2014 Fiscal Year Final Research Report
To provide a biomarker for predicting the therapeutic effect of chemotherapy to lung cancer harboring EGFR mutation.
| Project/Area Number |
24701037
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Clinical oncology
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| Research Institution | Kinki University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 化学療法 / 抗がん剤耐性 / EMT |
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| Outline of Final Research Achievements |
Non-small-cell lung cancer (NSCLC) has a poor prognosis and remains the leading cause of death related to cancer. The discovery of both activating mutations in the EGFR gene in 2004 and EML4-ALK in 2007 have been found. EGFR tyrosine kinase inhibitor (TKI) and ALK TKI results in dramatically high response rates and prolonged progression-free survival compared with standard chemotherapy in NSCLC patients harboring gene alteration.
However, almost patients eventually develop acquired resistance to these drugs within 1 year. In addition, 20%-30% of NSCLC patients with EGFR mutations do not show an initial response to EGFR-TKIs. Several mechanisms of acquired resistance to EGFR-TKIs were found but not all. We found that forkhead box Q1 (FOXQ1) is overexpressed in lung cancer and enhances tumorigenicity and tumor growth presumably through its angiogenic and antiapoptotic effects in this research. Furthermore, FOXQ1 has a role of regulating drug resistance and aggressiveness in lung cancer.
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| Free Research Field |
臨床腫瘍学
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