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Stephanie M. Tortorella

Researcher at University of Melbourne

Publications -  14
Citations -  1049

Stephanie M. Tortorella is an academic researcher from University of Melbourne. The author has contributed to research in topics: Warburg effect & Cancer. The author has an hindex of 10, co-authored 14 publications receiving 840 citations. Previous affiliations of Stephanie M. Tortorella include Monash University & Baker IDI Heart and Diabetes Institute.

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Cancer metabolism and the Warburg effect: the role of HIF-1 and PI3K

TL;DR: The molecular aspects of the Warburg effect are discussed with a particular emphasis on the role of the HIF-1 and the PI3K pathway, as well as the influence HIF has on cancer cell metabolism.
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Transferrin Receptor-Mediated Endocytosis: A Useful Target for Cancer Therapy

TL;DR: The main objective of this review is to evaluate the importance of the transferrin–transferrin receptor complex as a target for cancer therapy through extensive knowledge of both the physiological and pathological interactions between the complex and different cell types.
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Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition

TL;DR: The biochemical and biological properties of sulforaphane are discussed with a particular emphasis on the anticancer properties of the dietary compound, which possesses the capacity to intervene in multistage carcinogenesis through the modulation and/or regulation of important cellular mechanisms.
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The Warburg effect: molecular aspects and therapeutic possibilities

TL;DR: There is certainly a strong link between the genetic factors, epigenetic modulation, cancer immunosurveillance and the Warburg effect, which will be discussed in this review.
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Introduction to the molecular basis of cancer metabolism and the Warburg effect

TL;DR: Evidence indicates that the reasons as to why tumor cells undergo aerobic glycolysis include the shift in priority to accumulate biomass rather than energy production, the evasion of apoptosis as fewer reactive oxygen species are released by the mitochondria and the production of lactate to further fuel growth of tumors.