ChemoSen Cancer Research Results

ChemoSen, chemo-sensitization: Click to Expand ⟱
Source:
Type:
The effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them, which is known as “chemo-sensitization”.

Chemo-Sensitizers:
-Curcumin
-Resveratrol
-EGCG
-Quercetin
-Genistein
-Berberine
-Piperine: alkaloid from black pepper
-Ginsenosides: active components of ginseng
-Silymarin
-Allicin
-Lycopene
-Ellagic acid
-caffeic acid phenethyl ester
-flavopiridol
-oleandrin
-ursolic acid
-butein
-betulinic acid
Scientific Papers found: Click to Expand⟱
4760- antiOx,  Chemo,    Impact of antioxidant supplementation on chemotherapeutic efficacy: a systematic review of the evidence from randomized controlled trials
- Review, Var, NA
ChemoSen∅, There was no evidence of significant decreases in the efficacy of chemotherapy with antioxidant supplementation.
OS↑, There were some indications of improvements in survival, tumour response and incidence of toxicity, but studies were underpowered.
chemoP↑,

1999- Api,  doxoR,    Apigenin ameliorates doxorubicin-induced renal injury via inhibition of oxidative stress and inflammation
- in-vitro, Nor, NRK52E - in-vitro, Nor, MPC5 - in-vitro, BC, 4T1 - in-vivo, NA, NA
neuroP↑, APG has a protective role against DOX-induced nephrotoxicity
ChemoSen∅, without weakening DOX cytotoxicity in malignant tumors.
RenoP↑, potential protective agent against renal injury. attenuate renal toxicity in cancer patients treated with DOX.
selectivity↑, APG maintained the cytotoxicity of DOX to tumor cells but not to renal cells. APG alone exhibited a prominent cytotoxic effect on 4T1 cells (Fig. 9E), but not on normal renal cells, at the same concentration
chemoP↑, Furthermore, APG revealed a dose-dependent improvement in normal renal cells against DOX-induced injury (Fig. 9E), with an exacerbation observed in 4T1 cells
ROS↑, Our in vivo study revealed that DOX caused a severe reduction in SOD activity and GSH levels, accompanied by an increase in MDA, leading to the overproduction of ROS and induction of oxidative injuries.
*ROS∅, Noteworthily, these changes were suppressed by APG(meaning on normal cells), consistent with several previous reports
*antiOx↑, APG has a similar antioxidative role as NAC and scavenges DOX-induced oxygen radicals and inhibits apoptosis significantly, implying that antioxidative stress is one of the main mechanisms through which APG protects renal tubular cells against DOX cy
*toxicity↓, We confirmed that APG mitigated the toxicity of DOX on normal renal cells by inhibiting oxidative stress, inflammation, and apoptosis.

4762- CoQ10,    The role of coenzyme Q10 as a preventive and therapeutic agent for the treatment of cancers
- Review, Var, NA
*AntiCan↓, Coenzyme Q10 (CoQ10) is a naturally occurring component that performs an anticancer function by reducing oxidative stress.
*ROS↓,
chemoPv↑, As a defensive mechanism against oxidative stress elevation in the antioxidative level including CoQ10 is expected, and an increase in these agents can protect cells and organs from side effects of chemotherapeutic drugs.
TumCCA↑, CoQ10 may induce its antitumor effect through multiple mechanisms, including anti-oxidation, anti-inflammation, cell cycle arrest, promoting apoptosis, reducing cell proliferation, inhibiting angiogenesis, suppression of MMPs, and so on
Apoptosis↑,
TumCP↓,
angioG↓,
MMPs↓,
ChemoSen∅, The review points out that: Some studies show improved tolerance without reduced response (chatAI interpretation)

4763- CoQ10,  Chemo,  doxoR,    Effect of Coenzyme Q10 on Doxorubicin Cytotoxicity in Breast Cancer Cell Cultures
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549
ChemoSen∅, CoQ10 had no effect on the ability of doxorubicin to induce apoptosis or inhibit growth or colony formation in both cell lines tested when CoQ10 was applied over a wide dose range.
antiNeop∅, These results support the hypothesis that CoQ10 does not alter the antineoplastic properties of doxorubicin.
*cardioP↑, hypothesized that dietary supplementation of CoQ10 prior to and during doxorubicin treatment can prevent doxorubicin-induced cardiotoxicity by preventing or slowing the displacement of CoQ10 by doxorubicin metabolites.
Dose↝, A daily dose of 300 mg per day for 11 days has been shown to raise plasma CoQ10 concentrations by 300-400%
selectivity↑, CoQ10 increased the cytotoxic activity of doxorubicin in L-1210 leukemia cells and had no effect in Ehrlich ascites carcinoma cells.3
TumCG∅, CoQ10 does not antagonize the in vitro growth inhibition effect of doxorubicin
TumCG∅, The growth inhibition of doxorubicin alone for BT549 cell line of 53.1% was also not significantly altered by CoQ10 additions
Apoptosis∅, CoQ10 does not diminish apoptotic effect of doxorubicin

