Beginner's guide to genetics: Cancer genetics
BMJ 2005; 330 doi: https://doi.org/10.1136/sbmj.050252 (Published 01 February 2005) Cite this as: BMJ 2005;330:050252- Adrián J González, intern1,
- Juan J Morales, associate, researcher1,
- Leonora Luna, social worker1,
- Jazmín Arteaga, third year resident in medical genetics1,
- Osvaldo M Mutchinick, chief1
- 1Genetics Department, National Institute of Medical Sciences and Nutrition, Mexico
Cancer starts in a cell that loses genetic control. It always begins with one cell (an aberrant precursor) and then grows to give rise to a population of cells. This group of cells grow in a disorderly manner becoming different from the precursor. They have increased metabolism, divide rapidly, and develop certain characteristics, such as the ability to colonise new sites. These characteristics give cancerous cells an evolutionary advantage compared with normal cells.
DNA repair systems
Cells are constantly dividing. Genetic material is always duplicated and distributed in new cells. This high mobility of DNA increases the risk of mutations. Apart from the inherent risks involved in DNA duplication and cell division, carcinogens found in the environment--such as ultra violet radiation, hormones, or tobacco smoke--can disrupt the integrity of genetic information.
Often errors in DNA structure do not cause serious problems. Although changes in DNA occur every day, only one of 1000 accidental base changes remains as a mutation in DNA.1 This is thanks to DNA repair systems that detect errors and trigger enzyme mediated response that stop DNA duplication and repair the faulty section. Two of the most common DNA repair systems involve excision--one is the base excision repair and the other nucleotides excision repair. After recognition, both systems remove the deleterious base or segment, and using the other strand as a template, DNA polymerase adds corresponding nucleotides. DNA repair systems also induce some other responses to maintain healthy DNA--for example, they stimulate the cell cycle stop to allow DNA …
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