Atıf İçin Kopyala
Hassan Z., Schneeweis C., Wirth M., Veltkamp C., Dantes Z., Feuerecker B., ...Daha Fazla
BRITISH JOURNAL OF CANCER, cilt.118, sa.3, ss.366-377, 2018 (SCI-Expanded)
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Yayın Türü:
Makale / Tam Makale
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Cilt numarası:
118
Sayı:
3
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Basım Tarihi:
2018
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Doi Numarası:
10.1038/bjc.2017.421
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Dergi Adı:
BRITISH JOURNAL OF CANCER
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Derginin Tarandığı İndeksler:
Science Citation Index Expanded (SCI-EXPANDED), Scopus
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Sayfa Sayıları:
ss.366-377
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Anahtar Kelimeler:
MTOR, pancreatic cancer, therapeutic resistance, IN-VIVO, DUCTAL ADENOCARCINOMAS, FEEDBACK ACTIVATION, PRECLINICAL MODELS, CELL PLASTICITY, ONCOGENIC KRAS, LUNG-CANCER, TUMORIGENESIS, RESISTANCE, EGFR
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Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli:
Hayır
Özet
Background: Although the mechanistic target of rapamycin (MTOR) kinase, included in the mTORC1 and mTORC2 signalling hubs, has been demonstrated to be active in a significant fraction of patients with pancreatic ductal adenocarcinoma (PDAC), the value of the kinase as a therapeutic target needs further clarification.