Dan Wilson

Senior Member.
The Internet is full of web sites and articles that claim to be able to treat or "cure" cancer. Some claim that diet is the key, others say you can treat it with baking soda or marijuana products, and some clinics even sell their own alternative treatments to patients. Treatments taking the name of Essiac tea, Hoxsey therapy, Gerson therapy, Rick Simpson oil, and many more. Many of these methods can sound convincing, especially when dealing with a disease that comes with so much fear and despair. Even Steve Jobs chose to forego conventional treatment, which, unfortunately, likely cost him his life. None of the things I mentioned will cure cancer. There can be a variety of reasons why one treatment or another won't work but, rather than debunk each one individually, I think a general understanding of cancer and the real progress we have made in treating it can be all the knowledge one needs in order to see why these alternative cures simply won't work. Here, I want to provide a brief and general understanding of what cancer is, how it develops, and introduce the real success stories of cancer treatment.

What is cancer?
Cancer, to put it simply, is us. It is cells in our body that have suffered enough DNA damage to become overactive and unresponsive to the normal "stop" signals. Harold Varmus, a nobel laureate who, with Michael J. Bishop, demonstrated that cancer does come from within, said at a banquet speech in 1989:
...we have not slain our enemy, the cancer cell, or figuratively torn the limbs from his body. In our adventures, we have only seen our monster more clearly and described his scales and fangs in new ways - ways that reveal a cancer cell to be, like Grendel, a distorted version of our normal selves.
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This is the first reason caner is so difficult to treat. When we take medications to rid ourselves of unwanted guests, we might take an anti-bacterial drug that kills bacteria but leaves our cells alone. Similarly, those suffering from fungal infections might take anti-fungal drugs that kill the fungi but, again, leave our cells alone. These medications take advantage of evolutionary differences between our cells and invading pathogens. Now what happens when the invaders are not actually foreign or evolutionarily distant, but are our own cells? How do we target cancer without hurting healthy cells? This is an extremely complicated problem.

How does cancer develop?
Understanding the answer to this question is the key to seeing why cancer is so hard to treat. Our bodies are made up of tens of trillions of cells. These cells all communicate with each other, organize themselves into organs, follow very strict rules, and ultimately form a complex network of functions all to keep us alive. The mechanisms put into place for this to be possible are not foolproof. They can be damaged and break. Every day, the DNA in each and every cell is damaged in some way, whether it is through mistakes made during replication or exposure to carcinogens or mutagens. Although our bodies have mechanisms in place to correct this damage, some damage persists and once it makes it past all of the checkpoints the mutations can't be changed. Most damage is harmless and hits parts of the genome that serve no function, but sometimes the damage can hit a gene. If that gene is a proto-oncogene or tumor suppressor gene, that cell takes a step closer to becoming cancerous. When enough of the right damage accumulates over time, we get cancer. Given enough time, this means that for every multi-cellular organism, it is not a question of if cancer will develop, but when.
Much of the complexity of cancer can be described from the simple fact that this genetic damage that accumulates over time is random. This randomness makes every cancer different. One patient's prostate cancer is going to be different from another's lung cancer. That same patient's lung cancer, however, will also behave differently compared to another patient's lung cancer. While certain cancers of the same type might share themes, each and every cancer has its own unique set of mutations. Most of the time, getting cancer is not as simple as damaging one or two proto-oncogenes or tumor suppressor genes and it does not happen overnight. Cancers have many mutations in many genes gathered over many years. The nature of these mutations can influence the aggressiveness of cancer and its susceptibility to treatment. Breast cancer is a well-studied example of this.
Differing histopathological parameters such as receptor status (estrogen-receptor, progesterone-receptor, and/or ERBB2/HER2) contribute to diagnostic classification (Viale, 2012), and molecular profiling subdivides breast cancer into at least six subtypes (normal like, luminal A, luminal B, HER2 enriched, claudin low, and basal like). These expression profiles mostly reflect different clinical prognoses (Perou et al., 2000, Prat et al., 2010, Santagata et al., 2014, Sørlie et al., 2001, Sorlie et al., 2003) and to some extent responses to therapy (Troester et al., 2004), and integrated genomic and transcriptomic analysis of breast tumors has revealed further subgroups with distinct clinical outcomes (Curtis et al., 2012).
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To make things even more difficult, mutations continue to arise at a faster rate in cancer cells, so a single tumor could harbor cells with many different combinations of mutations. This is one major reason why so many patients relapse into cancer after what looked like a successful remission.

Considering how cancer develops, by accumulating irreversible mutations, it is easy to see how many alternative treatments (Essiac tea, Hoxsey therapy, Gerson therapy, etc.) won't work. Even cancer treatments that do work won't yield the same results on every kind of cancer or even every case of one particular cancer. In fact, designing a treatment that works has arguably been the biggest challenge ever in medicine, even back to the first medical records we have of cancer ever written in ancient Egypt. The complexities of cancer and difficulties involved in treating it makes it reasonable to say we may never cure every cancer. The knowledge accumulated in the past century, however, has led to incredible progress in treating and preventing cancer.

