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Prof Trevor Marshall
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http://bit.ly/8Lfj5y
"The renin-angiotensin pathway plays an important role in promoting cancer growth, explained Dr. Chae on December 11. The AT1 receptor is functionally expressed in several tumor types, including ovarian cancer. Prior retrospective studies have documented lower cancer incidence among users of ACE inhibitors/ARBs compared with nonusers, and 1 randomised trial showed a protective effect of these agents on the development of major skin cancers, he said. No studies, however, have looked at the relationship between ACE inhibitors/ARBs and cancer recurrence. For the study, Dr. Chae and colleagues reviewed the medical records of female patients diagnosed with stage II/III breast cancer at Albert Einstein between 1999 and 2005, and who later reached no evident disease (NED) after curative therapy. A user of ACE inhibitors/ARBs was defined as a patient who took the medication in the NED stage for at least 6 months. The mean follow-up period was 4.4 years and the maximum follow-up was 9.8 years. About one-fourth (23.3%) of the patients, overall, were prescribed an ACE inhibitor or ARB, including 49.0% of the 164 patients with hypertension. Fourteen percent (23/164) of the women who took either an ACE inhibitor or ARB developed a tumour recurrence, compared with 23.3% (125/541) of nonusers ([P = .01).
The 5-year disease-free survival was 0.85 in the ACE inhibitor/ARB users and 0.756 in the nonusers (P < .01)"

75 to 85% survival rate at 5 years. Interesting data in and of itself.

One of the problems with studies like this is that they clump all the drugs into one class - for example - 'ARBs' - without realizing that each of the ARB drugs is a little bit different. They also assume that ACEI have a similar mechanism of action - a sad commentary on the lack of precision in modern medicine.

Still - this is confirmation that Benicar should not increase the rate of relapse with cancers, even if it doesn't yet have the (study) strength to back up my suspicions as to why the MP has essentially wiped out metastasis in our cohort...

http://www.youtube.com/watch?v=y8AfUg3aJVk
 

Freddie Ash
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HI ALL

This is Fred in WV .  I just got my email from the Doctor's Guide today and that is the main story in it.  Thanks for posting that for all to see.  Another reason to take Benicar.

Remember, we are all in this together and I am pulling for us.

Your friend in Sarcoidosis

Freddie

Bane
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Impact of angiotensin I converting enzyme inhibitors and angiotensin II type 1 receptor blockers on survival in patients with advanced non-small-cell lung cancer undergoing first-line platinum-based chemotherapy.

http://www.ncbi.nlm.nih.gov/pubmed/19399518

Application of angiotensin II receptor blocker in prostate cancer

http://www.ncbi.nlm.nih.gov/pubmed/19348246

Ets-1 and hypoxia inducible factor-1alpha inhibition by angiotensin II type-1 receptor blockade in hormone-refractory prostate cancer.

http://www.ncbi.nlm.nih.gov/pubmed/19760626

Angiotensin II Type 1 Receptor Antagonist as an Angiogenic Inhibitor in Urogenital Cancer.

http://www.ncbi.nlm.nih.gov/pubmed/19463103

Synergistic inhibitory effect of gemcitabine and angiotensin type-1 receptor blocker, losartan, on murine pancreatic tumor growth via anti-angiogenic activities.

http://www.ncbi.nlm.nih.gov/pubmed/19578777

Ruth Goold
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And here is some info on (one of the) ways in which olmesartan (Benicar) mediates it's anticancer effects:

The Host Defense Peptide Cathelicidin Is Required for NK Cell-Mediated Suppression of Tumor Growth

http://www.ncbi.nlm.nih.gov/pubmed/19949065

And from the same issue of the Journal of Immunology, yet another study outlining a clever way in which intracelluar pathogens compromise the immune response (albeit, in mice in this case):

Dissemination of Mycobacteria to the Thymus Renders Newly Generated T Cells Tolerant to the Invading Pathogen

http://www.ncbi.nlm.nih.gov/pubmed/19949112

Happy Holidays,

Ruth

Prof Trevor Marshall
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Ah yes, the Thymus - so they can pervert the function of AIRE

Great find Ruth - I just hadn't put two and two together...
 
:)

ChrisMavo
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Great STUFF! 

So not only can we cure ourselves from chronic Th1 diseases... but we can protect ourselves from the Big C too....:D

Great stuff INDEED!!!

Phil Schoner
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Trevor,

You state "the MP has essentially wiped out metastasis in our cohort..."

