytics every day during the ADT cycle. Do you do something different? Since I'm also lazy, I'm looking for a shortcut to dosing & frequency rather than having to calculate half-lives, etc, etc.

[PCaWarrior in reply to Ichthus316]

PM me and I'll send you the link to the book. I update it a lot and added quite a bit since I put out the kindle one. The link is permanently to the working copy.

You could take them throughout the ADT cycle. Most of them are also ATR inhibitors (curc, EGCG, . ATRi might work best during SPA. Senolytics maybe should be taken during ADT only. So.... Punt? I don't worry about it. I just take em. Double down sometimes. How much of a difference does it make? My guess is not much.

[KocoPr in reply to Ichthus316]

What PCaWarrior said plus some of my herbs like skullcap are AR inhibitors or interfere with androgen or it’s receptors.

Many components of your TP53/senolytic formula inhibit AR, such as:

• Baicalein (from skullcap)

• Resveratrol

• Berberine

• EGCG

• Apigenin

• Quercetin

Taking these during the High-T phase would blunt the intended therapeutic effect of testosterone surges, interfering with cell cycle disruption and AR-driven apoptosis.

[Ichthus316 in reply to KocoPr]

Thanks KocoPr and PCaWarrior! I will adjust the timing of my senolytics to coincide with the low T phase of pBAT.

[PCaWarrior in reply to Ichthus316]

What wins? I play the averages a little and if undecided I do 50/50.

ATR inhibitors might synergize with SPA.

ATR inhibitors might synergize with ADT.

Senolytics might interfere with SPA.

Senolytics might synergize with ADT.

Most natural senolytics are also ATR inhibitors. Not all though. Fisetin appears to be a pretty good senolytic but not an ATRi.

So good and bad for SPA. How good and how bad? And does it depend on your PCa stage and __ - fill in the blank with billions of variables.

Good and good for ADT. Is this universal?

Lots of questions and not many answers.

I haven't been able to figure out the balance. So I use them every SPA pulse (sans Fisetin) and use them all during every ADT phase.

And if you really want to fine tune it, Oridonin is perhaps one of the best natural ATRis that we have (20-40mg). So, you could opt to do Oridonin during SPA and Fisetin/Curcumin/EGCG/Quercetin during ADT. Maybe throw some Oridonin in to a few ADT phases. I don't use Oridonin (yet). I'm not certain about the purity and how much overload I put on my kidneys.

I think I should write up my reasoning and doses in my book. Hard for me to keep track of this junk and as new research comes out it changes. Four years ago I wasn't using a PARPi and now I used one during SBRT and during almost every SPA pulse. New research and the ola+BAT clinical. Ola+BAT clinical poked holes in the hole BRCA needed for PARPi to work theory. And it added even more fuel to the BAT creates a state of BRCAness theory. We already had mechanistic, in vitro, and in vivo. Now we have human trials.

[PCaWarrior in reply to Ichthus316]

I am adding a more detailed explanation and a table of compounds, strengths, doses, etc to my book. This is the summary and I chose the substances based in part on this.

Summary of Key Interactions

1. ATR Inhibitors:

• SPA: Synergize by exacerbating DNA damage in repair-deficient tumors (e.g., ATM/TP53 mutants).

• ADT: Enhance cell death via dual suppression of DNA repair pathways.

2. Senolytics:

• SPA: Risk interference by prematurely clearing senescent cells critical for immune-mediated tumor suppression.

• ADT: Synergize by eliminating therapy-resistant senescent cells and reducing inflammation.

3. 5-AR Inhibition:

• SPA: Reduces DHT, blunting androgen-driven DNA damage efficacy.

• ADT: Augments androgen suppression, improving therapeutic outcomes.

[KocoPr in reply to KocoPr]

By the way the other skullcap baicalin is better than the lateriflora.

ChatGPT:

For prostate cancer (PCa) and your TP53-targeted, senolytic, and anti-androgenic strategy, the better skullcap species is:

⸻

1. Scutellaria baicalensis (a.k.a. Chinese skullcap)

Why it’s better for PCa:

• Baicalein + baicalin-rich: These flavonoids are:

• Anti-androgenic (AR signaling inhibition)

• Pro-apoptotic in prostate cancer cell lines (e.g., LNCaP, DU145)

• TP53 activators (induces wild-type p53 activity, suppresses mutant p53 in some models)

• Senolytic properties: In combination with other flavones (like fisetin)

PubMed support:

• Baicalein inhibits tumor proliferation via AR, PI3K/Akt, and TP53 pathways.

• Baicalin has shown synergistic effects with docetaxel and other therapies in PCa.

pubmed.ncbi.nlm.nih.gov/292...

pubmed.ncbi.nlm.nih.gov/183...

⸻

2. Scutellaria lateriflora (American skullcap)

Less targeted for PCa, but has:

• Mild GABAergic and antioxidant effects

• Useful as a calming adaptogen, and may enhance sleep, reduce anxiety, and complement nighttime oxidative stress recovery.

• You already use this in your tinctures, likely for flavonoid synergy in the TP53 + Senolytic Kill Blend (v2).

⸻

Verdict:

• For direct prostate cancer targeting, go with Scutellaria baicalensis.

• For nervous system support, GABA tone, or nighttime blend synergy: Scutellaria lateriflora still has value.

[PCaWarrior in reply to KocoPr]

Inhibits 5-AR so DHT decreases. Might be good during ADT but not during SPA.

[KocoPr in reply to PCaWarrior]

Yes i just used what i had in my herbal vault so next batch of liposomal will be scutellaria baicilensis

[PCaWarrior in reply to KocoPr]

Be kind of interesting to test out it's 5-ar inhibition. While T is still sort of high in the serum, but using an ARI to block the ARs, calculate what DHT should be. Then measure and see. Measure a baseline (with the same ARI and about the same T) so we know the approximate T->DHT conversion rate (typically 5%-10%) and then apply the numbers. That's all I'm doing with the D4A thing. DHT was only 3/4 of expected after day 1. 1/2 of expected on day 5.

What that would accomplish is that we might get an idea of whether or not we could use SB during SPA. And if it doesn't do anything to 5-AR I would question it's other effects.

Very strange to me that we don't hear more about D4A blocking DHT. That is obviously one of the ways by which AA works. It's an SOC drug so why doesn't the establishment tout it's benefits? The further I go into the weeds the more I question the training that the average doctor receives.

[podsart]

what happened to PTEN in your output?

[PCaWarrior in reply to podsart]

PTEN? It indicates that BAT might work better. But I don't have any actionable PTEN mutations. BRCA1/2, TP53, AR, ATM.

The top 4 mutations that might predict BAT response are BRCA2, TP53, AR, and ATM. I have mutations in all 4. But that is according to DTC and the effective VAF is different than the standard ctDNA tests. And the accuracy is lower. High for AR though.

[podsart]

thanks; DTC?, AR= androgen receptor?

[PCaWarrior in reply to podsart]

DTC is direct to the consumer. AR = androgen receptor.

[podsart]

thanks

[PCaWarrior in reply to podsart]

sure. i think that this DTC test is getting me ready to look into ctDNA test results when I get them.

DTC... I didn't know until yesterday that it means something so plain.

SNPs, variants, mutations... a whole field.