Can Cancer Be Cured With This New
July 1st, 2015 by Holly Cornish
It’s not often the words cure and cancer are mentioned in the same breath, but one conventional oncologist and scientist sees no reason to hold back.
“This is an unprecedented time of progress in the history of cancer medicine and cancer research.
“Cure is something I think we’re going to be increasingly able to talk about.”
Let me tell you first about the scientific developments that got this guy so excited. Then I’ll explain why he’s dead wrong and why the “breakthrough” is just more expensive, misguided hype from mainstream medicine.
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The bold assertion that a cure may be in sight comes from Johann de Bono, professor of experimental cancer medicine at Imperial Cancer Research (ICR) and honorary consultant in medical oncology at the Royal Marsden Hospital in London, England.
Taking part in a recent television documentary aired in the UK, he was very optimistic because of new targeted drugs designed for people with certain genetic mutations in their cancer.
The new focused therapy
These drugs are aimed at specific molecular targets within tumors that help block the changes in cancer cells which supposedly drive their growth and spread.
The targeted drugs are quite different from standard chemotherapy, which offers mainly a shotgun approach and therefore destroys healthy as well as cancer cells.
There are a number of good potential targets within a cancer cell (too many targets, as I’ll explain in a moment). Some proteins are only present in cancer cells or are much more abundant in them or have mutated. There may be chromosome abnormalities in cancer cells but not healthy cells.
Once a good target protein has been found, a drug can be devised to reduce its activity, block it from binding to a receptor that it would usually activate, or shut down particular pathways for tumor progression.
Breakthroughs in the understanding of human genetics have enabled scientists to map a cancer cell’s DNA quickly, cheaply and in greater detail than ever before. This “gene sequencing,” as it’s called, allows for an individualized treatment plan.
Cheap and available for all
Just a few years ago it was exotic and rare. Apple founder Steve Jobs, when he had cancer, reportedly spent hundreds of thousands of dollars to have his DNA sequenced. Now practically any cancer patient can afford it.
At the London cancer institute’s Tumor Profiling Unit the aim is to make cancer medicine as precise as possible for each patient, monitoring for molecular alterations and mutations as treatment progresses.
They are also developing techniques to look at blood DNA to represent all the different tumors in metastatic disease. Looking for cancer cells in the blood will allow for constant monitoring of the patient’s condition and enable the doctors to make adjustments to the therapy as needed.
Targeted therapies in lung cancer
In the documentary we were told that “in young and old some targeted treatments are producing spectacular results.”
An example was given of a ten-year-old girl with inflammatory myofibroblastic tumor. This rare and aggressive cancer was located in her chest and around her airway. Her condition was considered terminal.
DNA mapping revealed that she had a faulty gene called ALK that was driving the cancer. Mice bred to carry this mutation were tested to find a suitable drug that would hopefully work on human patients.
The drug she was given worked tremendously well, reducing the tumor by 60% on the initial scan. Ultimately the tumor became very small and inactive. She takes the drug by mouth a few times a day to keep the disease in check.
Anecdotes are fine if the treatment is conventional
When one or even large numbers of patients become cancer free thanks to alternative treatments, the finding is derided within the conventional medical community. It’s described as anecdotal, not worthy of consideration. Where, they ask, are the randomized, double-blind, placebo-controlled trials?
So now we have a one-patient anecdote used to tout a conventional treatment. Let’s have a look at the drug the little girl is taking, called ceritinib. This was approved by the FDA in 2014 for patients with non-small cell lung cancer (NSCLC) who have the faulty ALK gene and whose disease has progressed even though taking another targeted drug called crizotinib.
Crizotinib itself had a response rate of 60%, with an average progression-free survival of nine months. “Response” merely means the patient experienced some improvement, not total remission, and only six in ten enjoyed even that much benefit.
But there’s some bad news, as described in a recent medical journal: “Enthusiasm for crizotinib has been tempered, however, by the emergence of drug resistance.”
As for ceritinib — the new drug to be called in when crizotinib fails — the trial that led to its approval had 163 adult participants with an overall response rate of 55% and an average duration of response of 7.4 months.
“Like those treated with crizotinib, patients treated with ceritinib invariably relapse because of the emergence of resistance. To date, little is known about the mechanisms of resistance to next-generation ALK inhibitors such as ceritinib.”
