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Cancer Cells Have More Insulin Receptors

Why You Should Stay Away From Insulin Potentiation Therapy

Why You Should Stay Away From Insulin Potentiation Therapy

YourGuide to Quackery, Health Fraud, and Intelligent Decisions Insulin potentiation therapy (IPT) is one of several unproven,dangerous treatments that is promoted by a small group of practitionerswithout trustworthy evidence that it works. It is claimedto be effective against cancer, infectious diseases, arthritis,and many other conditions. Several patents have been issued, but patents are basedon whether or not something appears to be original. Proof of effectivenessis not required. IPT is based on the notion that intravenous insulin increases the effect of medications so that lower doses can be used. Its promoters suggest that somehow the insulin "opens the pores" of cells throughout the body so that certain drugs enter more easily. It is used mainly for treating cancer. The leading proponent is Stephen B. Ayre, M.D., of Burr Ridge, Illinois, who coined the treatment's name in 1986 [1]. In 2003, his Web site stated: The treatment . . . features an innovative low-dose chemotherapy protocol called Insulin Potentiation Therapy (IPT) that uses 75-90% less chemotherapy than the traditional treatment to destroy cancer cells. This low dose treatment causes little to none of the negative side effects such as loss of appetite, nausea, hair loss and fatigue. IPT was developed in Mexico City in 1932 by Dr. Donato Perez Garcia, Sr. and was used by him for decades to treat a wide variety of cancers, including cancers of the breast, lung and prostate. His son, Donato Perez Garcia Bellon, M.D., and his grandson, Donato Perez Garcia, Jr., M.D, followed Dr. Garcia in this work. Collaborating with these two physicians over the last 25 years, Dr. Ayre studied and researched IPT, resulting in their publication of scientific articles on the therapy in medical journals. Cancer cells have Continue reading >>

Insulin Receptor And Cancer

Insulin Receptor And Cancer

Abstract The widespread epidemic of obesity and type 2 diabetes has raised concern for the impact of these disorders as risk factors for cancer and has renewed the interest for studies regarding the involvement of hyperinsulinemia and insulin receptor (IR) in cancer progression. Overexpression of IR in cancer cells may explain their increased sensitivity to hyperinsulinemia. Moreover, IR isoform A (IR-A) together with autocrine production of its ligand IGF2 is emerging as an important mechanism of normal and cancer stem cell expansion and is a feature of several malignancies. De novo activation of the IR-A/IGF2 autocrine loop also represents a mechanism of resistance to anticancer therapies. Increasing knowledge of the IR role in cancer has important implications for cancer prevention, which should include control of insulin resistance and hyperinsulinemia in the population and meticulous evaluation of new antidiabetic drugs for their metabolic:mitogenic ratio. We are now aware that several anticancer treatments may induce or worsen insulin resistance that may limit therapy efficacy. Future anticancer therapies need to target the IR-A pathway in order to inhibit the tumor promoting effect of IR without impairing the metabolic effect of insulin. Introduction The insulin receptor (IR) and the IGF1 receptor (IGF1R), both evolved from a common ancestor gene, represent fundamental regulators of glucose metabolism and growth, respectively, in response to nutrient availability. It is now well established that deregulated expression of IGF1R and/or its ligands may have a role in cancerogenesis as well as in cancer progression and resistance to treatments. Recently, the concept that the IR may also be involved in cancer has rapidly evolved as the results of both epidemiological Continue reading >>

