DNArepair Cancer Research Results
DNArepair, DNA repair: Click to Expand ⟱
| Source: HalifaxProj(enhance) |
| Type: |
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⟱
ChemoSen↑, Beta-Caryophyllene (BCP), was highlighted in several recent preclinical studies to enhance chemo-sensitization in chemo-resistant tumors and to efficiently inhibit angiogenesis and cancer cells’ ability to invade and metastasize.
angioG↓,
TumCI↓,
TumMeta↓,
ROS↑, BCP seems to work as a dual modulator of oxidative stress, increasing reactive oxygen species (ROS) in cancer cells, and thus enhancing apoptosis, but reducing ROS in normal cells to protect them from damage
*ROS↓,
chemoP↑,
CB2 / CNR2↑, important issue in BCP is its ability to bind to the body’s cannabinoid receptor 2 (CB2), where it binds selectively to the CB2 receptors and not the CB1 receptor, which makes it non-psychoactive and therapeutically appealing.
Inflam↓, activation of the CB2 receptor by BCP can suppress pro-inflammatory cytokines production, helping to create an anti-tumor immune environment
AntiTum↑,
*BioAv↑, Beta-Caryophyllene, a food additive approved by the Food and Drug Administration, is efficiently absorbed in the gastro-intestinal tract and can penetrate the blood–brain barrier and has a well-established safety profile, making it an attractive biom
*BBB↑,
Apoptosis↑, Induces apoptosis and suppresses proliferative activity of lung cancer cells
TumCP↑,
TumCCA↑, Induces G1 cell cycle arrest by dysregulating cyclins and other molecules
RadioS↑, GBM: Works as a potential radiosensitizer for improving RT outcomes by inhibiting DNA repair, inducing apoptosis, and suppressing anti-apoptotic and survival pathways
DNArepair↓,
ROS↑, BC: Enhances sensitization and promotes the cigarette smoke condensate (CSC)-induced apoptosis in MDA-MB-468 cells, mainly by triggering oxidative stress and inhibition of STAT3
STAT3↓,
*BioEnh↑, BCP is considered a key component in black pepper’s ability to enhance nutrient absorption, including compounds like curcumin.
Pain↓, BCP in cloves further supports their role in pain management and infection prevention.
AntiBio↓,
ROS↑, selectively induce apoptosis and oxidative stress in cancer cells while sparing normal cells at lower concentrations.
Dose↝, I50, for many cancer cell lines typically ranges from 19 to 64 μM
NF-kB↓, Beta-Caryophyllene was reported to inhibit the central to the regulators of inflammation, NF-κB and MAPK pathways, leading to a decrease in pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) production
MAPK↓,
TNF-α↓,
IL1β↓,
IL6↓,
cl‑PARP↑, through increasing the levels of cleaved PARP, caspases and Bax, and the downregulation of Bcl-2, directly by interaction with CB2.
Casp↑,
BAX↑,
Bcl-2↓,
VEGF↓, BCP blocks migration of endothelial cells by inhibiting the secretion of VEGF, and thus blocking the activity of the tyrosine kinase VEGFR2
VEGFR2/KDR/Flk1↓,
MMP2↓, BCP can also prohibit the secretion of MMP-2, p-p38 and p-ERK
p‑p38↓,
p‑ERK↓,
EPR↑, BCP was suggested to accumulate in the cancer cell membrane, altering the cells’ permeability, leading to the accumulation of anticancer drugs, and consequently strengthening the drugs’ activity.
