As mentioned in this blog on several times, we are always on the lookout for interesting scientific studies related to the treatment of pancreatic cancer with alternative or complementary treatment approaches.
The July issue of the journal Oncology Reports features research by Chen and colleagues from the University of Kansas Medical Center looking at the effect of the naturally occurring extract of the Pao Pereira tree from the Amazon forests on pancreatic cancer cell lines and in mice. This is a follow-up to earlier work out of Columbia University in New York City suggesting that a couple of plant extracts containing beta-carbolines (including Pao Pereira) appeared to inhibit cancer cell lines.
The current study is somewhat elaborate. The Pao showed inhibition of all five of the pancreatic cancer cell lines that were studied. Also, the combination of Pao Pereira plus gemcitabine showed synergy in the inhibition of these cancer cell lines. Finally, Pao and gemcitabine alone and in combination were presented to live mice with pancreatic cancer tumors (PACN-1) which were then serially scanned. The Pao Pereira showed significant action in inhibiting tumor growth. And the combination of Pao Pereira coupled with gemcitabine showed even more apparent activity (inhibition).
This is the kind of serious science that we love to see with alternative therapies. It appears at this early stage that Pao Pereira is worthy of further study – possibly eventually making its way to clinical trials. There are many stages to this of course, but this research is a refreshing clean look at an interesting potentially effective “new” treatment agent for the treatment of pancreatic cancer.
Time (and future research) will tell …
Dale O’Brien, MD
Interesting research over recent years into risk factors for adenocarcinoma of the pancreas have yielded the usual suspects – and a number of somewhat surprising candidates for pancreatic cancer. These include the smoking of tobacco products, onset of diabetes, large intake of alcohol, pancreatitis, (possibly) obesity, ABO blood typing status, and even infections such as those that cause hepatitis and dental disease.
Also, increasingly there is work showing relationships between infectious agents and several other gastrointestinal cancers – agents including the hepatitis B and C viruses, human papilloma virus (HPV), Epstein-Barr virus, and Helicobacter pylori (a primary cause of peptic ulcers).
In a study released July 10, 2013 in the journal Carcinogenesis, Michaud of Brown University has published an intriguing article discussing infectious agents in the role of the origins of pancreatic cancer that particularly fingers the above noted Helicobacter pylori and Porphyrmomonas gingivalis – a the bacteria particularly associated with periodontal disease.
Michaud further discusses the possible complex interplay of risk factors, the human immune system, and the possible effect of an “outside” infective agent in the triggering of the onset of pancreatic cancer.
This work presents an altogether exciting and inclusive thesis. Again, early days – but hopefully this thoughtful synthesis will serve as an impetus to better tease out the role that infectious agents may play in the onset of pancreatic cancer.
Dale O’Brien, MD
There are few hard and fast rules for the medical treatment of patients with metastatic pancreatic neuroendocrine tumors. Two agents which have shown promise include everolimus (Afinitor – Novartis) and temozolomide (Temodar ~ Merck).
An article by Kulke and colleagues at Harvard Medical School and the associated Dana-Farber Cancer Institute in Boston as published in the June 3rd edition of the journal Cancer offers the results of a phase I/II clinical trial for a regimen consisting of a combination of the drug agents everolimus and temozolomide for the treatment of advanced neuroendocrine tumors.
In this study, 43 patients with diagnosed metastatic neuroendocrine tumors were given this regimen in two cohorts, and with an escalation of temozolomide dosage after safeties were observed. The progression-free survival median for patients was found to be 15.4 months. The overall median survival point was not reached. The temozolomide treatment was limited to a total duration of six months.
The authors suggest that the toxicity profile appeared to be reasonable. And thus, with apparent activity and tolerable side-effects, the everolimus and temozolomide combination may be appropriate for the treatment of advanced neuroendocrine tumors, and certainly merits further investigation including trying to discover whether the regimen improves survival over the use of each agent alone.
Dale O’Brien, MD