How To Outsmart Your Chemotherapy

How To Outsmart Your Chemotherapy

To discuss your treatment options call 480-657-7000 With the increasing amounts of cancer diagnoses, cancer patients have come to accept dangerous side effects and the often ineffective outcomes of conventional chemotherapy. Recent statistics provoke the question, "Could the treatment actually be worse than the condition?"While every patient is different, it is wise to consider all available treatment options and weigh their pros and cons including those associated with integrative cancer treatment plans.Aspects of Cancer Treatments to be Considered: Discovering lesser-known treatment options. How to avoid poor outcomes and side effects with cancer treatment and chemotherapy. Why many cancer patients fail to see results. A complete recovery plan to regain long-term health. Health Levels Diminished from Aggressive Chemotherapy In the standard treatment model, oncologists typically prescribe a high dose of chemotherapy for a span of several weeks, based upon the type and stage of cancer diagnosed. Research shows that there are glaring flaws with this approach: 1. Side Effects Chemotherapy prescribed in conventional cancer treatments can ravage the body's platelets, red blood cells and immune system. In doing so, secondary and tertiary effects often include: 2. Large Doses of Chemotherapy Followed by Recovery When chemotherapy is prescribed, the patient will receive several weeks of treatments followed by a typical three week recovery. Oftentimes, such practice leads to poor outcomes because: Cancer cells and their DNA are rapidly mutating and becoming more resistant to the treatment, particularly during the three week recovery period. If the chemotherapy is proven ineffective, as is often the case for late-staged cancers, the patient must then wait an additional three we Continue reading >>

Sugar And Cancer Growth Research

Sugar And Cancer Growth Research

Strategy for Selective Starvation of Cancer Cells According to researchers at the University of California, San Francisco, sugar poses a health riskcontributing to around 35 million deaths globally each year . So high is its toxicity that it should now be considered a potentially toxic substance like alcohol and tobacco. Its link with the onset of diabetes is such that punitive regulations, such as a tax on all foods and drinks that contain added sugar, are now warranted, the researchers concluded. They also recommend banning sales in or near schools, as well as placing age limits on the sale of such products. Sugar does not stop at diabetes, metabolic syndrome, hyper- and hypoglycemia, GERD and heart disease. Sugar and cancer are locked in a death grip yet oncologists often fail to do whats necessary to stop their patients from feeding their cancers with sweets. But mainstream medicine insists on promoting the belief that the link between certain types of food with an increased risk of cancer is weak or only nominally significant. They believe that research linking foodstuffs to cancer reveals no valid medical patterns. We find such superficial attitudes promoted in the medical pressall of which lack any kind of medical depth. An increasing number of medical scientists and many alternative practitioners know that the most logical, effective, safe, necessary and inexpensive way to treat cancer is to cut off the supply of food to tumors and cancer cells, starving them with a lack of glucose . The therapeutic strategy for selective starvation of tumors by dietary modification is one of the principle forms of therapy that is necessary for cancer patients to win their war on cancer. Researchers at Huntsman Cancer Institute in Utah were one of the first to discover that sug Continue reading >>

Frontiers | Insulin Receptor Isoform Variations In Prostate Cancer Cells | Endocrinology

Frontiers | Insulin Receptor Isoform Variations In Prostate Cancer Cells | Endocrinology

Front. Endocrinol., 28 September 2016 | Insulin Receptor Isoform Variations in Prostate Cancer Cells 1IGFs and Metabolic Endocrinology Group, School of Clinical Sciences, Southmead Hospital, University of Bristol, Bristol, UK 2Department of Biological, Biomedical and Analytical Sciences, Faculty of Health and Applied Sciences, University of the West of England, Bristol, UK 3Department of Clinical Oncology, Bristol Haematology and Oncology Centre, University Hospitals Bristol, Bristol, UK 4Department of Pathology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia 5Department of Cellular Histopathology, North Bristol NHS Trust, Bristol, UK Men who develop prostate cancer (PCa) increasingly have one of the co-morbidities associated with a Western lifestyle that are characterized by hyperinsulinemia, hyperglycemia and increased expression of insulin-like growth factors-I (IGF-I) and IGF-II. Each have been associated with poor prognosis and more aggressive cancers that exhibit increased metabolism and increased glucose uptake. The insulin receptor (IR) has two splice isoforms IR-A and IR-B: IR-A has a higher affinity for IGF-II comparable to that for insulin, whereas the IR-B isoform predominantly just binds to insulin. In this study, we assessed alterations in the IR-A and IR-B isoform ratio and associated changes in cell proliferation and migration of PCa cell lines following exposure to altered concentrations of glucose and treatment with IGF-II and insulin. We observed that where IR-B predominated insulin had a greater effect on migration than IGF-II and IGF-II was more effective when IR-A was the main isoform. With regard to proliferation IGF-II was more effective than insulin regardless of which isoform was dominant. We assessed the abundance of the IR Continue reading >>

