Xia, W, Liu, Z, Zong, R, Liu, L, Zhao, S, Bacus, SS, Mao, Y, He, J, Wulfkuhle, JD, Petricoin, EF, Osada, T, Yang, X-Y, Hartman, ZC, Clay, TM, Blackwell, KL, Lyerly, HK, and Spector, NL ."Truncated ErbB2 expressed in tumor cell nuclei contributes to acquired therapeutic resistance to ErbB2 kinase inhibitors". Molecular Cancer Therapeutics 10, no. 8 (August 2011): 1367-1374.
We next investigated how AEBP1 contributes to acquired resistance to BRAF inhibition.
Since histopathological examination of biopsy material is very important for the final diagnosis, accurate biopsy contributes to acquire the correct diagnosis of the lesion.
GPCR-like signaling contributes to acquired drug resistance after being mediated by Smoothened (SMO) via activating Gli, a canonical hedgehog (Hh) transcription factor [ 57].
In conclusion, the reciprocal positive regulation between Cx26 and PI3K/Akt signaling contributes to acquired gefitinib resistance in NSCLC cells by promoting EMT via a GJIC-independent manner.
In addition to nuclear ErbB-2 (p185ErbB-2) as an intact molecule, ErbB-2 (p95), which lacks the N-terminal extracellular domain, has also been found in the nucleus [ 69], where it contributes to acquired therapeutic resistance to ErbB-2 TKIs [ 70].
Thus we hypothesised that acquired methylation and associated gene silencing, particularly of the MLH1 promoter, during chemotherapy contributes to acquired platinum resistance in EOC and that this could be reversed by decitabine.
Therefore, these results reveal a novel PI3K/Akt-CREB-AEBP1-NF κB pathway whose activation contributes to acquired resistance to BRAF inhibition, and suggest that this pathway, particularly AEBP1, may represent a novel therapeutic target for treating BRAF inhibitor-resistant melanoma.
In this study, increased levels of Bcl-XL and Bcl2 were observed in A549-IRR cells as compared with A549 parental cells providing evidence that IR-enhanced Bcl-XL contributes to acquired radioresistance.
In summary, this study presents a novel PI3K/Akt-CREB-AEBP1-NF κB signaling pathway whose activation contributes to acquired resistance to PLX4032 in BRAF-mutant melanoma cells, and identifies AEBP1 as a potential therapeutic target for the treatment of BRAF inhibitor-resistant melanomas.
