Par4 Gene Cancer: Clinical Trials & Cancer Resistance

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Discussion Overview

The discussion centers around the par4 gene and its potential role in cancer resistance, particularly in the context of clinical trials and its mechanisms of action. Participants explore whether par4 can be effectively utilized in humans as it appears to be in mice, along with its implications for various types of cancer.

Discussion Character

  • Exploratory
  • Technical explanation
  • Debate/contested

Main Points Raised

  • Some participants inquire about existing clinical trials involving the par4 gene and its effectiveness in making humans more cancer-resistant, similar to observed effects in mice.
  • There is confusion regarding the full name of the par4 gene, with participants questioning whether it stands for Prostate Apoptosis Response-4 or Protease-activated receptor-4 (PAR4).
  • One participant notes that par4 does not kill all types of cancer cells but may interfere with signaling that promotes tumor growth, suggesting a potential broad application against various cancers.
  • Another participant references research indicating that par4 can suppress tumors and describes experiments where tumors in mice regressed after treatment with par4 adenovirus.
  • Questions arise about whether par4 needs to enter the nucleus of a cell to be effective, with references to conflicting statements about its mechanism of action.
  • One participant poses a question about the feasibility of forcing par4 into the nucleus using a viral vector if it is typically kept out of the nucleus in certain cancer cells.

Areas of Agreement / Disagreement

Participants express uncertainty regarding the mechanisms of par4, its effectiveness across different cancer types, and the necessity of nuclear entry for its function. There is no consensus on these points, and multiple competing views remain.

Contextual Notes

Limitations include unclear definitions of the par4 gene, unresolved questions about its mechanisms of action, and the dependence on specific experimental conditions that may not apply universally.

bioquest
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Are there any clinical trials or anything like that involving par4 gene and humans to make people more cancer-resistant, do you think it would work to make people cancer-resistant like it does in mice?

if there was a cancer resistant person do you think their white blood cells would cure cancer in mice like white blood cells from cancer resistant mice cure cancer in mice?
 
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Could somebody tell me what par4 stands for (the gene that makes things cancer-resistant) does it stand for Prostate Apoptosis Response-4 or does it stand for Protease-activated receptor-4 (PAR4)- could you let me know where you found out which one it stands for? I read that it can cure cancer/stop cancer from forming, does anyone know if it works for every type? I read that it worked for even aggressive types
 
So, par4 doesn't kill all typees of cancer cells, but maybe because it interfers with signaling that promotes tumor growth it could help stop all types of cancers?

http://www.nyas.org/annals/annalsExtra.asp?annalID=34the new york academy of science says

"Par-4 does not kill all types of cancer cells. In cancer cells that resist Par-4, such as hormone-dependent tumors, there is sufficient PKA to allow phosphorylation to take place, but Par-4 is still kept out of the nucleus, meaning the cell survives."

Tumors in mice regressed quickly after treatment
"Par-4 also works in other ways. Previous work showed that Par-4 can suppress tumors by interfering with signaling that promotes tumor growth. In one experiment, when Par-4 was purposely overexpressed in cancer cells, they were prevented from forming colonies in a soft agar medium. In another, tumors were started in mice and allowed to grow. Then the tumors were injected either with Par-4 adenovirus (a viral vector delivery system), or with a control viral vector. After about three weeks, all twenty of the tumors injected with Par-4 shrank markedly, while the other tumors continued to grow apace."

"The researchers named the region of Par-4 responsible for singling out cancer cells the Selective Apoptosis of Cancer (SAC) domain. The protein is being developed as a potential therapeutic agent against an array of cancers, not just tumors of the prostate. Says Rangnekar, "The best part is that despite the apoptotic effect in cancer cells, neither the SAC domain nor Par-4 induces apoptosis in normal cells—implying that treatment should be non-toxic and safe." Also, the fact that Par-4 targets cancer in different ways provides multiple opportunities for drug development."
 
Last edited:
sorry I can't edit posts

I mean does par-4 need to be in the nucleus of the cell to be overexpressed
because it says this
"Par-4 does not kill all types of cancer cells. In cancer cells that resist Par-4, such as hormone-dependent tumors, there is sufficient PKA to allow phosphorylation to take place, but Par-4 is still kept out of the nucleus, meaning the cell survives."
and then it says this

"Par-4 also works in other ways. Previous work showed that Par-4 can suppress tumors by interfering with signaling that promotes tumor growth. In one experiment, when Par-4 was purposely overexpressed in cancer cells, they were prevented from forming colonies in a soft agar medium. In another, tumors were started in mice and allowed to grow. Then the tumors were injected either with Par-4 adenovirus (a viral vector delivery system), or with a control viral vector. After about three weeks, all twenty of the tumors injected with Par-4 shrank markedly, while the other tumors continued to grow apace."

when the tumors were injected with the par-4 adenovirus/a control viral vector- did the par4 gene not need to get into the nucleus to work? Maybe par4 doesn't need to get into the nucleus if it interferes with signaling that inhibits tumor growth? Sorry for writing so much, thanks
 
My only question is:

could you force par 4 into the nucleus, with a virus or something, if it's kept out of the nucleus?
"In cancer cells that resist Par-4, such as hormone-dependent tumors, there is sufficient PKA to allow phosphorylation to take place, but Par-4 is still kept out of the nucleus, meaning the cell survives."
 

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