
EGFR Mutation Seen as Key Target for Successfully Fighting Lung Cancer, Mesothelioma
by Nancy Meredith
Once again researchers have shown that a lung cancer patient’s survival can be greatly increased by selecting a therapy that targets a specific genetic mutation, or biomarker, in the patient’s tumor. Researchers at Stanford University reported last week that early-stage non-small cell lung cancer (NSCLC) patients with mutations of the epidermal growth factor receptor (EGFR) protein gene treated with erlotinib had 2-year disease-free survival exceeding 90%. Patients with lung cancer and mesothelioma, a form of lung cancer where tumors invade the lining of the lungs, generally have a median survival rate of just one year.
Chemotherapy administered after surgery (adjuvant therapy), which is standard in lung cancer and mesothelioma treatments, has demonstrated a survival benefit, noted Joel Neal, MD, of Stanford University who presented the findings last week at the 2012 Chicago Multidisciplinary Symposium in Thoracic Oncology. But, he added, a substantial proportion of patients see a recurrence of the disease. Once cancer recurs, fewer treatment options are available to patients, and survival rates quickly decline.
Erlotinib Effective in Slowing Cancer Recurrence
With a goal to prevent cancer recurrence and to surpass an 86% two-year disease-free survival, Stanford researchers conducted a clinical trial using erlotinib on 36 patients with resected NSCLC, and an EGFR mutation, a protein that is overexpressed in most non-small cell lung cancers, and in some mesothelioma tumors, and causes the cells to divide and spread. Additional patient characteristics included: median age of 63; 75% of the patients were women; 44% had a history of smoking; 53% had stage I disease; 19% had stage II; and 28% had stage IIIa NSCLC.
Stanford researchers found that erlotinib appears to be “particularly effective” in patients with tumors containing particular mutated forms of EGFR. After a median follow-up of 2.7 years, the cohort had a two-year disease-free survival of 94%. Disease-free survival indicates the number of people with cancer who achieve remission, and they no longer have signs of cancer in their bodies.
Patients that stopped treatment of erlotinib saw a recurrence of the cancer within 3 to 24 months. The researchers concluded that continuing treatment beyond two years might afford ongoing protection against cancer recurrence.
EGFR Mutation Identified by ASCO as Treatment Indicator
Malignant peural mesothelioma is a cancer found in the outer lining of the lungs caused by inhaling asbestos fibers. Just as with NSCLC, there are a variety of chemotherapeutic agents that can be prescribed to fight mesothelioma, with the current standard of care a combination therapy utilizing pemetrexed and cisplatin.
As shown by this clinical trial finding the most effective therapy is critical for offering patients increased survival and a better quality of life during treatment.
Last year, the American Society of Clinical Oncology released a provisional clinical opinion (PCO) stating patients with EGFR may benefit from treatment with EGFR tyrosine kinase inhibitors (TKIs), such as, gefitinib (Iressa®, Astra Zeneca Pharmaceuticals) and erlotinib (Tarceva®, Genentech Inc). ASCO suggested oncologists check for an EGFR mutation before determining first-line therapy.
Gene therapy, which involves treatment of a disease by targeting specific genes or biomarkers unique to a disease, is seen as the next frontier of medicine. Continued research, such as this by Stanford, moves medicine closer to successfully treating cancers through patient-centric care.
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Mike is a licensed attorney and the former editor of North Carolina Lawyers Weekly and South Carolina Lawyers Weekly. He has contributed numerous articles to the North Carolina State Bar Journal and is a co-author of Capital Lawyers, a history of the Wake County (NC) Bar.
Gregory Froom is a licensed North Carolina attorney and the former editor of North Carolina Lawyers Weekly and South Carolina Lawyers Weekly.