Epidemiologically speaking, have we developed the percentages of expected cancer metastasis in the cohert versus the (nearly?) zero percent experienced?

Phil


Prof Trevor Marshall
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Phil,
Different sources have different expectations. The one that seems to be most reliable is an expectation of 10 % to 30% of autoimmune disease patients will die from cancer within a decade. This is also in line with the overall cancer death-rate in CFS patients.

I break this down to a year-by year average expectation of 1% to 3%. For our current reporting cohort size of 700+ this would lead to an expectation of 7 to 21 cases a year.

We are well below that :) :) Whether total cancers or just metastasizing cancers (the ones which lead to death) are considered in the total...

One of the biggest problems this cohort faces is that they are pushed (by oncologists) to accept treatments for a non-metastasizing tumor regardless of whether those treatments will exacerbate their underlying inflammatory disease, and thus eventually fuel the metastasis. We need to work on getting together enough case histories so that MP cohort members don't panic when Doc considers a potential "cancer" diagnosis.

We have been walking around for decades without the probing and testing and imaging that Doc has available these days. We should not be surprised if all this new technology finds tumors, some of which may have been there for years... The key is to focus on whether they present a future danger of spreading (metastasis)...

..Trevor..
 

Last edited on Sun Dec 20th, 2009 09:43 by Prof Trevor Marshall

Bane
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http://www.ncbi.nlm.nih.gov/pubmed/18677709

http://www3.interscience.wiley.com/cgi-bin/fulltext/121359256/PDFSTART

 

Last edited on Sun Dec 20th, 2009 09:40 by Bane

Joyful
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Bane, your link is to a pay-to-view article. :?

Would you care to summarize here?

Bane
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Joyful wrote: Bane, your link is to a pay-to-view article. :?

Would you care to summarize here?

"To investigate the effect of Ang-III on human prostate cancer cells, we applied it in LNCaP (androgen-dependent) and DU145 (androgen-independent) cells. As shown in Figure 2A,B, Ang-III treatment increased both prostate cancer cells in a dose-dependent manner. Because earlier reports indicated that Ang-III can bind to theAT1 receptor,which is predominantly for Ang-II (Fig. 1) [16], we investigated the effect of an AT1 receptor blocker on cell proliferation induced by Ang-III. Olmesartan is a selective blocker of the AT1 receptor and is widely used as anti-hypertensive agent. As shown in Figure 2A,B, olmesartan significantly suppressed the cell growth induced by Ang-III treatment in prostate cancer cells."

jrfoutin
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"75 to 85% survival rate at 5 years. Interesting data in and of itself.

"One of the problems with studies like this is that they clump all the drugs into one class - for example - 'ARBs' - without realizing that each of the ARB drugs is a little bit different.."


Along with lumping ARBs together, there is no discussion of atypical dose for any ARB. The study assumption for the full ARB set they lump is standard ARB dose, right?

The MP cohort daily ARB intake has always been on the line. With a void annual 7-21 cohort cancer record to date, might it be appropriate already--specific to study strength--to state more Benicar (typical MP dose levels with extra when needed) is simply not leading to cancer?

Thank you Dr Marshall and others for excellent discussion and links--Janet

Bane
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Dr Trevor Marshall wrote: Phil,
Different sources have different expectations. The one that seems to be most reliable is an expectation of 10 % to 30% of autoimmune disease patients will die from cancer within a decade. This is also in line with the overall cancer death-rate in CFS patients.

I break this down to a year-by year average expectation of 1% to 3%. For our current reporting cohort size of 700+ this would lead to an expectation of 7 to 21 cases a year.

We are well below that :) :) Whether total cancers or just metastasizing cancers (the ones which lead to death) are considered in the total...

One of the biggest problems this cohort faces is that they are pushed (by oncologists) to accept treatments for a non-metastasizing tumor regardless of whether those treatments will exacerbate their underlying inflammatory disease, and thus eventually fuel the metastasis. We need to work on getting together enough case histories so that MP cohort members don't panic when Doc considers a potential "cancer" diagnosis.

We have been walking around for decades without the probing and testing and imaging that Doc has available these days. We should not be surprised if all this new technology finds tumors, some of which may have been there for years... The key is to focus on whether they present a future danger of spreading (metastasis)...

..Trevor..
 


