Potential New Treatment Target Identified for Melanoma Skin Cancer

— New research from Western University has identified a potential new target for the treatment of melanoma, the deadliest of all skin cancers.
Silvia Penuela and Dale Laird have discovered a new channel-forming protein called Pannexin (Panx1) that is expressed in normal levels on the surface of healthy skin cells. But they found, in melanoma, Panx1 is over-produced to a pathological level.
The research is published in the August 17^th issue of the Journal of Biological Chemistry.
Malignant melanoma only accounts for four per cent of all skin cancers, and yet it's responsible for 79 per cent of skin cancer-related deaths. The World Health Organization says there are 200,000 cases of melanoma diagnosed each year and 65,000 melanoma-related deaths (2000 statistics).
"We think this over-production of Panx1 enables the melanoma to become very aggressive. The cells have these extra Panx1 channels and they can leave the primary tumor and invade other tissues," explained Laird, a Professor in the Department of Anatomy and Cell Biology.
"And when you find a protein that is highly up-regulated in a disease cell such as a melanoma, the question becomes, is there therapeutic value in targeting a drug to that protein to reduce its production or block its function. Would that be an effective treatment?"
"We now want to correlate our discovery to patient samples using the human melanoma bank through our collaboration with Dr. Muriel Brackstone and other clinicians at the London Health Sciences Centre, to see if this is a cancer marker," added Penuela, a Postdoctoral Fellow working in the Laird lab.
"So if a melanoma lesion has a lot of this protein, it might be a tool for prognosis, in saying this is more advanced, or going to be highly metastatic. And because it's on the skin, it would be more accessible for treatment."
Penuela suggests potential treatment might be in the form of a topical medication to use on melanoma lesions.

Missing Pieces of DNA Structure Is a Red Flag for Deadly Skin Cancer

— Melanoma is the most dangerous type of skin cancer and is the leading cause of death from skin disease. Rates are steadily increasing, and although risk increases with age, melanoma is now frequently seen in young people.

But what if we could pinpoint when seemingly innocuous skin pigment cells mutate into melanoma? Researchers at Brigham and Women's Hospital (BWH) have achieved this. Teams led by Yujiang Geno Shi, PhD, from BWH's Department of Medicine, and George F. Murphy, MD, from BWH's Department of Pathology have discovered a new biomarker for the lethal disease. The findings offer novel opportunities for skin cancer diagnostics, treatment and prevention.

The study will be published on Sept. 14, 2012 in Cell.

"Dr. Shi and colleagues have discovered an exciting new connection between the loss of a specific chemical mark in the genome and the development of melanoma," said Anthony Carter, PhD, of the National Institutes of Health's National Institute of General Medical Sciences, which mainly funded the research. "This work is a prime example of how basic research on mechanisms of epigenetic regulation can yield clinically significant insights that hold great promise for diagnosing and treating cancer."

The researchers found that certain biochemical elements in the DNA of normal pigment-producing skin cells and benign mole cells are absent in melanoma cells. Loss of these methyl groups -- known as 5-hmC -- in skin cells serves as a key indicator for malignant melanoma. Loss corresponded to more advanced stages of melanoma as well as clinical outcome.

Strikingly, researchers were able to reverse melanoma growth in pre-clinical studies. When the researchers introduced enzymes responsible for 5-hmC formation to melanoma cells lacking the biochemical element, they saw that the cells stopped growing.

"It is difficult to repair the mutations in the actual DNA sequence that are believed to cause cancer," said Christine Lian, MD, a physician scientist in the Department of Pathology at BWH and one of the lead authors. "So having discovered that we can reverse tumor cell growth by potentially repairing a biochemical defect that exists -- not within the sequence -- but just outside of it on the DNA structure, provides a promising new melanoma treatment approach for the medical community to explore."

Because cancer is traditionally regarded as a genetic disease involving permanent defects that directly affects the DNA sequence, this new finding of a potentially reversible abnormality that surrounds the DNA (thus termed epigenetic) is a hot topic in cancer research, according to the researchers.

In the United States, melanoma is the fifth most common type of new cancer diagnosis in men and the seventh most common type in women. The National Cancer Institute estimates that in 2012 there will be 76,250 new cases and 9,180 deaths in the United States due to melanoma.

The Shi laboratory pioneers studies in both basic chromatin biology and translational epigenetic research at the Endocrine Division, BWH Department of Medicine, and collaborates with Dr. Murphy's laboratory that focuses on melanoma biology in the Program for Dermatopathology, BWH Department of Pathology. This pre-clinical study, which shows a key role for epigenetics in melanoma development and progression, also enlisted the support of an international team of investigators.

The findings will provide insight for future functional, pre-clinical studies of 5-hmC in cancer biology.

Geneticists Verify Cholesterol-Cancer Link

— University of Rochester Medical Center scientists discovered new genetic evidence linking cholesterol and cancer, raising the possibility that cholesterol medications could be useful in the future for cancer prevention or to augment existing cancer treatment.

The data, published in the online journal Cell Reports, support several recent population-based studies that suggest individuals who take cholesterol-lowering drugs may have a reduced risk of cancer, and, conversely that individuals with the highest levels of cholesterol seem to have an elevated risk of cancer.

The cancer-cholesterol question has been debated since the early 20^thcentury, and along with it doctors and scientists have observed various trends and associations. However, until now genetic evidence directly linking cholesterol and malignancy has been lacking, said senior author Hartmut (Hucky) Land, Ph.D., Robert and Dorothy Markin Professor and chair, Department of Biomedical Genetics, and director of research and co-director of the James P. Wilmot Cancer Center at URMC.

Cholesterol is a fat-like substance supplied in foods and made in cells throughout the body. Too much cholesterol is bad for the heart and vascular system. It is typically measured as serum cholesterol by routine blood tests.

Unlike serum cholesterol that is bound to proteins, however, cholesterol also hides inside cells. While locked inside cell membranes before it is eventually exported, cholesterol has an impact on cell growth and survival. A gene, known as ABCA1, is at the crossroads of the process that shuttles intracellular cholesterol outbound.

Several years ago while conducting unrelated experiments that were published in the journal Nature, Land and colleagues first noticed the importance of ABCA1. At that time, they identified a network of approximately 100 so-called "cooperation response genes" that mediate the action of cancer genes. ABCA1 was found among these genes and is frequently turned off in presence of other mutant cancer genes.

In the latest investigation, Land and co-author Bradley Smith, Ph.D., a post-doctoral fellow in the Land lab, wanted to further understand the role of ABCA1 and cholesterol in cancer. They found that defective cholesterol exportation appears to be a key component in a variety of cancers.

The proper function of ABCA1 is critical for sensing of cell stress. If ABCA1 function is lost in cancer cells, cholesterol is allowed to build up in the cells' mitochondria, or energy centers, making their membranes more rigid. This in turn inhibits the function of cell-death triggers that normally become activated in response to cell stresses, as for example cancer gene activation. Therefore, when functioning properly, ABCA1 has anti-cancer activity -- in the sense that by keeping mitochondrial cholesterol low it protects the functioning of cellular stress response systems and acts as a barrier to tumor formation and progression.

Smith and Land also demonstrated that some of the relatively rare ABCA1 mutations found in human colon cancers by other investigators disabled the gene's ability to export cholesterol. And by re-establishing the cholesterol export function in human colon cancer cells, they inhibited the cells' ability to grow as cancers when grafted onto mice.

The URMC study, therefore, is the first to directly show how ABCA1 loss-of-function and cholesterol may play a role in cancer. "Scientifically it is very satisfying to have data that support longstanding ideas about cholesterol in the context of cancer," Land said. "Our paper provides a rationale for cholesterol targeting as a potentially fruitful approach to cancer intervention or prevention strategies."

Millions of Americans take cholesterol-lowering drugs or statins, as prescribed by physicians. Clinical trials also are evaluating statins as a tool against cancer, and some previous studies suggest that when used in combination with chemotherapy, statins might make chemotherapy more effective by sensitizing certain cancer cells to chemotherapy-induced cell death.

Land, however, urges caution and further study. Doctors do not know the appropriate statin dose for cancer prevention or treatment of cancer-related conditions. Side effects cannot be ignored either, and little research has distinguished between the responses among people who take statins.

"The link between cholesterol and cancer is clear," Land said, "but it's premature to say that statins are the answer."

The National Institutes of Health grants CA90663, CA120317 and CA138249 funded the research.

In Lung Cancer, Smokers Have 10 Times More Genetic Damage Than Never-Smokers

— Lung cancer patients with a history of smoking have 10 times more genetic mutations in their tumors than those with the disease who have never smoked, according to a new study from Washington University School of Medicine in St. Louis.

"None of us were surprised that the genomes of smokers had more mutations than the genomes of never-smokers with lung cancer," says senior author Richard K. Wilson, PhD, director of The Genome Institute at Washington University. "But it was surprising to see 10-fold more mutations. It does reinforce the old message -- don't smoke."

The study appears online Sept. 13 inCell.

