Response of Tumors to Therapy Studied by 31P Magnetic Resonance Spectroscopy

Karczmar, G. S.; Meyerhoff, Dieter J.; Speder, A.; Valone, Frank H.; Wilkinson, Michael; Shine, N.; Boska, Michael D.; Weiner, M W

doi:10.1097/00004424-198912000-00022

Cited by 9 publications

(5 citation statements)

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“…Our results also show that ATP content can rapidly drop in EATC in response to an energy supply shortage, perhaps due to the high ATP demand of malignant cells, thus confirming previous studies in vitro as well as in vivo [21,23,24].…”

Section: Discussionsupporting

confidence: 91%

“…As a consequence of the above analysis, one may advance the theory that in vivo the bioenergetic status of EAT was also maintained mainly by glycolysis, as reported for some other tumors ( [23], and references therein); in the opposite case, it should not drop once the cells are harvested because endogenous substrates are available, as shown above, and the O2 supply should not be lower than that in vivo.…”

Section: Discussionsupporting

confidence: 55%

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Metabolic pathways in Ehrlich ascites tumor cells recovering from a low bioenergetic status

Dell’Antone

1994

FEBS Letters

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Ehrlich ascites tumor cells were found to be in a low bioenergetic status, as evaluated by acridine orange uptake and ATP content, when resuspended in a glucose medium shortly after removal from the animal. Dye uptake as well as ATP content then increased for about 2 h at room temperature. This effect was only slightly inhibited by oligomycin. Cells resuspended in a glucose-free medium initially showed high dye uptake and ATP level, which were stable over time: in this case oligomycin caused a drop in both dye uptake and ATP level. The above findings, which are indicative of a marked Crabtree effect in Ehrlich ascites tumor cells, means that it is unlikely that limiting ADP and P, play an important role in the glucose-induced inhibition of oxidative phosphorylation in this system.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 55%

Metabolic pathways in Ehrlich ascites tumor cells recovering from a low bioenergetic status

Dell’Antone

1994

FEBS Letters

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“…ATP concentrations may be relatively low in certain areas of tumors themselves [35, 65,66,111]. Compromised blood supply to tumors results in oxygen-depleted areas of the tumors, associated with deprivation of nutrients and energy and a hostile metabolic microenvironment (i.e.…”

Section: The Anemia Hypothesismentioning

confidence: 99%

Fatigue associated with cancer and its treatment

Morrow

Andrews

Hickok

et al. 2001

Support Care Cancer

198

147

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Fatigue is often related to cancer, and that related to its treatment is the most commonly reported side effect of cancer treatment. It differs from that induced by other causes, such as sleep disturbance and exertion, as the latter are typically alleviated by a period of rest. In contrast to exercise-induced fatigue, the fatigue reported by cancer patients is usually described as an unusual, excessive, whole-body experience that is disproportionate or unrelated to activity or exertion and is not relieved by rest or sleep. Cancer-related fatigue is a subjective experience that has a clear detrimental effect on a cancer patient's quality of life and ability to sustain the usual personal, professional, and social relationships. The fatigue can be pervasive: cancer patients frequently report that fatigue begins with treatment, continues during the course of chemotherapy or radiation treatment, and declines somewhat - but frequently sustains at a higher-than-baseline rate - after treatment is over. It may also persist for several years even in patients with no apparent disease. While a number of researchers have speculated about the nature of cancer-related fatigue, there has been little systematic research on its etiology or treatment. In many aspects our knowledge of the fatigue mechanisms in cancer patients is at a similar stage to that reached in our understanding of anti-cancer therapy-induced nausea and vomiting about 20 years ago. This paper introduces four plausible hypotheses for the development of fatigue. Evidence available to support a role for anemia, adenosine triphosphate, vagal afferents, and the interaction of the HPA/cytokines and 5HT is discussed.

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“…2DG is a glucose analog that has a hydrogen in place of a hydroxyl group [57] . Hexokinase traps 2DG in the cell by adding a phosphate (2DG-P), which cannot continue in glycolysis as a substrate for phosphoglucose isomerase [58] , [59] , [60] , [61] . KCN binds the iron in cytochrome c and inhibits the mitochondrial electron transport chain from transferring electrons to oxygen and disrupts ATP production [62] .…”

Section: Methodsmentioning

confidence: 99%

Estrogen’s sex-specific effects on ischemic cell death and estrogen receptor mRNA expression in rat cortical organotypic explants

Trout,

McLouth,

Westberry

et al. 2024

Aging Brain

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Response of Tumors to Therapy Studied by 31P Magnetic Resonance Spectroscopy

Cited by 9 publications

References 0 publications

Metabolic pathways in Ehrlich ascites tumor cells recovering from a low bioenergetic status

Metabolic pathways in Ehrlich ascites tumor cells recovering from a low bioenergetic status

Fatigue associated with cancer and its treatment

Estrogen’s sex-specific effects on ischemic cell death and estrogen receptor mRNA expression in rat cortical organotypic explants

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