The development of new chemotherapy drugs that target cancerous tumor cells – while leaving healthy cells alone – has been a breakthrough in the cancer treatment field. However, these treatments have been shown to work only on a select few patients. Even when they do work, the tumor can create a resistance to the drugs, leaving the patient with fewer options. Several scientific research teams are working on new drugs that will work with a wider range of patients and target tumors before they can develop a resistance to the treatments.
The main component in the research behind these new cancer drugs comes from a deeper knowledge of how cancer cells come into being, grow, multiply and spread throughout the body. One study at the Massachusetts Institute of Technology examines lung cancer cells and how scientists can synthesize drugs that can target the tumors. The treatments can also be modified to help the patient as they proceed through the chemotherapy routines.
The MIT study takes a close look at a class of drugs known as “epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors”. Tyrosine kinase is a protein that functions as an “on/off” switch for many cell functions. When the proteins that regulate cell growth are permanently set in the “on” position, the cells can grow quickly and in uncontrolled ways, a common occurrence in cancer cells. Tyrosine kinase inhibitors act to slow down or stop the wild cell growth and stabilize or reduce the size of lung cancer tumors.
EGFR inhibitors are effective in less than 40 percent of all lung cancer patients. The drug’s effectiveness varies widely based on the patient’s medical history, smoking habits, race, gender and ethnicity. Dr. Philip Sharp, Professor at the Koch Institute for Integrative Cancer Research at MIT, said that laboratories around the world have “hundreds of drugs” that are in various stages of testing and development. “To personalize cancer care, we must interpret changes in (tumors) to predict the correct drug combination to use.”
Another factor in customizing cancer treatments is that some patients carry a mutation in the gene for EGFR, which makes the drugs more effective. The MIT study examined the differences between those patients and patients that did not respond to the drug. MIT researcher Doug Lauffenburger, along with a team of researchers, developed mathematical models to simulate the behavior of different types of cancer cells. The models revealed that the cancer cells that responded to the drug had a slower uptake of EGFR than the less responsive tumors.
While these methods require further verification, scientists are hopeful that the findings can lead to a possible screening test for lung cancer patients to determine the effectiveness of EGFR inhibitors in individual cases. Lauffenburger and his team also learned that the EGFR inhibitors could be more effective in certain cases when combined with another class of chemotherapy drug known as MEK inhibitors, which are often used to treat melanoma. In terms of tailoring drug combinations to individual patients, Dr. Sharp remarked that these findings “indicate that this is beginning to become possible.”
Sources: Technology Review, Medscape.com