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War on Cancer: Why Can't We Win?


Why Can’t We Win the War?

What can we learn from the “war on cancer” metaphor that has anything at all to do with cancer?

First, if it’s a war, then it’s a civil war – one part of us rebelling against another part of us.

What happens in a civil war? When the two sides fight, the whole country becomes devastated. We start talking about killing off whole populations of people –the Armenians in the Ottoman Empire during World War I, the Jews in Hitler’s Germany before and during World War II, ten years ago the Tutsi in Hutu-led Rwanda, currently the Darfuri in Sudan.

But in fact, it’s not only the “enemy” who die. Plenty of “friendly” troops also bite the dust. The countryside is devastated, crops are destroyed, and famine rules the land.

Is it so different with current cancer therapies?

  • We try to kill off a population of cells – the cancer cells – which originally developed from our own body cells. They are our cousins, our own tribe.
  • Chemotherapy often does a pretty good job at killing cancer cells. The problem is that is does an equally good, or sometimes even better, job of killing our own cells – our hair, our mucous membranes, our intestinal (GI) tracts, our bone marrow and immune system.
  • The GI tract is so injured and inflamed that it can no longer function to absorb water and nutrients, or discriminate between useful and not useful, so it ends up just excreting everything, with incapacitating diarrhea.
  • We lose weight – in medical terms, we develop cachexia – and are no longer able to maintain sufficient muscle mass to move around. Eventually we die of malnutrition – whether because we simply cannot absorb food, or because of some of the more extreme diets we try, in an effort to starve out the cancer cells.
  • Our bone marrow is so devastated that we no longer have sufficient shock troops to deal with infections that come down the pike. We die of chicken pox, or pneumonia, or infections caused by our own normally friendly intestinal bacteria.
  • We may survive the first round of the battle, only to develop a recurrence of the cancer – or a secondary cancer – years later, this time no longer responsive to the drugs that appeared to be effective on the previous round.

Why are we not winning this war?

Dr. Judy Garber, in an interview for the Boston Globe in April 2011, is quoted as saying: “Changing behavior turns out to be a whole lot harder than figuring out which molecule interferes with which gene. It’s not that people don’t want to, it’s just very hard to do. Patients always ask me: Isn’t there going to be a way to fix that gene? That’s going to take a while.”

Women from breast cancer prone families get the breast cancer about 10 years earlier than their mothers did. Same genes, different environment, different lifestyles.

Can we do anything about the genes? Probably not.

Can we do anything about our diet and lifestyle? Absolutely yes.

Should we be doing more frequent screening? To quote Dr. Garber again, “For many people it’s counterintuitive that more screening is not always better… [People] always feel they would be safer if we would just look more often but that’s not always the case. The more you look, the more you find, but not all you find is worth finding.”

In an article in Fortune magazine in 2004, Clifton Leaf, himself a Hodgkins Lymphoma survivor, writes: “Hope and optimism, so essential to this fight, have masked some very real systemic problems that have made this complex, elusive, relentless foe even harder to defeat. The result is that while there have been substantial achievements since the crusade began with the National Cancer Act in 1971, we are far from winning the war.”[1]

Mr. Leaf interviewed researchers, physicians and scientists, asking them to tell him what we could do to actually win the war. What he discovered was pretty appalling.

Virtually all these experts offered testimony that, when taken together, describes a dysfunctional “cancer culture”–a groupthink that pushes tens of thousands of physicians and scientists toward the goal of finding the tiniest improvements in treatment rather than genuine breakthroughs; that fosters isolated (and redundant) problem solving instead of cooperation; and rewards academic achievement and publication over all else.

At each step along the way from basic science to patient bedside, investigators rely on models that are consistently lousy at predicting success–to the point where hundreds of cancer drugs are thrust into the pipeline, and many are approved by the FDA, even though their proven “activity” has little to do with curing cancer.

Researchers talk about the heterogeneity of tumors – meaning that they can be composed of cells which have mutated DNA, each group of cells within a single tumor bearing a different genetic signature, making it extremely difficult to find a chemotherapeutic agent that will kill them all.

Eric Lander, of the Whitehead Institute’s Center for Genome Research in Cambridge, Mass, is quoted in the same article: “There are only, pick a number, say, 30,000 genes. They do only a finite number of things. There are only a finite number of mechanisms that cancers have. It’s a large number; when I say finite, I don’t mean to trivialize it. There may be 100 mechanisms that cancers are using, but 100 is only 100.”

But part of the problem is that the experiments are done on mice, not human beings. And despite the fact that both mouse and human are mammals, their genes are clearly different. The model is not a good model. Tumors grown experimentally in mice behave differently than tumors grown spontaneously in humans.

