The pancreas is a gland located behind the stomach. Its head is attached to the duodenum while its tail reaches the spleen. It contains two types of glands: exocrine glands that make enzymes to break down fats and proteins, and endocrine glands that make hormones insulin and glucagon to regulate sugar in the blood.

Cancer originating from the exocrine glands is said to be more aggressive of the two. However unless detected early and operated, pancreatic cancer at its metastasized stage is deadly because it is difficult to treat. It has a depressingly low survival rate – very few make it beyond 5 years after diagnosis, just 4 to 5 percent. The incidence of pancreatic cancer increases with age, usually between 50 and 80 years of age.

Strategies Against This Cancer

• Stop Smoking and Drinking – Smoking and alcohol are believed to increase the risk.

• Diet and Exercise – Eating a diet rich in clean and fresh fruits and vegetables, low in refined sugar and carbohydrates and exercising, cut risk.

• Colourful Flavonols – In a first of its kind study, researchers from the German Institute of Human Nutrition noted that flavonols helped cut pancreatic cancer risk by about 25 percent and 59 percent for smokers. The three types of flavonols analysed were: quercetin, found in apples and onions; kaempferol, present in spinach and cabbage; and myricetin, found in berries and red onions. Flavonols are a class of flavonoids, which are known for their powerful antioxidant properties.

• Vitamin D – Studies are showing a link between vitamin D and pancreatic cancer risk. Two studies from Harvard each found this correlation. One compared people taking 150 vs 600 international units (3.8 vs 15 mcg) vitamin D per day and reported a 40 percent lower cancer risk in people who took more vitamin D. The other study found a 35 percent lower risk for those with higher vitamin D blood levels. According to Vitamin D Council, taking 1000-4000 international units (25-100 mcg) daily of vitamin D may reduce pancreatic cancer risk.

An Alternative Treatment That Works

The Gonzalez regimen, named after Dr. Nicholas Gonzalez, is a nutritional protocol is based on the findings of Drs John Beard and William Donald Kelley. The therapy is focused on treating cancer, including pancreatic cancer and has achieved success. Testimonies of those who underwent this treatment have survived 5-15 years after diagnosis. The regimen involves a strict diet, taking enzymes and supplements, and using coffee enemas.

If all it takes is that we would change our unhealthy habits, take the right foods and supplements so as to reduce pancreatic cancer (or an other cancer) risk, prevention is within our reach and within our control.

In the case of prostate cancer, this has proved particularly challenging because of the extremely heterogeneous nature of the genetic alterations that underlie this disease. A prominent molecular target for prostate cancer therapy is the PI3K-AKT signaling pathway. A recent study of 218 prostate cancer tumors showed that 42% of the primary tumors and 100% of the metastases harbored genomic aberrations in that pathway.

The best-characterized genetic alteration in this pathway is in PTEN, which has been shown to be mutated and/or exhibit loss of heterozygosity in approximately 15% of localized prostate cancer and 30% of metastatic disease. Multiple small-molecule inhibitors of PI3K-AKT signaling have been developed and tested clinically. Although the results of early clinical trials are inconclusive, the therapeutic activities of PI3K-AKT inhibitors as single agents have generally been modest in patients with advanced prostate cancer. Thus, there is considerable effort to rationally integrate PI3K-AKT inhibitors into combination therapy protocols.

In recent issues of Cancer Cell, both report on having identified reciprocal feedback regulation between AR and PTEN loss/PI3K-AKT signaling in prostate cancer. By making effective use of the PB-Cre;Ptenlox/lox mouse model and carefully annotated human prostate cancer tissue samples, these two groups of investigators have made a seminal contribution to our understanding of the regulation of growth and survival signaling in prostate cancer cells and, by extension, to the rationale for use of specific combination therapy for advanced prostate cancer. Using similar experimental approaches, the loss of PTEN function sets into motion a series of molecular events that establish a linkage between two expansive signaling networks that exert control over the growth, survival, and differentiation of prostatic epithelial cells. Activation of PI3K-AKT signaling as a result of Pten mutation in the PB-Cre;Ptenlox/lox mouse leads to suppression of AR signaling.

