fatigue Cancer Research Results
fatigue, fatigue: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
fatigue↓, meta-analysis showed that the addition of Astragalus membranaceus to the control group was effective in reducing cancer-related fatigue
QoL↑, The current evidence is supportive of the efficacy of Astragalus membranaceus in patients with cancer-related fatigue and their quality of life,
Dose↝, Wang et al. study 16 showed that both doses of 500 mg and 250 mg were effective in improving fatigue.
*cachexia↓, The results of this process favored L-carnitine supplementation in patients with cancer-related cachexia.
*Apoptosis↓, inhibiting apoptosis or reversing inflammatory processes.
*Inflam↓,
QoL↑, This treatment increased plasma-free carnitine concentrations and significantly improved fatigue, which was assessed using the functional assessment of cancer therapy, fatigue, and quality of life questionnaire, as well as quality-of-life measu
Dose↝, placebo-controlled trial, in which 2 g per day of LC was administrated orally for four weeks among eligible patients.
Weight↑, advanced pancreatic cancer received either LC (4 g/day orally) or a placebo for 12 weeks. The results showed that body mass index, nutritional status (body cell mass and body fat), and quality-of-life parameters increased
OS↝, There was an insignificant increase in overall survival, a decline in length of hospital stays, and decrease in fatigue among the LC-treated patients.
fatigue↓,
eff↝, some dietary factors, such as food intake restriction and intake of LC and certain micronutrients (vitamin C, vitamin B6, and iron, which are required as cofactors for endogenous LC biosynthesis) may have some effects on the efficacy of LC sup
fatigue↓, carnitine supplementation has been tested in preliminary studies concerning human cachexia, resulting in improved fatigue and quality of life.
QoL↑,
*GSH↑, l-carnitine treatment improved the tumor-induced decrease in muscular glutamate and glutathione levels and the increased plasma glutamate levels in tumor-bearing rodents
Dose↝, Significant improvements in fatigue were also observed in a randomized phase III clinical trial, in which l-carnitine (4 g/day) was orally given to patients with advanced cancer
*memory↑, Bacopa monnieri has been used for centuries in Ayurvedic medicine, alone or in combination with other herbs, as a memory and learning enhancer, sedative, and anti-epileptic.
*neuroP↑, Brahmi as a lead formulation for treating neurological disorders and exerting cognitive-enhancing effects.
*cognitive↑,
*hepatoP↑, figure 1
*antiOx↑,
*AntiDiabetic↑,
*fatigue↓,
*GSK‐3β↓, figure 3
*PI3K↑,
*Akt↑,
*tau↓,
*ROS↓, The neuroprotective properties of these bioactive components include reduction of ROS, neuroinflammation, aggregation inhibition of amyloid-β and improvement of cognitive and learning behavior.
*Inflam↓,
Dose↝, 100-mg dose of a dry extract of U. tomentosa three times per day in patients with advanced solid tumors
QoL↑, Treatment improved the patients' overall quality of life (p=0.0411) and social functioning
fatigue↓, Use of cat's claw might be beneficial in patients with advanced cancer by improving their quality of life and reducing fatigue.
PDK1↓, classic DCA target, pyruvate dehydrogenase kinase
lactateProd↓, reduce lactic acid production which would push the cell towards oxidative phosphorylation: this would be the supposed function of dichloroacetate (DCA).
Apoptosis↑, They found that DCA induced apoptosis and decreased proliferation by restoring mitochondrial oxidative metabolism, without toxicity to normal cells.
TumCP↓,
selectivity↑,
other↝, many clinics, usually called “DCA Clinics” have opened, mainly in Canada and Germany.
Dose↝, DCA is sold over the counter and is produced by many laboratories. The quality of the product from these laboratories is not well established. These particulars explain many of the doubts about DCA’s real value as a therapeutic tool.
BioAv↑, DCA is an orally available molecule that is quickly and almost completely absorbed by the digestive system
Half-Life↓, With a 10 mg/kg infusion the maximum plasma concentration achieved was between 19.9 μg/ml and 24.7 μg/ml with a half life of only 20 minutes. If the infused dose was increased to 20 mg/kg the plasma concentration was between 57.3 and 74.9 μg/ml with
Glycolysis↓, facilitates the switch from a glycolytic to an oxidative metabolism.
OXPHOS↑,
Casp↑, onversion to an oxidative metabolism by DCA, is an increase in caspase-mediated apoptosis
i-pH↓, pHi decreases (at least temporarily).
