DNArepair Cancer Research Results
DNArepair, DNA repair: Click to Expand ⟱
| Source: HalifaxProj(enhance) |
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DNA repair is a crucial cellular process that maintains the integrity of the genome by correcting damage that can occur due to various factors, including environmental stress, radiation, and normal metabolic activities.
Radiation and Chemotherapy: These treatments often work by inducing DNA damage, and cancer cells with defective repair mechanisms may be more susceptible to these therapies.
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Scientific Papers found: Click to Expand⟱
*BioAv↑, another key property of allicin is its hydrophobicity, which allows it to be absorbed easily through the cell membrane without causing any physical or chemical damage to the phospholipid bilayer, thereby allowing its rapid metabolism to produce pharm
*cardioP↑, Allicin exhibits protective effects in multiple organ systems, including the brain, intestines, lungs, liver, kidneys, prostate, and heart.
*hepatoP↑,
*RenoP↑,
*Half-Life↝, half-life (t1/2)of allicin was 227 min–260 min. Because allicin is eliminated from the body by the respiratory tract, the concentration of allicin in lung tissue is significantly lower than that in the blood
*BioAv↓, We believe that the bioavailability of allicin is relatively low for the following reasons: At first, allicin is characterized by a distinctive garlic odor and chemical instability. It can be easily degraded under room temperature.
*neuroP↑, Neuroprotective activity
*cognitive↑, On the other hand, allicin improves cognitive deficits via Protein kinase R-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid-2-related factor 2 (NRF2) signaling pathway and c-Jun N-terminal kinase (JNK) signaling pathways
*ROS↓, They found that allicin suppressed ROS generation and decreased lipid peroxidation in 6-hydroxydopamine (6-OHDA)-induced Pheochromocytoma 12 (PC12) cells
*lipid-P↓,
*DNArepair↑, Allicin not only directly protects DNA, but also indirectly protects DNA through antioxidant activity and regulation of oxidizing enzymes
*ChemoSen↑, Allicin combined with other chemotherapy drugs showed a better anti-cancer effect
Risk↓, Meta-analyses of 118 observational studies of mortality in cancer patients give evidence consistent with reductions of about 20% in mortality associated with aspirin use.
*toxicity↓, Reasons against aspirin use include increased risk of a gastrointestinal bleed though there appears to be no valid evidence that aspirin is responsible for fatal gastrointestinal bleeding.
other↑, In conclusion, given the relative safety and the favourable effects of aspirin, its use in cancer seems justified, and ethical implications of this imply that cancer patients should be informed of the present evidence
*COX1↓, recent evidence highlights additional targets for aspirin in tackling cancer progression directly, irrespective of COX activity [3, 4]
TumCP↓, Such targets include energy metabolism involved in cancer proliferation, cancer associated inflammation [5] and platelet driven pro-carcinogenic activity [2].
DNArepair↑, beneficial effect of aspirin on colon cancer risk through an enhancement of DNA-repair mechanisms [2].
ChemoSen↑, ‘basic science’ basis to justify using aspirin as an adjunct to other pre-existing therapies (e.g., immunotherapy and cytotoxic chemotherapy) in the treatment of cancer progression and metastasis [2, 14].
other↓, Aspirin has been shown repeatedly to reduce thromboembolism, including in patients with cancer [15]
Dose↝, UT group received chemotherapy plus 300 mg of Uncaria tomentosa daily
*DNArepair↑, Uncaria tomentosa (Ut, Cat's claw) has antioxidant properties [10] and can stimulate DNA repair [11] and myelopoiesis
toxicity↝, Treatment with Ut did not alter liver function, defined as elevation of liver enzymes (alanine aminotransferase-ALT, aspartate aminotransferase-AST, γ glutamyl transpeptidase-GGT), and bilirubin levels, and kidney function
BioAv↝, consider the fact that all CRC patients in the present study underwent colectomy, which could interfere with the absorption of Ut.
eff∅, Ut at dose 300 mg dry extract daily is not effective in reducing the most prevalent adverse events due to treatment with 5FU/Leucovorin and oxaliplatin in patients with advanced CRC.
