Cromolyn and pancreatic cancer question

Cromolyn and pancreatic cancer question

My mom was recently diagnosed with pancreatic cancer. The chemo of
choice is Gemox, which is Gemcitibane with Oxyplatin (sp?). You may
know this is only moderately effective.

There was a study on mice at M.D. Anderson medical center in which
they realized Cromolyn, in combination with the Gemcitibane, had a
MUCH more powerful impact on the tumors than the Gemcitibane alone.


Since no human studies have been approved yet- I think they are
trying
to improve the method of delivering it to the tumor- it is
frustrating
to know that there is this OTC medication that could help her, and
almost certainly cant hurt (compared to the near-certain prognosis of
pancreatic cancer).


My question is, if we wanted to simply add OTC chromalyn (sold for
allergies and asthma) to her regimen, what is the best method to get
a substantial amount into her body. The inhaler, or should we try to
convince a doctor to prescribe the tablet (cromolyn sodium) that gets
mixed in water? I read that absorbtion through the intestines is only
1% which is why, perhaps, they are trying to work on delivery. Would
inhalation be more effective? They also have eyedrops which I assume
are not effectively absorbed?


Thanks. Below is some of the info from abstract.
-


Background: We previously found that S100P, a member of the S100
protein family, is expressed in more than 90% of pancreatic tumors
and
is associated with tumor growth and invasion. In the current study,
we
investigated the ability of the antiallergy drug, cromolyn, to block
S100P function. Methods: Interactions between cromolyn and S100P were
investigated using a drug affinity column and by examining cromolyn's
effects on coimmunoprecipitation of S100P and receptor for advanced
glycation end-products (RAGE). The effects of cromolyn on cell
growth,
invasion, and nuclear factor-B (NFB) activity of pancreatic cancer
cells with (BxPC-3 and MPanc-96) and without (Panc-1) endogenous
S100P
were investigated by cell proliferation assay, by cell invasion
assay,
and by luciferase reporter gene assay, respectively. The effects of
cromolyn on tumor growth in vivo were investigated in three
orthotopic
models (n = 20 mice per model) by administration of cromolyn (5 mg/kg
body weight, daily) with and without gemcitabine (125 mg/kg body
weight, biweekly), the drug currently used to treat pancreatic
cancer.
Tumor growth was assayed by reporter gene expression. All statistical
tests were two-sided. Results: S100P was retained on a cromolyn
affinity column. Cromolyn blocked the coimmunoprecipitation of S100P
and RAGE. In vitro, cromolyn (100 µM) inhibited S100P-stimulated
Panc-1 cell proliferation (S100P, mean = 0.93 U, versus S100P +
cromolyn, mean = 0.56 U, difference = 0.37 U; 95% confidence interval
[CI] = 0.24 to 0.49 U; P = .001, n = 3), invasion (S100P, mean =
58.0%, versus S100P + cromolyn, mean = 9.4%, difference = 48.6%; 95%
CI = 38.8% to 58.8%; P<.001, n = 3), and NFB activity (S100P, mean =
14 460, versus S100P + cromolyn, mean = 7360 photons/s, difference =
7100 photons/s; 95% CI = 3689 to 10 510 photons/s; P = .005, n = 3).
In vivo, cromolyn inhibited tumor growth in mice bearing tumor with
endogenous S100P (BxPC-3: control, mean = 1.6 x 109 photons/s, versus
cromolyn, mean = 4.4 x 108 photons/s, difference = 1.2 x 109 photons/
s; 95% CI = 6.2 x 108 to 1.6 x 109 photons/s; P<.001, n = 5;
MPanc-96:
control, mean = 1.1 x 1010 photons/s, versus cromolyn, mean = 4.8 x
109 photons/s, difference = 6.2 x 109 photons/s; 95% CI = 1.9 x 109
to
1.0 x 1010 photons/s; P = .009, n = 5) and increased the
effectiveness
of gemcitabine (BxPC-3: gemcitabine, mean = 9.2 x 108 photons/s,
versus combination, mean = 1.8 x 108 photons/s, difference = 7.4 x
108
photons/s; 95% CI = 4.5 x 108 to 1.0 x 109 photons/s; P<.001;
MPanc-96: gemcitabine, mean = 4.1 x 109 photons/s, versus
combination,
mean = 2.0 x 109 photons/s, difference = 2.1 x 109 photons/s; 95% CI
=
4.4 x 108 to 3.8 x 109 photons/s; P<.001). However, cromolyn had no
effect on growth of tumors lacking S100P (Panc-1). Conclusion:
Cromolyn binds S100P, prevents activation of RAGE, inhibits tumor
growth, and increases the effectiveness of gemcitabine in
experimental
models.

Re: Cromolyn and pancreatic cancer question

Since this study was only an experimental model, chances you get this
working as a therapy are about zero. There have always been promising
experimental models who didn't make it to a later stage, not to speak
of making it to the market.
If you really insist on this, talk to the chief of the oncology unit
of your mothers caretakers about this, this is the only option you
have.
I'm very sorry for your situation.

