A new view of cancer  pg. 3

COX-2 is not the only performer in this drama. During the past half-century, scientists have chronicled a burgeoning list of growth factors, cytokines, genetic switches and protein-chomping enzymes that play interacting—and overlapping—roles in inflammation and cancer.

These chemicals are generated in response to emergencies such as injuries and infection by a variety of cell types and through a variety of “signaling pathways,” including activation of the COX-2 enzyme and the resulting production of prostaglandins. They include:

  • Growth factors that trigger cell proliferation, and which block signals that otherwise would lead to cell death, a process known as apoptosis;
  • Enzymes that repair and “remodel” tissue after an injury, and which spur the growth of new blood vessels to feed it; and
  • Immune regulators, including cytokines, that call in the reinforcements of immune and inflammatory cells to fight infection and help heal wounds, and others that “call off the troops” to limit collateral damage to surrounding healthy tissue.

These pathways exist in exquisite balance. When the balance is tipped, or when certain genetic switches are turned on, certain growth factors and cytokines may be “over-produced” while others are suppressed. The result can be chronic inflammation, damage to tissues and abnormal growth. A growing number of scientists believe, therefore, that understanding the unique molecular and cellular “micro-environment” in which the tumor thrives is key to improving cancer therapy and prevention.

This is not an easy puzzle to solve. The “imbalance” of growth factors and cytokines that promotes cancer may differ depending on where in the body the tumor began and its stage of growth. The role of inflammation also may differ depending upon the circumstance.

In some cases, chronic inflammation may trigger tumor growth. Inflammatory cells, including mast cells, neutrophils and macrophages, can generate highly reactive molecules of oxygen and nitrogen that can literally punch holes in bacteria. Too much of this firepower, however, can damage the DNA of nearby cells, leading to out-of-control growth. Limiting inflammation in these cases could be an effective way to prevent the development of cancer.

Mutations in other cases may result from exposure to irradiation, carcinogenic chemicals or viral proteins. In this case, inflammation may be a “promoting” rather than initiating event. There is increasing evidence that the tumor can attract inflammatory cells, and use their growth-promoting factors to help it grow and spread. In this sense, the tumor “hijacks” the normal functions of inflammation for its own ends.

There is some evidence that tumor cells send out chemical signals—called chemokines—that attract inflammatory cells. According to one model, macrophages literally roll along the lining of blood vessels, following a trail of increasingly concentrated chemokines, like bloodhounds tracking a scent.

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