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Acquisition of cancer stem cell-like properties in non-small cell lung cancer with acquired resistance to afatinib.

Hashida S, Yamamoto H, Shien K, Miyoshi Y, Ohtsuka T, Suzawa K, Watanabe M, Maki Y, Soh J, Asano H, Tsukuda K, Miyoshi S, Toyooka S - Cancer Sci. (2015)

Bottom Line: Afatinib is an irreversible epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that is known to be effective against the EGFR T790M variant, which accounts for half of the mechanisms of acquired resistance to reversible EGFR-TKIs.In conclusion, we established afatinib-resistant cells and found that MET amplification, EMT, and stem cell-like features are observed in cells with acquired resistance to EGFR-TKIs.This finding may provide clues to overcoming resistance to EGFR-TKIs.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

No MeSH data available.


Related in: MedlinePlus

Copy number gains of MET and EGFR in EGFR-mutant lung cancer cell lines and their afatinib-resistant sublines. (a) The copy numbers of MET examined by real-time PCR were significantly amplified in HCC827-AR2, -AR3 and -ACR cells and slightly amplified in HCC4011-AR1 cells. (b) The copy number of EGFR in HCC827-ACR cells was approximately half of that in the parental cell line. All experiments were performed at least three times, and error bars indicate standard deviations.
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fig01: Copy number gains of MET and EGFR in EGFR-mutant lung cancer cell lines and their afatinib-resistant sublines. (a) The copy numbers of MET examined by real-time PCR were significantly amplified in HCC827-AR2, -AR3 and -ACR cells and slightly amplified in HCC4011-AR1 cells. (b) The copy number of EGFR in HCC827-ACR cells was approximately half of that in the parental cell line. All experiments were performed at least three times, and error bars indicate standard deviations.

Mentions: The T790M mutation was not detected in all 10 afatinib-resistant sublines by direct sequencing. The CNGs of MET were detected in HCC827-AR2 and HCC827-AR3 significantly and in HCC4011-AR1 slightly (Fig. 1).


Acquisition of cancer stem cell-like properties in non-small cell lung cancer with acquired resistance to afatinib.

Hashida S, Yamamoto H, Shien K, Miyoshi Y, Ohtsuka T, Suzawa K, Watanabe M, Maki Y, Soh J, Asano H, Tsukuda K, Miyoshi S, Toyooka S - Cancer Sci. (2015)

Copy number gains of MET and EGFR in EGFR-mutant lung cancer cell lines and their afatinib-resistant sublines. (a) The copy numbers of MET examined by real-time PCR were significantly amplified in HCC827-AR2, -AR3 and -ACR cells and slightly amplified in HCC4011-AR1 cells. (b) The copy number of EGFR in HCC827-ACR cells was approximately half of that in the parental cell line. All experiments were performed at least three times, and error bars indicate standard deviations.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4638008&req=5

fig01: Copy number gains of MET and EGFR in EGFR-mutant lung cancer cell lines and their afatinib-resistant sublines. (a) The copy numbers of MET examined by real-time PCR were significantly amplified in HCC827-AR2, -AR3 and -ACR cells and slightly amplified in HCC4011-AR1 cells. (b) The copy number of EGFR in HCC827-ACR cells was approximately half of that in the parental cell line. All experiments were performed at least three times, and error bars indicate standard deviations.
Mentions: The T790M mutation was not detected in all 10 afatinib-resistant sublines by direct sequencing. The CNGs of MET were detected in HCC827-AR2 and HCC827-AR3 significantly and in HCC4011-AR1 slightly (Fig. 1).

Bottom Line: Afatinib is an irreversible epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) that is known to be effective against the EGFR T790M variant, which accounts for half of the mechanisms of acquired resistance to reversible EGFR-TKIs.In conclusion, we established afatinib-resistant cells and found that MET amplification, EMT, and stem cell-like features are observed in cells with acquired resistance to EGFR-TKIs.This finding may provide clues to overcoming resistance to EGFR-TKIs.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic, Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

No MeSH data available.


Related in: MedlinePlus