TP53 missense mutation 11%: 21 months... - Advanced Prostate...

Advanced Prostate Cancer

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TP53 missense mutation 11%

wolverine11 profile image
33 Replies

21 months in, still hormone sensitive Lupron and zytiga....PSA 0.1 Stage 4 metastatic innumerable mets no visceral. Oncologist told me I have 11% TP53 Missense mutation????What effect will that have on me. Also report says I have low tumor burden, I would assume that's good. Overall Doc say I am doing great...Any info about this TP53 would be appreciated.....Thanks

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wolverine11
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Tall_Allen profile image
Tall_Allen

It's a very common mutation in people who have cancer. TP53 is a gene that repairs DNA mistakes. There are no medicines for it yet.

wolverine11 profile image
wolverine11 in reply to Tall_Allen

Thanks TA.... So if it cannot be eradicated. It will eventually grow and kill me??

Tall_Allen profile image
Tall_Allen in reply to wolverine11

There is no cure for metastatic prostate cancer - it is a managed disease. You may die of something else first.

wolverine11 profile image
wolverine11 in reply to Tall_Allen

Thanks TA

tango65 profile image
tango65

TP 53 gene is a tumor suppression gene and is frequently found in cancers. Missense indicates that the mutation makes a change in one amino acid of a particular protein.

TP53 gene is related to DNA repair and it has been called the guardian of the genome because impedes the division of a cell with abnormal genome.

medlineplus.gov/genetics/ge...

frontiersin.org/articles/10...

wolverine11 profile image
wolverine11 in reply to tango65

Thank you Tango65 The first article seems to indicate Tumor suppression is a good thing.I'm having trouble understanding the second article it seems to indicate faster progression of cancer. GREAT. Thanks to you & TA for your input

tango65 profile image
tango65 in reply to wolverine11

When is normal it is a tumor suppression gene. If there a mutation it does not work correctly.

I also have a tumor suppression gene that is mutated, PTEN. These are frequent mutations in cancers.

PC tumors with PT53 mutations have a good response to BAT

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

Even when your cancer is castration sensitive you could discuss with your MO or consult about the possibility of doing BAT since the cancer has a genome which favors the efficacy of this therapy.

wolverine11 profile image
wolverine11 in reply to tango65

Thanks Tango65. Interesting, when I asked my oncologist if Taxotere could kill this p53 gene she said yes. However, I googled info about p53 gene and the answer was consistent with TA no meds yet developed. I'll ask about BAT next visit with oncologist. Thanks again Tango65

tango65 profile image
tango65

You are welcome.

If I were in your situation I would consider BAT even when the cancer is mCSPC.

I believe (no data) that BAT is probably less risky in castration sensitive cancer since most of the cells which could reproduce with elevated testosterone are castration sensitive and it seems BAT has a tendency to destroy PT53 mutated cancer cells.

wolverine11 profile image
wolverine11 in reply to tango65

Thank you tango 65.. from what little I understand it works in about 15 to 20% of men. Is it testosterone that overwhelms the cancer and kills it if that's what I understand it to be on the other side of that is it could be like pouring gasoline on a fire so I'll have to find out more about it I appreciate you enlightening me about it.

cesces profile image
cesces

There are two types of tp53.

There is one type that is carried in all your cells.

There is another that is limited to only your cancer cells or a subset of your cancer cells.

Tp53 will inform your treatment decision in only one way.

BAT hormone therapy can be very effective, but unpredictabily so... except for Tp53 mutations. It tends to be a very effective treatment for them, with arguably less severe side effects than most alternative treatment options.

wolverine11 profile image
wolverine11 in reply to cesces

Thank you cesces, for the information. Also to tango 65 and Tall Allen . This has given me a better understanding of my cancer. The information on this site is pure gold thank you all so much. Will look more into BAT

cesces profile image
cesces in reply to wolverine11

Hard to find docs that do Bat.

Try Denemead and also Sartor at Tulane.

wolverine11 profile image
wolverine11 in reply to cesces

Thanks Cesces .....From what I know now, and hopefully learn more...I'll stay the course I'm on now,,,,If it ain't broke..... meaning having success with current treatments Thanks again.

Seasid profile image
Seasid in reply to cesces

the tp53 mutation is only 11% is it enough to justify BAT?

cesces profile image
cesces in reply to Seasid

I don't know.

I think that's a question for a doc with a lot of BAT treatment experience under their belt.