Overall, the analysis identified about 3,700 mutations across all 17 patients with non-small cell lung cancer, the most common type. Twelve patients had a history of smoking and five did not. In each patient who never smoked, the researchers found at least one mutated gene that can be targeted with drugs currently on the market for other diseases or available through clinical trials. Across all patients, they identified 54 mutated genes already associated with existing drugs.

"Whether these drugs will actually work in patients with these DNA alterations still needs to be studied," says first author Ramaswamy Govindan, MD, an oncologist who treats patients at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University. "But papers like this open up the landscape to understand what's happening. Now we need to drill deeper and do studies to understand how these mutations cause and promote cancer, and how they can be targeted for therapy."

Lung cancer is divided into two types -- small cell and non-small cell, the latter accounting for about 85 percent of all cases. Within non-small cell lung cancer are three further classifications. This current analysis included two of them. Sixteen patients had adenocarcinoma and one had large-cell carcinoma.

Govindan and Wilson also were involved in a larger genomic study of 178 patients with the third type, squamous cell carcinoma, recently reported in Nature. That study was part of The Cancer Genome Atlas project, a national effort to describe the genetics of common cancers.

"Over the next year or so, we will have studied nearly 1,000 genomes of patients with lung cancer, as part of The Cancer Genome Atlas," says Govindan, who serves as a national co-chair of the lung cancer group. "So we are moving in the right direction -- toward future clinical trials that will focus on the specific molecular biology of the patient's cancer."

Indeed, based on the emerging body of genetic research demonstrating common mutations across disparate cancer types, Wilson speculates that the field may reach a point where doctors can label and treat a tumor based on the genes that are mutated rather than the affected organ. Instead of "lung cancer," for example, they might call it "EGFR cancer," after the mutated gene driving tumor growth. Mutations in EGFRhave been found in multiple cancers, including lung, colon and breast.

This labeling is relevant, Wilson says, because today targeted therapies are approved based on the diseased organ or tissue. Herceptin®, for example, is essentially a breast cancer drug. But he has seen lung cancer patients with mutations in the same gene that Herceptin targets.

"For example, if genome sequencing revealed that a lung cancer patient has a mutation known to be sensitive to a drug that works in breast tumors with the same genetic alteration, you may want to use that agent in those lung cancer patients, ideally as part of a clinical trial," he says. "In the coming years, we hope to be treating cancer based more on the altered genetic make-up of the tumor than by the tissue of origin."

Lack of Oxygen in Cancer Cells Leads to Growth and Metastasis

— It seems as if a tumor deprived of oxygen would shrink. However, numerous studies have shown that tumor hypoxia, in which portions of the tumor have significantly low oxygen concentrations, is in fact linked with more aggressive tumor behavior and poorer prognosis. It's as if rather than succumbing to gently hypoxic conditions, the lack of oxygen commonly created as a tumor outgrows its blood supply signals a tumor to grow and metastasize in search of new oxygen sources -- for example, hypoxic bladder cancers are likely to metastasize to the lungs, which is frequently deadly.

A University of Colorado Cancer Center study recently published in the journal Cancer Research details a mechanism by which these hypoxic conditions create aggressive cancer, with possible treatment implications for cancers including breast, ovarian, colorectal, pancreatic, prostate, bladder and other cancers.

"We've known that the protein HIF-1a is overexpressed in hypoxic tumors. And we've known that the cancer stem cell marker CD24 is overexpressed in many tumors. This study shows a link between the two -- the HIF-1a of hypoxia creates the overexpression of CD24. And it's this CD24 that creates a tumor's aggressive characteristics of growth and metastasis," says Dan Theodorescu, MD, PhD, director of the University of Colorado Cancer Center and the paper's senior author.

Outgrowing the blood supply leads to tumor hypoxia, which leads to overexpression of HIF-1a, which signals the production of CD24, which makes tumors grow and metastasize. In addition to aggression, CD24 has also been shown to confer resistance to chemotherapy, allowing this small population of cells to regrow the tumor once chemotherapy ends, leading to relapse and disease progression.

"Now imagine we target CD24," Theodorescu says. "Either by removing a cell's ability to make CD24 or by killing cells marked by this protein, it's likely we could disarm this most dangerous population of cells."

Theodorescu and colleagues showed this by adjusting levels of HIF-1a and CD24 in cancer cell samples and animal models. With HIF-1a low and yet CD24 artificially high, cells retained the ability to grow and metastasize. With CD24 low and yet HIF-1a artificially high, cell survival and proliferation decreased.

"It seems CD24 overexpression in hypoxic cells drives growth and metastasis in these hypoxic tumors," Theodorescu says. "Now we have a rational target: CD24 for these hypoxic tumors."

Chemists Develop Nose-Like Array to 'Smell' Cancer

— In the fight against cancer, knowing the enemy's exact identity is crucial for diagnosis and treatment, especially in metastatic cancers, those that spread between organs and tissues. Now chemists led by Vincent Rotello at the University of Massachusetts Amherst have developed a rapid, sensitive way to detect microscopic levels of many different metastatic cell types in living tissue.

Findings appear in the current issue of the journal ACS Nano.

In a pre-clinical non-small-cell lung cancer metastasis model in mice developed by Frank Jirik and colleagues at the University of Calgary, Rotello's team at UMass Amherst use a sensor array system of gold nanoparticles and proteins to "smell" different cancer types in much the same way our noses identify and remember different odors. The new work builds on Rotello and colleagues' earlier development of a "chemical nose" array of nanoparticles and polymers able to differentiate between normal cells and cancerous ones.

Rotello explains, "With this tool, we can now actually detect and identify metastasized tumor cells in living animal tissue rapidly and effectively using the 'nose' strategy. We were the first group to use this approach in cells, which is relatively straightforward. Now we've done it in tissues and organs, which are very much more complex. With this advance, we're much closer to the promise of a general diagnostic test."

Until now the standard method for precisely identifying cancer cells used a biological receptor approach, a protein binding to a cancer cell wall. Its major drawback is that one must know the appropriate receptor beforehand. Rotello and colleagues' breakthrough is to use an array of gold nanoparticle sensors plus green fluorescent protein (GFP) that activates in response to patterns in the proteins found in cancer cells within minutes, assigning a unique signature to each cancer.

The chemist says, "Smell 'A' generates a pattern in the nose, a unique set of activated receptors, and these are different for every smell we encounter. Smell 'B' has a different pattern. Your brain will instantly recognize each, even if the only time you ever smelled it was 40 years ago. In the same way, we can tune or teach our nanoparticle array to recognize many healthy tissues, so it can immediately recognize something that's even a little bit 'off,' that is, very subtly different from normal. It's like a 'check engine' light, and assigns a different pattern to each 'wrong' tissue. The sensitivity is exquisite, and very powerful."

For this work, the researchers took healthy tissue and mouse tumor samples and trained the nanoparticle-GFP sensor array to recognize them and the GFP to fluoresce in the presence of metastatic tissue. Metastases are differentiated from healthy tissue in a matter of minutes, providing a rapid and very general means of detecting and identifying cancer and potentially other diseases using minimally invasive microbiopsies.

"It's sensitive to really subtle differences," says Rotello. "Even though two cheeses may look the same, our noses can tell a nicely ripe one from a cheese that's a few days past tasting good. In the same way, once we train the sensor array we can identify whether a tissue sample is healthy or not and what kind of cancer it is with very high accuracy. The sensitivity is impressive from a sample of only about 2,000 cells, a microbiopsy that's less invasive for patients."

In addition to the high sensitivity, the authors point out, their sensor is able to differentiate between low (parental) and high (bone, adrenal, and ovary) metastases, as well as between site-specific cells such as breast, liver, lung and prostate cancers.

"Overall, this array-based sensing strategy presents the prospect of unbiased phenotype screening of tissue states arising from genetic variations and differentiation state." Their next step will be to test the new sensor array method in human tissue samples, the researchers say.