COX2↑, DCA increases the expression of COX2 and the latter increases tumor resistance to DCA. Therefore, a possible integrated treatment could be COX2 inhibitor co-administered with DCA
Hif1a↓, DCA suppresses HIF-1α activity and angiogenesis through the inhibition of PDK-II
angioG↓,
HMG-CoA↓, figure 7
GSTZ1↓,
OCR↑,
lipoGen↓,
fatigue↓,
survivin↓, Survivin (an inhibitor of apoptosis) expression was decreased and miR-375 (a microRNA which acts as a tumor suppressor) levels were increased.
miR-375↑,
eff↓, African Americans are known to respond poorly to therapy compared with Caucasian American patients.
CSCs↓, DCA can inhibit the cancer stem cell like characteristics of the cells and strongly influenced the metabolic pathway of the cells causing a shift from glycolysis to oxidative phosphorylation.
TumAuto↑, DCA induced autophagy in human colon cancer cells with ROS production and mTOR inhibition,
mTOR↓,
TumCI↓, DCA induced apoptosis, inhibited invasion, and angiogenesis. In mouse experiments in vivo with the melanoma allografts, DCA reduced volume and weight of tumors.
TumVol↓,
TumW↓,
ATP↓, DCA alone reduced glycolytic activity and intracellular ATP levels and inhibited cellular growth in melanoma cells.
Warburg↓, DCA was also found to interrupt the Warburg effect and decreased proliferation.
eff↑, The co-application of metformin and DCA suppressed human liver cancer cell proliferation inducing apoptosis through inhibition of mTORC1 and increased ROS in vitro and in vivo
e-pH↑, when measuring extracellular pH in vivo found that an initial increase in extracellular pH of tumors in mice when treated with DCA.
eff↑, To avoid the development of this type of metabolic resistance DCA should be given simultaneously with other metabolic drugs such as metformin [327] or 2 deoxyglucose.
eff↑, chronic co-administration of DCA with sodium bicarbonate to tumor bearing mice prolonged survival
other↝, High doses of thiamin (vit B1) have effects similar to those of DCA: reduced PDH phosphorylation, reduced lactate prod and increased casp3 activity with reduced proliferation in colon cancer cells. can vitB1 replace DCA as a nontoxic PDK inhibitor?
RadioS↑, Dong et al. [380] found that DCA radiosensitized esophageal carcinoma cells in vitro and in vivo through increased ROS accumulation.
toxicity↓, 25 mg/Kg/day may show a mild sedative effect or drowsiness. The most serious published side effect is reversible peripheral neuropathy
Dose↝, 10 to 50 mg/kg body weight/day has been found to be a safe dose. However, single nucleotide polymorphisms (SNPs) in the gene of the enzyme GSTZ1 cause difficulties in establishing a universal dose [409] as noted above.
eff↑, There is strong evidence showing that the association of metformin and DCA has significant cytotoxic effects.
eff↑, To this approach we must add a third compound: a COX2 inhibitor like celecoxib to decrease COX2 expression induced by DCA.
eff↑, the triple association of DCA, metformin and celecoxib, which has never been experimentally tested in patients, deserves well planned phase II clinical trials.
toxicity↝, DCA will never become a stand-alone chemotherapeutic compound. The fundamental reason for this statement is that the drug can only reach micromolar blood concentrations without toxicity and requires millimolar levels to be cytotoxic.
eff↓, DCA should not be used in association with allopurinol, NSAIDs, or flavonoids because they reduce cellular DCA uptake.
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
miR-375↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
GSTZ1↓, 1, OXPHOS↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, OCR↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1, HMG-CoA↓, 1, lactateProd↓, 1, lipoGen↓, 1, PDK1↓, 1, Warburg↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 1, Casp↑, 1, survivin↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 2,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, mTOR↓, 1,
Migration(tgid=13) ⓘ
TumCI↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, Hif1a↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↑, 1,
Cellular Microenvironment(tgid=17) ⓘ
e-pH↑, 1, i-pH↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, Dose↝, 6, eff↓, 2, eff↑, 6, eff↝, 1, Half-Life↓, 1, RadioS↑, 1, selectivity↑, 1,
Functional Outcomes(tgid=23) ⓘ
fatigue↓, 5, OS↝, 1, QoL↑, 4, toxicity↓, 1, toxicity↝, 1, TumVol↓, 1, TumW↓, 1, Weight↑, 1,
Total Targets: 41
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, GSH↑, 1, ROS↓, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Apoptosis↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 1, PI3K↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Inflam↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
tau↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, cachexia↓, 1, cognitive↑, 1, fatigue↓, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 1,
Total Targets: 16
Scientific Paper Hit Count for: fatigue, fatigue
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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