415 Genetic Variability in Multi Drug Resistance Protein 1 (ABCC1/MRP1) and UDP-Glucuronosyltransferase-2B7 (UGT2B7) Are Highly Correlated with Severe Haematological Toxicity of Adjuvant FEC in Breast Cancer

2012 ◽  
Vol 48 ◽  
pp. S167 ◽  
Author(s):  
C. Vulsteke ◽  
D. Lambrechts ◽  
A.S. Dieudonné ◽  
S. Hatse ◽  
B. Brouwers ◽  
...  





2005 ◽  
Vol 12 (4) ◽  
pp. 999-1009 ◽  
Author(s):  
Jörg B Engel ◽  
Andrew V Schally ◽  
Gabor Halmos ◽  
Benjamin Baker ◽  
Attila Nagy ◽  
...  

The cytotoxic analog of bombesin (BN)/gastrin releasing peptide (GRP) AN-215 consisting of 2-pyrrolinodoxorubicin (AN-201), a superactive derivative of doxorubicin linked to a bombesin analog carrier, displays a high affinity to BN/GRP receptors and can be targeted to tumors that express these receptors. We evaluated the antitumor effect and the toxicity of AN-215 in 5 human breast cancer cell lines xenografted into nude mice. In addition, we measured the mRNA expression of multi drug resistance protein 1 (MDR-1), multi drug resistance related protein 1 (MRP-1) and breast cancer resistance protein (BCRP) by real-time PCR analysis after treatment with AN-215. All five cell lines expressed BN/GRP receptors, and AN-215 significantly (P<0.05) inhibited tumor growth in all models, while its cytotoxic radical AN-201 had no significant effect in four models. In MX-1 tumors, AN-201 had a significantly weaker antitumor effect than AN-215. The effect of AN-215 was nullified by a blockade of BN/GRP receptors with a bombesin antagonist. Low or no induction of MDR-1, MRP-1 and BCRP occurred after treatment with AN-215. In conclusion, targeted chemotherapy with the cytotoxic BN/GRP analog AN-215 strongly inhibits breast cancers that express BN/GRP receptors and might provide a new treatment modality for mammary carcinoma.



2010 ◽  
Vol 411 (1-2) ◽  
pp. 119-121 ◽  
Author(s):  
Wei-Xa Zhang ◽  
Hao Chen ◽  
Bing Chen ◽  
Qu Cai ◽  
Wei-Min Cai






2012 ◽  
Vol 83 (8) ◽  
pp. 1084-1103 ◽  
Author(s):  
Karthika Natarajan ◽  
Yi Xie ◽  
Maria R. Baer ◽  
Douglas D. Ross




2021 ◽  
Author(s):  
xingang wang ◽  
YAN ZHENG ◽  
YU WANG

Abstract Background and AimsPseudopodium-enriched atypical kinase 1 (PEAK1) has reported to be upregulated in human malignancies and related with poor prognosis. Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis and chemoresistance. However, the role of PEAK1 in breast cancer is not clear. Here, we investigated the PEAK1 expression in breast cancer and analyzed its relation with clinicopathological status and chemotherapy resistance to the neoadjuvant chemotherapy (NAC). We also investigated the role of PEAK1 on breast cancer cells in vitro and in vivo. MethodsImmunohistochemistry (IHC) was performed in 112 surgical resected breast cancer tissues. The associations between clinicopathological status, multi-drug resistance and PEAK1 expression were determined. Effect of PEAK1 overexpression or down-expression on proliferation, colony formation, invasion, migration, metastasis and Doxorubicin sensitivity in the MCF-7 cells in vitro and in vivo was detected. ResultsPEAK1 was overexpressed in breast cancer tissues and NAC -resistant breast cancer tissues. High PEAK1 expression was related with tumor size, high tumor grade, T stage, LN metastasis, recurrence, Ki-67 expression, Her-2 expression and multi-drug resistance. Targeting PEAK1 inhibited cell growth, invasion, metastasis and reversed chemoresistance to Doxorubicin in breast cancer cells in vitro and in vivo. ConclusionHigh PEAK1 expression was associated with invasion, metastasis and chemoresistance of breast cancers. Furthermore, targeting PEAK1 could inhibit cell growth and metastasis, and reverse chemoresistance in breast cancer cells, which provides an effective treatment strategies for breast cancer.



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