Cancer - A Synonym of Death

Cancer is not a new dub for the people breathing in the 21st century. It is as recurrent as our day to day usual activities. Every year about a million of new cases of cancer are diagnosed throughout the world. Most people loose their lives because of cancer. Treatment are available but there is still no 100% surety of recovery from cancer. Cancer influences almost every organ of human body transfiguring it into ruins in later stages.
Truly speaking cancer is not a single disease, but a heterogeneous group of disorders that are characterized by the presence of cells that loose control on normal cell division. Cancer cells divide rapidly and continuously resulting in formation of tumours that eventually strike healthy tissues. These tumourous cells travel across healthy cells creating tumours in them. The most frequent cancers include cancers of breast, lung, prostrate, blood, colon, rectum, pancreas, liver etc.
Formation of Tumour
Basically normal cells grow, divide, mature and die in response to a complex set of internal and external signals. A normal cell receives both stimulatory as well as inhibitory signals which are responsible for its growth, division and maturation. In case of a cancer cell, these signals get disrupted, so the cell divides abnormally at a higher rate. After losing normal control, the cancer cell loose its normal shape and forms a distinct mass what we call a 'tumour'. If the cells of a tumour remain localized it is termed a 'benign tumour' but if the cells invade other tissues, the tumour is termed as 'malignant tumour'. Cells that travel to other sites of the body, they form secondary tumours and have undergone 'metastasis'.
Cancer- The Genetic Aspect
Cancer is the culmination of abnormal cell growth so needs attention both publicly as well as scientifically. A number of theories have been put forward regarding cancer but now researchers realize that most if not all cancers arise from the defects in DNA> Previous views recommend the genetic origin of cancer. Many agents like ionizing radiations, chemicals that we come across result in episode of mutations that cause cancer. Some cancers are often syndicated with chromosomal abnormalities, about 90% of people with chronic myeloid leukemia bear a reciprocal trans location between chromosome 22 and chromosome 9> These observations accord clues for the genetic origin of cancer. In 1971 Alfred Knudson proposed a model for defining the genetic basis of cancer. His model id designated as 'Knudson multistep model of cancer', he was studying retinoblastoma- a cancer that develops in only one eye but occasionally appears in both> Knudson's proposal highlights that cancer is a multistep process requiring several mutations, if one or more mutations are inherited additional mutations are also obligatory to disclose a cancer and the cancer will run in families. His model has been confirmed today.
Cancer starts when a single cell is encountered with mutation and results in its abnormal growth. This cell divides and forms a clone of cells each carrying same mutation. An additional mutation that occurs in any of the clone cells may further enhance adroitness of these cells to burgeon and cells with both mutations become dominant. In this process, depicted as clonal evolution, the tumour cells gain more mutations that allow them to become increasingly aggressive in their proliferate aspects. The rate of clonal evolution depends upon the frequency of occurrence of new mutations. The genes that regulate DNA repair have also been found to get mutated in progressive cancer stages and inherited disorders of DNA repair are usually depicted by intensified incidences of cancer. Normally DNA repair mechanisms eliminate many of the mutations but cells with defective DNA repair systems are more likely to remain mutated including the genes that regulate cell division. Many cells are aneuploid and hence accelerate cancer progression.
Are Environmental Factors Also Responsible For Cancer?
Smoking is a good paradigm of environmental factor confronted with cancer strongly. Other environmental factors incorporate certain types of chemicals such as benzene (industrial solvent), benzo [a] pyrene (cigarette smoke), polychlorinated biphenyls (transformers and capacitors). Ultraviolet light, ionizing radiations, viruses are other carcinogens associated with cancer. Most environmental factors cause somatic mutations that quicken cell division.
Genes Contributing Cancer
The signals that regulate cell division fall under two categories: molecules that speed up cell division and others that inhibit it. Because cell division is perturbed by these two factors, cancer can arise from mutations in any of these two factors. Mutations in stimulatory genes are usually dominant and are termed 'oncogenes'. Oncogenes were first identified cancer causing genes discovered by Peyton Rous in 1909. Michael Bishop, Harold Varmus and their colleagues in 1975 discovered that genomes of all normal cells carry DNA sequences that are closely related to viral oncogenes. These cellular genes are termed as protoncogenes. THey are blameworthy for basic cellular functions of normal cells but when mutated they become oncogenes and produce cancer. Many oncogenes have been pinpointed by experiments in which selectted fragments of DNA are added to cells in a culture.
Tumour suppressor genes are more difficultly discerned than oncogenes as they inhibit cancer and are reccessive in action. One of the first tumour suppressor gene to be spotted out was that of retinoblastoma in 1985 by Raymond White and Webster Cavenne.
Alteration In Stucture And Number Of Chromosome Also Cause Cancer
Most tumours possess mutations. It is now clear that mutations in chromosomes appear to be both cause and be a result of cancer. At least three kinds of chromosome rearrangements- deletions, inversions and trans locations may be associated with cancer. Deletions may result in loss of one or more tumour suppressor genes. Inversions and trans locations may result in disruption of functions tumour suppressor genes and generation of fused proteins that may stimulate symptoms of cancer. Fusion proteins are generally formed in myelogenous leukemia, a form of leukemia affecting bone marrow cells. A third process by which cancer may arise due to chromosomal rearrangement is by the transfer of a potential cancer causing gene to a new location where it is activated by regulatory sequences, Burkitt lymphoma is common example.
Viruses Also Cause Cancer
About 95% of the women with cervical cancer are infected with human papiloma viruses (HPVs). Similarly, infection with the virus that causes hepatitis B increases the risk of liver cancer. Epstein-Barr virus causes mononucleosis embracing Burkitt's lymphoma. There are only few retroviruses that cause cancer in humans. Other human cancers are associated with DNA viruses which like retroviruses integrate into the host chromosome but disparate retroviruses donot reverse transcription.
Changes In DNA Methylation Are Often Associated With Cancer
In many cancerous cells the ornamentation of DNA methylation are found to be altered. In some cases, the DNA of cancer cells is over methylated (hypermethylated) or undermethylated (hypomethylated). Hypermethylation is seen to contribute to cancer by silencing the expression of tumour suppressor genes. However, hypomethylation also contributes to cancer requires further research. The role of DNA methylation is interesting because unlike other genetic changes DNA methylation is reversible. These types of reversible genetic alterations are called epigenetic processes.
The treatment of cancer is accessible at present inclusive of chemotherapy, bone marrow transplantation, radiotherapy etc. but the question to be 100% free from cancer still preponderates.