Transcriptome analysis revealed substantial overlap of up- and downregulated genes between intact male Pten/mice and castrated wild-type mice and also demonstrated that PTEN loss is associated with reduced AR signaling in PTEN-deficient human prostate tumors. These results, together with those of previous studies, show that the loss of PTEN function and activation of PI3K-AKT signaling plant the seeds for androgen-independent prostate cancer growth by establishing a castrate genetic program. Using both pharmacologic and genetic approaches, different mechanisms contribute to the repression of AR output. The PI3K-AKT, but not MEK signaling, is responsible for inhibiting AR signaling, and that this inhibition depends on upstream HER kinase inhibition. Using a PTEN re-expression approach, PTEN loss may suppress androgen-responsive genes through upregulation of Egr1 and c-Jun transcriptional coregulators and the catalytic subunit of Polycomb repressive complex 2, Ezh2. Thus, PTEN loss can lead to repression of AR signaling on two levels: upstream suppression of MAPK-stimulated HER kinase, and suppression/subversion of AR-mediated transcription through increased expression of transcriptional coregulators and a histone methyltransferase. Probing the castration response in PBCre; Ptenlox/lox mice, PB-MYC mice, and androgen-sensitive prostate cancer cells and analyzing a double-knockout mutant, PB-Cre; Ptenlox/lox;Arlox/Y, mouse and human prostate cancer samples led to the second crucial surprising finding-that castration or AR loss increased AKT phosphorylation.

An important note is that these two experimental approaches independently led to the identification of a reciprocal negative-feedback signal in thePB-Cre;Ptenlox/loxmodel and in androgen-sensitive human prostate cancer cell lines; that signal is AR-stimulated, FKBP5-mediated activation of the AKT phosphatase PHLPP, which suppresses AKT activities. On the basis of their results, both groups hypothesized that prostate cancers in a castrate state (or with low AR levels) have greater dependency on PTEN loss/ PI3K-AKTsignaling. Totest this hypothesis in vivo, in scientific synchrony, Carver and colleagues showed that a combination of BEZ235 (a dual PI3K and mTOR inhibitor) and castration resulted in dramatic reductions in tumor volume, in contrast to no effect of single-pathway therapy, in LNCaP xenografts and near-complete pathologic responses in the PB-Cre;Ptenlox/lox model; Mulholland and colleagues demonstrated that rapamycin (an mTOR inhibitor) treatment of castrated PB-Cre;Ptenlox/lox; Arlox/Y mice harboring prostate cancer resulted in significantly reduced proliferation and tumor burden when compared with castration alone. The reciprocal negative feedback that links the AR and PTEN loss/PI3K-AKT signaling networks is intriguing on many levels. However, the gene expression analysis does not exclude PI3K-AKT-independent, PTEN loss-mediated signaling as a mechanism underlying upregulation of EGR1, c-JUN, and EZH2, extending the linkage between the androgenic and PTEN loss/PI3K-AKT signaling.

It is well established that AR signaling promotes the growth and differentiation of prostate epithelial cells. The precision and coordination involved in androgenic regulation of prostatic growth, morphogenesis, and cytodifferentiation depends to a large extent on AR target gene activities, which are modulated by numerous coregulators.

A recent study showed that the TMPRSS2-ERG gene fusion product can disrupt androgenic signaling in prostate cancer cells through multiple mechanisms, including binding to AR target genes and induction of EZH2 expression, which in turn can suppress prostate cell differentiation. In addition, under some conditions, PI3K-AKT signaling can enhance AR activities and induce AR target genes, such as p21WAF/CIP, which is associated with androgen-independent growth of prostate cancer. In light of the new knowledge about this mechanistic framework that has resulted from the discovery of reciprocal negative feedback linking the AR and PI3K-AKT signaling networks, it may be possible to better characterize and delineate additional signaling pathways andidentifyadditional transcriptional coregulators and chromatin modifiers that underlie specific AR target gene functions related to androgen-dependent prostatic growth and/or differentiation and to androgen-independent growth in prostate cancer. The inexorable process of selection through which cancer cells develop resistance to all types of anticancer agents presents research and clinical oncologistswith a daunting task. Through their discovery of important reciprocal negative feedback involving AR and PTEN loss/PI3K-AKT signaling in prostate cancer.

Gd-T lymphocytes recognize small phosphorylated molecules or non-classical MHCI antigens in a non-MHC restricted manner, and B lymphocytes recognize tertiary or quaternary structures of antigens using immunoglobulins (Ig). A third type of recognition is used by cells of the innate immune system: natural killer (NK) and natural killer T (NKT) cells recognize lack of expression of self (missing self), i.e., absence or low cell-surface levels of MHCI and/or MHCII molecules Furthermore, antigen-presenting cells (APC) such as dendritic cells (DC), macrophages, and granulocytes can recognize non-self-structures via toll-like receptors (TLR) or C-type lectin receptors (CLRs).

