COX2 and BC a cumulative knowledge thread

[R.B.]

British Journal of Cancer (2006) 94, 346-350.
doi:10.1038/sj.bjc.6602942 Published online 17 January 2006

COX inhibitors and breast cancer

D Mazhar1, R Ang1 and J Waxman1

1Department of Cancer Medicine, Division of Medicine, Faculty of Medicine, Imperial College London, Room 1014 Garry Weston Centre, Hammersmith Campus, Du Cane Road, London W12 0NN, UK

http://www.nature.com/bjc/journal/v9.../6602942a.html

" Minireview

British Journal of Cancer (2006) 94, 346-350.
doi:10.1038/sj.bjc.6602942 Published online 17 January 2006

COX inhibitors and breast cancer

D Mazhar1, R Ang1 and J Waxman1

1Department of Cancer Medicine, Division of Medicine, Faculty of Medicine, Imperial College London, Room 1014 Garry Weston Centre, Hammersmith Campus, Du Cane Road, London W12 0NN, UK



Correspondence to: Professor J Waxman, E-mail: j.waxman@imperial.ac.uk

Received 3 October 2005; revised 6 December 2005; accepted 6 December 2005; published online 17 January 2006



"There is considerable evidence to suggest that prostaglandins play an important role in the development and growth of cancer. The enzyme cyclo-oxygenase (COX) catalyses the conversion of arachidonic acid to prostaglandins. In recent years, there has been interest in a possible role for COX inhibitors in the prevention and treatment of malignancy."

[R.B.]

Gurpreet Singh-Ranger1, Mohamed Salhab1 and Kefah Mokbel1, 2 Contact Information
(1) St George’s University of London, London, UK
(2) The London Breast Institute, The Princess Grace Hospital, 42-52 Nottingham Place, London, W1M 3FD, UK

Received: 28 May 2007 Accepted: 1 June 2007 Published online: 12 July 2007

http://www.springerlink.com/content/8310235677lm7875/

"Abstract There is a growing body of evidence that COX-2 expression s a fundamental step in breast cancer pathogenesis acting through prostaglandin-dependent and independent mechanisms. Epidemiological studies suggest that NSAIDs confer a moderate degree of benefit against breast cancer. However further work is required to establish how this enzyme system can be best manipulated for therapeutic benefit."

[R.B.]

REVIEW
Non-steroidal anti-inflammatory drugs for the prevention and treatment of cancer

* D. PEREG11Department of Internal Medicine A, Sapir Medical Center, Kfar Sava &
* M. LISHNER1,21Department of Internal Medicine A, Sapir Medical Center, Kfar Sava2Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv; Israel

*
From the 1Department of Internal Medicine A, Sapir Medical Center, Kfar Sava; and 2Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv; Israel

"Whilst their anti-inflammatory effect is well known, recent studies have demonstrated an unexpected effect in both the prevention and treatment of several types of cancer. The anticancerous effect of NSAIDs is believed to be mainly due to the inhibition of COX-2, which is overexpressed in many types of cancer and may play a major role in tumourigenesis."

[R.B.]

Effects of fatty acids and inhibitors of eicosanoid synthesis on the growth of a human breast cancer cell line in culture.
Rose DP, Connolly JM.

Division of Nutrition and Endocrinology, American Health Foundation, Valhalla, New York 10595.

http://www.ncbi.nlm.nih.gov/sites/en...t_uids=2224849

"Linoleic acid, an omega 6 FA, stimulated MDA-MB-231 cell growth with an optimal effect at a concentration of 0.75 microgram/ml, whereas oleic acid, an omega 9 FA, produced growth stimulation at 0.25 microgram/ml but was inhibitory at higher concentrations. Docosahexaenoic acid exhibited a dose-related inhibition of cell growth at concentrations ranging from 0.5 to 2.5 micrograms/ml; eicosapentaenoic acid, also an omega 3 FA, was less effective. Similar inhibitory effects occurred with saturated FAs. Indomethacin, which at high concentrations is an inhibitor of both the cyclooxygenase- and lipoxygenase-catalyzed pathways of eicosanoid synthesis, suppressed cell growth stimulation by an otherwise optimal dose of linoleic acid when present at 40 micrograms/ml. Experiments with piroxicam, nordihydroguaiaretic acid, and esculetin, other inhibitors of eicosanoid biosynthesis with varying selectivity for enzymes of the prostaglandin and leukotriene pathways, indicated that MDA-MB-231 cell growth was dependent on leukotriene rather than prostaglandin production."