Cancer is Not a Disease - It's a Survival Mechanism

It will perhaps astound you to learn that a person who is afflicted with the main causes of cancer (which constitute the real illness) would most likely die quickly unless he actually grew cancer cells. In this work, I provide evidence to this effect.
I further claim that cancer will only occur after all other defense or healing mechanisms in the body have failed. In extreme circumstances, exposure to large amounts of cancer-producing agents (carcinogens) can bring about a collapse of the body's defenses within several weeks or months and allow for rapid and aggressive growth of a cancerous tumor. Usually, though, it takes many years, or even decades, for these so-called "malignant" tumors to form.
Unfortunately, basic misconceptions or complete lack of knowledge about the reasons behind tumor growth have turned "malignant" tumors into vicious monsters that have no other purpose but to kill us in retaliation for our sins or abusing the body. However, as you are about to find out, cancer is on our side, not against us. Unless we change our perception of what cancer really is, it will continue to resist treatment, particularly the most "advanced" methods. If you have cancer, and cancer is indeed part of the body's complex survival responses and not a disease, as I suggest it is, you must find answers to the following pressing questions:
* What reasons coerce your body into developing cancer cells?
* Once you have identified these reasons, will you be able to change them? What determines the type and severity of cancer with which you are afflicted?
* If cancer is a survival mechanism, what needs to be done to prevent the body from taking recourse to such drastic defense measures?
* Since the body's original genetic design always favors the preservation of life and protection against adversities of any kind, why would the body permit self-destruction?
* Why do almost all cancers disappear by themselves, without medical intervention?
* Do radiation, chemotherapy and surgery actually cure cancer, or do cancer survivors heal due to other reasons, despite these radical, side-effect-loaded treatments?
* What roles do fear, frustration, low self-worth and repressed anger play in the origination and outcome of cancer?
* What is the spiritual growth lesson behind cancer?
To deal with the root causes of cancer, you must find satisfying and practical answers to the above questions. If you feel the inner urge to make sense of this life-changing event, (cancer that is), you most likely will recover from it. Cancer can be your greatest opportunity to help restore balance to all aspects of your life, but it can also be the harbinger of severe trauma and suffering. Either way you are always in control of your body.
To live in a human body, you must have access to a certain amount of life-sustaining energy. You may either use this inherent energy in a nourishing and self-sustaining or in a destructive and debilitating way. In case you consciously or unconsciously choose negligence or self-abuse over loving attention and self-respect, your body will likely end up having to fight for its life.
Cancer is but one of the many ways the body tries to change the way you see and treat yourself, including your body. This inevitably brings up the subject of spiritual health, which plays at least as important a role in cancer as physical and emotional reasons do.
Cancer appears to be a highly confusing and unpredictable disorder. It seems to strike the very happy and the very sad, the rich and the poor, the smokers and the non-smokers, the very healthy and the not so healthy. People from all backgrounds and occupations can have cancer. However, if you dare look behind the mask of its physical symptoms, such as the type, appearance and behavior of cancer cells, you will find that cancer is not as coincidental or unpredictable as it seems to be.
What makes 50% of the American population so prone to developing cancer, when the other half has no risk at all? Blaming the genes for that is but an excuse to cover up ignorance of the real causes. Besides, any good genetic researcher would tell you that such a belief is void of any logic and outright unscientific (as explained in the book).
Cancer has always been an extremely rare illness, except in industrialized nations during the past 40-50 years. Human genes have not significantly changed for thousands of years. Why would they change so drastically now, and suddenly decide to kill scores of people? The answer to this question is amazingly simple: Damaged or faulty genes do not kill anyone. Cancer does not kill a person afflicted with it! What kills a cancer patient is not the tumor, but the numerous reasons behind cell mutation and tumor growth. These root causes should be the focus of every cancer treatment, yet most oncologists typically ignore them. Constant conflicts, guilt and shame, for example, can easily paralyze the body's most basic functions, and lead to the growth of a cancerous tumor.
After having seen thousands of cancer patients over a period of three decades, I began to recognize a certain pattern of thinking, believing and feeling that was common to most of them. To be more specific, I have yet to meet a cancer patient who does not feel burdened by some poor self-image, unresolved conflict and worries, or past emotional trauma that still lingers in his/her subconscious. Cancer, the physical disease, cannot occur unless there is a strong undercurrent of emotional uneasiness and deep-seated frustration.
Cancer patients typically suffer from lack of self-respect or worthiness, and often have what I call an "unfinished business" in their life. Cancer can actually be a way of revealing the source of such inner conflict. Furthermore, cancer can help them come to terms with such a conflict, and even heal it altogether. The way to take out weeds is to pull them out along with their roots. This is how we must treat cancer; otherwise, it may recur eventually.
The following statement is very important in the consideration of cancer: "Cancer does not cause a person to be sick; it is the sickness of the person that causes the cancer." To treat cancer successfully requires the patient to become whole again on all levels of his body, mind and spirit. Once the cancer causes have been properly identified, it will become apparent what needs to be done to achieve complete recovery.
It is a medical fact that every person has cancer cells in the body all the time. These cancer cells remain undetectable through standard tests until they have multiplied to several billion. When doctors announce to their cancer patients that the treatments they prescribed had successfully eliminated all cancer cells, they merely refer to tests that are able to identify the detectable number of cancerous cells. Standard cancer treatments may lower the number of cancer cells to an undetectable level, but this certainly cannot eradicate all cancer cells. As long as the causes of tumor growth remain intact, cancer may redevelop at any time and at any rate.
Curing cancer has little to do with getting rid of a group of detectable cancer cells. Treatments like chemotherapy and radiation are certainly capable of poisoning or burning many cancer cells, but they also destroy healthy cells in the bone marrow, gastrointestinal tract, liver, kidneys, heart, lungs, etc., which often leads to permanent irreparable damage of entire organs and systems in the body. A real cure of cancer does not occur at the expense of destroying other vital parts of the body.
Each year, hundreds of thousands of people who were once "successfully" treated for cancer die from infections, heart attacks, liver failure, kidney failure and other illnesses because the cancer treatments generate a massive amount of inflammation and destruction in the organs and systems of the body. Of course, these causes of death are not being attributed to cancer. This statistical omission makes it appear we are making progress in the war against cancer. However, many more people are dying from the treatment of cancer than from cancer. A real cure or cancer is achievable only when the causes of excessive growth of cancer cells have been removed or stopped.
Power in the Word
Cancer is the second leading "cause" of death for Americans. According to the American Cancer Society, about 1.2 million cases will be diagnosed with cancer in the U.S. in 2008. More than 552,000 Americans will die of it. Among men, the top three cancer diagnoses are expected to be prostate cancer (180,400 cases), lung cancer (89,500 cases), and colorectal cancer (63,600). The leading types of cancer among women are breast cancer (182,800 cases), lung cancer (74,600), and colorectal cancer (66,600 cases).
Cancer is not just a word, but also a statement that refers to abnormal or unusual behavior of cells in the body. However, in quite a different context, cancer is referred to as a star sign. When someone tells you that you are a "cancer", are you going to tremble with fear of dying? It is unlikely, because your interpretation of being of the cancer sign does not imply that you have cancer, the illness. But if your doctor called you into his office and told you that you had cancer, you would most likely feel paralyzed, numb, terrified, hopeless, or all of the above.
The word "cancer" has the potential to play a very disturbing and precarious role, one that is capable of delivering a death sentence. Being a cancer patient seems to start with the diagnosis of cancer, although its causes may have been there for many years prior to feeling ill. Within a brief moment, the word "cancer" can turn someone's entire world upside down.
Who or what in this world has bestowed this simple word or statement with such great power that it can preside over life and death? Or does it really? Could it actually be that our collective, social belief that cancer is a killer disease, in addition to the aggressive treatments that follow diagnosis, are largely responsible for the current dramatic escalation of cancer in the Western hemisphere? Too far fetched, you might say! In this book, however, I will make the point that cancer can have no power or control over us, unless we unconsciously allow it to grow in response to the beliefs, perceptions, attitudes, thoughts, feelings we have, and the life choices we make.
Would we be just as afraid of cancer if we knew what caused it or at least understood what its underlying purpose is? Unlikely so! If truth were told, we would most probably do everything to remove the causes and, thereby, set the preconditions for the body to heal itself.
A little knowledge (which is what we call ignorance) is, in fact, a dangerous thing. Almost everyone, at least in the industrialized world, knows that drinking water from a filthy pond or polluted lake can cause life-threatening diarrhea, but still only few realize that holding on to resentment, anger and fear, or eating fast foods, chemical additives, and artificial sweeteners, is no less dangerous than drinking polluted water; it may just take a little longer to kill a person than tiny amoeba can.
Mistaken Judgment
We all know that if the foundation of a house is strong, the house can easily withstand external challenges, such as a violent storm. As we will see, cancer is merely an indication that there is something missing in our body and in life as a whole. Cancer shows that life as a whole (physical, mental and spiritual) stands on shaky grounds and is quite fragile, to say the least. It would be foolish for a gardener to water the withering leaves of a tree when he knows so well that the real problem is not where it appears to be, namely, on the symptomatic level (of withered leaves). By watering the roots of the plant, he naturally attends to the causative level, and consequently, the plant regenerates itself swiftly and automatically.
To the trained eye of a gardener, the symptom of withering leaves is not a dreadful disease. He recognizes that the dehydrated state of these leaves is but a direct consequence of withdrawn nourishment that they need in order to sustain themselves and the rest of the plant.
Although this example from nature may appear to be a simplistic analogy, it offers a profound understanding of very complex disease processes in the human body. It accurately describes one of the most powerful and fundamental principles controlling all life forms on the planet. However skilled we may have become in manipulating the functions of our body through the tools of allopathic medicine, this basic, highly evolved principle of evolution cannot be suppressed or violated without paying the hefty price of side-effect-riddled suffering and pain - physically, emotionally and spiritually.
I fervently challenge the statement that cancer is a killer disease. Furthermore, I will demonstrate that cancer is not a disease at all. Many people who received a "terminal" cancer sentence actually defied the prognosis and experienced total remission.
The Need for Answers
There is no cancer that has not been survived by someone, regardless how far advanced it was. If even one person has succeeded in healing his cancer, there must be a mechanism for it, just as there is a mechanism for creating cancer. Every person on the planet has the capacity for both. If you have been diagnosed with cancer, you may not be able to change the diagnosis, but it is certainly in your power to alter the destructive consequences that it (the diagnosis) may have on you. The way you see the cancer and the steps you take following the diagnosis are some of the most powerful determinants of your future wellness, or the lack of it.
The indiscriminate reference to "cancer" as being a killer disease by professionals and lay people alike has turned cancer into a disorder with tragic consequences for the majority of today's cancer patients and their families. Cancer has become synonymous to extraordinary suffering, pain and death. This is true despite the fact that 90-95 percent of all cancers appear and disappear out of their own accord. There is not a day that passes without the body making millions of cancer cells. Some people, under severe temporary stress make more cancer cells than usual and form clusters of cancerous cells that disappear again once they feel better. Secretions of the DNA's anticancer drug, Interleukin II, drop under physical and mental duress and increase again when relaxed and joyful. Thus, most cancers vanish without any form of medical intervention and without causing any real harm.
Right at this moment, there are millions of people walking around with cancers in their body without having a clue that they have them. Likewise, there are millions of people who heal their cancers without even knowing it. Overall, there are many more spontaneous remissions of cancer than there are diagnosed and treated cancers.
The truth is, relatively few cancers actually become "terminal." However, once diagnosed, the vast majority of all cancers are never even given a chance to disappear on their own. They are promptly targeted with an arsenal of deadly weapons of cell destruction such as chemotherapy drugs, radiation and the surgical knife. The problem with cancer patients is that, terrified by the diagnosis, they submit their bodies to all these cut/burn/poison procedures that, more likely than not, lead them to the day of final sentencing, "We have to tell you with our deepest regret there is nothing more that can be done to help you."
The most pressing question is not how advanced or dangerous a cancer is, but what we need to do to not end up dying from it. Why do some people go through cancer as if it were the flu? Are they just lucky or is there a mechanism at work that triggers the healing? In other words, what is that element that prevents the body from healing cancer naturally, or what is that hidden element that makes cancer so dangerous, if it is dangerous at all?
The answers to all these queries lie with the response of the person who has the cancer, and not with the degree of "viciousness" or advanced stage it appears to have progressed to. Do you believe that cancer is a disease? You will most likely answer with a "yes," given the 'informed' opinion that the medical industry and mass media have fed to the masses for many decades. Yet, the most pressing yet rarely asked question remains: "Why do you think cancer is a disease?" You may say: "Because I know cancer kills people every day." I would question you further: "How do you know that it is the cancer that kills people?" You would probably argue that most people who have cancer die, so obviously it must be the cancer that kills them. Besides, you may reason, all the expert doctors tell us so.
Let me raise another question, a rather strange one: "How do you know for sure that you are the daughter/son of your father and not of another man?" Is it because your mother told you so? What makes you think that your mother told you the truth? Probably because you believe her; and you have no reason not to. After all, she is your mother, and mothers do not lie about these things. Or do they? Although you will never really know that the person you believe to be your father is, in fact, your father, you nevertheless have turned what you subjectively believe into something that you just "know," into an irrefutable truth.
Although there is no scientific proof whatsoever that cancer is a disease (versus a survival mechanism), most people will insist that it is a disease because this is what they were told to believe. Yet their belief is only hearsay information based on other people's opinions. These other people heard it from someone else. Eventually, the "truth" of cancer being a disease can be traced to some doctors who expressed their subjective feelings or beliefs about what they observed and wrote about in some review articles or medical reports. Other doctors agreed with their opinion, and before long, it became a "well-established" fact that cancer is a vicious illness that somehow gets hold of people in order to kill them. However, the truth of the matter may be quite different.
Wisdom of Cancer Cells
Cancer cells are not part of a malicious disease process. When cancer cells spread (metastasize) throughout the body, it is not their purpose or goal to disrupt the body's vitals functions, infect healthy cells and obliterate their host (the body). Self-destruction is not the theme of any cell unless, of course, it is old and worn-out and ready to be turned-over and replaced. Cancer cells, like all other cells, know that if the body dies, they will die as well. Just because some people assume that cancer cells are there to destroy the body does not mean cancer cells have such a purpose or ability.
A cancerous tumor is neither the cause of progressive destruction nor does it actually lead to the death of the body. There is nothing in a cancer cell that has even remotely the ability to kill anything. What eventually leads to the demise of an organ or the entire body is the wasting away of cell tissue resulting from continued deprivation of nutrients and life force. The drastic reduction or shutdown of vital nutrient supplies to the cells of an organ is not primarily a consequence of a cancerous tumor, but actually its biggest cause.
By definition, a cancer cell is a normal, healthy cell that has undergone genetic mutation to the point that it can live in an anaerobic surrounding (an environment where oxygen is not available). In other words, if you deprive a group of cells of vital oxygen (their primary source of energy), some of them will die, but others will manage to alter their genetic software program and mutate in a most ingenious way: the cells will be able to live without oxygen and derive some of their energy needs from such things as cellular metabolic waste products.
It may be easier to understand the cancer cells phenomenon when comparing it with the behavior of common microorganisms. Bacteria, for example, are divided into two main groups, aerobic and anaerobic, meaning, those that need to use oxygen and those that can live without it. This is important to understand since we have more bacteria in our body than we have cells. Aerobic bacteria thrive in an oxygenated environment. They are responsible for helping us with the digestion of food and manufacturing of important nutrients, such as B-vitamins. Anaerobic bacteria, on the other hand, can appear and thrive in an environment where oxygen does not reach. They break down waste materials, toxic deposits and dead, worn-out cells.
The body sees the cancer as being such an important defense mechanism that it even causes the growth of new blood vessels to guarantee the much-needed supply of glucose and, therefore, survival and spreading of the cancer cells. It knows that cancer cells do not cause but, prevent death; at least for a while, until the wasting away of an organ leads to the demise of the entire organism. If the trigger mechanisms for cancer (causal factors) are properly taken care of, such an outcome can be avoided.
It is commonly believed that our immune system protects us against cancer. However, this is only partially true. On the one hand, the immune system readily destroys the millions of cancer cells that a healthy human body produces as part of the daily turnover of 30 billion cells. On the other hand, the immune system takes no action to eradicate cancer cells that develop in response to a build up of toxins, congestion and emotional stress.
Cancers and all other tissues in the body are larded with cancer-killing white cells, such as T-cells. In the case of kidney cancer and melanomas, for example, white cells make up 50 per cent of the mass of the cancers. Since these T-cells easily recognize foreign or mutated cell tissue such as cancer cells, you would expect these immune cells to attack cancer cells right away. However, the immune system allows cancer cells to recruit it to actually increase and spread the cancer to other parts of the body. Cancer cells produce specific proteins that tell the immune cells to leave them alone and help them to grow
Why would the immune system want to collaborate with cancer cells to make more or larger tumors? Because cancer is a survival mechanism, not a disease. The body uses the cancer to keep deadly carcinogenic substances and caustic metabolic waste matter away from the lymph and blood and, therefore, from the heart, brain and other vital organs. Killing off cancer cells would in fact jeopardize its survival. Cleansing the body of accumulated toxins and waste products through the various cleansing methods advocated in my book Timeless Secrets of Health and Rejuvenation (www.ener-chi.com) removes the need for cancer.
Cancer is not a disease; it is the final and most desperate survival mechanism the body has at its disposal. It only takes control of the body when all other measures of self-preservation have failed. To truly heal cancer and what it represents in a person's life we must come to the understanding that the reason the body allows some of its cells to grow in abnormal ways is in its best interest and not an indication that it is about to destroy itself. Cancer is a healing attempt by the body, for the body. Blocking this healing attempt can destroy the body. Supporting the body in its healing efforts can save it.