Activation of T cells, NKT, or NK cells happens via the interaction of activating receptors (KAR) associated with signaling molecules expressing immuno-tyrosineactivation- motif (ITAM) signal-motifs in their cytoplasmic region. T lymphocytes and NKT cells express T-cell receptor (TCR)/CD3 complexes, and T, NKT, or NK cells express KARs such as NKG2D associated with DAP10 signal-transduction molecules and Ly49D associated with DAP12 molecules. It appears that the high number (~10) of ITAMs associated with TCR molecules is necessary to avoid autoimmunity. Inhibition of cell activation by inhibitory receptors (KIRs) such as NKG2A/ CD94 is related to the expression by KIRs of ITIM inhibitory motifs in their cytoplasmic tails

Helper T (Th) cells trigger differentiation of precursor cells into CD8+ cytotoxic T lymphocytes (CTL) or antibody-producing B cells. The so-called Th1 cells induce preferentially the production of IL-2 and IFNg and the differentiation of CTL, whereas Th2 cells induce mostly the production of IL-4, IL-5, and IL-13 and the differentiation of B cells into antibody-producing plasma cells. When administered to elicit specific immune responses and memory but not tolerance, the antigens have to be presented in the form of cells, particles, or aggregates, or emulsified in adjuvants such as Freund’s adjuvants or aluminum salt precipitates. A unifying concept of these phenomena was proposed by late Charlie Janeway.

The innate immune system, NKT cells, NK cells, DC, macrophages, and granulocytes are activated by pathogenassociated molecular patterns (PAMPs) by means of TLR or CLRs. The DC differentiates from immature, phagocytosing cells to mature, non-phagocytosing cells with increased levels of co-stimulatory molecules such as MHCII, CD40, CD80, and CD86 and enhanced antigen-presenting activity. Cells from the innate immune system release inflammatory cytokines that induce the priming of CD4+ Th subpopulations (Th1, Th2, and Th17). Immediately after stimulation, NKT cells release preformed IFNg and IL-4 which direct Th1 and Th2 cell differentiation, respectively. IFNg triggers DC to produce IL-12, which induces preferential Th1-priming and NK cell production of IFNg and cytotoxicity. A subset of DCs, CD8+CD205+ dendritic cells, produces endogenous TGFb and is specialized to induce Foxp3+ Treg cells, whereas another subset, CD8 CD205 and DCIR-2+ (DC inhibitory receptor-2), participates in Th2 responses.

Although stimulation of the innate immune system may greatly help the initiation of adaptive cellular and humoral immune responses, over-activation of the innate immune system represents a risk due to a possible “fatal cytokine storm” However, the cytokine storm is prevented by CD4+ Th or CD8+ CTL, which down-regulate the activity of the innate immune cells by a cell-cell contact, MHC-dependent mechanism. It seems clear that memory T cells are derived from effector T cells by avoiding antigen-induced cell death. In contrast, the subdivision of CD4+ T cells into Th1, Th2, Th9, Th17, and Treg cells is more malleable and demonstrates more functional plasticity than previously thought.

Inexperienced, naive T cells appear to receive different types of “secondary education” when they encounter antigen at various regional sites including tumor micro environments. Besides possessing different effector functions, DC and T cells should be able to migrate to and within tissues. Adhesion via L-selectin induces rolling, activation, and transmigration via chemokine receptors such as CCR7. The interaction between CCR7 and its ligands, CCL19 and CCL21, may balance immunity and tolerance T lymphocytes do not react with self-structures that are expressed in normal physiological conditions, i.e., the organism is tolerant to self-structures.

However, thymus negative selection (central tolerance) is not infallible, and self-reactive Concepts and Ways to Amplify the Anti tumor Immune Response 99 T cells with low-avidity TCR do emigrate from the thymus. Such self-reactive T cells are regulated by CD4+CD25+ T regulatory (Treg) cells (peripheral tolerance). Thus, since many anti tumor immune responses are “autoimmune” reactions, these are often weak in both quantity and quality. It is important to distinguish between the following three levels of low responsiveness to malignant cells:

(1) tumor-specific T cells with high-avidity TCR have been eliminated in the thymus;

(2) tumor cells or their products may induce tolerance (in the sense of unresponsiveness), i.e., tumor-specific T cells are present but are rendered anergic;

(3) immune effectors recognize tumor cells but are prohibited from performing their natural function due to tumor-associated inhibitory molecules and/or cells.

The latter two phenomena are linked to the fact that resting DC or macrophages in the tumor induces and maintains peripheral tolerance and functional anergy in CD8+ T cells, NKT cells, and NK cells through PD-1 and CTLA-4-related mechanisms.

The acupoint used to treat nausea in all these diseases is always the same and does not vary according to personality the patient’s eating habits, etc. Scientific research in this field is developing rapidly, although at the moment auriculotherapy in cancer patients has proved especially useful for pain treatment.