How good are we at treating cancer?
Cancer today is treated one of three general ways; radiation, chemotherapy, and surgery. The most simple treatment for cancer is surgery, cutting out the malignant tissue solves the problem but in many cases that may not be an option. Radiation has also made improvements and has had success in treatments, but here we will focus on the progress of chemotherapeutic treatments.
When most people hear the word "chemotherapy," images of sick patients losing hair and becoming frail often come to mind. Chemotherapy is often thought of as a treatment that kills. This is because the drugs used in chemotherapy do also kill healthy cells. This goes back to the fact that cancer is us and, therefore, hard to target. In many cases, chemotherapy such as this is the best that can be done, but it has had a significant success rate in treating certain cancers. Cancer treatment, however, has become much more than toxic chemotherapy and radiation. Targeted therapies and smarter use of old chemotherapeutic drugs have yielded the following results. 80% of children with cancer in the U.S. will go on to live full lives. This is a massive improvement from survival rates of 50% in 1975. A more specific example, acute lymphoblastic leukemia (ALL) cases have gone from less than 10% survival in the 1960s to 90% in 2003-2009. In adults, 66% of men and 63% of women with cancer now survive 5 years after their diagnosis. Specific cases help to show the real success here. Breast cancer 5-year survival rate is up by 15.8% since 1975. Colorectal cancer 5-year survival is up by 17.9% since 1975. The most amazing success story is that of chronic myelogenous leukemia (CML) where 5-year survival is up by 45.3% since 1975. Again, much of these successes are thanks to new targeted chemotherapeutic strategies as well as emerging immunotherapeutic approaches. The success seen in CML patients is thanks in large part to the efforts of Brian Druker for the development of Gleevec, which targets a specific mutated protein found in most CML cases. Gleevec and many other targeted chemotherapy treatments do not result in the debilitating side-effects typically associated with chemotherapy.
CML: http://seer.cancer.gov/statfacts/html/images/longterm_line_graph/Longterm_LineGraph_Site_094_Sex_0.pngCML Incidence & Death Rates.png

With all of the success, it is important to keep things in perspective. Pancreatic, lung, and stomach cancers, for example, still have bleak outlooks. The stage of any cancer also matters. Most patients who's cancers progress to metastatic (stage IV) don't have much better prognoses than they might have had 50, 100, or even 4,000 years ago. Many questions still persist in basic cancer biology and countless clinical cases show cancers coming back after remission. Treating cancer is still one of medicine's biggest challenges. Researchers have been trying to make more drugs like Gleevec to target other cancers but, like I said, every cancer is different. What made Gleevec work so well against CML just doesn't apply to every cancer.
Lung and Bronchus Cancer:
Lung and Bronchus Cancer Incidence & Death Rates.png
Understanding how cancer works, the success we have already had with treatments, and how far we still have to go helps (I hope) to understand why alternative therapies don't work. Cancer is all of our cells' billions of years of evolution turned against us, it has mechanisms in place to effectively hide out from the immune system, develop resistance to drugs, and hijack the body's normal functions. The genetic mutations that cause cancer are irreversible and it is hard to get rid of them without causing harm to healthy cells. Alternative treatments, many of which actually claim to revert cancer cells back into healthy cells, do not address these fundamental challenges. A cancer cure will not come easily, but we have reason to believe that cancer might be curable one kind at a time. Wasting time, money, and lives on treatments we know don't work is something that can be avoided.
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Senior Member.
If there are substances that are carcinogens that make cells replicate faster than normal, or mutagens that cause more mutations, is there a possibility that there are some substances that do the opposite, such as prevent cells replicating too fast, or make them replicate slower? Such substances, if they DO exist and can be identified could therefore possibly have a preventative action, even if they can't be a cure.

Dan Wilson

Senior Member.
Such substances, if they DO exist and can be identified could therefore possibly have a preventative action, even if they can't be a cure.

Yes! Such things do exist but making them into cures or prevention methods is not so simple. Tumor suppressor genes code for proteins that are meant to prevent cancer. One of the most well-known ones that is commonly involved in cancer (>50% of cases) is p53. Different animals have evolved different mechanisms for preventing cancer. For example, a whale has many more cells than a human or a mouse, but their rate of cancer is more or less the same as ours. The reason they don't have more cancer is that they have mechanisms built into their genome to compensate for their large size. This gives us important insight into how cancer works but it is hard to directly translate knowledge like this into a preventative method or cure. As a preventative or cure, we would have to find a way of efficiently delivering these foreign proteins to multiple tissues in the body without eliciting an immune response. Gene therapy could be a feasible route, but it would difficult. The "ideal" cure in applying this kind of knowledge would be transgenic (genetically engineered) humans and we are probably still a long way from doing that.
Antioxidants help prevent cancer indirectly by reducing damage to DNA and cells caused by free radicals and are very much worth including in a healthy diet. They do not, however, prevent all damage in all tissues, so they cannot guarantee a cancer-free life nor can they do much to an already existing cancer.

Audrey Castle

New Member
Cancer is related to multiplication of cells and they multiply at very faster rate. The article is very informative for knowing the depth of the subject. Sometimes the symptoms are noticeable and sometimes the symptoms are not noticeable as in the case of my younger sister who was diagnosed with breast cancer. The question still prevails that is cancer fully treatable? But treatments like chemotherapy, surgery and radiotherapy at radiotherapy centers like Oceania Oncology, Advanced radiation Centers, MacArthur Cancer Service, James Cancer Hospital & Solve Research Institute and many more cannot be neglected as they have powerful results.

Dan Wilson

Senior Member.
The question still prevails that is cancer fully treatable?

In many cases, yes. In many others, however, the answer is still no. It really depends on the type and stage of the cancer. A breast cancer caught early can normally be easily removed with surgery but let the same breast cancer progress to metastasis where it spreads to other tissues and organs and there is little that can be done. Developing treatments for such stages of the disease is incredibly difficult for researchers and helping patients in that situation make decisions that will make the time they have left as comfortable as possible is just as challenging for medical doctors. It's really not an easy thing for anyone but we can look to the victories that have been made for hope.

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