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ARBs May Protect Against Breast Cancer Recurrence
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2   
 

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Bane
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 Posted: Wed Apr 28th, 2010 04:07

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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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 Posted: Wed May 12th, 2010 13:20

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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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 Posted: Wed May 26th, 2010 02:51

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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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 Posted: Fri Oct 1st, 2010 04:15

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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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 Posted: Sat Oct 2nd, 2010 05:31

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



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Living in the land of the lost. JUST OLMECIP 5 x a day.Sarcoidosis Dx.
Bone disintegration,lungs,joint/muscle/stomach pain, diarrhea,incontinence. Weakness on my left side sweats,fatigue,neuropathy,headaches,mood swings,cognitive diss.
Frans
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 Posted: Sun Oct 3rd, 2010 08:47

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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



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Prof Trevor Marshall
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 Posted: Sun Oct 3rd, 2010 09:04

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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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 Posted: Sun Oct 3rd, 2010 10:31

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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 10:33 by Sunset



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Nick B.
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 Posted: Mon Mar 11th, 2013 14:36

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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 14:55 by Nick B.



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Prof Trevor Marshall
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 Posted: Mon Mar 11th, 2013 18:47

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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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