Angiostop (Sea cucumber extract), Cancer, Research Genetic Cancer Centre (Greece)

Angiostop (Sea Cucumber Extract) Inhibits Multiple Cancer Targets and Addresses Many Limitations of Cancer Therapies

Tsu-Tsair Chi, NMD, PhD

Cancer has multiple cellular processes that allow it to thrive, proliferate, and spread. In order for a cancer therapy to be effective, it must be able to simultaneously address these processes. While there are many cancer therapies available in the market today, many of them have limitations, such as side effects, limited cancer targets, and more. Here we discuss Angiostop, a special sea cucumber extract, and how it can fill in the gaps that many conventional treatments are not able to provide.

Over the last two decades, various studies have explored and demonstrated the multiple mechanisms of sea cucumbers against cancer. This comes as no surprise for some cultures. In Chinese folk medicine, it has been an integral part of their therapies for centuries, primarily used as treatment for stomach ulcer and stomach cancer. It has also been studied for its effects on oral gingivitis, effectively reducing gum bleeding and other symptoms.¹ It was not until recent years that scientists have identified what makes sea cucumbers effective for cancer. Triterpene glycosides from sea cucumbers, in particular, have shown multiple anti-cancer mechanisms, such as angiogenesis inhibition, receptor tyrosine kinase inhibition, induction of apoptosis, and caspase activation. This makes Angiostop an attractive candidate for natural cancer therapy supplementation.

Angiostop Inhibits Angiogenesis

Angiogenesis is one of the main hallmarks of cancer as it is the formation of new blood vessels that drives tumor growth. Inhibiting angiogenesis has been a key strategy in order to reduce the size of tumors to make them operable or to reduce the chance of local relapse or metastasis.²

Studies have demonstrated that Angiostop inhibits angiogenesis. This mechanism starves tumors and eventually leads to cancer cell death (apoptosis). In vitro and in vivo studies have shown that Angiostop disrupts all three processes involved in angiogenesis: proliferation, migration, and tube formation.^3-6 This is more clearly illustrated in the following case report.

A 42-year-old female patient underwent chemotherapy for two months from April 11 to June 28, 2005. A mammogram and ultrasound right after that came back positive. Beginning June 28, she took Angiostop. After two months, her results have been remarkable. It appears angiogenesis has receded (see Figure 1).

FIGURE 1. Thermal image illustrating angiogenesis inhibition by Angiostop

C

B

A

April 11 June 28 August 24

Figure 1A. Angiogenesis is evident around the two breast tumors (represented by dark areas).

Figure 1B. Angiogenesis apparently increased around the area.

Figure 1C. Angiogenesis significantly reduced after taking Angiostop.

Angiostop Inhibits Tyrosine Kinase Receptors

We all have microscopic cancers waiting to grow. According to studies, about 40% of women between 40 and 50 years old have microscopic breast tumors. Fifty percent of men between 50 and 60 years old have microscopic prostate tumors, and 100% of people of 70 years old have microscopic thyroid tumors.⁷

Signals from microscopic cancers can prompt the body to release angiogenic factors, such as growth factors or tyrosine kinases. One of the reasons for Angiostop’s anti-angiogenic effect is its inhibition of growth factor receptors or tyrosine kinase receptors (RTKs) that promote proliferation, angiogenesis, invasion and metastasis and prevent apoptosis. Evidence shows that Angiostop can inhibit five different growth factors receptors:

• VEGFr

  – Vascular Endothelial Growth Factor Receptor

• EGFr

  – Epidermal Growth Factor Receptor

• PDGFr

  – Platelet-Derived Growth Factor Receptor

• FGFr

  – Fibroblast Growth Factor Receptor

• IGFr

  – Insulin-like Growth Factor Receptor

Angiostop was previously shown to inhibit four growth factor receptors or tyrosine kinase receptors (RTKs): VEGFr, EGFr, PDGFr and FGFr (Illustrated as rectangles in Figure 2).^3-4 Furthermore, Angiostop was also shown to suppress other RTKs involved in downstream VEGF signaling, such as Akt, ERK, FAK and paxillin (See Figure 2). This is significant because it means better suppression of angiogenesis and other cancer processes.