San


On Mar 27, 7:10 pm, Phil <thinkofanamef...@aol . com > wrote:
> My mom was recently diagnosed with pancreatic cancer. The chemo of
> choice is Gemox, which is Gemcitibane with Oxyplatin (sp?). You may
> know this is only moderately effective.
>
> There was a study on mice at M.D. Anderson medical center in which
> they realized Cromolyn, in combination with the Gemcitibane, had a
> MUCH more powerful impact on the tumors than the Gemcitibane alone.
>
> Since no human studies have been approved yet- I think they are
> trying
> to improve the method of delivering it to the tumor- it is
> frustrating
> to know that there is this OTC medication that could help her, and
> almost certainly cant hurt (compared to the near-certain prognosis of
> pancreatic cancer).
>
> My question is, if we wanted to simply add OTC chromalyn (sold for
> allergies and asthma) to her regimen, what is the best method to get
> a substantial amount into her body. The inhaler, or should we try to
> convince a doctor to prescribe the tablet (cromolyn sodium) that gets
> mixed in water? I read that absorbtion through the intestines is only
> 1% which is why, perhaps, they are trying to work on delivery. Would
> inhalation be more effective? They also have eyedrops which I assume
> are not effectively absorbed?
>
> Thanks. Below is some of the info from abstract.
> -
>
> Background: We previously found that S100P, a member of the S100
> protein family, is expressed in more than 90% of pancreatic tumors
> and
> is associated with tumor growth and invasion. In the current study,
> we
> investigated the ability of the antiallergy drug, cromolyn, to block
> S100P function. Methods: Interactions between cromolyn and S100P were
> investigated using a drug affinity column and by examining cromolyn's
> effects on coimmunoprecipitation of S100P and receptor for advanced
> glycation end-products (RAGE). The effects of cromolyn on cell
> growth,
> invasion, and nuclear factor-B (NFB) activity of pancreatic cancer
> cells with (BxPC-3 and MPanc-96) and without (Panc-1) endogenous
> S100P
> were investigated by cell proliferation assay, by cell invasion
> assay,
> and by luciferase reporter gene assay, respectively. The effects of
> cromolyn on tumor growth in vivo were investigated in three
> orthotopic
> models (n = 20 mice per model) by administration of cromolyn (5 mg/kg
> body weight, daily) with and without gemcitabine (125 mg/kg body
> weight, biweekly), the drug currently used to treat pancreatic
> cancer.
> Tumor growth was assayed by reporter gene expression. All statistical
> tests were two-sided. Results: S100P was retained on a cromolyn
> affinity column. Cromolyn blocked the coimmunoprecipitation of S100P
> and RAGE. In vitro, cromolyn (100 µM) inhibited S100P-stimulated
> Panc-1 cell proliferation (S100P, mean = 0.93 U, versus S100P +
> cromolyn, mean = 0.56 U, difference = 0.37 U; 95% confidence interval
> [CI] = 0.24 to 0.49 U; P = .001, n = 3), invasion (S100P, mean =
> 58.0%, versus S100P + cromolyn, mean = 9.4%, difference = 48.6%; 95%
> CI = 38.8% to 58.8%; P<.001, n = 3), and NFB activity (S100P, mean ==

> 14 460, versus S100P + cromolyn, mean = 7360 photons/s, difference =
> 7100 photons/s; 95% CI = 3689 to 10 510 photons/s; P = .005, n = 3).=

> In vivo, cromolyn inhibited tumor growth in mice bearing tumor with
> endogenous S100P (BxPC-3: control, mean = 1.6 x 109 photons/s, versus
> cromolyn, mean = 4.4 x 108 photons/s, difference = 1.2 x 109 photons/
> s; 95% CI = 6.2 x 108 to 1.6 x 109 photons/s; P<.001, n = 5;
> MPanc-96:
> control, mean = 1.1 x 1010 photons/s, versus cromolyn, mean = 4.8 x
> 109 photons/s, difference = 6.2 x 109 photons/s; 95% CI = 1.9 x 109
> to
> 1.0 x 1010 photons/s; P = .009, n = 5) and increased the
> effectiveness
> of gemcitabine (BxPC-3: gemcitabine, mean = 9.2 x 108 photons/s,
> versus combination, mean = 1.8 x 108 photons/s, difference = 7.4 x
> 108
> photons/s; 95% CI = 4.5 x 108 to 1.0 x 109 photons/s; P<.001;
> MPanc-96: gemcitabine, mean = 4.1 x 109 photons/s, versus
> combination,
> mean = 2.0 x 109 photons/s, difference = 2.1 x 109 photons/s; 95% CI
> =
> 4.4 x 108 to 3.8 x 109 photons/s; P<.001). However, cromolyn had no
> effect on growth of tumors lacking S100P (Panc-1). Conclusion:
> Cromolyn binds S100P, prevents activation of RAGE, inhibits tumor
> growth, and increases the effectiveness of gemcitabine in
> experimental
> models.