Immunological Similarities between Cancer and Chronic Fatigue Syndrome: The Common Link to Fatigue?

http://www.ncbi.nlm.nih.gov/pubmed/20032425

Bane
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Blocking Angiotensin II Type 1 Receptor Triggers Apoptotic Cell Death in Human Pancreatic Cancer Cells.

http://www.ncbi.nlm.nih.gov/pubmed/20118823

Angiotensin II regulates the expression of monocyte chemoattractant protein-1 in pancreatic cancer cells.

http://www.ncbi.nlm.nih.gov/pubmed/19816747

Inhibition of angiotensin II receptor 1 limits tumor-associated angiogenesis and attenuates growth of murine melanoma.

http://www.ncbi.nlm.nih.gov/pubmed/19771429

 

Bane
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Association of ACE inhibitors and angiotensin receptor blockers with keratinocyte cancer prevention in the randomized VATTC trial.

http://jnci.oxfordjournals.org/cgi/content/full/100/17/1223

"Among a high-risk group of veterans, users of ACE inhibitors or ARBs had a lower incidence of keratinocyte cancers than nonusers. The more pronounced reduction among those who initiated use during the study may indicate an immediate effect."

Bane
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Angiotensin II regulates the expression of monocyte chemoattractant protein-1 in pancreatic cancer cells.

http://www.ncbi.nlm.nih.gov/pubmed/19816747

In this study, we investigated the potential proinflammatory role of AngII in PDA through studying its effect on MCP-1. AngII significantly increased the expression of MCP-1 mRNA and protein in PDA cells and induced its promoter activity. Constitutive and AngII-induced MCP-1 transcription was inhibited by an AngII type 1 receptor (AT1R) blocker, but was unchanged by an AT2R blocker. AngII activated the phosphorylation of extracellular signal-regulated kinase (ERK)1/2, but not p38 or c-Jun NH2-terminal mitogen-activated protein kinases. Inhibition of ERK1/2 activation reduced the AngII-induced MCP-1 synthesis. AngII induced the activation and nuclear translocation of nuclear factor-kappaB (NF-kappaB), an effect that was inhibited by AT1R blockade. Inhibition of NF-kappaB by pyrrolidine dithiocarbamate decreased the AngII-mediated increase in MCP-1 mRNA. Our data provide a novel insight into an AngII-initiated signal transduction pathway that regulates MCP-1 as a possible inflammatory mechanism in PDA and suggest that AngII blockade may regulate chemokine-induced signal transduction to prevent or reduce inflammation in PDA.

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With respect to NFKB, I have a question that has been troubling me for some time.  While we know that inhibition of this transcription factor blocks the expression of various inflammatory cytokines, I believe the pathway is also required for Toll like receptor and NOD signalling. 

For example, if the VDR is activated, the intracellular pathogen recognition receptor NOD2 will be expressed.  However, if NOD2 senses bacteria, then it is unable to signal for the expression of human beta defensin 2 as this requires NFKB.  My unerstanding is that TLR2 also signals in a NFKB dependent manner.

That being said, I've read that the cathelecidin promoter has 3 VDREs and no NFKB sites.  Many viruses also rely upon NFKB signalling so blockade of this factor is probably beneficial in viral infection.

I wonder if one of the reasons that less frequent dosing is more painful for us (in addition to increased inflammatory cytokines) is due to heightened PRR signalling via a relaxed NFKB blockade.

So my question is if there is any concern about knocking out the TLRs and NODs via NFKB blockade?

 

Prof Trevor Marshall
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We don't 'blockade' NuclearFactor-kappaB, we just suppress its expression :) A body on Olmesartan  can still mount a robust defense, if attacked by acute pathogens :)
 

Phillyguy
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Fair enough!

Bane
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Role of renin-angiotensin system in prostate cancer

http://www.ncbi.nlm.nih.gov/pubmed/19692759

Although a low prevalence of cancer in hypertensive patients receiving angiotensin converting enzyme inhibitors was reported, the molecular mechanisms have not been elucidated.

 
Angiotensin II up-regulates PAX2 oncogene expression and activity in prostate cancer via the angiotensin II type I receptor.

http://www.ncbi.nlm.nih.gov/pubmed/19517575

CONCLUSIONS: Therefore, PAX2 may be a novel therapeutic target for the treatment of carcinomas such as prostate cancer via the down-regulation of its expression by targeting the AT1R signaling pathways.