The Role Of Insulin Receptor In Cancer

The Role Of Insulin Receptor In Cancer

University Magna Graecia of Catanzaro, Catanzaro, Italy. The IGF-I receptor (IGF-IR) and its ligands (IGF-I and IGF-II) play a physiological role in growth and differentiation and are also involved in cancer growth and progression. The insulin receptor (IR), which shares high homology with the IGF-IR, has a predominant role in glucose metabolism. However, several studies have convincingly shown that the IR pathway is more intimately involved in cancer development and progression than previously thought. Recent evidences showing that insulin resistance and hyperinsulinemia are important risk factors for cancer have renewed the interest for these studies. One mechanism explaining the increased sensitivity of malignant cells to hyperinsulinemia is the frequent IR overexpression in cancer cells. Moreover, cancer cells commonly show an altered IR gene splicing, with predominant expression of IR-A, one of the two IR isoforms. IR-A binds not only insulin but also IGF-II and, therefore, it competes with IGF-IR for IGF-II binding. IGF-II, via IR-A, stimulates subtly different signaling than insulin. IR-A overexpression and high IGF-II autocrine production are important factors for both normal and cancer stem cells expansion and are often present in dedifferentiated malignancies. Finally, IR overexpression enhances cell responsiveness to IGF-I and IGF-II by participating to the formation of hybrid IR/IGF-IR receptors, which bind both IGFs. Until very recently, only IGF-IR, but not IR, has been considered a target in cancer therapy. However, the results of the clinical first trials employing selective anti-IGF-IR drugs have been disappointing, with only a small subset of malignancies showing an objective response. Recent data have indicated that resistance to anti-IGF-IR drugs ma Continue reading >>

Insulin Potentiation Therapy

Insulin Potentiation Therapy

Insulin Potentiation Chemotherapy (IPT), also known as low dose chemotherapy, is one of the safest and most innovative approaches to treating cancer. It is a kinder, gentler way to fight cancer effectively, including particularly aggressive cancers such as lung cancer and colon cancer, but is also effective on a wide variety of cancer types. IPT is an alternative cancer treatment that has almost none of the side effects such as nausea, radical hair loss, liver damage, and DNA distortion that we see routinely with standard chemotherapy. The key to IPT as a cancer cure is the bodys own hormone insulin. To learn more about IPT , please take a moment to view a presentation on this treatment prepared by Dr. Frank George. This presentation includes the advantages of insulin potentiation therapy, case studies, and an outline of the 4-fold approach to IPT taken by the doctors at EuroMed Foundation. You may also visit our FAQ page for answers to commonly asked questions about IPT. Insulin manages the delivery of glucose across cell membranes into the cells. Cancer cells have 10-20 times more insulin receptors on their surface than normal cells. When insulin is released into the bloodstream by the pancreas in response to a meal, the insulin attaches to these receptors on the surface of the cell and, like a key fitting into a lock, opens channels in the cell wall to allow nutrients to go into the cell. Because cancer cells have more of these receptors, they compete for food better than normal cells. In this way, cancer cells thrive and normal cells are compromised. To find out more about how the EuroMed Foundation uses IPT as a cancer cure, request your free personal orientation online. One of our doctors will be happy to answer your basic questions in person or over the phone. Y Continue reading >>

