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Ana Milojkovic

Researcher at Max Delbrück Center for Molecular Medicine

Publications -  9
Citations -  4424

Ana Milojkovic is an academic researcher from Max Delbrück Center for Molecular Medicine. The author has contributed to research in topics: Apoptosis & Cytotoxic T cell. The author has an hindex of 6, co-authored 6 publications receiving 3525 citations. Previous affiliations of Ana Milojkovic include Charité.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Oncogene-targeting T cells reject large tumors, while oncogene inactivation selects escape variants in mouse models of cancer

TL;DR: Although drug-mediated oncogene inactivation selectively killed the cancer cells and left the tumor vasculature intact, which likely facilitated survival and growth of resistant clones, T(E) cell treatment led to blood vessel destruction and probably "bystander" elimination of escape variants, which did not require antigen cross-presentation by stromal cells.
Journal ArticleDOI

Apoptosis resistance, mitotic catastrophe, and loss of ploidy control in Burkitt lymphoma

TL;DR: The inverse relation of apoptosis and polyploidy induction by paclitaxel or nocodazole in BL is found and it should be of great importance to overcome therapy resistance and therapy-related events that result in ploidy changes and tumor progression.
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Systematic genetic dissection of p14ARF-mediated mitochondrial cell death signaling reveals a key role for p21CDKN1 and the BH3-only protein Puma/bbc3.

TL;DR: It is shown that p14ARF-induced mitochondrial apoptosis critically depends on the BH3-only protein Puma, and that the sensitivity of Puma-deficient cells to p14 ARF- induced apoptosis is fully restored by functional reconstitution ofPuma using a conditional adenoviral expression vector.