 

AGTR1 overexpression defines a subset of breast cancer and confers sensitivity to losartan, an AGTR1 antagonist.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2689309/

In addition to prioritizing ERBB2, we found AGTR1, the angiotensin II receptor type I, to be markedly overexpressed in 10-20% of breast cancer cases across multiple independent patient cohorts. Validation experiments confirmed that AGTR1 is highly overexpressed, in several cases more than 100-fold. AGTR1 overexpression was restricted to estrogen receptor-positive tumors and was mutually exclusive with ERBB2 overexpression across all samples. Ectopic overexpression of AGTR1 in primary mammary epithelial cells, combined with angiotensin II stimulation, led to a highly invasive phenotype that was attenuated by the AGTR1 antagonist losartan. Similarly, losartan reduced tumor growth by 30% in AGTR1-positive breast cancer xenografts. Taken together, these observations indicate that marked AGTR1 overexpression defines a subpopulation of ER-positive, ERBB2-negative breast cancer that may benefit from targeted therapy with AGTR1 antagonists, such as losartan.

 

Local angiotensin II-generation in human gastric cancer: correlation with tumor progression through the activation of ERK1/2, NF-kappaB and survivin.

http://www.ncbi.nlm.nih.gov/pubmed/19424575

Angiotensin II stimulates the cell proliferation in the AT1 receptor-positive OCUM2MD3 gastric cancer cell line and this proliferative effect of angiotensin II was inhibited by a specific AT1 receptor antagonist, candesartan.

 

Blockade of an angiotensin type I receptor enhances effects of radiation on tumor growth and tumor-associated angiogenesis by reducing vascular endothelial growth factor expression.

http://www.ncbi.nlm.nih.gov/pubmed/18691848

These results suggest that combination of radiation with AT1-R blockade markedly reduced the LLC growth rate, and that this was due to reduction of neovascularization by reducing VEGF levels. Combination therapy consisting of radiation and AT1R blockade may become an effective novel strategy for cancer treatment.

 

Potential role of Renin-Angiotensin-system for tumor angiogenesis in receptor negative breast cancer.

http://www.ncbi.nlm.nih.gov/pubmed/18395779

In conclusion, it is hypothesized that Angiotensin II may be involved in regulation of tumor angiogenesis especially in receptor negative breast cancer by regulation of angiogenesis associated genes via At(1)R. These findings are the first evidence for targeting tumor angiogenesis by inhibition of At(1)R in receptor negative human breast cancer cells and may lead to new therapeutical anticancer strategies based upon inhibition of At(1)R.

 

Angiotensin II induces oxidative stress in prostate cancer.

http://www.ncbi.nlm.nih.gov/pubmed/18314486

The hypothesis that angiotensin II has the potential to induce oxidative stress, which may be implicated in carcinogenesis of the prostate gland through long-term exposure to chronic inflammation is proposed.

Last edited on Fri Apr 2nd, 2010 12:51 by Bane

Bane
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White blood cell count and renin-angiotensin system inhibitors for the risk of cancer in type 2 diabetes.

http://www.ncbi.nlm.nih.gov/pubmed/19932519

In patients with WBC > or = 8.2 x 10(9) counts/L, use of RAS inhibitors was associated with 64% (31-81%) cancer risk reduction in multivariable analysis. CONCLUSIONS: In T2DM, increased WBC predicts cancer while use of RAS inhibitors may reduce cancer risks associated with high WBC count.

Bane
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Angiotensin II / Angiotensin II type I receptor (AT1R) signaling promotes MCF-7 breast cancer cells survival via PI3-kinase/Akt pathway.

http://www.ncbi.nlm.nih.gov/pubmed/20458733

Angiotensin II (Ang II) is a bioactive peptide of the renin-angiotensin system, acting not only as a vasoconstrictor but also as a growth promoter via Angiotensin II type 1 receptor (AT1R) in some cancer. In this study, we examined the mechanisms by which Ang II affected the cell proliferation in AT1R-positive MCF-7 human breast cancer cells. Ang II stimulated the growth of breast cancer cells in a dose- and time-dependent manner. The maximal proliferation effect on MCF-7 cells was obtained with 10-4 M Ang II at 24 h. Losartan (10-5 M,an AT1R antagonist) significantly decreased the level of Ang II-induced proliferative effects, whereas PD123319 (10-5 M,an AT2R antagonist) had no effects. Moreover, Ang II could significantly accelerate S-phase progression, which was inhibited by losartan (10-5 M) or LY294002 (50 microM, a PI3-kinase inhibitor). In addition, Ang II caused rapid activation of p-Akt in a dose- and time-dependent manner. 10-4 M Ang II induced a significant increase of p-Akt at 15 min. The peak level of p-Akt could be persisted for at least 6 h. Among the signaling molecules downstream of Akt, we revealed that Ang II also significantly upregulated CyclinD1, GSK3beta and downregulated p27. Pretreatment with losartan (10-5 M) or LY294002 (50 microM) could significantly suppress these effects of Ang II. These findings suggest that Ang II plays a role in the growth of AT1R-positive breast cancer cells through PI3-kinase/Akt pathway activation. Therefore, targeting Ang II/AT1R signaling could be a novel therapeutic for breast cancer.

