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Barbara Breznik

Researcher at University of California, Los Angeles

Publications -  38
Citations -  767

Barbara Breznik is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Stem cell & Cancer stem cell. The author has an hindex of 13, co-authored 30 publications receiving 374 citations. Previous affiliations of Barbara Breznik include Jožef Stefan Institute.

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Brain malignancies: Glioblastoma and brain metastases.

TL;DR: Focusing on one stromal component in the glioblastoma niches, the mesenchymal stem cells (MSCs), the major hindrance to metastatic progression of mCSCs seem to be crossing the blood-brain-barrier in brain metastases.
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Mesenchymal stem cells differentially affect the invasion of distinct glioblastoma cell lines.

TL;DR: It is demonstrated that MSC/glioblastomas cross-talk is different in the two glioblastoma cell phenotypes, which contributes to tumor heterogeneity.
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Cystatins in cancer progression: More than just cathepsin inhibitors.

TL;DR: Mechanistic studies of cystatin function revealed that they affect all stages of cancer progression including tumor growth, apoptosis, invasion, metastasis and angiogenesis, and involvement in anti-tumor immune response and signaling cascades leading to cancer progression designates cystatins as possible targets for development of new anti-Tumor drugs.
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Immunotherapy of Glioblastoma: Current Strategies and Challenges in Tumor Model Development

TL;DR: In this paper, the authors summarize the glioblastoma characteristics that drive tolerance to immunotherapy, the currently used immunotherapeutic approaches, and the most suitable tumor models to mimic conditions in brain malignant tumor patients.
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CCR5-Mediated Signaling Is Involved in Invasion of Glioblastoma Cells in Its Microenvironment.

TL;DR: Autocrine and paracrine cross-talk in glioblastoma and, in particular, gli oblastoma stem cells with its stromal microenvironment, involves CCR5 and CCL5, contributing to gliOBlastoma invasion, suggesting the CCL 5/CCR5 axis as a potential therapeutic target that can be targeted with repositioned drug maraviroc.