To an individual who becomes the cancer patient, the cancer may become evident in two ways. Either it affects the person's perception of their normal body - producing a change in their physiology, pain or a new symptom such as bleeding - or it becomes evident (apart from in cancers such as leukemias) as something that can be felt as a "lump". This is a tumour – a growth of tissue that can be felt as an abnormal mass or interferes with body function.

The tumour in an adult solid cancer such as carcinoma of the colon, breast or prostate usually appears as a firm pink or whitish nodule when is revealed by a surgeon. It looks very different from the surrounding tissue. This is because it is indeed very different from that tissue in its biochemistry and physical characteristics. Typically it is deficient in oxygen (hypoxic), has a fluid content that is slightly acidic (pH 6.8-7.0) and has raised fluid pressure. As well, because of its altered energy metabolism it has low levels of glucose and high levels of lactic acid (which contributes to the acidity). If we examine the tumour microscopically we find that the tissue has a higher proportion of the cells that gave rise to the cancer (typically epithelial cells, the kind of cells that protect a surface or line secretory glands in different organs), with a disordered array of supportive cells (''stroma'') and blood vessels. It’s a very abnormal tissue in addition to having abnormal cells.

For some years the Blay laboratory has been researching the changes in tissue biochemistry that as a result of this altered tissue physiology can change cell behaviour in a way that helps the cancer to grow, resist host defences, and spread. These include alterations in the molecules that underlie the framework of energy balance (such as the nucleosides and certain cellular enzymes) and a diverse array of small molecules that regulate many tissue functions called the eicosanoids. Such molecules can regulate proteins on the cancer cell surface that either help direct the cancer cells to other organs including two that we have studied, CD26 and CXCR4.

The results of this research open up the possibility that we could manipulate these mechanisms to downplay the role that they play in facilitating the spread of cancer. This is our current focus in study of the tissue microenvironment, both in the initial (primary) tumour and the secondary deposits (metastases) that are the result of cancer spread.