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This sensitization occurred as a consequence of parthenolide suppression of the activation of the nuclear transcription factor-kappaB (NF-B) and the sustained activation of the transcription factor regulator c-Jun N-terminal kinase (JNK)

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Although Sorafenib is a kinase inhibitor with multiple targets including RTKs and RAF, its treatment did not affect the total tyrosyl phosphorylation and ERK phosphorylation in TamR cells (Figure S5), indicating that inhibition of TamR ER+ breast cancer cell growth by Sorafenib under the concentration used is not through inhibition of RTKs and RAF

Winder-Patel, B