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From the Townsend Letter
July 2013

War on Cancer
FBI and FDA Raid a Laetrile-Using Clinic
by Ralph Moss, PhD
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On April 23, 2013, agents of the Food and Drug Administration (FDA), the Federal Bureau of Investigation (FBI), and the Oklahoma Medical Board raided an alternative cancer clinic in south Tulsa, Oklahoma. They descended on the Camelot Clinic, 6804 S. Canton St., because its owner, Maureen Long, was using laetrile (amygdalin) in the treatment of cancer patients.
FDA documents, obtained by a local television station, show that the government sent in an undercover agent in January 2012, posing as the husband of a cancer patient.
At this writing, the clinic remains closed.
FDA spokesman Christopher Kelly said, "We don't provide any comment on ongoing investigations." But sources told News On 6 that the reason for the raid was the clinic's use of the apricot kernel derivative, also sometimes known as vitamin B17.
"Listen, my wife's dying, and we don't want to go with chemotherapy and radiation," said a man at the scene, Sam Bass. He added that his wife, Yvonne, was battling a recurrent melanoma (a potentially deadly skin cancer). She had been cancer free for five years, but her cancer had come back.
Melanoma is frequently treated by repeated surgery, but this often falls short of a cure.
"She just couldn't tolerate the surgeries anymore, so we went natural, changed her diet," Bass said.
The couple said that they had been in Tulsa for eight days. As they were leaving the Camelot Clinic, the FDA and FBI agents showed up. Bass said the agents asked him to leave his wife's medication behind.
"For us, this was a hope and they took our hope away," said Bass, with simple eloquence. "They took our rights, in my opinion, for me and my wife to choose how to treat her." Later in the day, reporters saw federal agents carrying boxes from the business and loading them into official vehicles.
As for Bass, he said he did not know that laetrile was outlawed, but didn't care. Without it, he said, his wife may not survive her recurrent cancer.
"I just want my wife to get well. I've got three kids at home, they need their mom. I need my wife," he told the local reporters.
Thus, 60 years after first being denounced by the medical establishment, this persistent apricot kernel derivative continues to cause controversy in the US. There are many major issues raised by raids such as this: First, is there any possibility that an agent derived from apricot kernels could have efficacy of any sort against cancer? Second, do sane and sentient adults, such as the Basses, have the right, when confronted by recurrent cancer, to choose treatments that are not favored by the oncology community?

Get Ready for 'Precision Medicine'
On March 29, 2013, Science issued a Special Report on Cancer Genomics. In their introduction, the editors assert that the greatly reduced cost of sequencing a human cell's DNA, its genome, is leading to a "Medical Renaissance."
This reflects the prevailing view that the genetic basis of cancer is a cornerstone of modern cancer research. Ask most scientists the cause of cancer and they will say, "genetics." Cancer, they say, arises in our genes and so, logically, we have to analyze the total genome in order to devise effective treatments.
Genetic explanations are very old. A century ago, most scientists thought that cancer some sort of hereditary flaw that was passed along through the generations.
"Nothing about cancer is more generally accepted than its hereditary nature," wrote the famous pathologist James Ewing, MD, in 1922.
What Ewing was referring to was the view that cancer is inherited through the germ cells. (He himself remained skeptical.) But only 5% to 10% of tumors have a strong hereditary cause. In breast and ovarian cancer, for instance, the BRCA 1 and BRCA 2 genes are the exception, not the rule.
Geneticists then revived the somatic mutation theory (SMT) of Prof. Theodor Boveri. Today, when scientists say that cancer is genetic, they do not mean that it is predominantly hereditary (Siteman 2013). They mean that cancers arise in body cells that have acquired a series of mutations. These turn the mutated cell into an "early founder cell of a tumor" (Fey 2004).

Prof. Swanton Shakes Biologists
Science described a revealing report on the work of Charles Swanton, MD, showing that "tumors are a mosaic of different cells" (Gerlinger 2012). This revelation, Science said, has "shaken cancer biologists and clinicians" (Kaiser 2013). Swanton showed that a single person's kidney cancer was extremely diverse in genetic makeup. Add distant metastases and you have a veritable ecosystem of abnormalities. Other patients with the same diagnosis had radically different genes. Targeting one or a few genetic abnormalities, then, is not likely to have much clinical impact.
Genetic analysis was supposed to simplify the chaotic appearance of cancer and "provide temporary relief from this angst" of not knowing where cancer was coming from, to quote Dr. Edison T. Liu, president and CEO of the Jackson Laboratory, Bar Harbor, Maine.
"But what briefly seemed tidy quickly became messy again," said Liu. Greater knowledge revealed a "surprising fact ... every tumor contains hundreds of thousands of mutations, most of which affect only a small percentage of the cancers in any tumor type."
Yes, you read that right: hundreds of thousands of mutations!

