Biosignalling (Cell Division)

Certain genes, when mutated, can lead to cancer. The abnormal alleles encode proteins that are more active than normal proteins, promoting rapid cell cycle advancement. Typically, a mutation in only one copy is sufficient to promote tumor growth and is therefore considered dominant. Tumor suppressor genes, like p53, encode proteins that inhibit the cell cycle or participate in DNA repair processes.2 They normally function to stop tumor progression, and are sometimes called antioncogenes. Mutations of these genes result in the loss of tumor suppression activity, and therefore promote cancer. The body’s cells, especially the skin and blood cells, are produced anew on a daily basis. Their total number must be kept constant and so a mechanism must be in place to maintain a balance and remove any redundant cells. This mechanism, programmed cell death (PCD) or apoptosis, is an orderly, highly regulated process that functions to keep normal cell division in check. Inadequate PCD can lead to the spread of cancer or, for instance, babies born with fingers still joined. Responding to signals arising from outside and within the cell to initiate PCD, the cell undergoes a reduction in size as its components break down and condense. These cell fragments (apoptotic bodies) become enclosed in a membrane, walling them off and preventing them from damaging nearby cells. Phagocytic cells then engulf and destroy the fragments. Mutated genes that cause cancer are termed oncogenes.2 Oncogenes primarily encode cell cycle-related proteins. Before these genes are mutated, they are often referred to as proto-oncogenes.

 

References

1) Maton A, Hopkins JJ, LaHart S, Quon Warner D, Wright M, Jill D (1997). Cells: Building Blocks of Life. New Jersey: Prentice Hall. pp. 70–4

2) Wilbur, Beth, editor. The World of the Cell, Becker, W.M., et al., 7th ed. San Francisco, CA; 2009.

3) Kent, M. (2000). Advanced Biology. Pages 246 -247. Oxford University Press.

4)  M.B.V. Roberts, J. M. (1985) Biology for CXC. Pages 266 – 267. Cheltenham: Thomas Nelson and Sons Limited.

5)  Slack, J.M.W. (2013) Essential Developmental Biology. Wiley-Blackwell, Oxford.

6) Hayflick L; Moorhead PS (December 1961). “The serial cultivation of human diploid cell strains”. Exp. Cell Res. 25: 585–621.

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