The detection of a specific genetic mutation may help identify liver cancer patients who are at a higher risk of experiencing a cancer recurrence following surgery, according to a recent article published in the Archives of Surgery. Patients with this mutation may benefit from additional and/or more aggressive therapy to help prevent the return of cancer.
Individualizing treatment strategies according to differing biological characteristics of cancer is emerging as a new focus in the treatment of cancer. There are two important benefits of individualizing therapy: 1) the achievement of optimal treatment strategies for each patient, and 2) the sparing of some patients from unnecessary treatment. Since cancer responds differently to treatment according to unique and differing biological properties, therapies must be tailored accordingly in order to produce optimal treatment outcomes.
The liver is the largest organ in the body and is responsible for over 500 functions, including the secretion of glucose, proteins, vitamins and fats, the production of bile, the processing of hemoglobin and the detoxification of numerous substances. Primary liver cancer, sometimes called hepatocellular carcinoma, starts in cells of the liver and can spread, through blood or lymph vessels, to different parts of the body. The treatment of liver cancer depends on the size, and specific stage, or extent of the cancer. Currently, the only curative treatment option for liver cancer is surgical removal of the cancer (resection). However, many patients experience a cancer recurrence following surgery. This has resulted in extensive ongoing research efforts to determine factors associated with an increased risk of developing a recurrence, and thus enable treatment to become more individualized.
Many different types of cancers develop due to a mutation (alteration) in a certain gene called the p53 gene. This gene, sometimes called the “cell suicide” gene, keeps normal cell replication under strict control. If there is an abnormality in a cell, the p53 gene normally stops replication of this damaged cell, inhibiting further progression of any detrimental abnormality. However, in cells that have a mutation with their p53 gene, there is no restraint on abnormal replication, leading to uncontrolled, rapid growth of the cells – the hallmark trait of cancer.
Researchers from Taipei, Taiwan recently conducted a clinical trial evaluating the implications of a p53 mutation in liver cancer patients. All of the patients had comparable extent of their disease. These patients had their cancer surgically removed and then tested to determine if the certain mutation existed in the cancer cells. Nearly 70% of all the patients tested positive for a mutation within their p53 gene. Interestingly, 93% of the men in this study tested positive for the mutation while not one woman carried the mutated gene. There was a significant correlation between the presence of a p53 mutation and a cancer recurrence following surgery. In addition, the survival duration for patients with a p53 mutation was significantly shorter than patients who did not carry the mutation.
These results imply a positive association between the existence of a mutated p53 gene and a higher chance of experiencing a cancer recurrence in liver cancer patients. Patients carrying this mutation may benefit from additional therapy following surgery in order to reduce the chance of a recurrence. However, these results are not definitively conclusive and further clinical trials will help determine the true association between this genetic mutation and its implications in liver cancer patients. Researchers will continue to define relationships between varying factors and individual cancer characteristics in order to provide the optimal treatment for each patient.
Patients with liver cancer may wish to speak with their physician about the risks and benefits of participating in a clinical trial further evaluating p53 mutation associations or other promising treatment approaches. (Archives of Surgery, Vol 135, pp 1329-1333, 2000)