P-gp/ABCB1↓, direct inhibition of P-glycoprotein (P-gp/ABCB1) and multidrug resistance-associated protein 1 (MRP1/ABCC1), which are overexpressed in resistant tumors
MRP1/ABCC1↓,
*NRF2↑, Importantly, BCP’s selective antioxidant activity—activating Nrf2 in normal cells while increasing ROS in cancer cells—minimizes off-target toxicity,
*antiOx↑,
AntiTum↑, Formononetin elicits antitumorigenic properties in vitro and in vivo by modulating numerous signaling pathways to induce cell apoptosis (by intrinsic pathway involving Bax, Bcl-2, and caspase-3 proteins)
Apoptosis↑,
BAX↑,
Bcl-2↓,
Casp3↑,
TumCCA↑, cell cycle arrest (by regulating mediators like cyclin A, cyclin B1, and cyclin D1),
cycA1/CCNA1↓,
CycB/CCNB1↓,
cycD1/CCND1↓,
TumCP↓, suppress cell proliferation [by signal transducer and activator of transcription (STAT) activation, phosphatidylinositol 3-kinase/protein kinase-B (PI3K/AKT), and mitogen-activated protein kinase (MAPK) signaling pathway],
VEGF↓, inhibit cell invasion [by regulating growth factors vascular endothelial growth factor (VEGF) and Fibroblast growth factor 2 (FGF2), and matrix metalloproteinase (MMP)-2 and MMP-9 proteins].
FGF↓,
MMP2↓,
MMP9↓,
eff↑, Co-treatment with other chemotherapy drugs such as bortezomib, LY2940002, U0126, sunitinib, epirubicin, doxorubicin, temozolomide, and metformin enhances the anticancer potential of both formononetin and the respective drugs through synergistic effec
ChemoSen↑,
chemoPv↑, Compiling the evidence thus far highlights the potential of formononetin to be a promising candidate for chemoprevention and chemotherapy.
p‑Akt↓, downregulation of EphB3, p-AKT, p-P13K, p-STAT3, inhibition of cyclin D1, MMP2/9
p‑STAT3↑,
TumCMig↓, MDA-MB-231-luc and 4T1 Inhibition of cell migration and invasion, elevation of TIMP-1 and TIMP-2, and suppression of PI3K/AKT signaling
TumCI↓,
TIMP1↑,
TIMP2↑,
PI3K↓,
Akt↓,
Dose↝, formononetin is administered into the mice intraperitoneally or intragastrically, mainly at doses between 10 and 60 mg/kg for 2–3 weeks via intraperitoneal route and between 15 and 100 mg/kg for more than a month via intragastric route
TumCG↓, In general, the formononetin treatment suppresses xenograft tumor growth in terms of tumor weight and volume, and also inhibits tumor invasiveness and angiogenesis.
TumW↓,
TumVol↓,
angioG↓,
Casp3↑, After exposure to formononetin, expression levels of cleaved caspase-3 and -9 in ovarian cancer cells increased in a dose-dependent manner
Casp9↑,
cl‑PARP↑, leading to the cleavage of poly(ADP-ribose) polymerase (PARP), which results in the inability to repair damaged DNA
DNArepair↓,
MMP↓, significant loss of mitochondrial membrane potential of approximately 457% (P < 0.001) and 265% (P < 0.001) in ES2 and OV90 ovarian cancer cells was observed upon exposure to 40 µM formononetin
BAX↑, expression of Bax protein surged upon formononetin treatment, while Bcl-2 protein level decreased
Bcl-2↓,
DR5↑, formononetin displayed high affinity and steric compatibility to death receptor 5, which could be activated to mediate the TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis
ROS↑, Formononetin can also induce the apoptotic pathway via the overexpression of reactive oxygen species (ROS) and disturbance of the intracellular antioxidant system.
eff↓, abrogated with the use of antioxidants such as N-acetyl-L-cysteine (NAC) and glutathione (GSH), suggesting that formononetin induces apoptosis via ROS production.
p‑ERK↓, formononetin was demonstrated to be a promising molecule that inhibits the phosphorylation of ERK1/2 itself as well as the phosphorylation of downstream ERK substrate (P90RSK)
PTEN↑, Besides the inhibition on AKT activity, formononetin upregulated PTEN expression in bladder cancer T24 cell.
