When an imaging test shows a mass, or a biopsy confirms that a tumour is malignant, the biological process has usually been underway for some time. This has consequences for how prevention is understood, although routine clinical consultations rarely have enough time to explain it in detail.

Throughout life, all of us produce cells with genetic errors. The immune system and DNA repair mechanisms remove most of them before they ever form a lesion. Having cells with mutations, therefore, is not the same as having cancer. The environment in which a cell lives, tissue oxygenation, chronic inflammation and the chemical exposures accumulated over the years can all influence whether a genetic alteration remains contained or eventually escapes tissue control.

Having cells with mutations is not the same as having cancer.

Cellular regulation can also be influenced by compounds that activate the cell’s own defence pathways. Early detection and established oncological treatment remain essential when they are needed, but before that point there is a period in which biological prevention still has a place, even if conventional medicine often has little time to describe it.

Paul Talalay brought this question into the laboratory. A pharmacologist at Johns Hopkins University, trained in biochemistry and with earlier work on enzymes and steroid hormones, he began studying in the 1990s whether compounds found in cruciferous vegetables could activate cellular defence enzymes with the same rigour used to assess a candidate drug. That line of research led him to sulforaphane.

The cancer research became more concrete in Qidong, a region of China where dietary exposure to aflatoxins had long been associated with a high incidence of liver cancer. Talalay, Fahey, Kensler and other researchers carried out randomised clinical trials there using broccoli sprout beverages. In the decades that followed these interventions, together with other public health measures, liver cancer mortality in the region declined significantly. Sulforaphane was one part of that documented history, although it cannot explain the whole decline.

In 2015, Cancer Prevention Research published a French clinical trial involving 78 men with biochemical recurrence of prostate cancer after prostatectomy, whose PSA levels had begun to rise again. For six months, some participants received 60 mg of sulforaphane daily, while others received placebo. PSA doubling time, an indicator of how quickly the disease may progress, was longer in the sulforaphane group: 28.9 months, compared with 15.5 months in the placebo group. The primary endpoint was not fully met, but the secondary findings were solid enough to justify further studies using higher doses.

Cancer is a process in which the body is involved for much longer than is usually explained. Diet and other daily exposures may influence the conditions around damaged cells before the disease becomes detectable. Studying these preventive mechanisms helps shift attention to an earlier stage, when tissue repair, defence and regulation may still affect the course of the process.