Seven Secrets About Breast Cancer

Secret #1 The Money Spent On Research Into Breast Cancer Is Not Ensuring That Less Women Get Breast Cancer.
Secret #2 You Do Need To Act Against Getting Breast Cancer Before You Reach 50 And You Cannot Rely On Mammograms.
Secret #3 You Are At Risk Of Getting Breast Cancer Even If You Don't Have It In Your Family.
Secret #4 Most Of The Money Spent On Research Is Not Going Into Prevention To Ensure That Less Women Suffer The Devastating Effects Of Breast Cancer In The Future.
Secret #5 Most Women Are Not Breast Aware And Are Afraid Of Breast Cancer.
Secret #6 Women Are Not Given Lots Of Advice On How They Can Protect Their Breasts Against Breast Cancer.
Secret #7 Most Women Do Not Appreciate How Important Their Breasts Are And Do Not Do Everything They Can To Look After And Protect Them.
The above "secrets" are things which are not commonly known by most women and may be surprising to you. In this article, I intend to shed light on these facts and allow women to make up their own minds how they approach their breast health.
SECRET #1 THE MONEY SPENT ON RESEARCH INTO BREAST CANCER IS NOT ENSURING THAT LESS WOMEN GET BREAST CANCER.
The Pink Ribbon and Breast Cancer Awarenss Month was introduced in the US in 1985 and introduced to the UK in 1993. The Pink Ribbon Foundation is fronted by the Estee Lauder group of companies (known for cosmetics and skincare).
Since then the pink ribbon symbol has become synonymous with breast cancer and during the past 15 years billions of pounds have been raised in its name. Every October the world celebrates Breast Cancer Awareness Month and fund raising during that month is phenomenal. All the breast cancer charities vie with each other to see who can come up with the most innovative "pink" fundraising. They run pink parties and sell pink products in order to raise money. Many companies take part and do special promotions during October for their preferred charity. "Pink" is big business.
So with all this money being raised during October and also at other times during the year through events like charity runs and walks, is there an impact on the breast cancer rates in the UK and around the world? Are they coming down? Are fewer women suffering from the devastating effects of breast cancer?
Unfortunately, the answer is 'no'.
In the UK, from 1993-2004, breast cancer incidence has increased 18.5%, that is 1% per year. 1 in 9 women will get the disease during their lifetime with current projections of 1 in 7 by 2010. 45,500 women were diagnosed in 2005, which equates to 125 women every day. Worldwide more than a million women are diagnosed with breast cancer every year. It is also projected that breast cancer rates will rise most in developing countries, where women do not have access to top quality care and where they can also be treated as outcasts in certain societies.
Breast cancer survival rates have improved. Every year more than 12,300 women and 70 men die from breast cancer. Since the peak in the late 1980s breast cancer death rates have fallen by a third. Breast cancer drugs have helped to save women's lives but, as with any drugs, can have long-term side affects. Also the cost of these drugs puts great strain on the NHS. If breast cancer rates continue to increase as they have been doing, then, according to Professor Karol Sikora as reported in the Daily Mail on 09/09/08, "the next generation of drugs would keep patients alive longer, but could swallow half of the current NHS cancer budget within four years. (this refers to all cancer drugs at a cost of £50 billion).
With the billions being raised by people around the world in the name of breast cancer, is it right that actually more women are getting this devastating disease every year?
SECRET #2 YOU DO NEED TO ACT AGAINST GETTING BREAST CANCER BEFORE YOU REACH 50 AND YOU CANNOT RELY ON MAMMOGRAMS.
Women in the UK are offered breast screening by mammogram every three years from the age of 50. This is because breast cancer is still more common in women over 50 but also because the breast tissue of younger women is denser and, therefore, makes it more difficult for a mammogram to pick up on a potential breast lump.
However, this could be giving the message to younger women that they don't need to check their breasts themselves. Based on my experience during my breast health talks, very few younger women check their breasts. The main reasons for this are that no-one has shown them how to, they don't know what to do, they think that they only need to worry if breast cancer is in the family (see Secret #3) or they are afraid that they might find something.
For a younger woman it is even more important to check her breasts from her mid-twenties as breast cancer in younger women is usually much more aggressive as the breast cancer cells can multiply more rapidly than in older women. If girls were taught by their mothers to check their breasts from their mid-twenties, they would not be afraid - it would just be part of their general regime of looking after themselves. Also they would feel confident about what to do. Breast self-examination is easy to do once you have been shown how and there are even devices on the market which can help you do so with confidence and greater accuracy.
Breast cancer is the biggest killer of women aged 35-54, which means it makes sense for women in this age bracket to do everything they can to protect their breasts.
Furthermore, I do not believe that we should rely on mammograms either. Women are only screened every three years and, usually, a mammogram can only detect a breast tumour once it has been growing for 8 years. By the time the tumour reaches 10 years, it could be too late. The other thing to remember is that a mammogram can only screen the part of the breast which can be put into the "clamp". It cannot screen under the armpit or between the breasts for example.
Lastly, there is growing concern over the safety of mammograms. The following are extracts from an article written by Peter Leando PhD.
"Controversy has raged for years as to whether the risks related to the radiation exposure suffered from mammography are justified by the benefits gained ...... new evidence relating to the particular type of radiation used and the hard evidence relating to the clinical benefits of mammography have caused a serious re-evaluation of the justification of mammography as a screening test.
Radiation from routine mammography cannot be directly compared to other types of X-ray like chest X-ray etc because they are very different types of radiation.
The comparisons that have been used between a chest x-ray and mammography, 1/1,000 of a rad (radiation-absorbed dose) for a chest X-ray and the 1 rad exposure for the routine four films taken of both breasts for a mammographic screening exam results in some 1,000 times greater exposure. (This refers to the US, where they do four-way screening. In the UK typically only two-way screening is offered.)
This is considered a significant risk factor when extended over a ten year screening period and a potential accumulative dose of 10 rads. Unfortunately this is not the major risk posed by the particular type of radiation used by mammograms, mammography X-rays use a low energy form of ionising radiation that causes greater biologic damage than the high energy X-ray. The very low energy electrons affect the density of ionisation tracks that pass through the tissue, which can cause complex damage to the DNA and carcinogenic changes.
The radiation used by mammography is almost 5 times more effective at causing cancer." So, women do need to start checking their breasts from their early twenties and we cannot rely on mammograms 100%, particularly for younger women who would have a greater exposure to radiation during their lifetime if they were offered mammograms from a younger age. Also mammograms do not detect Inflammatory Breast Cancer (IBC) which is a much rarer form of the disease and does not involve a lump. This would only detected by a woman looking for changes to her breasts and reporting them to her doctor.
SECRET #3 YOU ARE AT RISK OF GETTING BREAST CANCER EVEN IF YOU DON'T HAVE IT IN YOUR FAMILY.
Amongst the hundreds of women I have talked to about breast health, the vast majority were under the false impression that breast cancer is primarily hereditary. They were surprised to hear that fewer than 10% of cases occur to women who have breast cancer in the family.
In fact, every woman is at risk and should take control of her own breast health to give herself the best possible chance of prevention or early detection.
The other most common acknowledged risk factors are:

