When it’s Time to Put Your Pancreatic Cancer Patients on a Diet

Last week, I had a discussion with a friend and colleague regarding our work and its application to cancers of almost every stripe. During our chat, I received a call from the infusion center requesting the clarification of an order. I responded to the nurse’s inquiry and returned to our conversation. Apropos, my guest inquired whether I ‘d had much success in pancreatic cancers. I smiled and explained that the call I had just received was regarding a patient with that exact diagnosis who is now approaching the one-year anniversary of our first meeting in June 2010.

At 59 years of age, the patient found himself diagnosed with pancreatic carcinoma that had virtually overtaken his liver. Visits to his oncologist and subsequent second opinions at UCLA and City of Hope offered few options. He returned to my care and we conducted a biopsy to examine his drug response profile. The patient could hardly have been more ill. Uncontrollable pain, abdominal distention, a liver that extended almost to his pelvic brim and tumor markers in the thousands that were doubling ever one to two weeks. We certainly had our work cut out for us.

I remember starting his treatment and leaving town for a week to attend the American Society of Clinical Oncology meeting in Chicago. After my departure, I was informed that his CA 19.9 (on his first cycle of therapy) had continued upward, cresting at 6,000 (normal is 0 — 30). I was greatly disappointed by the news. Pancreatic cancer is hard to treat, but I had felt confident that this patient would respond. And then, his pain diminished and he started winding off the industrial doses of narcotics that he had once required. His appetite and exercise tolerance both improved as well. The tumor markers began falling precipitously. And, over the coming month, that giant liver returned to normal.

The best news was the PET/CT that confirmed his dramatic response. The better news still, the subsequent PET/CT that revealed virtually complete resolution of all measurable disease. Oh, and yes, the normalization of the tumor markers.

I turned to my guest and said, “Yes, we can even fix pancreatic cancer in some patients. Would you like to meet one?” We walked together to the infusion center and I introduced the patient to my friend. As the patient sat receiving the final hydration of his, now maintenance, therapy, I realized how much weight he had gained. In fact, I said only half jokingly, “I’m going to have to put you on a diet.”

Now, there’s a change, a pancreatic cancer patient a year after diagnosis for whom my principle current concern is his weight gain. Weight Watchers anyone?

About Dr. Robert A. Nagourney
Dr. Nagourney received his undergraduate degree in chemistry from Boston University and his doctor of medicine at McGill University in Montreal, where he was a University Scholar. After a residency in internal medicine at the University of California, Irvine, he went on to complete fellowship training in medical oncology at Georgetown University, as well as in hematology at the Scripps Institute in La Jolla. During his fellowship at Georgetown University, Dr. Nagourney confronted aggressive malignancies for which the standard therapies remained mostly ineffective. No matter what he did, all of his patients died. While he found this “standard of care” to be unacceptable, it inspired him to return to the laboratory where he eventually developed “personalized cancer therapy.” In 1986, Dr. Nagourney, along with colleague Larry Weisenthal, MD, PhD, received a Phase I grant from a federally funded program and launched Oncotech, Inc. They began conducting experiments to prove that human tumors resistant to chemotherapeutics could be re-sensitized by pre-incubation with calcium channel blockers, glutathione depletors and protein kinase C inhibitors. The original research was a success. Oncotech grew with financial backing from investors who ultimately changed the direction of the company’s research. The changes proved untenable to Dr. Nagourney and in 1991, he left the company he co-founded. He then returned to the laboratory, and developed the Ex-vivo Analysis - Programmed Cell Death ® (EVA-PCD) test to identify the treatments that would induce programmed cell death, or “apoptosis.” He soon took a position as Director of Experimental Therapeutics at the Cancer Institute of Long Beach Memorial Medical Center. His primary research project during this time was chronic lymphocytic leukemia. He remained in this position until the basic research program funding was cut, at which time he founded Rational Therapeutics in 1995. It is here where the EVA-PCD test is used to identity the drug, combinations of drugs or targeted therapies that will kill a patient's tumor - thus providing patients with truly personalized cancer treatment plans. With the desire to change how cancer care is delivered, he became Medical Director of the Todd Cancer Institute at Long Beach Memorial in 2003. In 2008, he returned to Rational Therapeutics full time to rededicate his time and expertise to expand the research opportunities available through the laboratory. He is a frequently invited lecturer for numerous professional organizations and universities, and has served as a reviewer and on the editorial boards of several journals including Clinical Cancer Research, British Journal of Cancer, Gynecologic Oncology, Cancer Research and the Journal of Medicinal Food.

4 Responses to When it’s Time to Put Your Pancreatic Cancer Patients on a Diet

  1. Gary Brutsch says:

    Dr N

    On behalf of Amber and Mark’s family, I would like to thank you for your thoughtful concern regarding Mark’d health challenges.

    Your professional insight allowe us to make some very difficult decisions.

    These decisions, although painful were made with the knowledge that we had exhausted our options, and that Mark would benefit from the results of our decisions.

    Thank you

    Gary Brutsch……Amber Wynn

  2. Dr. Nagourney,

    Have you looked at low dose naltrexone for pancreatic cancer. Dr. Berkson in New Mexico has a patient with pancreatic cancer with liver mets 9 years out now. He came to his clinic when he was told to get his things in order by his oncologists in a major medical center. LDN upregulates the P16 and P24 cell inhibition pathways to prevent cancer cell reproduction. Dr. ian Zagon has identified this metenkephaliin pathway in 90% of the human cancer lines. It costs about 20 dollars a month and there are no side efffects. There is more to this and would be glad to talk to you about it. There is another new cancer therapy too that is totally harmless I uust learned about. Chemo is not effective in most cases as you know. It does not get to the root of the problem. The stem cells are still left intact.

    • Thank you for your comment. I am aware of the use of Naltrexone as a cancer therapy. It is a very interesting concept that connects the cell surface receptors for the opioids (met-enkephalin, etc.) to downstream signaling for cell proliferation and survival. Naltrexone has the advantage of superior oral bio-availablity (over the related Naloxone). While Naltrexone may have some agonist (potentiating) effects at high doses, it is mostly an opioid antagonist. Thus, it would appear that tonic opioid inhbition is the mode of action. The reports by Berkson (more recently addtional cases have been added) are extremely intriguing. As opiods are widely used in oncology the implications could be important. While I am far from expert in this area, I would speculate that this pathway may be operative in some patients. Again, with each patient manifesting their own unique cascade of cell signaling that can be perturbed by different classes of agents, including possibly the opioid antagonists. As the response rates for my patients who have used Naltrexone have been less dramatic, it may be that a small subset of patients have disease features that render them the best candidates. The tumor suppressive influences may be at the level of proliferation inhbition, but It could be of interest to more formally test this and related compounds to determine whether that subset can be identified in a laboratory platform.

      Thank you again for your interesting comment.

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