I am posting about two items today. Originally, I was going to post only about Turkey Rhubarb (don’t you love that plant name?). But the “turkey” post brought me to reflect on another topic, i.e., conventional versus alternative approaches to the treatment of MM. First things first, though.

1. Turkey Rhubarb? A friend recently sent me a 2005 study by an MD Anderson research team on plant polyphenols and chemosensitization, which I am going through bit by bit. The bit I looked at yesterday concerns an active component of Turkey Rhubarb (scientific name: Rheum palmatum) called emodin. By the way, the roots and rhizomes of this plant have been used in traditional Chinese and Japanese medicine for centuries. And its extract, emodin, has many medicinal properties; for instance, it is antiaggregant, anti-inflammatory, antimutagenic, antiseptic, antitumour, antiviral, cathartic, cytotoxic, purgative, immunosuppressive, antispasmodic, styptic and viricidal!

The abstract of the above-mentioned MD Anderson study can be seen at: http://tinyurl.com/2k3pea The full study reports that emodin may sensitize cancer cells to chemotherapy, and also kills human promyeloleukemic HL-60 cells in vitro. The MD Anderson researchers examined the effects of emodin on a variety of cancers, from lung to breast cancer, but I found no mention of MM.

So does this extract have any connection to MM? You betcha! 😉 A quick online search took me to the March 2007 issue of Molecular Cancer Therapeutics, which features a study titled: Emodin has a cytotoxic activity against human multiple myeloma as a Janus-activated kinase 2 inhibitor (http://tinyurl.com/38a7om). I wanted to understand what Janus-activated kinase 2, or JAK2, meant, so I looked it up and found the following study: http://tinyurl.com/225l93, according to which IL-6 and the subsequent JAK- dependent signaling pathways are essential for MM cell proliferation. Okay, so anything that inhibits that process is absolutely brilliant! Back to the Molecular Cancer Therapeutics abstract. It concludes that emodin inhibits interleukin-6 €”induced JAK2/STAT3 pathway selectively and induces apoptosis in myeloma cells via down-regulation of Mcl-1, which is a good target for treating myeloma. Taken together, our results show emodin as a new potent anticancer agent for the treatment of multiple myeloma. This all sounds very promising. I just hope more studies are done on this compound, as well as on many others!

2. Conventional/Alternative Food for Thought. However, more importantly, the opening statement of the MD Anderson study abstract provides some serious food for thought: The treatment of cancer with chemotherapeutic agents and radiation has two major problems: time-dependent development of tumor resistance to therapy (chemoresistance and radioresistance) and nonspecific toxicity toward normal cells. Many plant-derived polyphenols have been studied intently for their potential chemopreventive properties and are pharmacologically safe. This is not a new issue for me. I have been thinking along the same lines in recent months. And apparently, I am not the only one, as you will see below

One of the main problems with MM is that eventually the nasty malignant cells become resistant to chemotherapy. Unlike curcumin (just as an example!), conventional treatments do not have the ability to distinguish between normal and cancerous cells. What I hope to achieve with my alternative research is to develop a non toxic but effective alternative protocol that will target only my malignant cells, leaving my normal cells alone.

When I read about what is going on in the conventional MM treatment world, even my non-medical, non-scientific brain is able to figure out that the idea of a multi-pathway attack seems to be the predominant current approach. In other words, conventional chemotherapy drugs are given mainly in combination, not one at a time. And in fact, this morning I read some of the findings of the 11th International Myeloma Workshop just held in Kos, Greece (it ended yesterday). The most effective treatments for patients with relapsed MM, according to the IMF write-up (http://tinyurl.com/3atnmj), are as follows: a. Revlimid plus Dexamethasone; b. Velcade (bortezomib) plus cyclophosphamide and prednisone, and c. Velcade, Revlimid and a steroid. The list of current MM conventional clinical trials (about 300 or so) consists mostly of combinations of various drugs, many of which have been around for some time.

These findings lead me to believe that I am on the right track, except that in my case I want to find a protocol that I can keep modifying, if necessary, in order to keep engaging my MM cells in a sort of battle, but at the same time confounding them–attacking them from different pathways. If my approach works, great. If not, I will find something else (how about that for a positive thought on a sunny Sunday morning?). Only time will tell if my approach is correct, but, as usual, I remain confidently and stubbornly cheerful! Have a great Sunday! 🙂