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Constadina Arvanitis

Researcher at Northwestern University

Publications -  19
Citations -  2228

Constadina Arvanitis is an academic researcher from Northwestern University. The author has contributed to research in topics: Oncogene & Carcinogenesis. The author has an hindex of 12, co-authored 17 publications receiving 2066 citations. Previous affiliations of Constadina Arvanitis include Stanford University & Children's Memorial Hospital.

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MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer

TL;DR: It is reported that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers and how oncogenic inactivation may reverse tumorigenesis in the most clinically difficult cancers is shown.
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Sustained Loss of a Neoplastic Phenotype by Brief Inactivation of MYC

TL;DR: It is demonstrated that brief inactivation of MYC results in the sustained regression of tumors and the differentiation of osteogenic sarcoma cells into mature osteocytes, raising the possibility that transient in activation ofMYC may be an effective therapy for certain cancers.
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Dasatinib synergizes with doxorubicin to block growth, migration, and invasion of breast cancer cells.

TL;DR: Combination treatment with doxorubicin resulted in synergistic growth inhibition in all cell lines and blocked the migration and invasion of the highly metastatic, triple-negative MDA-MB-231 cell line, warrants the re-evaluation of dasatinib as an effective agent in multi-drug regimens for the treatment of invasive breast cancers.
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Conditional transgenic models define how MYC initiates and maintains tumorigenesis.

TL;DR: Conditional transgenic mouse model systems are tractable methods to precisely dissect how and when the inactivation of MYC might be effective in the treatment for human cancer.
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Developmental context determines latency of MYC-induced tumorigenesis.

TL;DR: The tetracycline regulatory system is used to generate transgenic mice in which the expression of a c-MYC human transgene can be conditionally regulated in murine hepatocytes and it is found that apoptosis is not a barrier to MYC inducing tumorigenesis.