EGFR Gene Signature Predicts Non-Small Cell Lung Cancer Prognosis
Main Category: Lung CancerAlso Included In: Cancer / Oncology; Genetics
Article Date: 13 Jan 2010 - 3:00 PDT
Epidermal growth factor receptor (EGFR) is a validated therapeutic target for non-small cell lung cancer. Researchers have now discovered a 93-gene signature that is associated with the presence of EGFR mutations in tumors from lung cancer patients and is a favorable prognostic marker in patients with early stage lung cancer.
"We hope this mutation signature will be able to define patients with these tumor types who will then respond to EGFR inhibition," said Pierre Saintigny, M.D., Ph.D., a research scientist at the University of Texas M. D. Anderson Cancer Center.
Data presented at the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer have immediate clinical implications. The EGFR-mutation signature will be evaluated as a predictor of response in the BATTLE (Biomarker-integrated Approaches of Targeted Therapy for Lung Cancer Elimination) I trial, which will be presented later this year.
For the current study, the researchers conducted messenger RNA expression profiling on 195 human lung adenocarcinoma samples. They found a 93-gene signature that identified the presence of EGFR mutation and was validated in multiple cohorts of lung cancer patients. Furthermore, the presence of this gene signature was significantly correlated with drug sensitivity to erlotinib and gefitinib in non-small cell lung cancer cell lines.
Saintigny said the EGFR-mutation signature may help guide medical treatment decisions, may provide prognosis information beyond EGFR-mutation status and may give some biological insights in EGFR-mutant tumors.
Source
American Association for Cancer Research (AACR)
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MLA
16 Feb. 2012. <http://www.medicalnewstoday.com/releases/175825.php>
APA
http://www.medicalnewstoday.com/releases/175825.php.
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Problem With Mutation Or Amplification Studies
posted by Gregory D. Pawelski on 18 Jan 2010 at 4:31 pmGene signature prediction examines a single process within the cell or a relatively small number of processes. The aim is to tell if there is a theoretical predisposition to drug response. It involves the use of dead, formaldehyde preserved cells that are never exposed to targeted drugs. It cannot tells us anything about uptake of a certain drug into the cell or if the drug will be excluded before it can act or what changes will take place within the cell if the drug successfully enters the cell.
It cannot discriminate among the activities of different drugs within the same class. Instead, it assumes that all drugs within a class will produce precisely the same effect, even though from clinical experience, this is not the case. Nor can it tell us anything about drug combinations. Cancer is a complex disease and needs to be attacked on many fronts.
Cancer cells have many mutations in many different pathways, so even if one route or two is shut down by a targeted treatment, the cancer cell may be able to use other routes. What do you do when there are too many receptors and the cancer cell still continues to grow and divide?
Molecular diagnostics often have been mostly or totally ineffective at identifying clinical responders to the various therapies. Genetic profiles are able to help doctors determine which patients will probably develop cancer and those who will most likely relapse, however, it cannot be suitable for specific treatments for individual patients.
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