Bane
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Keratinocyte cancer prevention with ACE inhibitors, angiotensin receptor blockers or their combination in renal transplant recipients.

http://www.ncbi.nlm.nih.gov/pubmed/20497756

Skin cancer (SC) is the most frequent malignancy after renal transplantation (RT), especially squamous and basal cell carcinoma. The observation that angiotensin II is a potent angiogenic and growth factor raises the possibility that blocking its effects could reduce the incidence of skin cancer. Objectives: To evaluate the incidence of keratinocyte cancer in RT recipients, the timing of occurrence of the skin events after RT; to compare the incidence of SC in our RT recipients and in RT patients on angiotensin converting enzyme inhibitors (ACEi), angiotensin receptor blockers therapy (ARBs) and their combination. Risk factors were also evaluated. Results: During follow up, 52 of 565 patients (9.2%), 38 males 14 females, developed SC at a median time of 59 months (range 29 - 74) after RT. 12 of 52 patients (23%) with SC were on ACEi, ARBs therapy or their combination. The incidence was significantly lower in user patients compared to non user (5.6% and 11.4% respectively). BCC was the most frequent type of keratinocyte cancer in non users and in users. No association with incidence of BCC or SCC was observed for other classes of antihypertensive drugs (calcium antagonists, beta-blockers, alpha-blockers). Conclusion: This study confirms that RT patients are at high risk of SC. The use of ACEi or ARBs is associated with an approximately two-fold reduced risk of Keratinocyte cancers compared to non users in RT recipients. We did not observe an association between the incidence of SC and the use of other classes of antihypertensive drugs. Any chemoprotective effect of these agents may reflect inhibition of the growth factor activity of angiotensin II. Use of ACEi or ARBs, when this is possible, should be considered in RT patients with multiple risk factors.

Bane
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Angiotensin II induces tumor progression and fibrosis in intrahepatic cholangiocarcinoma through an interaction with hepatic stellate cells.

http://www.ncbi.nlm.nih.gov/pubmed/20878072

http://en.wikipedia.org/wiki/Cholangiocarcinoma

Intrahepatic cholangiocarcinoma (ICC) is characterized as a highly fatal tumor with poor prognosis because of its strong progression, early invasion, widespread metastasis and rich cancerous stroma. Although it is widely accepted that fibroblasts facilitate stromal fibrosis and tumor progression, the mechanisms of the interaction between cancer cells and activated fibroblasts have not been fully elucidated thus far. In this study, we demonstrate the presence of angiotensin II (AngII) in ICC tissues and explore the interaction between hepatic stellate cells (HSCs) and ICC cells as one of the sources of stromal fibrosis and tumor progression through the interaction of the AngII/AngII type 1 receptor (AT-1) axis. The concentrations of AngII in ICC tissues were significantly higher than those of HCC and normal liver. Two human ICC cell lines (HuCCT-1, CCKS-1) and a human HSC cell line (LI-90) expressed AT-1 mRNA and protein. The proliferative activity of ICC cells and HSCs to which AngII was added dose-dependently increased and AT-1 antagonist inhibited the proliferative effects. HSCs to which AngII was added showed a higher expression of α-smooth muscle actin (α-SMA, a marker of activated HSCs and myofibroblasts), glial fibrillary acidic protein (GFAP, a specific marker of HSCs) and collagen type I than control cells. AT-1 antagonist also inhibited the activation and transformation of HSCs stimulated by AngII. These findings suggested that locally formed AngII in ICC tissues plays a role in the proliferation and activation of ICC cells and HSCs expressing AT-1 as a growth factor in autocrine and paracrine fashions. Our mechanistic findings provide the first insight into an autocrine and paracrine AngII-initiated signaling pathway that regulates ICC proliferation and fibrosis.

jlunn247
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So   often the different imunosuppressors are just bioactive for a group of similar types of disease?

