The Genetics Behind Cancer
By Tsering Sherpa
The term “cancer” does not only seem daunting to the general public, it is also considered a formidable opponent to scientists and clinical researchers. The affliction cancer has caused humanity for the past thousand of years has yet to be relieved. Research for cancer treatments has come a long way since the past 250 years, including the establishment of the National Cancer Institute in 1937 under President Franklin D. Roosevelt and the 1971 establishment of the National Cancer Act under President Nixon. However, in comparison to the late 20th century, we have been exploring and releasing many new treatments more rapidly. Many of the general treatment options available to the public include treatments found in the 20th century, including surgery, radiation therapy, immunotherapy, and many others. Starting in the late 90s, scientists shifted their focus to studying anticancer genes (coinciding with the boom in genetics research, including the Human Genome Project), which are genes that specifically destroy tumor cells without harming normal cells when expressed. This catalyzed a new wave of experiments that studies anticancer genes in organisms other than humans to obtain a better understanding of how to use modified gene therapy to treat cancer with less severe effects.
In 1977, Richard Peto formulated a paradox, an observation that within the same species, the incidence of cancer does not correlate with the number of cells in an organism. This turned to the possibility of evolutionary considerations causing a variance in cellular carcinogenesis rates and poses the question- can we use the mechanisms that other organisms have to find a more efficient way to treat cancer? Recently, the Heterocephalus glaber, known as the naked mole rat, has been popular in different studies. They have been found to be resistant to cancer due to production of a high quantity of hyaluronic acid. The amount of hyaluronic acid in naked mole rats is about five times larger than in humans, and this large amount acts as a cage outside of the extracellular matrix and isolates any tumor development. This high molecular mass hyaluronan is produced by mutations in the HAS2 gene. Although scientists have found that all African mole rats share some mutations in the HAS2 gene, naked mole rats have a unique combination that contributes to their resistance to cancer and defy signs of aging.
It has also been suggested that a redundancy of tumor-suppressor genes (TSG) is a possible explanation for Peto’s paradox. This explanation has been supported with the recent observation that elephants possess 20 copies of the p53 anticancer gene. Humans only have one p53 gene. The p53 gene is responsible for quickly repairing damaged DNA.