It can be said that every cell is a ticking time bomb of cancer. Isn't it odd then, that whales display similar cancer rates to their mammalian relatives, despite having up to 108 times as many cells? (Bredberg, 2009). This is exactly the paradox that baffled Dr. Richard Peto in the 1970's. The term 'Peto's Paradox' has been coined to describe this observation. Peto's Paradox is also very applicable to elephants, which led a group of evolutionary biologists to investigate. He states 'the mechanisms by which large bodied animals evolved enhanced cancer resistance are unknown' (Sulak, et. al, 2015). His team obtained the genomes of several elephants and other mammals, and noted a significant difference in the p53 gene, which codes for a tumor
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Inactivating mutations of the p53 gene are found in almost all tumors. Furthermore, if a human has even one mutant copy of the gene at birth, they have a 50% chance of cancer by age 30 (compared to a chance of 1% for individuals with two working copies) (Lustbader et al 1992). The protein works by binding to a specific site on DNA, which leads to the expression of another protein, p21. P21 interacts with a protein involved in cell division, stopping the process (Genes and Disease, 1998). Having nearly 20 copies of this gene would help elephants combat the proportionally higher number of tumors they …show more content…
Does p53 'hold the cure for cancer', as the Telegraph article states? The answer is a resounding 'maybe'. It turns out p53 has been a topic of research for many years. A 2000 study at Baylor determined that there was evidence of 'clinical activity' of p53 gene therapy (Nemunaitis, 2000). A 2001 in vitro study in Japan showed that gene therapy, in conjunction with radiotherapy, had 'remarkable synergistic effects in human prostate cancer cells' (Sasaki, 2001). Yet another study lasting from 2001 to 2003 in Beijing noted that patients treated with p53 gene therapy saw the rate of tumor disappearance increase by 231% (Zhang et al. 2005). Legions of clinical trials in the East returned remarkable results for p53 gene therapy. Consequently, the Chinese FDA approved the treatment, under the trade name 'Gendicine', in 2004 (Jia, 2007). The Gendicine has been very effective in its use, but hasn't been the cut-and-dry 'cure' - it is merely another weapon in our arsenal of treatment
Inactivating mutations of the p53 gene are found in almost all tumors. Furthermore, if a human has even one mutant copy of the gene at birth, they have a 50% chance of cancer by age 30 (compared to a chance of 1% for individuals with two working copies) (Lustbader et al 1992). The protein works by binding to a specific site on DNA, which leads to the expression of another protein, p21. P21 interacts with a protein involved in cell division, stopping the process (Genes and Disease, 1998). Having nearly 20 copies of this gene would help elephants combat the proportionally higher number of tumors they …show more content…
Does p53 'hold the cure for cancer', as the Telegraph article states? The answer is a resounding 'maybe'. It turns out p53 has been a topic of research for many years. A 2000 study at Baylor determined that there was evidence of 'clinical activity' of p53 gene therapy (Nemunaitis, 2000). A 2001 in vitro study in Japan showed that gene therapy, in conjunction with radiotherapy, had 'remarkable synergistic effects in human prostate cancer cells' (Sasaki, 2001). Yet another study lasting from 2001 to 2003 in Beijing noted that patients treated with p53 gene therapy saw the rate of tumor disappearance increase by 231% (Zhang et al. 2005). Legions of clinical trials in the East returned remarkable results for p53 gene therapy. Consequently, the Chinese FDA approved the treatment, under the trade name 'Gendicine', in 2004 (Jia, 2007). The Gendicine has been very effective in its use, but hasn't been the cut-and-dry 'cure' - it is merely another weapon in our arsenal of treatment