So the “spectacular results” mentioned in the documentary may be true for a lucky few, but not so spectacular for everyone else.
Also, while NSCLC represents 85% of all cancers of the lung, the ALK gene is mutated in only about 5% of them. The drug therefore will only benefit a small fraction of those with lung cancer.
This is a miniature cancer breakthrough, if you want to call it a breakthrough at all. What’s more, other targeted drugs for other types of cancer have run up against the same wall. This has been known for years. Yet targeted drugs continue to be proclaimed as the new “hope for a cure.”
Targeted therapies for prostate & ovarian cancer
For more examples of how limited these therapies are, let’s look at the other end of the age spectrum. The UK television documentary featured a man in his early 80s suffering from prostate cancer that had spread to the bone. His disease had remained stable for over a year with enzalutamide taken as oral tablets. This drug targets androgen receptors to inhibit their signaling ability.
He felt well during the treatment and was able to carry on with life as normal. This was a wonderful result for him personally.
Now let’s look at the study which led to its approval. Of the 1,199 patients in the trial, those taking the active drug lived on average 4.8 months longer than did those taking the placebo.
In another trial of 1,717 patients, the average survival for those taking enzalutamide was four months longer than the patients given the placebo.
While any extension of life for someone with advanced disease is welcome, I’m not sure that “spectacular” is an appropriate term to apply when only a few will see their lives extended much beyond what most other patients experience.
Another drug described as “spectacular in many ovarian cancer patients” was olaparib. This drug targets the BRCA oncogene found in 5% of breast and 10% of ovarian cancers.
In the trial, those with advanced ovarian cancer lived on average 7.1 months longer than did patients in the placebo group. A few lucky patients gained five extra years before relapsing.
The pattern with these targeted drugs in late stage cancer is the same. The drug is appropriate for only a small subset of patients — those with a certain mutation — among all those who have that type of cancer. Most patients will benefit by a number of months; only the fortunate few will see their lives extended by years. None appear to be cured.
“Resistance is inevitable”
The documentary did not hide the problem of resistance. Dr Udai Banerji put it this way.
“For a lot of our targeted treatments the cancer shrinks very quickly and in about 8 to 9 months or sometimes a year and a half the cancer stops responding.
“Resistance is inevitable, it’s going to happen. We have a huge effort trying to understand cancer evolution and the more you understand it, you can predict the next step the cancer is going to take.”
To be fair to Professor de Bono, he held out hope of cures becoming a possibility for “small numbers of patients.” For many he believed cancer could become a chronic illness that people are able to live with for many years, like high blood pressure or diabetes.
He was optimistic, but this optimism isn’t borne out by the results of targeted drug trials to date.
Although cancer is described as a genetic disease, it would be more accurate to call it a gene-related disease — and not all that related, either. According to some researchers, “Only 5–10% of all cancer cases can be attributed to genetic defects, whereas the remaining 90–95% have their roots in the environment and lifestyle.”
Don’t put your faith in the
gene-mutation theory of cancer
Long-time readers of this newsletter know I believe the gene theory of cancer is on the wrong track. The flaws in the gene theory have been confirmed by Professor Thomas Seyfried of Boston College in his landmark book The Metabolic Theory of Cancer.
The kind of gene-targeting drugs that so excite Professor de Bono don’t cure cancer quite simply because cvancer isn’t caused by gene mutations. Damaged genes are, at most, a sideshow. Cancer is almost certainly caused by malfunctions in a cell’s mitochondria or “energy factories.”
A typical cancer cell has not one but tens of thousands of DNA mutations. Some cancer cells are damaged in more than 100,000 places. And each type of cancer has a different set of mutations. Cancer cells are rarely identifiable, much less treatable, based on their mutation profile. And there’s isn’t a chance in the world that we can come up with 10,000 drugs to target 10,000 different mutations.
In short, the approach Professor de Bono advocates will do little to reduce cancer deaths. But it’s very successful at soaking up billions of research dollars and tons of media attention.
It would seem more sensible to focus research on the 90% plus, rather than the small numbers that will be candidates for targeted therapies.
With 30,000 different genes in each of our cells; with unstable cancer cells that create more genetic errors every time they copy themselves; with a disease that rapidly changes, it may be that cancer will always stay one step ahead of targeted therapies.
It seems to me the current enthusiasm for these treatments is based more on hope than expectation.