Around one in three of us will be diagnosed with cancer during our lifetime. But research over the last couple of decades has led some researchers to the uncomfortable conclusion that as we age perhaps all of us develop hidden, or ‘covert’, cancer.
This is the subject of an interesting review
published in Nature Reviews Cancer
by Professor Mel Greaves
here at The Institute of Cancer Research in London. By defining ‘covert’ cancer as “a [growth] or tumour that is considered to be either malignant [or a] recognised precursor to malignant cancer”, Professor Greaves refers to many intriguing studies that have shown that many people have cancer without knowing they have it.
Many of these are post mortem studies, in which researchers look for cancer in the bodies of people who have died of accidental or non-cancerous causes. These studies have shown that pre-malignant lesions – essentially tumours that have not yet become cancerous – are present in a surprisingly large number of people.
Professor Greaves highlights a study
that detected pre-malignant lesions in the prostates of some men as early as in their twenties. The study reported that as men age, the prevalence of pre-malignant lesions increases until most men in their seventies or eighties have a hidden prostate cancer.
But why should the development of cancers, whether malignant or hidden, be such a common occurrence in humans? Professor Greaves, who is Director of the ICR’s new Centre for Evolution and Cancer, argues that it’s all to do with our lifestyles. Humans today live ‘risky’ lifestyles, examples of cancer risks include the inhalation of carcinogens through smoking, excessive UV exposure to white skin and the persistent hormonal drive of breast and ovarian tissue without the breaks applied by early pregnancy or breast-feeding.
Couple this with the error prone nature of cellular replication and our increasingly long lives during which genetic mutations can build up, and it seems inevitable the we will all develop some form of cancer in our lifetime.
This raises problems for population screening – if everyone develops some form of pre-cancerous lesion, how do clinicians differentiate between those that will remain indolent and those that will become malignant?
The new Centre for Evolution and Cancer
here at the ICR will use Charles Darwin’s theory of evolution via natural selection to help pin-point which pre-cancerous lesions are more likely to become malignant.
One way of doing this will be to measure the level of genetic diversity within a tumour. The greater the genetic diversity of cells within a tumour, the more likely it is that some of those cells will be selected for, leading to the evolution of a malignant cancer. By developing tools to measure the genetic diversity within a tumour, researchers at the Centre will be able to determine which precancerous lesions are more likely to become malignant. With this understanding, researchers hope to develop treatments that slow down or impede the evolution of malignant cancers.
Professor Greaves gives a striking example
of one such treatment. Non-steroidal anti-inflammatory drugs – a class of drugs of which aspirin and ibuprofen are members – reduce the development of overt cancer from pre-malignant lesions in the oesophagus by limiting the level of genetic diversity within the lesion.
“It is something of an irony of modern day oncology,” concludes Professor Greaves. “That the drug that does rather effectively restrain cancer is the oldest and cheapest that we have – aspirin.”
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