Insulin Potentiation Therapy - Welcome To Cancer Cure Foundation

Insulin Potentiation Therapy - Welcome To Cancer Cure Foundation

Information from Steven Ayre's website: Chemotherapy drugs are powerful cell-killing agents. In current medical practice, getting these drugs into the inside of cells where they do their work requires that they be administered in doses high enough to force them across the membranes of cancer cells. A major drawback to this dosing strategy is a serious dose-related side effect profile frequently seen with anticancer drugs. This happens because chemotherapy agents do not discriminate between cancer cells and other normal cells in the patient's body. They kill both kinds of cells, therefore there are side effects. With recent advances in our understanding of the inner workings of cancer cells, it is now possible to avoid the dose-related side effects of chemotherapy, while at the same time increasing the effectiveness and specificity of these agents in killing cancer cells. The key to this is an innovative strategy for drug delivery called Insulin Potentiation Therapy (IPT). Readers will recognize insulin as being the hormone used to treat diabetes. Secreted by the pancreas in healthy people, insulin is a powerful hormone with many actions in the human body, a principal one being to manage the delivery of glucose across cell membranes into cells. Insulin communicates its messages to cells by joining up with specific insulin receptors scattered on the outer surface of the cell membranes. Every cell in the human body has some of these receptors, with there being from one hundred to one hundred thousand of them per cell. One might well ask, "What does any of this have to do with cancer cells?" It is a well-known scientific fact that cancer cells have a voracious appetite for glucose. Glucose is their unique source of energy, and because of the relatively inefficient way canc Continue reading >>

Does Sugar Feed Cancer? |what Happens In The Cells

Does Sugar Feed Cancer? |what Happens In The Cells

Does sugar feed cancer? Sugar, in the form of glucose, is used by all cells as the body’s primary source of fuel. It is like the gas/petrol in a car. It powers our movements, thoughts, and more or less everything that we do. If sugar is so vital, how can it feed cancer? The majority of carbohydrates in our diet contain glucose. Glucose is easily absorbed in the body, and once absorbed into the blood stream, it is either used immediately to make energy – especially in brain cells – or it is converted into glycogen and stored. A door with a lock and key For glucose to get from the blood into the cells, it needs the help of insulin. Insulin, a hormone produced in the pancreas, moves glucose into the cells of your body for fuel, or into the liver to be stored as glycogen. To understand how insulin and glucose work together, it can be helpful to think of a door with a lock and key. The lock/key hole represent the insulin receptors on the membrane of cells, and the key to the door of the cell is insulin. Take a look at the diagram above. When blood glucose levels rise after eating, the pancreas secretes insulin. The insulin binds (attaches) to the insulin receptors on the surface of cells (i.e., the key fits into the specific lock) and the door opens into the cell. This allows glucose to enter the cell and be utilized as fuel. When the glucose has entered cells, the blood glucose level drops. At the same time, the pancreas stops secreting insulin and the ‘doors’ into the cell are ‘locked’ again. When we eat a diet with minimal refined sugars, exercise regularly, and have sufficient vitamins and minerals, we can properly maintain our blood sugar levels. The lock gets stuck However, if our diet is high in sugars and refined carbohydrates, or we aren’t sleeping w Continue reading >>

Obesity And Cancer, A Case For Insulin Signaling

Obesity And Cancer, A Case For Insulin Signaling

Cell Death & Disease volume 6, page e2037 (2015) Obesity is a worldwide epidemic, with the number of overweight and obese individuals climbing from just over 500 million in 2008 to 1.9 billion in 2014. Type 2 diabetes (T2D), cardiovascular disease and non-alcoholic fatty liver disease have long been associated with the obese state, whereas cancer is quickly emerging as another pathological consequence of this disease. Globally, at least 2.8 million people die each year from being overweight or obese. It is estimated that by 2020 being overweight or obese will surpass the health burden of tobacco consumption. Increase in the body mass index (BMI) in overweight (BMI>25 kg/m2) and obese (BMI>30 kg/m2) individuals is a result of adipose tissue (AT) expansion, which can lead to fat comprising >50% of the body weight in the morbidly obese. Extensive research over the last several years has painted a very complex picture of AT biology. One clear link between AT expansion and etiology of diseases like T2D and cancer is the development of insulin resistance (IR) and hyperinsulinemia. This review focuses on defining the link between obesity, IR and cancer. Hyperinsulinemia, along with the other obesity-related factors, is linked to the development of several types of cancers. Insulin, signaling through insulin receptor A, has direct oncogenic effects on cancer cells. Insulin-lowering drugs, such as metformin, may prove to be useful in lowering insulin levels and insulin resistance, decreasing body weight and improving cancer outcomes in patients with obesity and type 2 diabetes. How are the PI3K-AKT and the Ras-MAPK pathways regulated by INSR-A in normal epithelial cells and in cancer? How should obesity and T2D be treated in order to minimize the risk of cancer development, spe Continue reading >>

