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Cancer, we now know, is a disease caused by the uncontrolled growth of a single cell. This growth is unleashed by mutations—changes in DNA that specifically affect genes that incite unlimited cell growth. In a normal cell, powerful genetic circuits regulate cell division and cell death. In a cancer cell, these circuits have been broken, unleashing a cell that cannot stop growing.
These tumors could also spread from one site to another, causing outcroppings of the disease—called metastases—in distant sites, such as the bones, the brain, or the lungs.
From several tons of pitchblende, four hundred tons of washing water, and hundreds of buckets of distilled sludge waste, they finally fished out one-tenth of a gram of the new element in 1902.
Down to their innate molecular core, cancer cells are hyperactive, survival-endowed, scrappy, fecund, inventive copies of ourselves.
“Traditional epidemiology,” Hunter reasoned, “is concerned with correlating exposures with cancer outcomes, and everything between the cause (exposure) and the outcome (a cancer) is treated as a ‘black box.’ . . . In molecular epidemiology, the epidemiologist [will] open up the ‘black box’ by examining the events intermediate between exposure and disease occurrence or progression.”