FIGURE 2. Angiostop’s Multiple Pathways of Suppressing Cancer

Angiostop Shown to Inhibit IGFr, FGFr, VEGFr in Colon Cancer

The Research Genetic Cancer Centre (RGCC), 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 shared that Angiostop is a very potent extract, effective on six to seven different types of cancer that they have tested, including breast, lung, prostate, colorectal, pancreatic, and liver cancer. 
He provided one of the chemosensitivity assessment results (see Figure 3). In colon cancer cells of a patient, Angiostop inhibited IGFr, FGFr and VEGFr by 19%, 24% and 26%, respectively. In cancer genetic testing, a drug or supplement with an inhibition rate of more than 10% is considered an excellent anti-cancer agent.

FIGURE 3

.

Example of Research Genetic Cancer Centre (RGCC) Analysis shows Angiostop’s Effect on

FGFr, VEGFr, IGFr, Caspase 3 in Colon Cancer Patient

The Insulin-like Growth Factor (IGF) has become a worthwhile cancer target in recent years. It is elevated in almost all 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, IGFr.

The chemosensitivity test results provided by RGCC are of great significance because there has yet to be an approved IGFr inhibitor. In order to better manage cancer, IGFr also needs to be inhibited.

Many studies have shown that hyperinsulinemia, as well as insulin resistance and hyperglycemia, is associated with increased cancer risk (see Table 1).^7-12 Colorectal cancer risk, for example, increases by 17% to 42%. Gastric cancer risk increases by up to 101%, breast cancer by up to 300% and endometrial cancer by up to 4500%. IGFr, which is promoted by increased insulin levels, therefore needs to be inhibited in order to reduce these risks.

The chemosensitivity test provided by RGCC is of great significance because there has yet to be an approved IGFr inhibitor. In order to better manage cancer, IGFr is an important target.

Blocking Multiple RTKs for Better Cancer Management

Blocking multiple RTKs has been shown to better fully suppress cancer. This is because most cancer processes like angiogenesis, proliferation, invasion, metastasis, and apoptosis are not associated with only one but multiple RTKs. For instance, VEGFr is a very important target, involved in all of the cancer processes. It is the RTK mainly responsible for new blood vessel growth from tumors. If not inhibited, more blood vessels can proliferate from the tumor, continually feeding its growth. Many of the targeted drugs have VEGFr as the primary target; however, blocking VEGFr alone may not be enough to fully suppress cancer. Cancer cells express multiple RTKs at the same time. For example, breast, prostate, lung, colorectal, ovarian, brain, and pancreatic cancer express all five RTKs.

One disadvantage of available cancer therapies is the limited number of RTK targets. This may only lead to partial suppression and could explain poor patient prognosis and/or recurrence. For instance, let us look at this breast cancer case report.

F. Akbarpour, MD, from California, has an 81-year-old female patient with breast cancer. She had a mastectomy but the cancer recurred as angiosarcoma in the breast. She was given Sutent (25 mg/day) with no apparent effect. The dose was doubled, but still there were no results. Then Dr. Akbarpour reduced the Sutent dose and added Angiostop. After about four months, the angiosarcoma cleared.

Sutent is a targeted drug that inhibits VEGFr and PDGFr, but it does not inhibit EGFr, FGFr, and IGFr. This explains why Sutent had limited effect even after doubling the dose. It was only after adding Angiostop that the desired results were achieved. Similar results were seen in the following case:

R. Abraham, MD, from California, has a male patient in his 60s with kidney cancer. He took Sutent, which reduced his tumor to only 2 cm. Then he added Angiostop and Revivin. After approximately four months, the tumor reduced to one cm. After a year, the tumor cleared.

Again, kidney cancer expresses all five RTKs. The addition of Angiostop provided a synergistic effect with Sutent, leading to better prognosis.

Another example is a lung cancer patient who took Tarceva, an EGFr inhibitor drug and the best targeted drug for lung cancer, along with Angiostop, Myomin, and other cancer supplements, Revivin, Asparagus Extract, and Reishi Spore Extract. Lung cancer is also related to high estrogen so in the following case, Myomin, a natural aromatase reducer, was also recommended.¹³

Antoine E., a 60-year-old male from Florida, was diagnosed with primary pulmonary adenocarcinoma in his lung in 2010 at age 53. Surgery removed the mass. However, within two years, the cancer recurred and spread from his left lung to his right lung and chest cavity. The large mass in his chest cavity was increasing at a rapid rate. At that time, it had grown to the size of a grapefruit and considered inoperable Stage 4 adenocarcinoma. He was given three to six months to live. He underwent chemotherapy. In April 2012, he added Angiostop, Revivin, Reishi Spore Extract, Asparagus Extract, Myomin and OxyPower. He also took Tarceva. In December 2013, his PET scan revealed no tumor. He continues to take the supplements and Tarceva and is determined to be cancer free. In his words, his oncologist told him, “I am their only patient on Tarceva living that long. Tarceva is only good for nine months before patients acquire drug resistance.

