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CANCER: WHAT CAUSES MALFUNCTION IN ONCOGENES AND TUMOUR SUPPRESSOR GENES?
It is clear that a number of crucial control elements called genes within the cell have to be altered before it becomes cancerous. What we have not yet said is how these alterations that produce the malfunctioning genes actually occur. A few of the processes that damage the genetic material are well understood, but most can only be described in very general terms. A small number of well-understood examples comes from the study of rare inherited cancers like retinoblastoma. Here it is easy to understand how the inheritance of an abnormal gene from parents can put the child at risk of developing a cancer. There are other examples of inherited cancer patterns. Perhaps the most closely studied is a condition (called familial polyposis coli) in which multiple growths occur in the bowel, many of them turning into cancers. Here again, the inheritance of an abnormal gene from parents puts the patient at risk of developing a cancer. However, we have already said that cancers that clearly run in families represent a small minority. Studying them has given important insights into how cancers develop but cannot tell us what happens for most common cancers where no clear family pattern exists. For these cancers it is likely that the oncogenes and tumour suppressor genes are damaged by factors present in the environment. There are very many chemicals which are known to damage DNA, our genetic material.
Such substances are usually referred to as mutagens (that is mutation-generating) and when they are capable of causing cancer they are called carcinogens (that is cancer-generating). We believe that exposure of normal cells to damaging substances in the environment produces the changes in oncogenes and tumour suppressor genes that lead on to the development of a cancer. We know that many of the environmental factors which appear to be associated with the development of cancers, each of which will be discussed in some detail in subsequent chapters, are capable of damaging DNA. We do not yet know which environmental factors cause consistent damage to particular oncogenes or whether the damage can (often) occur in many different oncogenes. Perhaps, when we do have this knowledge, the process of preventing cancer will become much simpler to plan and explain. For the time being, the new biology has provided us with an understanding of how cancers grow and what the essential targets for carcinogens are. It has not yet filled in all the gaps to explain step by step the link between cancer-causing substances in the environment and the development of the cancer in the patient.
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Cancer