Hif1a↓, The inhibition of AKT pathway by formononetin was mediated through the attenuation of HIF-α expression and inflammatory cytokines release
eff↑, Formononetin was shown to potentiate bortezomib-induced apoptosis in multiple myeloma
eff↑, synergistic effect was evident between formononetin and metformin in cancer treatment.
ChemoSen↑, sensitivity of glioma cells towards doxorubicin was shown to be enhanced by co-treatment with formononetin
HDAC↓, formononetin in doxorubicin-treated glioma cells was associated with formononetin’s suppressive effect on the histone deacetylase (HDAC) 5 expression
*BioAv↑, Due to its lipophilic nature, formononetin is rapidly absorbed into the gut via passive diffusion, with a peak absorption at 30 min ().
*Half-Life↝, Formononetin was determined to have a half-life of ∼2–3 h after oral administration and ∼2 h after intravenous administration
*BioAv↝, At oral administration of formononetin at 20–50 mg/kg, the peak plasma concentration was achieved between (Tmax) 0.5–1 h, while the maximum plasma concentration (Cmax) was determined ranging from 62 nM (17 ng/ml) to 302 nM (81 ng/ml).
*BioAv↑, Meanwhile, the Cmax of 1,302.8 nM (349.5 ng/ml) and 16,956.6 nM (4,548.5 ng/ml) was achieved after intravenous administration of formononetin at 4 and 10 mg/kg, respectively
*BioAv↑, rapidly metabolized and extensively converted into its metabolites daidzein and conjugates of daidzein and formononetin to be excreted, which makes it poorly bioavailable.
*eff↑, Drug delivery systems are strategies employed to overcome the low bioavailability and low water solubility of formononetin to achieve its pharmacological efficacy at minimum dose
RadioS↑, Hyperthermia has long been known as a radio-sensitizing agent that displays anti-tumor effects, and has been developed as a therapeutic application.
DNArepair↓, The mechanisms of hyperthermia-induced radio-sensitization are highly associated with inhibition of DNA repair.
Dose↑, Significant differences in cellular toxicity attributable to hyperthermia at and above 42.5°C were observed.
NA↑, As an adjunct to radiotherapy and chemotherapy, hyperthermia enhances the therapeutic efficacy against both primary and recurrent tumors.
RadioS↑, The present review explores the mechanisms underlying the synergy between radiotherapy and hyperthermia, while reviewing the outcomes of relevant clinical trials.
DNArepair↓, Key mechanisms of action include inhibition of DNA repair, reduction of hypoxic tumor cell populations, enhancement of drug uptake and improved perfusion and oxygenation.
Hypoxia↓,
EPR↑,
LC↑, Its application has improved both local control and overall survival (OS),
OS↑,
*toxicity↓, Randomized clinical trials (4–6) have demonstrated that combined therapy effectively prolongs disease-free survival and ensures local tumor control without added toxicity.
Dose↝, fever-range temperatures (39–40°C), moderate heating to induce cellular stress (41–43°C) and high-intensity thermal ablation >43°C for cell destruction.
BloodF↑, Hyperthermia is particularly toxic to cells in acidic environments (29), and increased blood flow helps clear acidic metabolites, restore normal extracellular pH
pH↝,
Imm↑, Under heat stress, tumor cells release heat shock protein 70 (HSP70), triggering antitumor immune responses
HSP70/HSPA5↑,
RadioS↑, mild hyperthermia (HT) represents an old, but recently revived opportunity to increase the efficacy of radiotherapy (RT) without increasing side effects, thereby widening the therapeutic window.
DNArepair↓, associated to DNA damage and repair, hypoxia, stemness and immunostimulation.
Hypoxia↓,
CSCs↓, Some evidences suggests that HT may be able to radiosensitize CSCs, as well as quiescent tumor cells,
Imm↑, Heat-induced activation of the immune system is mediated by heat shock proteins (HSPs); they increase antigen presentation and maturation of dendritic cells,
pH↝, regains a normal oxygen partial pressure (pO2), a normal concentration of nutrients and a normal pH, which reverse the established radioresistance
HSPs↑,
ROS↑, Hyperthermia potentializes the effects of irradiation by reducing DNA damage repair, increasing oxygen levels by vessel dilation, increasing ROS,
eff↑, An increasing number of preclinical and clinical studies are focusing on heating tumors with nanoparticles
LC↑, moderate RHT in improving local tumour control, survival outcomes and quality of life scores were observed across the different cancer subsites with minimal increase in toxicities.