Trillions of mice have been cured by experimental cancer drugs. But not trillions of humans.

So is the fault in the FDA which approves drugs based on drug trials in these flawed models? Or is the fault in the pharmaceutical companies which use the flawed models in their applications to the FDA?

It is not generally the original cancer that kills the patient, but rather the fact that cancer cells crawl or are surgically spilled into the bloodstream or into the lymph nodes and spread to distant organs. This process is called metastasis, and it is almost always metastatic disease that kills the individual, not the original tumor.

So why are we not researching the process of metastasis? We could be (a) discovering whether metastasis is an issue in any given patient, by means of testing of circulating tumor cells or (b) figuring out ways to prevent metastatic cells from latching on to new tissues and invading them.

In 2004, Mr. Leaf writes: “There are probably good biomarkers–proteins, perhaps, circulating in the body–that can tell us that cancer cells have begun the process of spreading to other tissues. As of yet, though, we don’t know what they are.”

In fact, tests of circulating tumor cells have been available in Europe and in Greece for many years.

RGCC was established in 2004 by Dr. Ioannis Papasotiriou in northern Greece. This laboratory has developed a method to identify, isolate and sort cells from peripheral blood, and to determine whether they are simply circulating tumor cells, or whether they also have cancer stem cell characteristics. Stem cells are the ones capable of migrating into distant tissues to create new and often genetically different tumors. They also have a way to grow the cells which are isolated, so that they can be tested against chemotherapeutic and so-called alternative, or botanical and biologic agents. Thus it is possible to get a very good idea as to which agents can be the most helpful in any given patient.[2]

Biofocus is a German laboratory which provides molecular analysis to determine whether circulating tumor cells are likely to be sensitive to specific families of chemotherapeutic and alternative agents. This lab provides an indirect test, but unlike the RGCC lab does not grow the circulating cells in tissue culture for direct analysis of kill rate.

Neither of these tests is accepted in the United States as valid, or even helpful, in determining potential chemotherapy for a patient with cancer. Insurance does not cover them, and few oncologists are guided by the results.

A search of PubMed for the terms “cancer stem cell” and “chemosensitivity” brings up on 1408 articles, the oldest published in 1976, most published since 2000. One article published in 2011 compared genetic tumor markers with actual tissue culture chemosensitivity testing, and concluded that actual chemosensitivity testing was significantly better at predicting patient response to drugs than were the genetic markers.[3]

And we still have hardly any options for testing chemosensitivity in the United States. We who use this form of testing[4] are forced to send our specimens outside the country in order to get this valuable information.

How can we possibly win this “war on cancer” if we cannot define the condition of the enemy, or its number, or its weak points? If we wait for the tests to be validated by multiple placebo controlled double blind studies, we are liable to wait for many years before we see any meaningful data.

In the meantime, over 1500 people are dying of cancer every day[5], many of treatment-related complications. If they have to die, at least they could die of something that has been shown to have some relevance to their particular individual tumor cells.

What if we are fighting the wrong war? What if the cancer is actually trying to send us a message? If we shoot the messenger, we’re liable never to hear the message it was trying to convey.

“I never asked to have cancer!” I hear you say.

“I am offended.”

“I can’t believe you would be so cruel, or so unthinking, or so uncompassionate, or so mean, or so small-minded as to suggest that I had some part to play in the development of my cancer.”

And yet…

“I know that I brought this on myself.” – from a patient with ovarian cancer who said she had pushed herself beyond her own limits. If we can agree that illness arises in the emotional body – as many would say – then it behooves us to help our patients find those areas in which they have unfinished business, so that they can make the choice whether to let it go, or to hang on to it.

Not that letting go of the issues that troubles them is necessarily a cure – in the physical body – for cancer. Sometimes the disease is just too far advanced for the best of our medical science to reverse. But, at the very least, there may come some peace, some resolution of an issue that has troubled them all their lives, and some hope for the future.

We only have control over our own actions, not those of anyone else – not our children, not our spouses, not our employers, not the person who denigrated or ignored our very existence.

We do have control over our own actions. We can choose to hold on to those old hurts. We can also choose to let them go. Whether we do so in life, or as we are approaching death is less important than what we choose to do, and what we choose to carry with us into the next life. We have the choice.

[1] Downloaded from 8/26/2012. Why we’re losing the war on cancer [and how to win it].[2] See for further information, and for papers published in the peer-reviewed literature.[3] Arienti C, Tesei A, Zol W et al. Peritoneal carcinomatosis from ovarian cancer: chemosensitivity test and tissue markers as predictors of response to chemotherapy. J Transl Med. 2011; 9: 94. doi: 10.1186/1479-5876-9-94.[4][5] Downloaded 8/26/2012 from the American Cancer Society website