P-100 Phase IB study of sorafenib + evofosfamide in patients (pts) with advanced hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC): NCCTG N1153 (Alliance)

Borad, Mitesh J.; Renfro, Lindsay A.; Foster, Nathan R.; Martin, P; Alberts, Steven R.; Hubbard, Joleen M.; Silva, A.; Halfdanarson, Thorvardur R.; Byrne, Thomas; Erlichman, Charles

doi:10.1093/annonc/mdw199.95

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“…In rabbits bearing the HCC VX2 tumor model, the treatment combination of TACE and evofosfamide showed enhanced antitumor efficacy with respect to TACE or evofosfamide alone [ 169 ]. Evofosfamide was tested in a phase Ib trial in combination with sorafenib in patients with advanced HCC [ 200 ]. A list of the proposed combination treatments tested in vitro and/or in vivo is reported in Table 1 .…”

Section: Targeted Therapies For Metabolic Pathwaysmentioning

confidence: 99%

Glucose Metabolism and Oxidative Stress in Hepatocellular Carcinoma: Role and Possible Implications in Novel Therapeutic Strategies

Mossenta

Busato

et al. 2020

Cancers

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Hepatocellular carcinoma (HCC) metabolism is redirected to glycolysis to enhance the production of metabolic compounds employed by cancer cells to produce proteins, lipids, and nucleotides in order to maintain a high proliferative rate. This mechanism drives towards uncontrolled growth and causes a further increase in reactive oxygen species (ROS), which could lead to cell death. HCC overcomes the problem generated by ROS increase by increasing the antioxidant machinery, in which key mechanisms involve glutathione, nuclear factor erythroid 2-related factor 2 (Nrf2), and hypoxia-inducible transcription factor (HIF-1α). These mechanisms could represent optimal targets for innovative therapies. The tumor microenvironment (TME) exerts a key role in HCC pathogenesis and progression. Various metabolic machineries modulate the activity of immune cells in the TME. The deregulated metabolic activity of tumor cells could impair antitumor response. Lactic acid–lactate, derived from the anaerobic glycolytic rate of tumor cells, as well as adenosine, derived from the catabolism of ATP, have an immunosuppressive activity. Metabolic reprogramming of the TME via targeted therapies could enhance the treatment efficacy of anti-cancer immunotherapy. This review describes the metabolic pathways mainly involved in the HCC pathogenesis and progression. The potential targets for HCC treatment involved in these pathways are also discussed.

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Section: Targeted Therapies For Metabolic Pathwaysmentioning

confidence: 99%