Dino F. is a 51-year-old male from Florida who started weekly testosterone injections and the HCG diet. His testosterone was 350 and PSA was 3.0. After a year, his testosterone shot up to 1400 and his PSA to 5.9. He was then diagnosed with prostate cancer. He took Angiostop, Myomin, Revivin and other supplements for one-and-a-half years. At age 51, his PSA has reduced to 2.8, and he also lost 78 lbs (see Table 2).

Table 2. Reduction of PSA and Weight in Prostate Cancer Patient

In the case above, this patient may well have a microscopic prostate tumor already and testosterone therapy may have been the trigger for the growth, causing the increase in PSA level. Taking Angiostop definitely helped reduce growth, as evidenced by the decrease in PSA. Since prostate cancer is an estrogen-responsive condition, Myomin also contributed to the reduction.

Angiostop Induces Cancer Apoptosis

When cells are no longer needed by the body, they die a natural death in a process called apoptosis. Cancer cells, however, have a defective apoptosis mechanism that allows them to be immortal, accumulate, and eventually form a tumor. Research from the last few years has revealed that sea cucumber activates caspases and proteins that induce apoptosis and it also inhibits proteins that block apoptosis.

Caspases are a member of the cysteine-aspartic acid protease family and are the primary regulators of cancer apoptosis or cell death. In cancer cells, missing or deficient caspases can give them immortality and make them resistant to cancer drugs. Either activating or inhibiting these caspases is an important cancer therapy mechanism.

Studies demonstrate that Angiostop activates not only Caspase 3, as seen in the RGCC test (Figure 3), but also Caspase 7, 8, and 9, enabling it to more effectively induce apoptosis (Illustrated as ovals in Figure 2).^15-18

In addition, Angiostop also acts on other types of proteins that affect the apoptosis process. Cancer thrives when there are more proteins that block apoptosis than proteins that promote apoptosis. Angiostop has been shown to tip this balance in favor of apoptosis: it inhibited proteins that block apoptosis, such as Bcl-2 and survivin, while promoting pro-apoptotic proteins like Bax and BAD.^15,18-20

Other Mechanisms

Angiostop has other mechanisms that are worth mentioning.

• Inhibiting the Topoisomerase 2-alpha enzyme – Angiostop is able to attack cancer at the DNA level by inhibiting the topoisomerase 2-alpha enzyme. But unlike topoisomerase 2-alpha inhibitor chemotherapy drugs, like Adriamycin or Vincristine, Angiostop does not have toxic effects.²¹

• Activating the Tumor Suppressor, PTEN – In about 70% of prostate cancer patients, the tumor suppressor PTEN (Phosphatase and tensin homolog) is missing so cell proliferation occurs. PTEN is also deficient in breast, lung, brain, kidney, pancreatic, and endometrial cancer. Angiostop has been shown to activate PTEN (illustrated as a hexagon in Figure 2), blocking cell proliferation and other related processes.¹⁵

• Antagonizing Prostaglandin E2 (PGE2) Receptors – A 2012 National Institutes of Health (NIH)-grant supported study at the University of Maryland Greenebaum Cancer Center found sea cucumber to reduce the risk of metastasis by antagonizing Prostaglandin E2 (PGE2) receptors, EP2 and EP4 (illustrated as diamonds in Figure 2).²² This leads to reduced tumor growth and metastasis.