What Is The Role Of Insulin In Tumors/cancer Development?

What Is The Role Of Insulin In Tumors/cancer Development?

Actually, many factors potentially contribute to the role of insulin in the development and progression of cancer. These include hyperinsulinemia and insulin-like growth factor I, hyperglycemia, dyslipidemia, inflammatory and angiogenic adipokines and cytokines, and the gut microbiome Epidemiological studies have shown that hyperinsulinemia and hyperglycemia associated with type 2 DM are linked to an increased risk of several types of cancer, especially the liver and pancreas. Hyperinsulinemia and the exposure of the liver to high insulin concentrations in the portal circulation plays the major role. This is because insulin binds to and activates the related insulin-like growth factor-I (IGF-I) receptor (80% homology with insulin receptor. This leads to more potent mitogenic and transforming activities. moreover, insulin decreases IGF-I-binding proteins (IGF-BP1) resulting in increased free IGF-I, the biologically active form of the growth factor. Besides, The action of insulin in malignant cells is favored by mechanisms acting at both the receptor and post-receptor level. Insulin receptors are overexpressed in cancer cells. The IR may be expressed in two different isoforms, A and B. In malignant cells, IR isoform A (IR-A) expression is predominant and its activation, in contrast to the IR-B isoform, causes more mitogenic than metabolic effects. By binding to the overexpressed IR-A, insulin may favor cancer progression and facilitates the growth of tumors by increasing cell proliferation. Continue reading >>

The Insulin Receptor: A New Target For Cancer Therapy

The Insulin Receptor: A New Target For Cancer Therapy

The Insulin Receptor: A New Target for Cancer Therapy 1Endocrinology Unit, Department of Clinical and Experimental Medicine, University Magna Graecia of Catanzaro, Catanzaro, Italy Edited by: Annamaria Anita Livia Colao, University Federico II of Naples, Italy Reviewed by: Eva Surmacz, Temple University, USA; Jean-Yves Scoazec, Universit Lyon 1, France *Correspondence: Antonino Belfiore, Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Catanzaro, Campus Universitario, Viale Europa, localit Germaneto, 88100 Catanzaro, Italy. e-mail: [email protected] This article was submitted to Frontiers in Cancer Endocrinology, a specialty of Frontiers in Endocrinology. Received 2011 Aug 19; Accepted 2011 Nov 19. Copyright 2011 Malaguarnera and Belfiore. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License , which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. This article has been cited by other articles in PMC. A large body of evidences have shown that both the IGF-I receptor (IGF-IR) and the insulin receptor (IR) play a role in cancer development and progression. In particular, IR overactivation by IGF-II is common in cancer cells, especially in dedifferentiated/stem-like cells. In spite of these findings, until very recently, only IGF-IR but not IR has been considered a target in cancer therapy. Although several preclinical studies have showed a good anti-cancer activity of selective anti-IGF-IR drugs, the results of the clinical first trials have been disappointing. In fact, only a small subset of malignant tumors has shown an objective response to these therapies. Development of resistance to anti Continue reading >>

Part 2: Cancer & Nutrition Does Sugar Feed Cancer?

Part 2: Cancer & Nutrition Does Sugar Feed Cancer?