• Age - breast cancer is more common in women over 50
• Early puberty - it is worrying that puberty is starting younger, with most girls starting their periods at primary school
• Late pregnancy - many woman are opting to have children later
• Late onset menopause
• Not having children and not breastfeeding - this was known as early as the 18^th century when a doctor in Italy noticed that nuns had higher levels of breast cancer than the general population
• Being overweight - this applies mainly to post-menopausal women
• Alcohol - over-consumption increases the risk of breast cancer

Acknowledged risk factors account for around 50% of breast cancer cases. For the remainder, there are no definite reasons.
There are a growing number of scientists, commercial companies and individuals who believe that this remaining 50% is due to the rise of the number of chemicals which have been introduced over the past 50 years. They are used in our food, in our toiletries, in the workplace, in our clothes, in our furnishings - in fact, in every aspect of our lives. Many of these chemicals are endocrine disrupting chemicals (EDC's), also known as hormone disruptors or oestrogen mimickers. In simple terms, they act like oestrogen in our bodies and could be responsible for changing our delicate hormone balance which controls events like pregnancy, puberty, menopause.
An interesting example of the levels of oestrogen of British women was examined in a collaborative study undertaken in the late 80's between Oxford University, the Chinese Academy of Preventive Medicine Beijing, Guys, and the Dept. of Preventive Medicine, L.A., California. They compared blood-serum concentrations of hormones linked to breast cancer between women in rural China and in Britain. The results showed that British women who are exposed to toxic chemicals in their everyday lives had increasingly higher levels of oestradiol (oestrogen) than women living a rural lifestyle in China (see table below).
On this theme, the Guardian online reported on 22/05/07 that 'Beijing blames pollutants for rise in killer cancers'.
Oestradiol levels higher in British women by: Age 35 - 44 36% Age 45 - 54 90% Age 55 - 64 171%
SECRET #4 MOST OF THE MONEY SPENT ON RESEARCH IS NOT GOING INTO PREVENTION TO ENSURE THAT FEWER WOMEN SUFFER THE DEVASTATING EFFECTS OF BREAST CANCER IN THE FUTURE.
As we know, billions of pounds are raised every year worldwide in the name of breast cancer and most of this money is received by the mainstream breast cancer charities. In my opinion, the areas which should be targeted by these funds are prevention, treatment and care. You would probably expect these areas, at least, to be treated with equal importance and the funds available allocated accordingly.
Let's first take a look at the mainstream breast cancer charities in this country, namely Cancer Research UK (who obviously deal with all cancers), Breakthrough Breast Cancer, Breast Cancer Campaign and Breast Cancer Care.
Cancer Research UK has done a huge amount of research into breast cancer and their website has a wealth of useful information with a lot of detail on breast cancer. Their slogan is 'Together We Will Beat Cancer'. The charity offers funding schemes to scientists. Their research strategy is directed at reducing mortality from cancer and more women are surviving breast cancer than ever before. Cancer Research UK is looking trying to prevent breast cancer in women known to be at high risk of developing it (approx 10% of sufferers). Doctors have looked into using tamoxifen and other hormone blocking drugs such as anastrozole (Arimidex) to lower the risk of breast cancer in women with a strong family history. This work has to be done very carefully. These women are healthy and the treatment aimed at preventing breast cancer must not risk their health in other ways.
Breakthrough Breast Cancer supports a programme of cutting-edge biological research to reach their vision of 'a future free from the fear of breast cancer'. Breakthrough set up the UK's first dedicated breast cancer research centre in 1999, the Breakthrough Toby Robins Breast Cancer Research Centre. Breakthrough is funding The Generations Study whosepurpose is primarily to investigate environmental, behavioural, hormonal and genetic causes of breast cancer, and secondarily to investigate the causes of other cancers and diseases, by means of a UK cohort study to be established of more than 100,000 women in the UK aged 18 years and older at entry.
However, when you look at environmental factors as a possible risk factor, it seems to be dismissed because it is too difficult to research due to the huge amount of chemicals to which we are exposed in our everyday lives. You can read more at their website under "risk factors".
As I have mentioned, I am one of the many people who believe that certain chemicals which act like oestrogen in our bodies are a contributing factor in rising breast cancer rates. I am disappointed to see that Breakthrough are not even including this as a possible risk factor, particularly as we know that excessive oestrogen has been linked to breast cancer cell growth.
Breast Cancer Campaign cites its mission is to beat breast cancerby funding innovative world-class research to understand how breast cancer develops, leading to improved diagnosis, treatment, prevention and cure. The charity is supporting 97 projects worth over £12.8 million in 41 locations throughout the UK. Over the past 13 years, Campaign has awarded 232 grants with a total value of over £23 million to universities, medical schools / teaching hospitals and research institutes across the UK. Campaign's breast cancer research gap analysis document has been published by the open access journal Breast Cancer Research. The document entitled 'Evaluation of the current knowledge limitations in breast cancer research: a gap analysis' is the product of two and a half year project. It involved around 60 of the key breast cancer scientists in the UK.
Through their website, they sell products of various types and the companies who own those brands donate part of their profits to the Campaign. They include things like lip gloss, perfume, toiletries, clothing and stationery. Some of us would say that many of the products include harmful ingredients and are not actually contributing to the breast health of the ladies buying them! I was also disappointed that, although they mention prevention in their mission statement, I have one of their leaflets that shows prevention only receives 1% of their budget.
Breast Cancer Care, as its name suggests, is primarily concerned with the care and treatment of ladies going through breast cancer. It provides invaluable information and support.
I applaud all of these organisations who are dedicated to their work to help us understand and treat breast cancer.
However, I still believe that the risk factor of certain chemicals affecting our delicate hormone balance should be taken seriously and that all the available research should be studied. It is important to note that only 50% of breast cancer cases can be put down to one of the acknowledged risk factors. What is this remaining 50%? What has changed in our world over the past 50 years? It is also interesting that other countries are recognising the dangers of these chemicals and banning substances. I also believe in adopting the 'precautionary principle', which means that if there is a doubt over the safety to public health, then we should not wait until it is too late but take action as soon as possible. It has also been proved that there are alternatives to these potentially harmful chemicals when we see the growing number of companies who are selling safer food, cosmetics and toiletries.
This is why I am an active supporter of Breast Cancer UK, the only charity whose main focus is primary prevention. We are determined that breast cancer should be a 'preventable' disease not an 'inevitable' one. There is lots of research available on the link between endocrine disrupting chemicals and breast cancer. It is time that this was taken into account when looking at breast cancer risk factors.
SECRET #5 MOST WOMEN ARE NOT BREAST AWARE AND ARE AFRAID OF BREAST CANCER.
Despite the huge focus on being breast aware, particularly during Breast Cancer Awareness month in October, the majority of women are not breast aware. In fact, most women pay little attention to their breasts and do very little to look after them, except maybe during breastfeeding. Our breasts represent our femininity - they make us feel sexy and they nourish our children. Yet most women don't even know what their breasts feel like, let-alone check them for anything unusual.
It is so important that women take control of their own breast health by undertaking monthly self-examination to check for any changes. If they find a lump and go to their doctor straight away, the chances are the lump will be benign (80% are) or, if it is cancerous, they are giving themselves the best possible chance of recovery. At Stage One, women have around a 95% chance of surviving beyond 5 years. At Stage One the lump is less than 2cm and has not spread to the lymph nodes or anywhere else in the body. At Stage Four this survival rate drops to 1 in 10. The average size of lump discovered accidentally by women who don't check their breasts regularly is approximately 3.6 cm.
I have spoken with hundreds of women through my breast education work and most women do not check their breasts because they don't know what to do, they don't realize that all women are at risk, they don't know about the four stages of breast cancer and the corresponding survival rates, they don't really think about the need to do anything to look after their breasts or they are afraid that they might find something.
According to research by Breast Cancer Campaign, breast cancer is the most feared disease amongst women. Fear is usually due to a lack of knowledge. This is certainly the case here. If women understood everything detailed here, they would want to give themselves the best chance of survival should they get the disease. The current approach to women's breast health obviously isn't getting through, which is why I believe it is time to get women to take control themselves and empower other women to do the same.
SECRET #6 WOMEN ARE NOT GIVEN LOTS OF ADVICE ON HOW THEY CAN PROTECT THEIR BREASTS AGAINST BREAST CANCER.
In the past, GP surgeries used to run Well Woman clinics where any woman could go and see a doctor or nurse and be given advice about looking after herself with practical information like being shown how to check her breasts. Very few surgeries offer these clinics now. This is one of the reasons that I started my Breast Health Presentations. I talk to women in the workplace or in other gatherings and empower them with information, which helps to remove some of their fear. I also show them how to check their breasts and talk to them about their bra-wearing habits, how to avoid harmful chemicals in their everyday lives and how to benefit from detoxifying breast massage.
As we know, breast cancer is the most feared disease amongst women and understanding how it develops, the risk factors and, most importantly, how to protect against it, will make women feel more in control and positive towards their breast health.
During October and other events during the year, the focus is on breast cancer rather than breast health. I am one of those people who believe that the more you focus on something negative, the more you will get of it. This is why it is time to change that focus.
I believe that it is definitely time for women to take their breast health into their own hands, which is why I have launched my new campaign "Healthy Breasts For Every Woman". You can read more at www.healthybreastscampaign.co.uk.
SECRET #7 MOST WOMEN DO NOT APPRECIATE HOW IMPORTANT THEIR BREASTS ARE AND DO NOT DO EVERYTHING THEY CAN TO LOOK AFTER AND PROTECT THEM.
As I mentioned before, most women give very little thought to their breasts. They get up in the morning and they may give them a wash in the shower. They then shove them into a cage we call a bra (and most women wear a bra that doesn't fit them properly) and forget about them for the rest of the day. It is amazing that we live in a society which is obsessed with breasts and women do very little to protect this most precious part of their body. It is also amazing that women spend a fortune on looking after every other part of their body with creams and lotions and forget about their breasts! I know that once women understand more about breast health and don't feel so helpless in the face of breast cancer that they do want to be proactive and take control of their breast health.