What About Targeted Agents?
The dozen or so "targeted" agents approved by the FDA have side effects, some of which are serious. If you put 2, 3, or 10 of these new drugs together, you may get a plethora of interactions that make a mockery of the idea of "precision medicine."
In the same issue of Science, Prof. Bert Vogelstein of Johns Hopkins University drew a picture of the "cancer genome landscapes." He and his coauthors are geneticists, not skeptics. Yet they write that "in common solid tumors such as those derived from the colon, breast, brain, or pancreas, an average of 33 to 66 genes display subtle somatic mutations. ..." And certain tumor types display many more mutations. Melanomas and lung tumors contain 200 important mutations per tumor. Lung cancers from smokers have 10 times as many mutations as those of nonsmokers.

How Effective is Tarceva?
The data that have accumulated since the introduction of the first "targeted" agents do not lead to confidence in the efficacy of this type of treatment for common types of cancer.
For example, EGFR (epithelial growth factor receptor) kinase is often mutated in non-small cell lung cancer (NSCLC). Oncologists currently have at their disposal two EGFR inhibitors: gefitinib (trade name Iressa) and erlotinib (Tarceva). In the US, about 15% of patients with NSCLC harbor EGFR mutations.
Yet, according to the American Society of Clinical Oncology (ASCO)'s Guidelines: "As of yet, there is no evidence of an overall survival (OS) benefit from selecting treatment based on performing this testing [of EGFR mutations]" (Keedy 2011).
FDA approved gefitinib (Iressa) for the treatment of lung cancer in May 2003. Two years later, in June 2005, it issued an alert withdrawing approval, due to lack of evidence that the drug actually extended life. In an unusual decision, FDA stated: "The medicine should be used only in cancer patients who have already taken the medicine and whose doctor believes it is helping them. New patients should not be given Iressa® because in a large study Iressa® did not make people live longer" (2005).
Erlotinib (Tarceva) then replaced gefitinib as the treatment of choice for EGFR-positive lung cancer. But serious questions remain. How effective is erlotinib (Tarceva) as a treatment for this disease?
In the topical clinic trial, which tested first-line erlotinib in patients with advanced non-small cell lung cancer unsuitable for standard chemotherapy, the median overall survival did not differ significantly between the two groups. Survival in the erlotinib (Tarceva) group was 3.7 months vs. 3.6% in the placebo group. In patients who did not develop a rash, survival was 30% less than doing nothing (placebo)!
These patients were not prescreened for the presence of EGFR mutations. Vogelstein warns:
Before instituting treatment with such agents, it is imperative to determine whether the cancer harbors the mutations that the drug targets. Only a small fraction of lung cancer patients have EGFR gene mutations or ALK gene translocations, and only these patients will respond to the drugs. Treating lung cancer patients without these particular genetic alterations would be detrimental, as such patients would develop the toxic side effects of the drugs while their tumors progressed. (2013)
But what actually happened when one restricts use of erlotinib to the minority of patients who have these telltale mutations? Not much. Here are the results of the EURTAC trial, also published in Lancet Oncology. "At data cutoff, median PFS [progression-free survival] was 9.7 months in the erlotinib [Tarceva®] group, compared with 5.2 months ... in the standard chemotherapy group ... " (Rosell 2012).
This study says nothing about overall survival (OS): there is a big difference between progression-free survival (PFS) and more meaningful overall survival. However, even when treatment is restricted to the EGFR group the increase in progression-free survival in this clinical trial was only about 4 months.
Results like this show why it is difficult to accept the current dogma that cancer is a genomic disease that it will be largely solved through drugs chosen by the genomic analysis of tumors. All that will be accomplished by the total genomic analysis of tumors is discovery of myriad new mutations, each of which will then have to be treated with its own drug.