OS↑,
QoL↑,
toxicity↓,
Dose↝, Various heating methods include direct (e.g., intracavitary and whole-body waterbed), infrared, perfusional (e.g., isolated limb perfusion, intravesical and intraperitoneal), nanoparticles, ultrasound and regional radiofrequency (RF) radiation
Dose↝, Moderate HT is usually described at a range of 39–44 °C a
ROS↑, Figure 1
DNArepair↓,
EPR↑,
DNAdam↑,
HSP70/HSPA5↑,
BloodF↑,
Hypoxia↓,
RadioS↑, Mild hyperthermia (mHT, 39–42 °C) is a potent modality when combined with existing radio-, chemo-, or immunotherapy, leading to enhanced microcirculatory blood flow and improved tumor oxygenation
ChemoSen↑, Hyperthermia enhances cytotoxicity of anticancer drugs:
Imm↑,
BloodF↑,
Hypoxia↓, HT-induced improvements of tumor oxygenation status (“reversal of tumor hypoxia”) a
Dose↝, Mild hyperthermia (mHT, 39–42 °C) is a potent cancer treatment modality when delivered in conjunction with radiotherapy.
DNArepair↓, Hyperthermia inhibits DNA repair enzymes: In the upper range of mHT (41–43 °C), several DNA damage repair enzymes responsible for the repair
e-pH↓, Tissue exposure to mHT triggers a series of events that aggravate tumor tissue acidosis (pH↓), finally reaching extracellular pH values of ≈ 6.20:
HDAC↓, Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI).
TumCCA↑, phenylbutyrate treatment that results in reduced proliferation and cell-cycle arrest in G1 or G2 phases.
P21↑, common sequela of phenylbutyrate treatment is the upregulation of p21,
Dose↝, In prostate cancer, phenylbutyrate at clinically achievable concentrations (0.1 mM-8 mM),
Telomerase↓, butyrate or its derivatives was also evident in several other types of cancers and was associated with loss of telomerase activity
IGFBP3↑, Upregulation of insulin-like growth factor binding protein 3 (IGFBP-3) is another unique antiproliferative mechanism of sodium butyrate in breast cancer cells
p‑p38↑, Phenylbutyrate and its derivatives upregulated p21, gelsolin, phosphorylated p38, JNK, and ERK (MAPK pathway members), Bax, caspases-3,
JNK↑,
ERK↑,
BAX↑,
Casp3↑,
Bcl-2↓, downregulated Bcl-X L , Bcl-2, cytochrome c, FAK, and survivin
Cyt‑c↝,
FAK↓,
survivin↓,
VEGF↓, Butyrate treatment reduced the level of vascular endothelial growth factor (VEGF)
angioG↓,
DNArepair↓, Inhibition of DNA Repair.
TumMeta↓,
HSP27↑, Moreover, butyrate treatment in colorectal cancer cells resulted in an acute stress response that was associated with HSP27 activation, activation of ASK1 (MAP3K) and p38 MAPK pathway consequently.
ASK1↑,
ROS↑, Also it resulted in elevated cellular levels of reactive oxygen species (ROS) in oral and tongue cancer cells.
eff↑, phenylbutyrate enhanced the cytotoxicity of temozolamide in malignant glioma cells via suppression of the endoplasmic reticulum stress revealed by the decreased expression of GRP78 and GADD153.
ER Stress↓,
GRP78/BiP↓,
CHOP/DDIT3↑, GADD153
AR↓, Sodium butyrate treatment of prostate cancer cells was associated with downregulation of androgen receptor
other?, lots of references in this paper.
