Gene ral Hea lth Multicellular organisms appeared on earth 700 millions years ago. Since then, organisms and their DNA have continuously evolved and in the process mistakes or mutations have occurred. While the processes of evolution and mutation have led to the development of modern man and indeed all of the natural world in which we live today, it could be argued that mutations have also led to the evolution of cancers. Medical scientists have concluded the presence of cancer is an inevitable consequence of our make-up, as a multicellular sexually reproductive organism and consequently cancer is “a statistical inevitability of nature”. While DNA has evolved over millions of years our understanding of cancers has evolved only over the last two centuries. We have gone from the days of the ancient Greeks, who explained cancers as the result of unbalanced “black bile” that also produced depression (equally lethal in some cases); to the days of the medieval physicians who used magic and prayers to “control the demons” that caused “diseases with no cure”; to the present day, when researchers have unscrambled the genetic code of DNA and the secrets of genes to completely map the human genome and the cancer genome. And with this greater understanding has come improved management and treatments of specific type of cancers. Take, for instance, colorectal cancer - medical specialists are now able to look inside the heterogeneity of colon cancers and identify different subtypes of disease categorised according to their gene expression, mutations, pathways alterations, RNA or protein expression. They have found five subtypes. The first subtype affects predominantly the right colon and is more common in older people and females. A significant proportion has hypermutation, microsatellite instability MSI, BRAF mutation and immune activation. The second subtype affects mainly the left colon. These cancers are microsatelite stable MSS, have high chromosomal instability CIN, p53 mutation, overexpression of epithelial markers, MYC and WNT pathway activation. The third subtype also has epithelial markers as well as a heterogeneous CIN and MSI. Many are K ras mutant and more frequently overexpress IGFBP 2. The fourth subtype usually affects young people and presents in advanced states. These have mesenchymal expression, TGFB and VEGF pathway activation and NOTCH 3 overexpression. The fifth group have immune and stromal infiltration and variable epithelial mesenchimal activation. Researchers now have evidence that not all colorectal cancers are equal. Each subtype responds differently to treatment and patients with the different colorectal cancer subtypes have different prognoses. pindaramagazine.com.au Pindara Magazine 23
Pindara Private Hospital Magazine - Issue Five
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