Breast cancer is one of the most widespread cancers among women worldwide. In the US, it is the most common, and the leading cause of cancer related deaths among women between 45 – 64 years of age (Clegg et al., 2002; Ward et al., 2008). Early detection and improved treatment procedures have resulted in gradual decline in the number of deaths caused by the disease since 1990. Nevertheless, in 2009, the estimated death toll for the disease was 40,170 (American Cancer Society, 2009). The gravity of the disease therefore demands further research towards its early diagnosis, and for evaluating the prognosis of its course.
Breast cancer is a heterogeneous disease characterized by the complex interplay of molecular, genetic and physiological factors. Identification of some common characteristics, such as c-erb-b2/her-2 neu oncogene expression (Jimenez et al., 2000; Kallioniemi et al., 1991), mutations in the BRCA-1 (Miki et al., 1994; Welcsh et al., 2002), BRCA-2 genes (Venkitaraman, 2002), as well as ER/PR status (Ferno et al., 1990; Warnberg et al., 2001; Xu et al., 2003); have provided approaches for intervention. However, the totality of the molecular factors that contribute to the onset and progression of breast cancer remains uncertain. Continuing investigation into the heterogeneous tumor microenvironment is important not only in identifying additional molecular pathways that are involved in the onset and progression of the disease, but also to guide possible therapeutic approaches.
Cancer is characterized by several distinct features including uncontrolled cell division, resistance to growth inhibitors, evasion of apoptosis, invasion of distant tissues, ability to induce angiogenesis and immortality (Hanahan and Weinberg, 2000). Numerous reports (Coussens and Werb, 2002; Kim et al., 2009; Mantovani et al., 2008) indicate that inflammation is associated with the onset and progression of cancer, and it has been shown that along with genetic alterations, cancer cells also depend on the inflammatory microenvironment for the progression of metastasis (Kim et al., 2009).
The principal mechanism leading to pain and inflammation is the arachidonic acid (AA) pathway. AA is typically bound to the membrane phospholipids and is released by a group of enzymes known as the phospholipases A2’s. AA acts as the precursor of the group of bioactive lipids collectively known as the eisosanoids. There have been several reports that AA and the eicosanoids are intimately linked to cancer biology...