Risk↓, CRMs were well tolerated, and metformin and aspirin showed the most promising effect in reducing cancer risk in a selected group of patients.
AMPK↑, the increased AMP levels activate AMPK
Akt↓, This activation results in the inhibition of AKT and mTOR pathways
mTOR↓,
SIRT1↑, energy deficit also activates the SIRT pathways, which downregulates HIF1α, and the Nrf2 pathway
Hif1a↓,
NRF2↓,
SOD↑, enhances antioxidant defenses (e.g., superoxide dismutase SOD1 and SOD2)
ROS↑, Additionally, in prostate cancer (PC) [55] and triple-negative breast cancer (TNBC) [56] cell lines glucose restriction (GR) has been shown to trigger an increase in ROS, leading to cell death.
IGF-1↓, CR decreases poor prognosis markers such as IGF1, pAKT, and PI3K
p‑Akt↓,
PI3K↑,
GutMicro↑, induces changes in the gut microbiome linked to anti-tumor effects
OS↑, Incorporating a nutraceutical regimen like CR or KD with CT has reduced tumor growth and relapse and improved the survival rate
eff↝, type of dietary intervention, with FMD being the first option, followed by KD and CR last. FMD has been considered the most cost-effective and applicable because it does not completely restrict food intake.
ROS↑, findings consistently indicating that dietary restrictions render highly proliferative tumor cells more susceptible to oxidative damage
TumCCA↑, CR has been reported to induce cell cycle arrest in the G0/G1 phases , enabling cells to undergo DNA repair more efficiently and diminishing DNA damage by CRT
*DNArepair↑,
DNAdam↑, In contrast, tumoral cells, which have an altered cell cycle, are unable to repair DNA, leading to cell death
chemoP↑, Studies suggest that fasting before or during chemotherapy may induce differential stress resistance, reducing the adverse effects of chemotherapy and enhancing the efficacy of drugs.
ChemoSen↑,
*DNArepair↑, (1) repairing DNA damage in normal tissues (but not tumor cells);
*Apoptosis↓, preventing apoptosis-mediated damage to normal cells;
*CD8+↑, depleting regulatory T cells and improving the stimulation of CD8 cells;
UPR↑, accumulating unfolded proteins and protecting cancer cells from immune surveillance
eff↝, discuss how ‘fasting-mimicking diet’ as a modified form of fasting enables patients to eat a low calorie, low protein, and low sugar diet while achieving similar metabolic outcomes of fasting.
TumAuto↑, upregulating autophagy flux as a protection against damage to organelles and some cancer cells;
Remission↑, tumor remission rate in the MLT group was significantly higher than that in the control group
OS↑, MLT group had an overall survival rate of 28.24% (n=294/1,041), which was greatly increased compared with the control group (RR =2.07; 95% CI, 1.55–2.76; P<0.00001; I2=55%)
neuroP↑, MLT could effectively reduce the incidence of neurotoxicity
VEGF↓, by the downregulation of vascular endothelial growth factor (VEGF)
KISS1↑, MLT could suppress the metastasis of triple-negative breast cancer by inducing KISS1 expression
TumCP↓, MLT can significantly inhibit the proliferation of cancer cells
ChemoSideEff↓, while reducing the incidence of side effects in chemotherapy or radiotherapy
radioP↑, In the 20 randomized trials included, MLT was beneficial to reduce multiple side effects of radiotherapy and chemotherapy
Dose∅, mostly 20 mg/day and taken orally and taken at night, respectively
*ROS↓, Preclinical experimental research has confirmed that MLT was capable of scavenging ROS and repairing damaged DNA to exert antitumor effects
DNArepair↑,
ROS↑, The mechanisms of MLT exerting antitumor effect might involve with other pathways, such as antiangiogenesis and pro-oxidant
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1/CCND1↓,
CDK4↓,
CycB/CCNB1↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated
Imm↑, A less recognized, albeit even more essential role of selenite is in its stimulation of the cellular immune system
angioG↑, certain studies indicate that selenite may inhibit angiogenesis, and help to repair the damaged DNA fragments.