Angiostop’s multiple mechanisms are illustrated in Figure 2. In the tyrosine kinase pathway (illustrated as rectangles in Figure 2), Angiostop blocks important RTKs such as VEGFr, EGFr, FGFr, PDGFr, IGFr, Akt, ERK, FAK and paxillin. Therefore, it can affect gene regulation and reduce cell proliferation, migration, and angiogenesis. Furthermore, its activation of several caspases and other apoptosis factors like Cytochrome C, BAD and Bax (seen as ovals in Figure 2), makes it effective in inducing cancer apoptosis. Through the PGE2 pathway, it antagonizes the receptors EP2 and EP4 (seen as diamonds in the figure) to block tumor growth and metastasis. Finally, it activates the tumor suppressor PTEN (seen as a hexagon in Figure 2) that is missing in many types of cancer. Activation of PTEN can also contribute towards caspase activation and apoptosis through Akt signaling.

Case Analysis: Triple Negative Breast Cancer Case

F. Mercado, MD, from Sanoviv Medical Institute, has a 52-year-old female patient with Grade 3 ER negative, PR negative and HER2 negative (triple negative) invasive ductal carcinoma in her right breast. She had a lumpectomy in September 2016 and was recommended full dose chemotherapy; however, she opted for natural therapies and took Angiostop and Revivin immediately after her lumpectomy. Her Circulating Tumor Cells (CTCs) level then was 9.4 cells/7.5ml (see Table 3). By January 2017, her CTC was zero. All other cancer markers, CEA, CA 15-3 and CA 27-29, are normal. Barb, Table 3 can be deleted (all info is in the text); but we’d have to renumber the remaining Tables and text.

Table 3. Circulating Tumor Cancer Cells Reduced in Triple Negative Cancer Patient

This patient’s favorable response to Angiostop and Revivin are explained by her RGCC genetic testing results, which assessed her risk using certain cancer markers. Her results showed that she is at high risk for angiogenesis-related markers, VEGFr, FGFr and PDGFr (see Table 4). Indeed, Angiostop inhibits these markers. Her proliferation-related marker EGFr is at 50%, which puts her at high risk. Again, this RTK is inhibited by Angiostop. Furthermore, she was at high risk for certain markers that target the cell cycle rate. Revivin, another supplement she is taking, targets the G1 to S phase of the cell cycle, thereby interrupting uncontrolled cell replication. Her assessment results indicated that her hormone receptors are normal, which is expected of triple negative breast cancer cases. If her hormone receptors were positive, Myomin, a natural aromatase reducer, would have been recommended.

All these assessment results serve to illustrate that, because Angiostop and Revivin address many facets of her cancer, especially the markers for which she is at high risk, she then achieved favorable results (i.e., reduction of CTC).

Table 4. RGCC Assessment of Results for Triple Negative Breast Cancer Patient

Case Analysis: Leiomyosarcoma Patient

RGCC results can be a useful tool in assessing a patient’s potential response to therapeutics, especially Angiostop. We demonstrate it in the following case. A 44-year-old female patient had a chemosensitivity RGCC test after surgery and chemotherapy. Her CTC was still above normal at 7.6 cells/7.5 ml even after conventional treatment. Her RGCC results (see Table 5) provide clues as to which other therapies might be effective for her. Assessment of her results shows that there are many markers that Angiostop can address. For instance, she tested high risk for the angiogenesis and proliferation markers, VEGFr, FGFr, PDGFr, EGFr and IGF-r1. Angiostop inhibits all of these markers. Additionally, Angiostop promotes the pro-apoptotic marker, Bax, and inhibits the anti-apoptotic marker, Bcl-2, both of which were high risk on this patient’s results. The tumor suppressor gene, PTEN, is also promoted by Angiostop. So, based on the assessment, Angiostop would be a good candidate therapy for this patient because it can potentially suppress multiple cancer pathways for which she is at high risk.

Table 5. RGCC Assessment of Results for Leiomyosarcoma Patient

Case Analysis: Fallopian Tube Cancer Patient

Similarly, a 58-year-old female patient with fallopian tube cancer underwent surgery and had subsequent chemotherapy. After she finished chemotherapy treatments in April 2015, her RGCC genetic testing results showed she was still at high risk for certain markers. Table 6 highlights the markers that are at high risk. Among these markers, Angiostop can address VEGFr, FGFr, PDGFr, Bcl-2 and PTEN. It can also address Bax but this patient was low risk for it in this instance. So, based on these results, Angiostop would again be a good candidate for this fallopian tube cancer patient.