Phytotherapy deserves a separate mention because herbal medicine is the discipline that comes closest to the natural conventional medicine as it is based of course on the use of chemicals present in plants, with organic farming activities. Besides, just think that 30 – 40% of conventional drugs derived from herbal substances. Herbal medicine is the medical discipline so using medicinal plants and derivatives in prevention and treatment of diseases, in relation to the pharmacological properties of chemical constituents present in the plant, or better in the preparation used. It does not follow diagnostic or therapeutic methods different from those of scientific medicine. The medicinal plant, so it can simply be considered, a container of chemicals, sometimes isolated and used as such in therapy, in other cases the source of raw material for the production of drugs or as a basis for the production of herbal medicines themselves. Herbal medicine is a discipline particularly promising for the cure cancer, both as a preventive measure or as a complementary therapy to chemo and radiotherapy or surgery. It is used as an immunostimulant, for treatment of gastrointestinal disorders and radiodermatitis and to combat certain symptoms such as fatigue, depression, constipation, etc.

There are also many studies that confirm the pre-clinical anticancer activities of substances present of many plants. The substances of plant origin may also be toxic, causing serious interactions with pharmaceutical drugs taken concurrently, or be responsible for allergic reactions. For these reasons, suitable extracts must always be used, quality controlled, standardized active ingredients, purified from useless or dangerous, and used only with medical prescription. For example, cancer patients often use honey and aloe smoothies (presented as a miracle cure for cancer!), not knowing that just some substances present in the plant cut the effectiveness of Chemotherapy.

Cancer vaccines are beginning to gain more interest in the medical community. Research into cancer vaccines is continuing to grow and many clinical trials are currently underway. The premise behind a cancer vaccine is to help the body’s immune system fight off and protect itself from any type of infectious agents, including cancer cells. The FDA has in fact already approved of two vaccines. One is known as Gardasil, which protects against the human papillomavirus. The other is a prostate cancer vaccine known as Provenge. Clinical trials are using vaccines to treat lymphomas, breast, brain, kidney, melanoma, leukemia, prostate, pancreatic, lung, kidney and cervical cancers and well as solid tumors.

Cancer vaccines work by protecting the body from infection. They are based on antigens that are commonly carried by infectious agents. These antigens are easy for the immune system to recognize as foreign. One particularly powerful cancer vaccine that can potentially outsmart the cancer cell is known as a dendritic cell vaccine.

The Problem with Cancer Cells and How Dendritic Cell Vaccines Can Help: The immune system often does not “see” cancer cells as dangerous or foreign, as it generally does with microbes. Therefore, the immune system does not mount a strong attack. Cancer cells develop genetic changes that create a “chemical message”. This can essentially trick the killer T cells of the body to not mount an assault against them because they cannot recognize them as dangerous. So although the body will attack the cancer cells the immune system may not do so as strongly as it does when it detects various other rogue cells.

The immune system contains Dendritic cells: These cells help to identify pathogens in the body. In a healthy immune system there are specific cells whose sole purpose is to defend the body against disease. Additionally, these specialized cells maintain a “memory” and will be able to recognize dangerous microbes or cells if they ever return again. The concept of the dendritic cell vaccine is to work with this natural response that already occurs in the human body. Dendritic cells will locate viruses and cancerous cells. Once identified they will produce the antigen to the body’s t-lymphocyte cells. These t-lymphocytes will then begin to multiply and attack the invading cells.

The Dendritic Cell Vaccine: The dendritic cell vaccine became approved for use by the FDA in 2010 and is in clinical trials. This vaccine involves a very specific process. Dendritic Blood cells are extracted from a patient and then processed in a laboratory setting to produce them in large amounts. They are then exposed to the antigens of the patient’s cancer cells. Then the cells are reinjected back into the patient where they are attempting to program the cells to now respond more aggressively against the cancerous cells.

The Dendritic Cell Vaccines Stimulates the immune system. The vaccine is designed to activate the B and T killer cells to recognize and attack the cancer cells. B cells work by making an antibody which destroys bad cells. Killer T cells will make the invader cell self destruct through a process known as “apoptosis”. The dendritic cell acts in a supporting role to the B and killer T cells by helping to activate them more effectively.

Potential Side Effects: Dendritic Vaccines are generally considered safe but may have side effects depending on individual response. These can include itchiness or rash, weakness or more seriously, occasionally breathing difficulties. Any treatment that impacts on the immune system may of course carry more serious risks although not common which can be life threatening.

Combining Conventional Treatments with Dendritic Cell Vaccines: Many of the current clinical trials are using the vaccine in combination with traditional therapies such as chemotherapy, radiation and surgery. Some trial results are indicating an overall increase in the effectiveness of other treatments. Research is being conducted to determine when a cancer vaccine works best when given along with conventional therapies in order to produce optimal immune system responses.

The Future: Much research is being conducted to understand just how cancer cells are able to avoid or even suppress a powerful immune system attack on them. Work is being done on developing vaccines and other mechanisms to override this response of the immune system. Combining a vaccine such as the dendritic cell vaccine with such other novel treatments may be able to greatly improve the ability of the body to find and destroy the cancer cells. As more and more cancer vaccines are being developed researchers are hopeful to one day be able to provide more answer to this suffering with cancer.

