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Pseudostratified, Metaplastic, Dysplastic, and Carcinomatous Nasal Mucosa in Nickel Workers: A Study by Scanning Electron, Transmission Electron, and Light Microscopy
Published in Gerd Reznik, Sherman F. Stinson, Nasal Tumors in Animals and Man, 2017
Albrecht Reith, Jean-Paul Riguat, Morten Boysen, Per Marton
The findings of remarkable mitochondrial changes, expressed in the organelle enlargement and cristae reduction in dysplasia, are interesting in the context of the known biochemical changes in the respiratory chain of malignant cells as recently again described by Racker and Spector38 and first postulated in the Warburg hypothesis of malignant transformation.39 Very few cancer-related electron microscopic studies exist using morphometry, and in one — relevant in this context — the reduction of mitochondria was observed after treating hamster cheek pouch with dimethylbenz(a)anthracene (DMBA).33
The Warburg effect: essential part of metabolic reprogramming and central contributor to cancer progression
Published in International Journal of Radiation Biology, 2019
Peter Vaupel, Heinz Schmidberger, Arnulf Mayer
Warburg’s interpretation of his pioneering experimental data (‘Warburg hypothesis’) was originally questioned by Chance and Castor (1952), Chance (1953) and Chance and Hess (1956, 1959), showing that intact and functional cytochromes detected in most tumor cells clearly speak against a general mitochondrial dysfunction. In addition, Weinhouse (1956, 1976), Aisenberg (1961), Vaupel (1974, 1977), Shapot (1976), Shapot and Vaupel (1976), Zu and Guppy (2004), Kim and Dang (2006), Moreno-Sanchez et al. (2007), Christofk et al. (2008), Potter et al. (2016) and a series of other authors provided substantial evidence that oxidative phosphorylation (OXPHOS) and a normal Krebs cycle (TCA cycle) persist in the vast majority, if not in all malignant tumors, that is, most cancers exhibit the Warburg effect while retaining mitochondrial respiration (for reviews, see e.g. Koppenol et al. 2011;Vaupel and Mayer 2012).
The influence of ketogenic therapy on the 5 R’s of radiobiology
Published in International Journal of Radiation Biology, 2019
Radiation oncologists are well aware of the value of FDG-PET (2-deoxy-2-[18F]fluoro-D-glucose positron emission tomography) for tumor imaging and radiotherapy (RT) treatment planning purposes. Regions of high FDG uptake are frequently boosted with higher doses simultaneously with the basic (planning target volume) dose application (Figure 1), and various measures of FDG uptake have been used to predict outcomes after RT (El Naqa 2014). It is important to recall that the utility of FDG-PET is based on a phenomenon systematically investigated nearly 100 years ago by Otto Warburg and coworkers (Warburg et al. 1924, 1926). Warburg measured a several-fold increased glucose uptake and lactate release of tumor tissue compared to normal tissue even in the presence of oxygen which is now referred to as the Warburg effect or aerobic glycolysis. He later proposed that damaged respiration would be the cause for this glycolytic phenotype (Warburg 1956). This “Warburg hypothesis” (which should not be confused with the Warburg effect) has gained support from detailed studies of tumor mitochondrial structure and metabolism (López-Ríos et al. 2007; Hall et al. 2013; Gabriel et al. 2017).
The Warburg hypothesis and weak ELF biointeractions
Published in Electromagnetic Biology and Medicine, 2020
Recently, there has been increasing discussion (Epstein et al. 2017; Esparza-Molto and Cuezva 2018; Jiang et al. 2015; Moreno-Sanchez et al. 2014; Pokorny et al. 2017; Sullivan and Chandel 2014) concerning the relevance of Warburg’s observation to cancer production and/or treatment. This, despite the fact that the Warburg Hypothesis tells us nothing about the cause of cancer cells, but merely how their energy content is derived. Nevertheless the possibility exists that the inefficient rate of ATP inclusion in cancer cells may reflect problems with ATP Synthase itself. This in turn might conceivably implicate ATPS dysfunction as a reason for mitochondrial-linked disease, and perhaps even as a potential contributing factor to oncogenesis.