Table 6. RGCC Assessment of Results for Fallopian Tube Cancer Patient

In all three case analyses and RGCC test results (see Tables 4, 5 and 6), angiogenic growth factors VEGFr, FGFr, PDGFr, EGFr, IGFr and ERK1 as well as proliferation stimuli are almost always at high risk and are therefore important targets that need to be inhibited. In the triple negative cancer case, VEGFr, FGFr, PDGFr, EGFr and ERK1 are all overexpressed. In the leiomyosarcoma case, VEGFr, FGFr, PDGFr, and IGFr are all highly expressed. The tumor suppressor gene PTEN is also missing. In the fallopian tube cancer case, VEGFr, FGFr, and PDGFr are also overexpressed and the PTEN gene missing. These factors all stimulate angiogenesis and proliferation. Since the treatments that these patients received (e.g., chemotherapy or surgery) do not address them all, Angiostop would be a good recommendation since it inhibits these markers (See Figure 2).

Furthermore, apoptosis-related markers are also not addressed by these patients’ conventional treatments. Angiostop, however, can inhibit anti-apoptotic markers like Bcl-2 and promote pro-apoptotic markers like Bax (see Figure 2). Bcl-2 is at high risk in both the leiomyosarcoma and fallopian tube cases while Bax is at high risk in the leiomyosarcoma case.

Angiostop with Surgery

Angiostop is recommended before and after cancer surgery or any invasive procedure. Many cancer patients develop resistance to chemotherapy or oral cancer drugs, or their cancer recurs after a time. One of the underlying reasons behind that is their cancer was not fully suppressed in the first place because most therapies attack cancer through a single pathway. Taking Angiostop or adding Angiostop to their current cancer regimen may be a more effective approach to fully suppressing cancer.

An angiogenesis inhibitor like Angiostop may be necessary for individuals undergoing cancer surgery or any other type of invasive procedure, such as biopsy, lumpectomy, endoscopy or colonoscopy. There is evidence that the chance of the cancer recurring and spreading increases after surgery. In fact, one study shows that the risk of recurrence and metastasis is 50% within two years after breast, colon, and lung cancer surgery, etc. Researchers recommend an angiogenesis inhibitor before and after surgery to minimize this recurrence.²³

Cancer cells can grow exponentially and are quickly triggered by angiogenic stimulators, so angiogenesis needs to be quickly suppressed. In any type of surgery or invasive procedure (e.g., biopsy, colonoscopy, endoscopy, and so on), the healing process triggers the release of angiogenic stimulators. If there are any cancer cells, then these factors can trigger growth.

Angiostop Safety

Angiostop with or without conventional cancer therapy has minimal toxicity and can be recommended for long-term use. Conventional cancer therapies are often recommended to patients in combination in order to suppress cancer from different angles. For instance, chemotherapy is given with radiation. Or even targeted drugs like Tykerb must be used with Femara for breast cancer. Angiostop has a synergistic effect with conventional therapies.

As presented here, Angiostop has multiple mechanisms and is able to address cancer’s many processes like angiogenesis, apoptosis, and metastasis. In the first case report, for example, Angiostop by itself was able to reduce angiogenesis in a breast tumor patient (see Figure 1). When used in combination with conventional cancer therapies, Angiostop has been shown to enhance their effect, as seen in the case reports presented in an earlier section. In Dr. Akbarpour’s or Dr. Abraham’s cases, for example, their patients had better prognosis once Angiostop was added to Sutent.

Angiostop’s synergistic effect with conventional cancer treatments has been studied as well. In pancreatic cancer, sea cucumber was found to enhance the effect of gemcitabine, a chemotherapeutic agent. In fact, the combination was more effective than either one alone.²⁴ In addition, it also enhanced the anticancer activity of cisplatin, another chemotherapeutic agent, with no side effects.¹⁶ We see evidence of this in the following case report.

G. Farkas, MD, from California, has a patient with colorectal cancer that metastasized to the liver and lung. After using Avastin with 5FU for three treatments in a five-week period, his CEA reduced from 8 to 6.9. Then he added Angiostop. After four weeks, his CEA level further dropped to 3.6 (see Table 7). Barb, this Table is also not imperative; info in text. (But it is a sponsored article….)