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in-vitro, |
BC, |
MCF7 |
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in-vitro, |
BC, |
MDA-MB-468 |
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in-vitro, |
Nor, |
MCF10 |
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Apoptosis↑, NaBu induced a dose and time-dependent cell toxicity in breast cancer cells which was related to the cell cycle arrest and induction of apoptosis.
i-ROS?, NaBu-elicited apoptosis was accompanied by the elevated level of ROS
Casp↑, increased caspase activity
MMP?, reduced mitochondrial membrane potential (Δψm) in MCF-7 and MDA-MB-468 cells
selectivity↑, and with no effect on the above mentioned factors in MCF-10A cells.
*ROS∅, however the level of ROS production was remained approximately unchanged in MCF-10A cells.
HDAC↓, Sodium butyrate (NaBu), one of the well-studied HDACi, is a short-chain fatty acid and the byproduct of carbohydrate metabolism in the gut
DNArepair↓, Sodium butyrate including the inhibition of DNA double strand break repair and stress oxidative
Casp3↑, effect of sodium butyrate on the cell cycle distribution, intracellular formation of Reactive oxygen species (ROS), the caspase 3 and 8 activity,
Casp8↑,
*toxicity↓, MCF-10A cells were treated with the same concentrations of sodium butyrate (0.1–20 mM) for 24, 48, 72 h and the subsequent cytotoxic effect was significantly lower comparing to the breast cancer cells.
TumCCA↑, significant elevation in the percentage of accumulated cells in the sub-G1 phase which was observed in MCF-7 and MDA-MB-468 cells however the effect of sodium butyrate on MCF-10A cell cycle distribution was inconsiderable
*antiOx↑, Reserpine is a natural indole alkaloid isolated from Rauwolfia serpentina and has potent antioxidant, antimicrobial, and anti-mutagenic properties.
*AntiBio↑,
TGF-β↓, reserpine inhibits TGF-β dependent Smad2/3/4 phosphorylation, thereby blockage Smad3/Snail activation and Smad2/4 nuclear translocation.
p‑SMAD3↓,
p‑SMAD2↓,
p‑SMAD4↓,
SMAD3↓,
Snail↓,
ERCC1↓, downregulating ERCC1, XPF, Ku70, DNA-PKcs, PCNA, cyclin D1, HIF-1α, IL-6, Mcl-1
ERCC4/XPF↓,
Ku70/XRCC6↓,
PCNA↓,
cycD1/CCND1↓,
Hif1a↓,
IL6↓,
Mcl-1↓,
BAX↑, stimulates Bax, cytochrome C, Apaf-1, caspase-9, caspase-3 and PARP protein expressions.
Cyt‑c↑,
APAF1↑,
Casp9↑,
Casp3↑,
PARP↑,
DNArepair↓, therapeutic potential of reserpine in inhibiting DNA repair, cell proliferation, and invasion
TumCP↓,
TumCI↓,
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in-vivo, |
Melanoma, |
B16-F10 |
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xCT/SLC7A11↓, Sulfasalazine is an inhibitor of xCT that is known to increase cellular oxidative stress, giving it anti-tumor potential.
ROS↑,
RadioS↓, radio-sensitizing effect of sulfasalazine using a B16F10 melanoma model.
GSH↓, Sulfasalazine decreased glutathione concentrations and resistance to H2O2 in B16F10 melanoma cells, but not in mouse embryonic fibroblasts.
selectivity↑,
DNArepair↓, It inhibited cellular DNA damage repair and prolonged cell cycle arrest after X-irradiation.
