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Anamaria Brozovic
Researcher at Stanford University
Publications - 46
Citations - 1746
Anamaria Brozovic is an academic researcher from Stanford University. The author has contributed to research in topics: Chemistry & Apoptosis. The author has an hindex of 16, co-authored 39 publications receiving 1197 citations. Previous affiliations of Anamaria Brozovic include University of Mainz & University of Ljubljana.
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Journal ArticleDOI
The multi-factorial nature of clinical multidrug resistance in cancer.
Yehuda G. Assaraf,Anamaria Brozovic,Ana Cristina Gonçalves,Dana Jurkovicova,Aija Linē,Miguel Machuqueiro,Simona Saponara,Ana Bela Sarmento-Ribeiro,Cristina P.R. Xavier,M. Helena Vasconcelos,M. Helena Vasconcelos +10 more
TL;DR: This review aims to bring together these multidisciplinary and interdisciplinary features of MDR cancers by deciphering the molecular mechanisms underlying anticancer drug resistance, to pave the way towards the development of novel precision medicine treatment modalities that are able to surmount distinct and well-defined mechanisms of antic cancer drug resistance.
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The relationship between cisplatin-induced reactive oxygen species, glutathione, and BCL-2 and resistance to cisplatin
TL;DR: This review focuses on the relationship between glutathione and BCL-2 and their protective role in cDDP-induced reactive oxygen species formation and cD DP resistance.
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Activation of mitogen-activated protein kinases by cisplatin and their role in cisplatin-resistance.
Anamaria Brozovic,Maja Osmak +1 more
TL;DR: Current knowledge concerning the role of MAPK family members in cell response to cDDP, as well as their role in cisplatin-resistance are summarized.
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Tumor microenvironment and epithelial mesenchymal transition as targets to overcome tumor multidrug resistance
TL;DR: Evidence for TME components as causative factors of EMT and anticancer drug resistance is summarized, concluding that EMT signaling simultaneously increases MDR.
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Long‐term activation of SAPK/JNK, p38 kinase and fas‐L expression by cisplatin is attenuated in human carcinoma cells that acquired drug resistance
Anamaria Brozovic,Gerhard Fritz,Markus Christmann,Jochen Zisowsky,Ulrich Jaehde,Maja Osmak,Bernd Kaina +6 more
TL;DR: It is shown that ACR is due to a lower level of induced apoptosis, and sustained SAPK/JNK and p38 kinase activation may be a general mechanism of cDDP‐induced cell death.