In Part 1 of my Does Sugar Feed Cancer? series exploring the connection between sugar and cancer, I answered the questions What is one connection between sugar and cancer? And should I be on a Ketogenic diet? To find out the answers to these questions and learn how you can take action to reduce your cancer risk, click here . In Part 2, I will continue to explore the relationship between sugar and cancer to help guide you in understanding how your food choices can impact your cancer risk. I believe there are incremental changes you can make in your diet and lifestyle that will reduce your risk of developing cancer. These changes work through a variety of channels including supporting your immune system, reducing chronic inflammation and acting on cancer cells directly. I want you to understand these channels because I think this will lead to greater appreciation for the power that food has on cancer risk. These changes that you can make will also boost your overall health and vitality, while allowing you to overcome your fear and thrive after cancer. To join a group of cancer thrivers who meet regularly to learn more about this topic and get support with their food and lifestyle goals, you are invited to join my Thriving After Cancer Coaching and Support Program by following this link . In todays blog, I will explore the Insulin and Diabetes Connection to Cancer How are insulin levels connected to cancer? How do I use this information to reduce my risk? Are these two seemingly different conditions related? According to the author of several papers on the connection, having diabetes will put a person at higher risk of developing certain cancers. These are cancers of the liver, pancreas, kidney, endometrium, colon or rectum, bladder, non-Hodgkins lymphoma and breast. What Continue reading >>

Overexpression Of The Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth

Overexpression Of The Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth

Overexpression of the Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth Contributed equally to this work with: Chun-Fang Wang, Guo Zhang, Li-Jun Zhao Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Contributed equally to this work with: Chun-Fang Wang, Guo Zhang, Li-Jun Zhao Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Contributed equally to this work with: Chun-Fang Wang, Guo Zhang, Li-Jun Zhao Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Affiliation: Department of Obstetrics and Gynecology, Peking University Peoples Hospital, Peking University, Beijing, China Epidemiological studies have demonstrated that type 2 diabetes mellitus (T2DM) and hyperinsulinemia are associated closely with endometrial carcinoma risk, although the molecular mechanism remains unclear. Insulin receptor isoformA expression is upregulated in many cancer cells and tissues, which suggests that IR-A-mediated signaling pathways may have important implications for cancer pathogenesis. We measured the expression of insulin receptor isoforms (IR-A and IRB in the normal endometrium tissues, the endometrial carcinoma tissues and the endometrial carcinoma cell lines. We found that the tota Continue reading >>

Insulin, Insulin Receptors, And Cancer.

Insulin, Insulin Receptors, And Cancer.

1. J Endocrinol Invest. 2016 Dec;39(12):1365-1376. Epub 2016 Jul 1. Vigneri R(1)(2)(3)(4), Goldfine ID(5), Frittitta L(6)(7). (1)Endocrinology, Garibaldi-Nesima Medical Center, Via Palermo 636, 95122, Catania, Italy. [email protected] (2)Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy. [email protected] (3)Humanitas, Catania Cancer Center, Catania, Italy. [email protected] (4)CNR, Institute of Bioimages and Biostructures, Catania, Italy. [email protected] (5)University of California, San Francisco, CA, USA. (6)Endocrinology, Garibaldi-Nesima Medical Center, Via Palermo 636, 95122, Catania, Italy. (7)Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy. Insulin is a major regulator of cell metabolism but, in addition, is also agrowth factor. Insulin effects in target cells are mediated by the insulinreceptor (IR), a transmembrane protein with enzymatic (tyrosine kinase) activity.The insulin receptor, however, is represented by a heterogeneous family ofproteins, including two different IR isoforms and also hybrid receptors resultingfrom the IR hemireceptor combination with a hemireceptor of the cognate IGF-1receptor. These different receptors may bind insulin and its analogs withdifferent affinity and produce different biologic effects. Since many years, itis known that many cancer cells require insulin for optimal in vitro growth.Recent data indicate that: (1) insulin stimulates growth mainly via its ownreceptor and not the IGF-1 receptor; (2) in many cancer cells, the IR isoverexpressed and the A isoform, which has a predominant mitogenic effect, ismore represented than the B isoform. These characteristics provide a selectivegrowth advantage to malignant cells when exposed to insulin. For this r Continue reading >>

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