TumCCA↑,
H2O2↑, SAS decreases cellular GSH and increases H2O2 cytotoxicity in B16F10 cells
Dose↝, At lower SAS concentrations (10–100 μM), we did not observe any increase in intracellular ROS. At higher concentrations of SAS (800–1,000 μM), intracellular ROS increased approximately 2.3-fold in B16F10 cells
HK2↓, When TRAMP mice were given 6 μmol/mouse (1 mg/mouse) three times a week for 17–19 weeks, the prostate tumor expression of glycolysis-promoting enzymes such as (HKII), 2 (PKM2) and (LDHA) was decreased by 32–45%
PKM2↓,
LDHA↓,
Glycolysis↓, These results provide evidence that sulforaphane suppresses in vivo glycolysis in prostate cancer cells
LAMP2↑, The study shows that 10–20 μM of sulforaphane significantly increased lysosome-associated membrane protein 2 (LAMP2) in the cell lines
Hif1a↓, sulforaphane has been shown to suppress HIF-1α
DNAdam↓, SFN causes DNA damage and prevents DNA repair in prostate cancer cell
DNArepair↓,
Dose↝, 5 to 100 mg/kg of sulforaphane reduce tumors in animal models [ 5 , 19]. For a 70 kg human,
this translates to 350–7000 mg/kg, which is significantly above the upper threshold of
tolerable doses
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↓, 1, ERCC4/XPF↓, 1, Ku70/XRCC6↓, 1, LC↑, 2, NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
GSH↓, 1, H2O2↑, 1, ROS↑, 8, i-ROS?, 1, xCT/SLC7A11↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP?, 1, MMP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ERCC1↓, 1, Glycolysis↓, 1, HK2↓, 1, LDHA↓, 1, PKM2↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↑, 3, ASK1↑, 1, BAX↑, 5, Bcl-2↓, 4, Casp↑, 2, Casp3↑, 5, Casp8↑, 1, Casp9↑, 2, Cyt‑c↑, 1, Cyt‑c↝, 1, DR5↑, 1, JNK↑, 1, MAPK↓, 1, Mcl-1↓, 1, p‑p38↓, 1, p‑p38↑, 1, survivin↓, 1, Telomerase↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other?, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, ER Stress↓, 1, GRP78/BiP↓, 1, HSP27↑, 1, HSP70/HSPA5↑, 2, HSPs↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LAMP2↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, DNAdam↑, 1, DNArepair↓, 12, PARP↑, 1, cl‑PARP↑, 2, PCNA↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 2, P21↑, 1, TumCCA↑, 5,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, ERK↑, 1, p‑ERK↓, 2, FGF↓, 1, HDAC↓, 3, IGFBP3↑, 1, PI3K↓, 1, PTEN↑, 1, STAT3↓, 1, p‑STAT3↑, 1, TumCG↓, 1,
Migration(tgid=13) ⓘ
FAK↓, 1, MMP2↓, 2, MMP9↓, 1, p‑SMAD2↓, 1, SMAD3↓, 1, p‑SMAD3↓, 1, p‑SMAD4↓, 1, Snail↓, 1, TGF-β↓, 1, TIMP1↑, 1, TIMP2↑, 1, TumCI↓, 3, TumCMig↓, 1, TumCP↓, 2, TumCP↑, 1, TumMeta↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EPR↑, 3, Hif1a↓, 3, Hypoxia↓, 4, VEGF↓, 3, VEGFR2/KDR/Flk1↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CB2 / CNR2↑, 1, IL1β↓, 1, IL6↓, 2, Imm↑, 3, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Cellular Microenvironment(tgid=17) ⓘ
pH↝, 2, e-pH↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 4, Dose↑, 1, Dose↝, 9, eff↓, 1, eff↑, 5, MRP1/ABCC1↓, 1, RadioS↓, 1, RadioS↑, 5, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 1, BloodF↑, 3, IL6↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiTum↑, 2, chemoP↑, 1, chemoPv↑, 1, OS↑, 2, Pain↓, 1, QoL↑, 1, toxicity↓, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 122
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, NRF2↑, 1, ROS↓, 1, ROS∅, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 4, BioAv↝, 1, BioEnh↑, 1, eff↑, 1, Half-Life↝, 1,
Functional Outcomes(tgid=23) ⓘ
toxicity↓, 2,
Total Targets: 12
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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