NKX2-1/TITF1/TTF-1-Induced ROR1 is required to sustain EGFR survival signaling in lung adenocarcinoma (Q24308684)

GOA release 2020-03-11

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Takashi Takahashi

11

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author name string

Tomoya Yamaguchi

1

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Kiyoshi Yanagisawa

2

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Ryoji Sugiyama

3

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Yasuyuki Hosono

4

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Yukako Shimada

5

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Chinatsu Arima

6

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Seiichi Kato

7

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Shuta Tomida

8

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Motoshi Suzuki

9

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Hirotaka Osada

Ror1, a cell surface receptor tyrosine kinase is expressed in chronic lymphocytic leukemia and may serve as a putative target for therapy

10

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language of work or name

English

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publication date

20 March 2012

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published in

Cancer Cell

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volume

21

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issue

3

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page(s)

348-61

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Akt activation by growth factors is a multiple-step process: the role of the PH domain

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Genomic profiling identifies TITF1 as a lineage-specific oncogene amplified in lung cancer

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Thyroid transcription factor-1 (TTF-1/Nkx2.1/TITF1) gene regulation in the lung

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Antisera induced by infusions of autologous Ad-CD154-leukemia B cells identify ROR1 as an oncofetal antigen and receptor for Wnt5a

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Modeling oncogene addiction using RNA interference.

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Src kinase activation by direct interaction with the integrin β cytoplasmic domain

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Regulation of Akt/PKB activation by tyrosine phosphorylation

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Interaction between Src and a C-terminal proline-rich motif of Akt is required for Akt activation

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MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling

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Lineage-specific dependency of lung adenocarcinomas on the lung development regulator TTF-1

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Unique cell surface expression of receptor tyrosine kinase ROR1 in human B-cell chronic lymphocytic leukemia.

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Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

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