David A. Gewirtz

TL;DR: The differential impact of autophagy on distinct phases of tumorigenesis is discussed and the implications of this concept for the use of Autophagy modulators in cancer therapy are discussed.

TL;DR: It is suggested that DNA strand breaks fail to fully account for the antiproliferative activity of doxorubicin in the MCF-7 breast tumor cell line, and compromised DNA synthesis associated with interference with DNA unwinding may contribute to growth inhibition in MCf-7 cells exposed to doxorbicin.

TL;DR: In this paper, preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.

TL;DR: This commentary/review advances the premise that autophagy is actually populated by at least two additional players, and is now term the cytostatic form of autophagic in that its activation results in prolonged growth inhibition as well as reduced clonogenic survival but in the absence of actual loss of cell viability through apoptosis or necrosis.

TL;DR: The term "accelerated senescence" will be used in the consideration of the morphological, biochemical, and molecular aspects of treatment-inducedsenescence, its relationship to classical replicative senescENCE, its prevalence in clinical specimens and the implications of accelerated senescences for the outcome of cancer therapy.