DNArepair↑,
NK cell↑, most important function of this compound in the fighting of cancer may be the direct activation of natural killer (NK) cells.
ROS↑, thus selenite Se4+ exhibits an ability to undergo oxidation and reduction reactions (the so-called redox reactions)
AntiCan↑, It should be emphasized that the use of high doses of sodium selenite exhibits promising anticancer effects, as described in numerous preclinical studies
selectivity↑, Numerous studies demonstrated higher selenite cytotoxicity against cancer cells when compared to normal cells, using a comparable dose of this element
ER Stress↑, sodium selenite can cause cell death by an independent pathway of mitochondrial apoptosis, endoplasmic reticulum stress (caused by the presence of (non)unfolded proteins), processes of autophagy, or necrosis.
TumAuto↑,
necrosis↑,
toxicity↝, Sodium selenite may be toxic when taken orally at higher doses, yet it is well tolerated by other routes such as intravenous, intraperitoneal and/or transdermal
Dose↑, As demonstrated recently by Swedish scientists, considerably higher doses of selenium are well tolerated by patients with cancer, in the case when sodium selenite is administered intravenously.
Showing Research Papers: 1 to 8 of 8
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
NRF2↓, 1, ROS↑, 4, SOD↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, CAIX↑, 1, SIRT1↑, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 2, p‑Akt↓, 1, Apoptosis↑, 1, BAX↑, 1, Bcl-2↓, 1, Casp3↑, 1, Casp9↑, 1, JNK↑, 1, MAPK↑, 1, necrosis↑, 1, p27↑, 1,
Transcription & Epigenetics ⓘ
KISS1↑, 1, other↓, 1, other↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 2,
DNA Damage & Repair ⓘ
DNAdam↑, 1, DNArepair↑, 4, P53↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 2, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
IGF-1↓, 1, IGF-1R↓, 1, mTOR↓, 1, PI3K↓, 1, PI3K↑, 1, PTEN↑, 1, STAT3↓, 1, TumCG↑, 1,
Migration ⓘ
E-cadherin↑, 1, MMP13↓, 1, MMP2↓, 1, MMP9↓, 1, Treg lymp↓, 1, TumCP↓, 3, TumMeta↑, 1, Vim↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, Hif1a↓, 2, NO↓, 1, VEGF↓, 2,
Barriers & Transport ⓘ
GLUT1↑, 1, GLUT3↑, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↑, 1, COX2↓, 1, FOXP3↓, 1, IL6↓, 1, IL8↓, 1, Imm↑, 1, NF-kB↓, 1, NK cell↑, 2, T-Cell↑, 1, Th1 response↑, 1, TNF-α↑, 1,
Hormonal & Nuclear Receptors ⓘ
RANKL↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↝, 2, ChemoSen↑, 3, Dose↑, 1, Dose↝, 1, Dose∅, 2, eff↑, 1, eff↝, 2, eff∅, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1, IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, chemoP↑, 1, ChemoSideEff↓, 2, neuroP↑, 1, OS↑, 3, radioP↑, 2, Remission↑, 1, Risk↓, 2, toxicity↝, 2,
Total Targets: 87
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
Catalase↑, 1, GPx↑, 1, GSH↑, 1, lipid-P↓, 1, ROS↓, 3, SOD↑, 1,
Cell Death ⓘ
Apoptosis↓, 1,
DNA Damage & Repair ⓘ
DNArepair↑, 4,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, ChemoSen↑, 1, Half-Life↝, 1,
Functional Outcomes ⓘ
cardioP↑, 1, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 1, RenoP↑, 1, toxicity↓, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 20
Scientific Paper Hit Count for: DNArepair, DNA repair
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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