It is an silent epidemic that affects everyone because it respects no one. All of us know people who have cancer, people looking for ways of curing cancer; and for a lot of us, sadly, even people that are close to us and even loved ones.

CHEMOTHERAPY
The most popular (and accepted) method for curing cancer is chemotherapy. Why? Because ever since we were little kids, we were taught that if we are sick, we go to the doctor. And here’s one more thing we “learned,” the doctor is always right. Now, for 99% of sicknesses and diseases, they know exactly what they’re talking about. And even when they talk about cancer, they know all the why’s and how-to’s of the disease, the cells, etc. But when it comes to curing cancer, this is where the knowledge stops.

For starters, here is the dictionary definition:

Chemotherapy – The treatment of disease by the use of chemical substances, esp. the treatment of cancer by Cytotoxic and other drugs.

“Cytotoxic” literally means toxic to cells. This means that chemotherapy is actually KILLING your cells. Now, granted, they are targeting the cancer cells, but here’s the logic. Imagine a group of people, about a hundred of them, gathered in a small room. There are 5 of them that need to be eliminated. Now imagine chemotherapy as a grenade thrown into the crowd. Oh sure, you might kill the 5, but what happens to the 95?

Doctors might disagree with me on this reasoning, but it is what it is. They have to promoting chemotherapy because as of now there is still no known procedure or perfect way of curing cancer. They have to introduce toxic chemicals to the cancer patient to kill the cancer cells. The Doctor’s Hippocratic Oath says, “Do no harm.” Uhm, I guess there are exceptions.

IF NOT CHEMOTHERAPY, THEN WHAT?
Common sense tells us that the way to restore life is by using life-restoring treatments and medicine. Then why in the world are we not including this to the methods of curing cancer?

The hospitals, doctors, and even the government have promoted and accepted that chemotherapy is the ONLY way to extend or lengthen the life of the patient; it is the most scientifically accepted way of curing cancer (sic).

Believe me when I say that there are other solutions. Chemotherapy is basically – to slowly kill you for the purpose of killing your disease (do you realize how stupid that sounds?).

It is time for a revolution. A healing revolution.

We have been taught, indoctrinated, and essentially told that doctors (and even nurses, in some cases) know what’s best for us, especially when it comes to the well-being of our bodies. And to be fair, most of the time they really do know all the facts and figures and solutions and outcomes of the sickness or disease we are afflicted with. Most of the time…

Everybody knows what a cancer is, right? Next to AIDS, cancer is the most-feared condition there is. Unfortunately for us, a lot of our experiences with cancer are with someone close to us or even a loved one who is suffering from it and are looking for various ways of curing cancer.

The next few paragraphs will probably turn you off and make you stop reading the rest of this article, but I believe it is my responsibility to report this.

Curing cancer has always been guesswork. Yes, you read that right, guesswork. The reason is that if it is not guesswork and the solution is already out there, why in the world are saying that it is still an incurable disease?

Nobody knows how to eliminate the cancer cells and replace them with new ones, without killing the patient, nobody. That is the plain and simple truth.

Cancer – Through a Different Perspective

Here is an interesting proposition; and this will go against everything that you have learned about cancer and about what you think the “experts” (i.e. doctors) know about it.

For decades, we have viewed cancer as a sickness, an illness, a disease; when in actuality, it is not. It is a symptom. A manifestation. An indicator. “Of what?” you ask. I’m glad you did.

Our body is so complex that even centuries of research and study can’t fully comprehend what it is capable of. Our body has natural antibodies that fight toxins. Natural soldiers that drive out anything that is surplus in our body, from vitamins, minerals, toxins; even the type that causes cancer.

Simply put, a lump or tumor is basically a balloon that contains all the bad toxins. And this balloon is devotedly keeping the deadly toxins from spreading throughout the body via the bloodstream. This is the good news.

Now the bad news. When we notice the lump, we see a doctor. Doctor wants to be “sure” what it is (which means he has no idea and just wants more information and data), so he orders a biopsy.

Going back to our “balloon” illustration, having a biopsy is like bursting that balloon just to make sure that air is definitely what’s inside. Now imagine what happens to the air in the balloon when it bursts. Right! It spreads everywhere and anywhere.

A friend of mine named Karen put a comment on Facebook the other day saying when are they going to find a cure for cancer as my close neighbour has just been diagnosed with it. She said I wish it was very soon so it will help my dear friend and neighbour.

Knowing a little more than Karen about the subject and what’s going on in the cancer industry I felt compelled to reply but in a personal email to her. This is what I said, I’m sorry to hear about your neighbour but there are two answers to your question. Firstly if you are waiting for a drug to be developed to cure cancer then the answer is never but if you are prepared to step outside of our current ways of treating cancer then the answer is, we already have a cure. Let me explain.