What You Should Know About Breast Cancer

Breast cancer is the most common malignancy in women and the second leading cause of cancer death, exceeded only by lung cancer in 1985. One woman in eight who lives to age 85 will develop breast cancer at some time during her life.
At present there are over 2 million women living in the United States who have been treated for breast cancer. About 41,000 women will die from the disease. The chance of dying from breast cancer is about 1 in 33. However, the rate of death from breast cancer is going down. This decline is probably the result of early detection and improved treatment.
Breast cancer is not just a woman's disease. The American Cancer Society estimates that 1600 men develop the disease yearly and about 400 may die from the disease.
Breast cancer risk is higher among those who have a mother, aunt, sister, or grandmother who had breast cancer before age 50. If only a mother or sister had breast cancer, your risk doubles. Having two first-degree relatives who were diagnosed increases your risk up to five times the average.
Although it is not known exactly what causes breast cancer; sometimes the culprit is a hereditary mutation in one of two genes, called BRCA1 and BRCA2. These genes normally protect against the disease by producing proteins that guard against abnormal cell growth, but for women with the mutation, the lifetime risk of developing breast cancer can increase up to 80 percent, compared with 13 percent among the general population. In effect, more than 25 percent of women with breast cancer have a family history of the disease.
For women without a family history of breast cancer, the risks are harder to identify. It is known that the hormone estrogen feeds many breast cancers, and several factors - diet, excess weight, and alcohol consumption - can raise the body's estrogen levels.
Early Signs
Early signs of breast cancer include the following:
- A lump which is usually single, firm and most often painless is detected.
- An area of the skin on the breast or underarm is swollen and has an unusual appearance.
- Veins on the skin surface become more prominent on one breast.
- The affected breast nipple becomes inverted, develops a rash, changes in skin texture, or has a discharge other than breast milk.
- A depression is found in an area of the breast surface.
Types and Stages of Breast Cancer
There are many different varieties of breast cancer. Some are fast-growing and unpredictable, while others develop more slowly and steady. Some are stimulated by estrogen levels in the body; some result from mutation in one of the two previously mentioned genes - BRCA1 and BRCA2.
Ductal Carcinoma In-Situ (DCIS): Generally divided into comedo (blackhead), in which the cut surface of the tumor shows extrusion of dead and necrotic tumor cells similar to a blackhead, and non-comedo types. DCIS is early breast cancer that is confined to the inside of the ductal system. The distinction between comedo and non-comedo types is important, as comedocarcinoma in-situ generally behaves more aggressively and may show areas of micro-invasion through the ductal wall into surrounding tissue.
Infiltrating Ductal: This is the most common type of breast cancer, representing 78 percent of all malignancies. On mammography, these lesions can appear in two different shapes -- stellate (star- like) or well circumscribed (rounded). The stellate lesions generally have a poorer prognosis.
Medullary Carcinoma: This malignancy comprises 15 percent of breast cancers. These lesions are generally well circumscribed and may be difficult to distinguish from fibroadenoma by mammography or sonography. With this type of breast cancer, prognostic indicators estrogen and progesterone receptor are negative 90 percent of the time. Medullary carcinoma usually has a better prognosis than other types of breast cancer.
Infiltrating Lobular: Representing 15 percent of breast cancers, these lesions generally appear in the upper outer quadrant of the breast as a subtle thickening and are difficult to diagnose by mammography. Infiltrating lobular can involve both breasts (bilateral). Microscopically, these tumors exhibit a linear array of cells and grow around the ducts and lobules.
Tubular Carcinoma: This is described as orderly or well-differentiated carcinoma of the breast. These lesions make up about 2 percent of breast cancers. They have a favorable prognosis with nearly a 95 percent 10-year survival rate.
Mucinous Carcinoma: Represents 1-2 percent of carcinoma of the breast and has a favorable prognosis. These lesions are usually well circumscribed (rounded).
Inflammatory Breast Cancer: This is a particularly aggressive type of breast cancer that is usually evidenced by changes in the skin of the breast including redness (erythema), thickening of the skin and prominence of the hair follicles resembling an orange peel. The diagnosis is made by a skin biopsy, which reveals tumors in the lymphatic and vascular channels about 50 percent of the time.
Stages of Breast Cancer
The most common type of breast cancer is ductal carcinoma. It begins in the lining of the ducts. Another type, called lobular carcinoma, arises in the lobules. When cancer is found, the pathologist can tell what kind of cancer it is - whether it began in a duct (ductal) or a lobule (lobular) and whether it has invaded nearby tissues in the breast (invasive).
When cancer is found, special lab tests of the tissue are usually done to learn more about the cancer. For example, hormone (estrogen and progesterone) receptor tests can help determine whether hormones help the cancer to grow. If test results show that hormones do affect the growth of the cancer (a positive test result), the cancer is likely to respond to hormonal therapy. This therapy deprives the cancer cells of estrogen.
Other tests are sometimes done to help predict whether the cancer is likely to progress. For example, x-rays and other lab tests are done. Sometimes a sample of breast tissue is checked for a gene, known as the human epidermal growth factor receptor-2 (HER-2 gene) that is associated with a higher risk that the breast cancer will recur. Special exams of the bones, liver, or lungs are done because breast cancer may spread to these areas.
A woman's treatment options depend on a number of factors. These factors include her age and menopausal status; her general health; the size and location of the tumor and the stage of the cancer; the results of lab tests; and the size of her breast. Certain features of the tumor cells, such as whether they depend on hormones to grow are also considered.
In most cases, the most important factor is the stage of the disease. The stage is based on the size of the tumor and whether the cancer has spread. The following are brief descriptions of the stages of breast cancer and the treatments most often used for each stage. Other treatments may sometimes be appropriate.
Stage 0
Stage 0 is sometimes called non-invasive carcinoma or carcinoma in situ. Lobular carcinoma in situ (LCIS) refers to abnormal cells in the lining of a lobule. These abnormal cells seldom become invasive cancer. However, they are an indicator of an increased risk of developing breast cancer in both breasts. The treatment for LCIS is a drug called tamoxifen, which can reduce the risk of developing breast cancer. A person who is affected may choose not to have treatment, but to monitor the situation by having regular checkups. And occasionally, the decision is made to have surgery to remove both breasts to try to prevent cancer from developing. In most cases, removal of underarm lymph nodes is not necessary.
Ductal carcinoma in situ (DCIS) refers to abnormal cells in the lining of a duct. DCIS is also called intraductal carcinoma. The abnormal cells have not spread beyond the duct to invade the surrounding breast tissue. However, women with DCIS are at an increased risk of getting invasive breast cancer. Some women with DCIS have breast-sparing surgery followed by radiation therapy. Alternatively, they may choose to have a mastectomy, with or without breast reconstruction (plastic surgery) to rebuild the breast. Underarm lymph nodes are not usually removed. Also, women with DCIS may want to talk with their doctor about tamoxifen to reduce the risk of developing invasive breast cancer.
Stage I and II
Stage I and stage II are early stages of breast cancer in which the cancer has spread beyond the lobe or duct and invaded nearby tissue.
Stage I means that the tumor is about one inch across and cancer cells have not spread beyond the breast.
Stage II means one of the following:
The tumor in the breast is less than 1 inch across and the cancer has spread to the lymph nodes under the arm.
The tumor is between 1 and 2 inches (with or without spread to the lymph nodes under the arm).
The tumor is larger than 2 inches but has not spread to the lymph nodes under the arm.
The treatment options for early stage breast cancer are breast-sparing surgery followed by radiation therapy to the breast, and mastectomy, with or without breast reconstruction to rebuild the breast. These approaches are equally effective in treating early stage breast cancer. (Sometimes radiation therapy is also given after mastectomy.)
The choice of breast-sparing surgery or mastectomy depends mostly on the size and location of the tumor, the size of the breast, certain features of the cancer, and how the person feels about preserving the breast. With either approach, lymph nodes under the arm usually are removed.
Chemotherapy and/or hormonal therapy after primary treatment with surgery or surgery and radiation therapy are recommended for stage I and most frequently with stage II breast cancer. This added treatment is called adjuvant therapy. Systemic therapy sometimes given to shrink the tumor before surgeries called neoadjuvant therapy. This is given to try to destroy any remaining cancer cells and prevent the cancer from recurring, or coming back, in the breast or elsewhere.
Stage III
Stage III is also called locally advanced cancer. In this stage, the tumor in the breast may exhibit the following:
More than 2 inches across and the cancer has spread to the underarm lymph nodes.
The cancer is extensive in the underarm lymph nodes.
The cancer is spreading to lymph nodes near the breastbone or to other tissues near the breast.
Inflammatory breast cancer is a type of locally advanced breast cancer. In this type of cancer, the breast looks red and swollen (or inflamed) because cancer cells block the lymph vessels in the skin of the breast.
Patients with stage III breast cancer usually have both local treatment to remove or destroy the cancer in the breast and systemic treatment to stop the disease from spreading. The local treatment may be surgery and/or radiation therapy to the breast and underarm. The systemic treatment may be chemotherapy, hormonal therapy, or both. Systemic therapy may be given before local therapy to shrink the tumor or afterward to prevent the disease from recurring in the breast or elsewhere.
Stage IV
Stage IV is metastatic cancer. The cancer has spread beyond the breast and underarm lymph nodes to other parts of the body.
The treatments for stage IV breast cancer are chemotherapy and/or hormonal therapy to destroy cancer cells and control the disease. Patients may have surgery or radiation therapy to control the cancer in the breast. Radiation may also be useful to control tumors in other parts of the body.
Recurrent Cancer
Recurrent cancer means the disease has returned in spite of the initial treatment. Even when a tumor in the breast seems to have been completely removed or destroyed, the disease sometimes returns because undetected cancer cells remained somewhere in the body after treatment.
Most recurrences appear within the first 2 or 3 years after treatment, but breast cancer can recur many years later.
Cancer that returns only in the area of the surgery is called a local recurrence. If the disease returns in another part of the body, the recurrence is called metastatic breast cancer. The patient may have one type of treatment or a combination of treatments for recurrent cancer.