Table 7. CEA level reduced in Patient taking Angiostop with Avastin and 5FU

In this case, the patient was taking Avastin, a VEGFr inhibitor drug, while undergoing chemotherapy (5FU). Although the combination therapy did reduce the patient’s cancer marker, CEA, the addition of Angiostop provided much faster results, reducing the CEA level to 3.6.

Angiostop is also a well-tolerated supplement with minimal or no side effects. In the cisplatin study, there was no evidence of side effects when used in combination.¹⁶ In a pancreatic cancer study, it did not show any sign of acute toxicity or side effects.²⁵

Anecdotal evidence shows that patients can also take it for a long period of time with no side effects and still get results unlike many cancer drugs. Many drugs prolong survival only for a short period of time. For instance, Nexavar, a multiple RTK inhibitor for kidney, liver, and thyroid cancer, increases survival by only three months. Tarceva, an EGFR inhibitor drug, is typically effective for nine to ten months. After that, it loses its effect. This was seen in Antoine’s lung cancer case. According to his doctor, he is his only patient on Tarceva who has lived this long. This may be attributed to the addition of Angiostop.

Another case shows how long-term use of Angiostop, with or without conventional therapy, can still be effective.

A 70-year-old from California was a smoker. At age 64 in June 2011, he found blood in the stool and immediately started taking the supplements Angiostop, Myomin, and Revivin. In September 2012, at age 65, a test found he had lung cancer and had subsequent surgery. The surgeon was amazed that the lung cancer did not metastasize. In March 2013, he was diagnosed with colon cancer and two sections of his colon were removed. He added Tarceva in Jan 2015 but continued to take Angiostop and Myomin. All this time his CEA has been well managed (see Table 8).

Sep 2012 – Lung cancer surgery

Apr 2013 – Colon cancer surgery

Table 8. CEA Levels of Lung and Colon Cancer Patient

Jan 2015 – Took Tarceva, Angiostop and Myomin

Apr 2013 – Took Angiostop and Myomin

Jun 2011 – Took Angiostop, Revivin, Myomin

Angiostop, when taken at the first sign or symptom of a problem, can be very beneficial, just like in the case above. This patient had already started taking it in June 2011 even before diagnosis. He also took Myomin and Revivin, supplements that have beneficial properties for cancer. Blood in the stool suggests a colon condition, which can be mitigated by estrogen dominance. Myomin is an aromatase reducer supplement that corrects estrogen dominance.¹⁴ Revivin, on the other hand, causes cell cycle arrest to block uncontrolled cell replication.

So, taking all these supplements helped manage different aspects of the abnormal growth. By the time he was diagnosed, the cancer had not metastasized at all. It is also important to note that he only added Tarceva after he has been on Angiostop for a few years. But for the past four years at least, his CEA has been under control and his quality of life was not compromised.

Summary

Currently, common conventional cancer treatments usually involve a combination of surgery, chemotherapy, radiation, targeted drugs, and immunotherapy. While each has its benefits, each also comes with limitations. Adding Angiostop (sea cucumber extract) to conventional cancer therapy can help address some of these limitations.

• It addresses cancer targets simultaneously:

  • It inhibits angiogenesis by blocking several RTKs (VEGFr, EGFr, PDGFr, FGFr, IGFr). In fact, Johns Hopkins reports inhibiting angiogenesis is the best strategy for cancer prevention in order to cut nutrition supply to cancer cells. IGFr is an especially important target because there is no IGFr inhibitor drug approved.

  • It induces cancer cell death (apoptosis) through caspase activation.

  • It antagonizes PGE2 receptors to reduce tumor growth and metastasis

  • It activates PTEN to inhibit cell proliferation.

  • It attacks cancer at the DNA level by inhibiting the topoisomerase 2-alpha enzyme.

• It can be used by itself or in combination with conventional cancer therapies. In fact, studies show that the combination has synergistic effects. Angiostop before and after surgery or any invasive procedure can also have benefits in reducing the risk of recurrence and metastasis.

• Long-term use can still potentiate effects unlike other drugs that are only effective for a limited time.

• It is well-tolerated with minimal or no side effects.

Angiostop is indeed an attractive candidate for cancer therapy supplementation. Clinical studies are, of course, necessary to fully establish Angiostop’s mechanisms, but preliminary studies already show that Angiostop inhibits pathways that allow cancer cells to proliferate and tumors to grow; and, at the same time, it promotes pathways that allow cancer cells to die.

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