When developing complimentary strategies to treat cancers one way is to understand the action of the drug used to treat it and then look at research into nutrients/supplements and herbs that work on the same cell signalling pathways. An example of this approach is the drug Lapatinib. It works upon the cell signaling proteins that are over-expressed in certain kinds of cancer cells. To be exact, according to Wikipedia, Lapatinib is an epidermal growth factor receptor (EGFR) and HER2/neu (ErbB-2) dual tyrosine kinase inhibitor.
Lapatinib (INN) or lapatinib ditosylate (USAN), also known as GW572016, is an anti-cancer drug developed by GlaxoSmithKline (GSK) as a treatment for solid tumours such as breast and lung cancer. It was approved by the FDA on March 13, 2007, for use in patients with advanced metastatic breast cancer in conjunction with the chemotherapy drug Capecitabine (Xeloda TM). It is marketed by GSK in the U.S. as Tykerb and in Europe as Tycerb. Lapatinib is a once-daily oral drug indicated for women who have received prior treatment with the intravenous drug Trastuzumab (Herceptin TM) and cancer drugs called taxanes and anthracyclines. [1]
In patients with HER2+ metastatic breast cancer that has progressed following treatment with regimens that included an anthracycline, a taxane, and trastuzumab; randomized clinical trial has demonstrated that the addition of lapatinib to capecitabine delayed the time of further cancer growth compared to capecitabine alone.What if there are natural products that could have similar action?
Here are some links to herbs that work on the same and additional cell signalling pathways to Lapatinib:- Adv Exp Med Biol. 2007;595:1-75.
Curcumin: the Indian solid gold.
Curcumin exhibits activities similar to recently discovered tumor necrosis factor blockers (e.g., HUMIRA, REMICADE, and ENBREL), a vascular endothelial cell growth factor blocker (e.g., AVASTIN), human epidermal growth factor receptor blockers (e.g., ERBITUX, ERLOTINIB, and GEFTINIB), and a HER2 blocker (e.g., HERCEPTIN). Considering the recent scientific bandwagon that multitargeted therapy is better than monotargeted therapy for most diseases, curcumin can be considered an ideal "Spice for Life".
Natural health products that inhibit angiogenesis: a potential source for investigational new agents to treat cancer-Part 2.
Juravinski Cancer Centre and McMaster University (Department of Medicine), Hamilton, Ontario.
The herbalist has access to hundreds of years of observational data on the anticancer activity of many herbs. Laboratory studies are expanding the clinical knowledge that is already documented in traditional texts. The herbs that are traditionally used for anti-cancer treatment and that are anti-angiogenic through multiple interdependent processes (including effects on gene expression, signal processing, and enzyme activities) include Artemisia annua (Chinese wormwood), Viscum album (European mistletoe), Curcuma longa (curcumin), Scutellaria baicalensis (Chinese skullcap), resveratrol and proanthocyanidin (grape seed extract), Magnolia officinalis (Chinese magnolia tree), Camellia sinensis (green tea), Ginkgo biloba, quercetin, Poria cocos, Zingiber officinalis (ginger), Panax ginseng, Rabdosia rubescens hora (Rabdosia), and Chinese destagnation herbs. Natural health products target molecular pathways other than angiogenesis, including epidermal growth factor receptor, the HER2/neu gene, the cyclo-oxygenase-2 enzyme, the nuclear factor kappa-B transcription factor, the protein kinases, the Bcl-2 protein, and coagulation pathways. Quality assurance of appropriate extracts is essential prior to embarking upon clinical trials. More data are required on dose-response, appropriate combinations, and potential toxicities. Given the multiple effects of these agents, their future use for cancer therapy probably lies in synergistic combinations. During active cancer therapy they should generally be evaluated in combination with chemotherapy and radiation. In this role, they act as modifiers of biologic response or as adaptogens, potentially enhancing the efficacy of the conventional therapies or reducing toxicity. Their effectiveness may be increased when multiple agents are used in optimal combinations. New designs for trials to demonstrate activity in human subjects are required. Although controlled trials may be preferable, smaller studies with appropriate endpoints and surrogate markers for anti-angiogenic response could help to prioritize agents for larger, resource-intensive phase iii trials.
