Cancer Biology - molecular biology of cancer cell and therapy

Most human neoplasms are monoclonal in origin, i.e. they arise from genetic mutations within a single affected cell; however, over subsequent divisions heterogeneity develops through the accumulation of further abnormalities. The genes most commonly affected can be characterized as those controlling cell cycle check points, DNA repair and DNA damage recognition, apoptosis, differentiation, and growth signalling. Proliferation may continue at the expense of differentiation, which together with the failure of apoptosis leads to tumour formation with the accumulation of abnormal cells varying in size, shape and nuclear morphology as viewed down the light microscope.

The kinetics of cancer cell growth appear to be exponential; however, the doubling times of human tumours are enormously variable. Mutations are common in the genes controlling a series of intracellular proteins, such as the cyclins and cyclin-dependent kinases, and oncogenes products such as c -myc , and the ras proteins that regulate proliferation. Proliferation may also be abnormal due to defects in the nuclear enzyme telomerase, contact with other cells, nutrient supply or cytokine signalling. Telomerase is an enzyme that prevents the normal shortening of DNA with each cell division that leads to senescence. Persistent telomerase activity helps to maintain the neoplastic state in cancer cells.

Cancer Tip Prostate Specific Antigen (PSA) has been called the most important tumor marker in oncology. Certainly in prostate cancer, it has revolutionized our ability to detect the disease early, as well as follow the course of the disease in patients after being treated with different therapies.

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Health Tip Tiny airborne droplets rapidly spread viral infections if an infected person coughs or sneezes and another person breathes these in. This photograph shows how far droplets are sprayed by a sneeze.

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