The reason why researchers haven’t succeeded in finding a cure despite looking for more than 40 years is that cancer is a disease caused by both toxins and deficiencies and it’s impossible to cure that with a drug. You can only cure deficiencies within the body by correcting them.

One example is scurvy which is also a deficiency disease and the only way to cure that is by eating something that contains the missing vitamin which is vitamin C. Pellagra and Pernicious Anaemia are two other deficiency diseases which were common many years ago and these can never be solved with a drug.

Also there is too much at stake in stopping the status quo with our treatments today because they are making too much money at present from the way they are treating cancer with surgery, radiation and especially chemotherapy. The cold hard facts are that cancer and other degenerative diseases are big business. Do you really think that pharmaceutical companies want someone to find an inexpensive natural, non toxic treatment to cure cancer?

Back in 1971 when Richard Nixon was in power in America, he declared war on cancer and allocated millions of dollars for cancer research. What they are searching for is a drug they can patent that will work more effectively than current treatments of radiation and chemotherapy in which they can profit from. Some of the latest cancer drugs are Avastin for colon cancer, Herceptin for breast cancer and Gleevec for chronic myeloid leukaemia. These drugs aren’t cures but only there to prolong life and they all cost approximately 4000 dollars a month.

Remember the pharmaceutical industries are one of the largest and most profitable businesses in this world and if people took prevention measures to stay healthy, this would impinge on their profits. Drug companies don’t profit from cures, they need us coming back over and over again,

Dr Linus Pauling who in his lifetime won 2 Nobel prizes stated that most cancer research is largely a fraud and that the major cancer research organizations are derelict in their duties to the people who support them. The people who support them are of course the tax payers and those who donate money for cancer research

I know it’s a brave choice to step outside of our current way of treating cancer but there has always been a way to cure the disease and that is to correct the reasons why it first grew which deals with the deficiency. It’s only then that the body will self heal and remove the cancer naturally. Everybody has a self-healing mechanism called the immune system so all you have to do is to use it.

I am hoping that one day in the not too distant future, this way of treating cancer will be incorporated into our mainstream treatments and one would hope that, the power of the internet with the knowledge that’s now available to help people, might do that.

Our cancer industry nowadays is controlled by power and greed and nothing except money is to be gained by pretending that the battle against cancer is slowly but surely being won.

Effective cancer immunotherapy induces the killing of tumor cells by cytotoxic T lymphocytes (CTLs), resulting in tumor regression and a survival benefit for patients. Malignant tumors are often characterized by an intense proliferative capacity, and local to systemic invasiveness, and these lethal characteristics have rendered surgical resection, radiation treatment, and chemotherapy ineffective for many cancer patients. Tumors are also replete with antigens, resulting in immune recognition and significant immune-cell infiltrates, but tumor cells create microenvironments (e.g., production of immunosuppressive cytokines) that suppress anticancer activity. The potential for the innate immune system to react specifically and systemically against local and metastatic lesions, and to obtain memory that may prevent tumor recurrence has inspired the development of immunotherapies that seek to reprogram anticancer responses. A key challenge is to formulate treatment modalities that provide specific and persistent immunostimulation to sustain immune attack against tumor cells (predominantly by CTLs) until patients’ tumors are completely cleared

Current immunotherapeutic approaches are of two main types: cancer vaccines and adoptive T cell transfer. Cancer vaccines introduce tumor-associated antigens at the vaccine site and seek to cause tumor regression by relying on a cascade of events that are orchestrated by dendritic cells (DCs). Innate antigen recognition and processing is the responsibility of DCs, which, upon activation, have a potent ability to present tumor-antigens processed onto major histocompatibility complexes (MHC), and to translate pathogenic danger signals (e.g., lipopolysaccharides and bacterial DNA) into the expression of specific stimulatory molecules and cytokines. Activated DCs then migrate to lymphoid tissues to interact with nave T cells by presenting MHC-antigen peptides and immunostimulatory cytokines, which signal and propagate antigen-specific T cell differentiation and expansion The type and potency of the T cell response elicited by activated DCs, and, by extrapolation, cancer vaccines, depends on several factors: the type of antigen (endogenous versus exogenous), the microenvironment of the DC-antigen encounter, the extent of DC activation and the number of DCs that stimulate CTL differentiation and expansion. In contrast to vaccines, adoptive T cell transfer bypasses antigen delivery and mediators of T cell activation, by transfusing autologous or allogenic T cells that have been modified in ex vivo cultures and selected to target specific cancer antigens.

