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Personalized Patient Sensitivity Testing Confirms Angiostop's Efficacy
ANGIOSTOP'S TARGETS:
** Tysorine Kinase
Receptors (RTKs)
** Patient Case Report:
Angiostop Reduced VEGF
in wet AMD
** Insulin-Like Growth
Factor (IGF)
** Caspases and
Cytochrome C
** Patient Case Report:
Lung Cancer Patient
after 8 Years on
Angiostop and other
supplements
Angiostop References
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DR. CHI'S SEMINAR IN AUGUST |
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August 13-14, 2016
Anaheim, CA
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UPCOMING TRADE SHOWS & CONVENTIONS |
Please visit our booth at the following convention(s).
ANMA CONVENTION
August 26- 28, 2016
Westgate Resort & Casino
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Booth #215
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for more details
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PATIENT SCREENINGS IN YOUR AREA |
May 5-7
Costa Mesa, CA
Depke Wellness Center
(949) 954-6226
May 19-21
Aiea, HI
Yoza Chiropractic
(808) 488-6330
May 26-27
Lake Mary, FL
Holistic Options
(407) 333-1059
May 28-31
Tampa, FL
Abby's Health & Wellness
(813) 265-4951
June 10-11
Orland Park, IL
Rozich Chiropractic
(708) 460-0011
June 13-17
East Lansing, MI
Wycoff Wellness
(517) 333-7270
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DR. CHI'S LECTURE SCHEDULE |
Listen to Dr. Chi speak about Physical Analysis and other topics. Most of these lectures are FREE, so do not miss them!
May 5, 6:30 pm
Costa Mesa, CA
Depke Wellness Center
(949) 954-6226
May 18, 6:00 pm
Aiea, HI
Yoza Chiropractic
(808) 488-6330
May 26, 6:30 pm
Lake Mary, FL
Holistic Options
(407) 333-1059
May 30, 6:30 pm
Tampa, FL
Abby's Health & Wellness
(813) 265-4951
June 10, 6:30 pm
Orland Park, IL
Rozich Chiropractic
(708) 460-0011
June 14, 6:00 pm
East Lansing, MI
Wycoff Wellness
(517) 333-7270
Please call the sponsors above for details about the lecture.
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NEW POSTER |
A must-have for all practitioners!
If you already have the original set of 3 posters, get this NEW Fingernail and Tongue Analysis poster now with tons of new images, such as cherry angiomas, acanthosis nigricans, xanthomas and more!
Or if you do not have any of these, get the complete set!
The posters are a valuable addition to any practitioner's office
GET THEM NOW!
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PRODUCT UPDATES |
We would like to inform all customers that the following products are no longer available:
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Please update your inventory records accordingly.
Please click here for the updated product list
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CONTACT US |
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1435 N. Brasher Street
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Personalized Patient Sensitivity Testing Confirms Angiostop's Effect on RTKs and Caspases
At the recent International Integrative Oncology Conference in mid-April, we were excited to find out yet another proof of Angiostop’s efficacy. Angiostop is a special sea cucumber extract that has multiple pathways that lead to cancer suppression.
A nurse from OH who used Angiostop before told Dr. Chi he should submit it for testing at the Research Genetic Cancer Centre (RGCC). The centre, headquartered in Greece, specializes in medical genetics and performs personalized sensitivity testing on circulating tumor cells (CTCs) from actual cancer patients. Dr. Ray Hammond, DC, NMD, Director of the US Division in Texas, said there’s no need to submit it for testing; they already know Angiostop’s efficacy. For the last 3 to 4 years, over 350 doctors have sent their cancer patients’ blood samples with drugs or supplements for testing. According to the results, it is a very potent extract, effective on 6-7 different types of cancer that they have tested so far, including breast, lung, prostate, colorectal, pancreatic and liver cancer.
He went on to show Dr. Chi one of the assessment results (Figure 1 above). In colon cancer cells of a patient, Angiostop produced a 24% and 26% inhibitory effect on FGF-r and VEGFR-r, respectively. In addition, it increased Caspase 3 and Cytochrome C activity, thereby inducing apoptosis in cancer cells. In addition, Angiostop also tested over 40% sensitivity in pancreatic cancer.
This new report reinforces what we have already presented in the last issue of the newsletter: Angiostop targets two hallmarks of cancer, namely angiogenesis and its ability to avoid apoptosis.
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Tysorine Kinase Receptors (RTKs)
Growth factors have been well-studied molecular targets of cancer agents. We have already known that Angiostop inhibits four growth factor receptors or tyrosine kinase receptors (RTKs): VEGFR, EGFR, FGFR and PDGFR. Figure 2 illustrates immunoblot detection of RTK phosphorylation, indicating that they are inhibited (Reference:
Cancer Cell Biology & Therapy. Aug 2005; 4(8): 874-882). Furthermore, in the same study, Angiostop was also shown to suppress other RTKs involved in downstream VEGF signaling, such as Akt, ERK, FAK and paxillin (blue rectangles in Figure 3).
This is reinforced by the test results in Figure 1, with a 24% inhibitory effect on FGFR and 26% inhibitory effect on VEGFR. Multiple RTK targets make Angiostop wide-ranging and more effective in inhibiting angiogenesis, cell proliferation, and cell migration (Figure 3).