Seasid profile image
Seasid in reply to cesces

if you have only 11% mutations of p53 ? 30% would be better? I am also not a doctor. I belive BAT should be more appropriate later when a percentage of the mutations increase? I wouldn't rush myself until other therapies work? I belive BAT is recommended by professor Sartor if you never had any symptoms. I read this on this forum. But by time xou you could develop some symptoms and maybe the percentage of the mutations will go up. Interesting. Bottom line i have to make a decision. I am always thinking thet some doctors would like to try out some new ideas.

wolverine11 profile image
wolverine11 in reply to Seasid

Thank you...

cesces profile image
cesces in reply to Seasid

I think you can try it with no percentage.

There is no substitute for clinical experience.

You really need to get one or more second opinions before pulling the trigger.

Seasid profile image
Seasid in reply to cesces

i am a slow mover and my cancer is also moving slowly. I just hope that it will not catapult itself into a stratosphere.

cesces profile image
cesces in reply to Seasid

Not so long ago the published a mathematical paper applicable to fighting mutating cancer as well as Covid.

When choosing between slow escalation or punctuated intense stacks, you are better off putting your resources into the punctuated attacks.

I believe clinical trials are confirming this to be true. And standards of practice are following. Such as using stronger more potent combinations of treatment earlier as opposed to sequencing them over time.

Seasid profile image
Seasid in reply to cesces

i had 4 x 68GA PSMA PET scans (164 MBq each) every 15 days from day zero. At day zero I received Degarelix injection. After around 2 months from day zero i received 6 cycles of Docetaxel chemotherapy.

wolverine11 profile image
wolverine11

That biopsy of 11% missense TP53 was taken about 3 days after starting ADT. Please correct me if I am wrong. I think I saw on Pubmed? Men on ADT had a much higher % something like 38% of TP53 which was much higher than men not on ADT. I believe they used the word ,astounded. Since I only had been on ADT 3 days my P53 now could be much higher. Sorry I don't have that study. I was doing alot of searching about this P53. I informed my 2 sisters there is a 50% chance they may have this gene. Thank you guys for your input

Seasid profile image
Seasid in reply to wolverine11

i know someone who also had around 10 % of mutations of the tp53.

Tall Allen said to me that BAT only extends the effectiveness of Enzalutamide but it didn't extend the overall survivor.

wolverine11 profile image
wolverine11 in reply to Seasid

Well That's good to Know bad news....My nadir PSA is 0.1 I have a low tumor burden which hopefully will increase my OS Although read low tumor burden mutations not so good immunotherapy treatments. Thanks

Seasid profile image
Seasid in reply to wolverine11

i agree with you in not to change a treatment if it is still working. Standard of care first and don't rush enjoy your low PSA and low volume. Don't make yourself available to clinical trials until the standard of care works. They wanted to put me on Olaparib and Abiraterone when my PSA gets up to 1. (PROPEL trial)

Then I read that Olaparib is a toxic medication and now I will maybe start at some point Enzalutamide and when it fails I would do cabazitaxel chemotherapy somewhere far in the future and maybe continue with Abiraterone (in UK and Australia when Enzalutamide fails the health system wouldn't pay for Enzalutamide or Abiraterone again even if it would work after chemotherapy. Good to know.

wolverine11 profile image
wolverine11 in reply to Seasid

Good Advice, I will stay with SOC for as long as is effective....Good luck to you

Seasid profile image
Seasid in reply to wolverine11

you are doing great.i read your profile even ALP is a normal range now. Are they giving you bone medication? Did you have a bone density scan? Be extremely careful not to have falls.

wolverine11 profile image
wolverine11 in reply to Seasid

Thank you, yes I had bone scan in April 2021 have some ostopenia -1.7 left femor Have been taking Alendronate oral weekly for about 6 months

Seasid profile image
Seasid in reply to wolverine11

i thought that with prolia (denosumab) subcutaneous injections every six months your ALP would drop very low. I myself are not geting prolia as my ALP is 55.

wolverine11 profile image
wolverine11 in reply to Seasid

Hmm, My oncologist talked about some form of injections for my bones when I become resistant( hopefully not for a long time).

Seasid profile image
Seasid in reply to wolverine11

i am also not rushing with denosumab. Professor Sartor recommends prolia injections every six months.

Seasid profile image
Seasid in reply to wolverine11

information about your bone medication from Mayo clinic:

mayoclinic.org/drugs-supple...

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