Although cancer vaccines and adoptive T cell transfers have induced CTL responses to specific tumor-associated antigens, and tumor regression in a subset of cancer patients, these treatments have failed to confer reproducible survival benefit. Clinical tests of cancer vaccines have utilized a variety of methods to deliver antigen, including delivery of bulk antigen in the form of tumor lysates and irradiated tumor cells or patient-derived DCs pulsated with tumor antigen in ex vivo cultures. Adjuvants and toll-like receptor (TLR) agonists are often mixed into vaccines to provide danger signals (factors associated with infectious microenvironments) in order to enhance DC maturation and amplify effector responses. However, the limitations of current approaches include short term antigen presentation and immunostimulation due to short, in vivo half-lives (within tissues and immune cells), and in the case of DC or T cell transplantation therapies, there is a rapid loss in cell viability and no control over cell function upon transplantation. The indiscriminate targeting and rapid loss of bioavailability and bioactivity in relation to current therapies likely reduces their efficiency, which limits DC and CTL activation resulting in transient to ineffective tumor attack. Intuitively, persistent induction of antitumor CTL activity is required to mediate tumor regression, and to clear large tumor burdens.

The development and application of immunologically active biomaterials that specifically target DCs and T cells, and regulate their responses to antigens and tumors are interest of study in present day Immunotechnology, which involves two biomaterial approaches that enable specific and sustained regulation of immune activity, and controlled immunostimulation: drug delivery and three-dimensional cell niches. Biopolymers of many different types have been formulated into particulate systems that control the bioavailability, the pharmacokinetics and the localization of proteins and nucleic acids, and we will discuss work to develop material vectors Immunologically for antigen and adjuvants with DC targeting ability. Moreover, as an alternative to approaches that utilize ex vivo cell manipulation (e.g., DC-based vaccines and Adoptive T cell transfer), biomaterials have been fashioned into biofunctional, three-dimensional matrices that create distinct, immunostimulatory microenvironments and regulate DC and T cell trafficking and activation in situ.

We also highlight the use of these delivery systems and niches to prime DC and T cell responses to tumors in animal models, and the prospects for their clinical impact in cancer immunotherapy. Sources and Inspiration for Biomaterials Biomaterials are derived from various combinations of natural or synthetic components, and, by definition, are intended to interact with biological systems. Biomaterials have historically been designed to augment cellular behavior that promotes tissue regeneration e.g., skin grafts or to replace tissue function [e.g., stents and prosthetics]; traditionally, these materials were fabricated to minimize host inflammatory and immune responses, due to their potentially destructive affects. However, our understanding of immunological regulation has progressed tremendously alongside the development of materials science, and at their intersection emerges the possibility to employ immunologically active biomaterials for cancer immunotherapy. In this section we discuss the sources and raw materials for the fabrication of biomaterial systems and the inspiration underlying their design as drug delivery agents and synthetic extracellular matrices to control cell processes.

Raw Materials

Nature provides numerous sources of structural proteins and polysaccharides, derived from plants and animals, that may be modified into immuno-active biomaterials. Natural materials, including collagen protein derived from the connective tissue of animals, chitosan polysaccharides extracted from the exoskeleton of crustaceans and alginate polysaccharides isolated from seaweed, have been fashioned into gels and utilized as drug delivery devices or as depots for cell transplantation. These materials have been utilized in the clinic for cosmetic and wound care applications with established biocompatibility. Further, the concentrations, molecular weight and crosslinking density of collagen, chitosan and alginate macromolecules can be modified to develop gels with defined degradation rates, stiffness, and functional groups, which can influence the release kinetics or binding of immunostimulatory biomolecules for drug delivery, or the viability and activation state of cells interacting with the material matrix.

Biodegradable devices may also be fabricated from a variety of synthetic polymers, and are frequently used as drug delivery vehicles. Polyglycolide (PGA), polylactide (PLA), and their copolymers polylactide-co-glycolide (PLG) which degrade, by hydrolysis, into the natural metabolites, lactic and glycolic acid, have been widely used in the clinic setting as biodegradable sutures, and are commonly fabricated into particulate systems for the controlled delivery of biomolecules. Polyanhydrides are another class of biodegradable materials that have been utilized as drug delivery vehicles, such as wafers for the clinical delivery of chemotherapeutic agents at the site of glioblastoma resection and as investigative vaccine carriers. In addition, liposome particles (phospholipid bilayers) and block copolymers with hydrophobic and hydrophilic domains are assembled into vesicles or micelle carriers that encapsulate proteins and nucleic acids to protect them from in vivo degradation and for their controlled release.

Controlled Delivery and Cell Targeting

Engineering solutions are needed for delivering therapeutic biomolecules to specific sites of treatment with controlled kinetics, which has inspired the development of biomaterials as delivery vehicles. Molecular therapeutics form the basis for the prevention and treatment of many human diseases; however, their use is limited by short in vivo half-lives which limits their bioavailability to target cells and tissues. Therefore, in some cases, multiple, systemic administrations of therapeutic molecules are utilized to prolong therapeutic stimulation but this increases nonspecific cell/tissue exposure and may cause severe adverse reactions, which limits the time-course and benefit of treatment.