'Arms Race' Grips War on Cancer: Cornell and Sloan Ready for Battle
Weill Cornell Medical College/New York-Presbyterian Hospital is building a $650 million research tower to process genetic information about patients. Memorial Sloan-Kettering Cancer Center, across the street, has completed a $550 million tower for the same purpose.
The same thing is going on at Harvard Medical School, Phoenix Children's Hospital, Beth Israel Deaconess Hospital, and Johns Hopkins Medical School. Everyone wants in on the gold rush of genomic sequencing. Not long ago Steve Jobs paid $100,000 to have his genome sequenced. The price now is $5 to $10,000. Before the year is out, the cost may dip below $1000. The New York Times called this rush to provide genomic sequencing "an arms race within the war on cancer," driven by the fact that the "medical establishment is moving toward the routine sequencing of every patient's genome." According to advocates, the goal is "precision medicine." Notice how last year's slogan, "personalized medicine," has already become outdated!
This is an enormously expensive addition to medicine, just at a time when the country is trying to get its health costs under control. But is this really about improving patient well-being, or about providing fabulous profit opportunities to hospitals, laboratories, and drug companies, who will provide new "targeted" drugs based on the ensuing tsunami of data?
In a New York Times op-ed last month, oncologist and former White House adviser Ezekiel K. Emanuel, MD, noted: "Of the 13 anticancer drugs the Food and Drug Administration (FDA) approved in 2012, only one may extend life by more than a median of six months. Two extended life for only four to six weeks. All cost more than $5,900 per month of treatment" (2013).
We will see an explosion of such drugs in the near future. But whether they will positively affect patients' overall survival (OS) remains to be seen.

Metabolic Treatments Go Begging
I suggest that more attention be paid to treatments that influence abnormal tumor metabolism. Targeting metabolism has the virtue of simplicity. Decades ago the Nobel laureate Otto Warburg, MD, PhD, showed that most cancer cells produce a significant amount of their energy via glycolysis (fermentation), rather than only through the oxidation in the mitochondria, as happens for the most part in normal cells. This fundamental fact (the basis of the PET scan) creates an opportunity to design treatments to attack a wide variety of tumor types, without the need for "precision medicine" that target an individual tumor's extensive and erratic genetic variations.
An undue emphasis on cancer genomics is having a harmful effect on other promising avenues of treatment. Metabolic treatments go begging, while the major cancer centers spend billions to process a flood of genetic information of dubious importance. This is an unsustainable development.

Emanuel EJ. A plan to fix cancer care. New York Times. March 23, 2013.

Ewing J.
Neoplastic Diseases. 2nd ed. Philadelphia: Saunders; 1922:105.

FDA. Gefitinib (marketed as Iressa) information. FDA Alert (6/2005) [Web page].

FDA, FBI, Oklahoma Medical Board investigation shuts down Tulsa cancer clinic Camelot Cancer Care [online article]. Available at Accessed April 24, 2013.

Fey MF. The biology of cancer. In: Cavalli F, Hansen HH, Kaye SV, eds.
Textbook of Medical Oncology. 3rd ed. Boca Raton: CRC Press; 2004.

Gerlinger M, Rowan AJ, Horswell S, et al. Intratumor heterogeneity and branched evolution revealed by multiregion sequencing.
N Engl J Med. 2012;366(10):883–892.

Kaiser J. The downside of diversity.
Science. 2013;339(6127):1543–1545.

Keedy VL, Temin S, Somerfield MR, et al. American Society of Clinical Oncology provisional clinical opinion: epidermal growth factor receptor (EGFR) Mutation testing for patients with advanced non-small-cell lung cancer considering first-line EGFR tyrosine kinase inhibitor therapy.
J Clin Oncol. 2011;29(15):2121–2127.

Marte B. Milestone 2: (1890) Cancer as a genetic disease: lack of principles [online article]. Nature.

Rosell R, Carcereny E, Gervais R, et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial.
Lancet Oncol. 2012;13(3):239–246.

Siteman Cancer Center. Information about hereditary cancers [online article]. 2013. 173.

Vogelstein B, Papadopoulos N, Velculescu VE, et al. Cancer genomic landscapes.
Science. 2013;339:1546–1558.

Ralph W. Moss, PhD, is the author of 12 books on cancer-related topics. The former science writer at Memorial Sloan-Kettering Cancer Center, for 35 years Moss has investigated the validity of many cancer treatments. He currently directs the Moss Reports, a library of reports for patients on over 200 different cancer diagnoses.


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