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Hi all !

This is not exactly the right thread, but I came across an article that fits the MP Pathogenesis regarding cancer:

The following stood out for me:
"This work suggests that significant tumor growth probably requires the slow and steady accumulation of multiple mutations in a cell over a number of years"

- http://tinyurl.com/2db345r

(http://www.sciencedaily.com/releases/2010/09/100928111124.htm)

Best, Frans

Prof Trevor Marshall
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They are getting closer :)

http://www.biomedcentral.com/1471-2407/10/483

"From this study, we conclude that there is a deregulation of the Vitamin D signalling and metabolic pathways in breast cancer, favouring tumour progression. Thus, during mammary malignant transformation, tumour cells lose their ability to synthesize the active form of Vitamin D and respond to VDR-mediated Vitamin D effects, while increasing their ability to degrade this hormone."
 

Sunset
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Dr. Trevor Marshall wrote:

They are getting closer

http://www.biomedcentral.com/1471-2407/10/483

"Vitamin D is a lipid soluble substance that belongs to the family of secosteroid hormones."


It helps when researchers conducting a study understand that the "Vitamin" in Vitamin D is a misnomer!

Last edited on Sun Oct 3rd, 2010 09:33 by Sunset

Nick B.
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[Successful]  Treatment of infantile haemangioma [in human babies] with captopril [an ACE inhibitor].
 
Source:  http://www.ncbi.nlm.nih.gov/pubmed/22533490
 
Abstract
BACKGROUND:
Infantile haemangioma (IH) has recently been reported as an aberrant proliferation and differentiation of a primitive mesoderm-derived haemogenic endothelium regulated by the renin-angiotensin system (RAS), leading us to propose angiotensin converting enzyme (ACE) as a potential therapeutic target.

OBJECTIVES:

To present initial results of our open-labelled observational clinical trial using captopril, an ACE inhibitor (ACEi), in the treatment of problematic proliferating IH.

METHODS:

After initial screening investigations, infants with problematic IH were admitted for initiation of captopril with a 0·1 mg kg (-1) test dose orally, followed by 0·15 8-hourly over 24 h. This was then followed by dose escalation to 0·3 mg kg (-1) 8-hourly for another 24 hours. The dosage was increased to 0·5 mg kg (-1) 8-hourly 1 week later, if a noticeable involution had not already occurred. The response of IH to captopril was documented clinically and photographically before and after treatment and any side-effect was recorded.

RESULTS:
Two boys and six girls aged 5-22 weeks (mean 12·9) with problematic IH were recruited with the lesions located in nasal tip (n = 1), cervicofacial (n = 3), periorbital (n = 1) and perineal (n = 2) areas, and shoulder (n = 1). Transient mild renal impairment occurred in one subject but resolved spontaneously. No other complication was observed. The IHs in all patients responded to captopril at a dosage of 1·5 mg kg(-1) daily which led to a dramatic response in three, moderate response in two, and slow response in three patients. Continued involution of IHs was observed during the follow-up period of 8-19 months (mean 15·8) in all subjects. Treatment was ceased at 14 months of age in seven patients with no rebound growth. In the remaining patient, rapid healing occurred with ongoing gradual reduction in the size and colour of a large ulcerated retroauricular lesion following 5·5 months of treatment. The lesion was excised to address its persistent distortion of the ear.

CONCLUSIONS:

The response of IH to an ACEi supports a critical role for the RAS in IH and represents a paradigm shift in the understanding and treatment of this enigmatic condition.
© 2012 The Authors. BJD © 2012 British Association of Dermatologists.
 
I have a full copy of this paper,  if Dr Marshall is interested in reading it.  :)

 
Cheers
 
Nick

Last edited on Mon Mar 11th, 2013 13:55 by Nick B.

Prof Trevor Marshall
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I attended a presentation at the Salk Institute several weeks ago where a research group  reported that a VDR agonist was effective in-vitro against Pancreatic cancer... And that the VDR was responsible for expressing a majority of the anti-metastasis pathways in man... Their work hasn't been published yet, but coming soon to a journal near you...

Meanwhile, I feel a lot more confident in my analysis of the pathology reports from MP members showing essentially no metastasis in those members still on the MP... Sadly, we have seen several cases of cancer apparently starting, or re-starting, after members stopped the MP...
 



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