Biomaterials are now tailored with defined physical properties such as degradation mechanisms and rates, and specialized surface characteristics, that protect encapsulated bioactive molecules against degradation in vivo, control their release kinetics and allow for specific cellular targeting in vivo. To efficiently target therapeutic agents (e.g., immunostimulatory cytokines), researchers are developing sophisticated micro- and nano-particulate systems that carry particular surface molecules (e.g., antibodies) Immunologically to recognize and bind to specific cells. The size and surface properties of these particulate systems are also modified to control particle localization within specified tissues and body compartments (e.g., lymphoid tissues). Material carriers are not only designed to encapsulate and protect proteins and nucleic acids from degradation in vivo, but they may also be designed with specific degradation properties allowing the delivery of its bioactive load at specific tissue locations or, for intercellular delivery, at defined intervals within the cell-internalization pathway.

Synthetic ECMs

The natural extracellular matrix (ECM), in structure and function, has inspired the development and application of three-dimensional biomaterial systems that produce distinct microenvironments that transmit chemical and mechanical cues to cells in situ. The interstitial space of tissues contains fibrous ECM proteins (for example, collagens and laminins), and gels of polysaccharides like glycosaminoglycan and heparin sulfate.

The ECM presents a variety of cell adhesion ligands, provides support and anchorage for cells, regulates cellular communication/migration, and sequesters a wide range of cellular growth factors – to act as a local depot. The ECM components and the corresponding degradative enzymes are produced by resident cells in response to local stimuli (e.g., inflammation), which may cause ECM remodeling and a redistribution of cell signals until homeostasis is reachieved between cells and matrix. Thus, the ECM interacts dynamically with cells to regulate their processes, and this ability may be translated to biomaterial systems.

Three-dimensional biomaterial constructs are now engineered to provide the necessary structural support as synthetic ECMs for cell transplantation and delivery, as long-term depots for the controlled presentation of bioactive molecules, and as niches with controlled microenvironments that regulate cell function. The porosity and degradation rate of these materials may be optimized to provide a residence for cells, and to regulate host cell infiltration or cell deployment for therapy. Adhesion ligands may be patterned onto biomaterial surfaces to orient the spatial distribution of cells and cell-cell communication like immune synapes.

Cancer today is well understood, there is no mystery to the disease and all cancers appear for a reason. It is not caused by bad genes or something beyond our control. It appeared because of a weakened immune system, our built in repair system that keeps us healthy, which didn’t stop normal body cells from mutating and becoming cancerous. There are many changes you can make to help rid the body of any of these unwanted growths and especially to stop it spreading. To survive cancer it’s important to make these changes.

It is well known that what you eat can have a profound effect on strengthening the immune system. I know people don’t want to change the food they eat, they just want to take a pill but unfortunately that approach doesn’t work with degenerative diseases such as cancer. There are many changes you can make to the way you live and especially the food you choose to eat which will increase your odds of success in overcoming the disease.

How did we ever believe that when someone is diagnosed with cancer, there are only three ways to treat it? Not only are these ways toxic to the human body and causing harm, they are not even effective. The cancer industry is built on the foundation of just treating the symptoms while doing virtually nothing to treat the actual cause of the problem which is far more important.

Our orthodox medical system is extremely powerful, has virtually no competition which is dangerous for the user, and because of the vast amounts of money spends on advertising their drugs, has a huge control over the media. Today we are being educated about cancer from television and newspapers so be wary. Many of the facts about the disease we hear or read are not true and we are paying the price with our lives.

For instance dealing with only the symptom which is the cancer growths themselves is often of little help if it’s only going to return again. The growth is only a symptom and not the problem and the only way to fix the problem is to deal with the initial cause or the reason why cancer first appeared. To do this, all you need is knowledge and it does make a difference.

Healthy people don’t get cancer because healthy people eat mainly fresh food including raw food; they drink water to hydrate the body. They get adequate amounts of sunshine for the important vitamin D we need and they get plenty of exercise, rest and fresh air. These are called the necessities of life and will solve any problem caused by a degenerative disease. Remember the human body has amazing powers of restoration but it needs your help.

Another fact you won’t be told, it is vitally important for cancer patients to limit their refined sugar intake as cancer cells create energy to grow and spread by fermenting sugar. This fact has been known for over 80 years yet our doctors today are ignorant of this. Also the chemicals that are in circulation nowadays are not well regulated and many of them are causing us harm.

The solution is to change the factors that led to the cancer in the first place. In the long term it’s the only thing that really works.