How Cancer Arises?

Cancer can be explained as a disease when a group of unnatural cells grow uncontrollably by disregarding the standard rules of cellular division. Normal cells are constantly governed by signals that dictate whether the cell should try to portion, differentiate into another cell or die. Cancer cells create a degree of autonomy by these signals, resulting in uncontrolled growth as well as proliferation. If this proliferation is permitted to continue and distribute, it can become fatal. In actuality, almost 90% involving cancer-related deaths are because of tumour spreading — a procedure called metastasis.

The foundation of modern cancer biology rests on a simple principle — virtually all mammalian cells share similar molecular networks that control cell proliferation, differentiation and cell death. The prevailing theory, which underpins research into the genesis and treatment of cancer, is that normal cells are transformed into cancers as a result of changes in these networks at the molecular, biochemical and cellular level, and for each cell there is a finite number of ways this disruption can occur.

Phenomenal advances in cancer research in the past 50 years have given us an insight into how cancer cells develop this autonomy. We now define cancer as a disease that involves changes or mutations in the cell genome. These changes (DNA mutations) produce proteins that disrupt the delicate cellular balance between cell division and quiescence, resulting in cells that keep dividing to form cancers.


Cancer is clonal in origin

Current dogma states that cancer is a multi-gene, multi-step disease originating from a single abnormal cell (clonal origin) with an altered DNA sequence (mutation). Uncontrolled proliferation of these abnormal cells is followed by a second mutation leading to the mildly aberrant stage. Successive rounds of mutation and selective expansion of these cells results in the formation of a tumour mass.


Subsequent rounds of mutation and expansion leads to tumour growth and progression, which eventually breaks through the basal membrane barrier surrounding tissues and spreads to other parts of the body (metastasis). Death as a result of cancer is due to the invading, eroding and spread of tumours into normal tissues due to uncontrolled clonal expansion of these somatic cells.


Evidence for the clonal expansion model can be demonstrated with a simple but striking clinical example. The enzyme, glucose-6-phosphate dehydrogenase (G6PD) has two forms, G6PD-A and G6PD-B, which differ from each other by 1 single amino acid. Some people have cells that contain either type A or type B but no cell contains both, hence tissues are a mosaic of cells with these two types. Individuals who develop Chronic Myeloid Leukaemia (CML – a blood cancer) contain cancerous myeloid cells which all contain only one type of the enzyme, either type A or type B, but never both, clearly demonstrating that cancers are clonal in origin.


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