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Angiostop Reduces VEGF in Wet AMD, an Angiogenesis-related Condition
In addition, we see how much Angiostop reduced VEGF in wet age-related macular degeneration (AMD), a condition that also involves angiogenesis and is characterized by elevated VEGF. This case report confirms Angiostop’s effect on VEGFR presented in Figure 1 and Figure 2.
S. Pouira, MD (United Kingdom) has a 71 y/o/f patient with wet macular degeneration. She had started on Avastin ophthalmic injections in June 2010. Avastin is a VEGFR inhibitor. The injections were given once a month to each eye and carry the risk for infection which always worried her. In Sep 2011, her VEGF was high at 570 despite the injections. Three months later, in December 2011, she added Angiostop. By March 2012, she has not required Avastin injections in the left eye and her VEGF level reduced to 510 (Table 1). By June 2012, she has not required Avastin injections in the right eye. In August 2012, her VEGF level reduced further to 445, now within the normal range. Both eyes can see clearly now. Angiogenesis is triggered by VEGFR, EGFR and FGFR. So inhibiting all these RTKs is important in more effectively suppressing angiogenesis. Avastin inhibits only VEGFR while Angiostop inhibits all three RTKs, making it a more complete angiogenesis inhibitor. This explains why it was able to help the wet macular degeneration patient so much better than Avastin did.
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Insulin-like Growth Factor (IGF)
Insulin-like Growth Factor (IGF) has also become a worthwhile cancer target in recent years. It is elevated in several types of cancer, including colorectal, breast and prostate cancer. Specifically it promotes cell cycle progression, angiogenesis and inhibition of apoptosis through activation of its receptor, IGF-R. In the test results in Figure 1, we see that Angiostop inhibits IGF-R by 19%, thereby blocking tumor survival and growth.
This occurs because IGF-R inhibition blocks Akt signaling, which is involved in both the RTK and Caspase pathways (please see Figure 3). In our last newsletter issue, we discussed that increased Akt expression inhibits the BAD protein, preventing it from triggering apoptosis and allowing cancer cells to survive. Akt signaling also promotes cell proliferation and angiogenesis by increasing COX-2 and PGE2 expression. Therefore, through inhibition of IGF-R, Angiostop blocks angiogenesis and induces apoptosis.
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Caspases and Cytochrome C
Cancer cells become “immortal” because of mechanisms that allow them to avoid apoptosis. Caspases (Cysteine-aspartic acid protease) are proteins that initiate and execute the apoptosis process. However, caspases are either lost or deficient in many types of cancer. Again referring to the test results in Figure 1, Angiostop is reported to increase Caspase 3. This supports the more recent studies showing that sea cucumber (Angiostop) activates Caspase 3, 7, 8 and 9. By activating caspases, Angiostop can trigger apoptosis and induce cancer cells to die.
Cytochrome C (Cyt C) is a hemeprotein in the inner membrane of mitochondria also involved in the initiation of apoptosis. Normally, Cyt C is released into the cytoplasm by the Bax protein, binds with the apoptotic protease activating factor and then activates Caspase 9 (see Figure 3). However, cancer cells are able to protect themselves from apoptosis by blocking the release of Cyt C through the Bcl protein. We see in Figure 1 that Angiostop also increases Cyt C activity, meaning it is able to promote Cyt C which then stimulates Caspase 9 and the consequent apoptosis process.
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Lung Cancer Patient: Progress after 8 Years
In the last newsletter, we discussed the multiple pathways by which Angiostop targets cancer. It inhibits several RTKs. It activates caspases and Cytochrome C. It antagonizes prostaglandin E2 (PGE2) receptors, EP2 and EP4. It also promotes the tumor suppressor, PTEN. Combining all these different functions makes Angiostop a more targeted and wide-ranging supplement for cancer management. We see proof of this from a lung cancer patient’s case.
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A. E., a 63 y/o/m from CA, is a conductor from Argentina who was a heavy smoker. In December 2004, Dr. Chi told him he has a risk for lung and prostate cancer through the Fingernail and Tongue Analysis. He tool Angiostop, Revivin, Reishi Spore and Asparagus Extract in 2005 for about 6 months but stopped because he didn’t feel he had an immediate need of them. In December 2008, he was indeed diagnosed with Stage 3.5 lung cancer. On January 3, 2009, he came back to Dr. Chi and told him about the diagnosis. The 7cm tumor in his left lung was located near a major artery, making it difficult to operate. He immediately started Angiostop, Revivin, Reishi Spore Extract and Asparagus Extract along with chemotherapy and radiation. After about 5 months, he had surgery to remove half of his left lung. He had radiation after that and still continued with the supplements for a total of 3 years and was doing well. In December 2015, he was diagnosed with prostate cancer, confirming what Dr. Chi predicted in 2004. So he took Angiostop again with Myomin. His PSA reduced from 5.7 to 3.5 after 4 months. He is now doing great (see picture above).
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Angiostop's Multiple Cancer Pathways
Cancer cells have many factors that are viable targets of cancer therapy, as we have seen through the studies above. Angiostop (sea cucumber) addresses these factors and suppresses cancer through different mechanisms (Table 2).
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