Double Drug Combo Could Shut Down Abnormal Blood Vessel Growth That Feeds Disease

A new study by researchers at Weill Cornell Medical College shows combining two already-FDA approved drugs may offer a new and potent punch against diseases in which blood vessel growth is abnormal -- such as cancer, diabetic retinopathy, macular degeneration and rheumatoid arthritis.
Their study, published in the Sept. 11 issue of the journal Developmental Cell, is the first to show that a protein, sphingosine 1-phosphate receptor-1 (S1P1), is a key player in angiogenesis -- the growth process of new blood vessels in the body from pre-existing vessels. S1P1, previously known to modulate immune system function, is the target of the approved drug fingolimod used to treat the autoimmune neurological disease multiple sclerosis.
Researchers have discovered that S1P1 works hand-in-hand with vascular endothelial growth factor (VEGF), which stimulates blood vessel growth. VEGF is the target of a number of different cancer drugs that have not proven to be as effective as originally envisioned in shutting down the excess blood vessels that provide nutrients to growing tumors and other diseases that rely on extra blood supply.
"The body needs to make new blood vessels that transport oxygen and blood. We now know that VEGF starts the process of sprouting new blood vessels from existing vessels, and S1P1 finishes it," says Dr. Timothy Hla, professor of pathology and laboratory medicine and director of the Center for Vascular Biology at Weill Cornell.
"Angiogenesis is abnormal in many diseases; by targeting both S1P1 and VEGF, it may be more effective to strike out disease than using just VEGF inhibitors alone," he says.
Not only are VEGF inhibitors currently used to treat cancer, these drugs are also used to block excessive angiogenesis in the eyes of diabetics and vascular proliferation that occurs in the wet form of age-related macular degeneration. "We are intrigued to see what the potential for treating these eye diseases would be if S1P1 axis was also targeted," Dr. Hla says.
In rheumatoid arthritis, which is driven by reactive and inflammatory immune cells, a S1P1 inhibitor could block both immune and blood vessel-related mechanisms, and therefore may be beneficial, based on the study's findings. In addition, Dr. Hla points out that while the existing approved S1P1 inhibitor fingolimod has had some adverse effects in some multiple sclerosis patients, there are new inhibitors of S1P1 being developed by many companies that could also be tested in combination with a VEGF inhibitor for treating these diseases.
An Antenna that Senses Blood Flow
Angiogenesis is needed for many normal tissue growth, repair and regenerative processes, which ultimately results in increased blood flow and oxygenation of tissues.
The Hla laboratory has long been interested in defining the molecular mechanisms of the angiogenic process, in which endothelial cells from pre-existing blood vessels sprout, move and then change to form new vascular channels. Dr. Hla was first to identify S1P1 as a key angiogenic response gene, and he also successfully cloned and characterized the receptor.
In this study, the research team shows that as new blood vessel networks form, the resulting blood flow activates S1P1 on the surface of endothelial cells and relays signals inside these cells to stabilize new blood vessel networks.
"The S1P1 molecule acts like an antenna to sense blood flow. If blood flow is reduced, then normal S1P1 signaling is interrupted, destabilizing blood vessel formation, causing the endothelium to undergo an inflammatory process," Dr. Hla says. "This happens in many diseases with abnormal vessels, including rheumatoid arthritis, psoriasis and even cancer."
In their laboratory studies, the researchers found that blocking S1P1 resulted in abnormal endothelial function and blood vessel growth. Inhibiting S1P1 causes new vessels to leak and become unstable. Blocking S1P1 would be beneficial, for example, to cut off the blood supply feeding a cancerous tumor, researchers report.
"This research defines one of the fundamental mechanisms of blood vessel growth that is vital to normal health and that also fuels many diseases," he says. "This research could ultimately lead to our ability to better modulate blood vessel health and growth, especially in diseases that depend on extra blood to sustain them."
The study was supported by grants from the National Institutes of Health.
Dr. Hla's co-authors include Bongnam Jung, Dr. Hideru Obinata, Dr. Sylvain Galvani, Dr. Karen Mendelson, Dr. Bisen Ding, Dr. Shahin Rafii and Dr. Todd Evans from Weill Cornell; Dr. Athanasia Skoura from Pfizer Inc.; and Dr. Bernd Kinzel and Dr. Volker Brinkmann from Novartis Institutes for Biomedical Research in Basel, Switzerland.