4768- CoQ10,    Role of coenzymes in cancer metabolism
- Review, Var, NA
Risk↓, Deficiency of NADH dehydrogenase ubiquinone 1 subunit (Ndufc2), a subunit of CI, has been found in diabetes, cancer, and stroke
*ROS↓, CoQ10 function as an intracellular antioxidant preventing mitochondrial membrane proteins and phospholipids from free radical-induced oxidative damage
AntiCan↑, CoQ10 supplementation has found beneficial effects in diabetes [137,138], huntington's disease [139], coronary heart disease [140,141], congestive cardiac failure [142], fibromyalgia [143,144], and cancer
TumMeta↓, In addition, they observed that the patients with metastasis had lower CoQ10 levels than those who did not
ROS↑, It has been shown in an in vitro study on C57BL/6 mice that treatment with 100 μM CoQ10 for 72 h. can significantly alleviates pancreatic fibrosis by the ROS-triggered PI3K/AKT/mTOR signaling pathway
TumCG↓, Another in vitro and in vivo study on melanoma cells demonstrated that treatment with CoQ10 inhibit cell growth, induce apoptosis and prevent metastasis through suppression of the Wnt/β-catenin signaling pathway
Apoptosis↑,
TumMeta↓,
Wnt↓,
β-catenin/ZEB1↓,
TumCG↓, CoQ10 significantly lowered the growth of prostate cancer cells without affecting non-cancer prostate cells
selectivity↑,
RadioS↑, human glioblastoma cells with CoQ10 combined with radiation therapy and temozolomide, sensitized cells to radiation-induced DNA damage and potentiates temozolomide cytotoxicity
ChemoSen↑,
H2O2↓, In vitro study suggests that treatment of breast cancer cell lines with CoQ10 significantly decrease intracellular H2O2 content and inhibit MMP-2 activity leading to lower invasion and metastasis
MMP2↓,
cardioP↑, acute reversible depression of myocardial function and a chronic irreversible cardiomyopathy were prevented by different doses of CoQ10
ChemoSen∅, a recent study demonstrated that CoQ10 did not inhibit doxorubicin induced cytotoxicity in breast cancer cell lines [
Dose↝, 59 patients undergoing chemotherapy were enrolled and provided with CoQ10 (30 mg), branch chain amino acids (2500 mg), and carnitine (50 mg) for 21 days.

2251- MF,  Rad,    BEMER Electromagnetic Field Therapy Reduces Cancer Cell Radioresistance by Enhanced ROS Formation and Induced DNA Damage
- in-vitro, Lung, A549 - in-vitro, HNSCC, UTSCC15 - in-vitro, CRC, DLD1 - in-vitro, PC, MIA PaCa-2
RadioS↑, enhanced cancer cell radiosensitization associated with increased DNA double strand break numbers and higher levels of reactive oxygen species upon BEMER treatment relative to controls
DNAdam↑,
ROS↑,
ChemoSen∅, Intriguingly, exposure of cells to the BEMER EMF pattern failed to result in sensitization to chemotherapy and Cetuximab
Pyruv↓, levels of pyruvate, succinate, aspartate and adenosindiphosphate (ADP) were significantly downregulated after BEMER therapy whereas serine showed significant upregulation
ADP:ATP↓,
ROS↑, BEMER therapy increases ROS levels leading to radiosensitization via increased induction of DSBs

4747- Se,  Chemo,  antiOx,    Phase I trial of selenium plus chemotherapy in gynecologic cancers
- Trial, Ovarian, NA
*toxicity↓, The maximum tolerated dose of selenium was not reached
ChemoSen∅, Selenium had no effect on carboplatin pharmacokinetics.
RAD51↓, Correlative studies showed post-treatment downregulation of RAD51AP1, a protein involved in DNA repair, in both cancer cell lines and patient tumors.
other↝, Overall, the addition of selenium to carboplatin/paclitaxel chemotherapy is safe and well tolerated, and does not alter carboplatin pharmacokinetics. A 5000 μg dose of elemental selenium as selenious acid is suggested as the dose to be evaluated in a


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↓, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Pyruv↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   Apoptosis∅, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   RAD51↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 2,   TumCG∅, 2,   Wnt↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMPs↓, 1,   TumCP↓, 1,   TumMeta↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   ChemoSen∅, 7,   Dose↝, 2,   RadioS↑, 2,   selectivity↑, 3,  

Functional Outcomes ⓘ

AntiCan↑, 1,   antiNeop∅, 1,   cardioP↑, 1,   chemoP↑, 2,   chemoPv↑, 1,   neuroP↑, 1,   OS↑, 1,   RenoP↑, 1,   Risk↓, 1,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 2,   ROS∅, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   cardioP↑, 1,   toxicity↓, 2,  
Total Targets: 6

Scientific Paper Hit Count for: ChemoSen, chemo-sensitization
3 Chemotherapy
3 Coenzyme Q10
2 Anti-oxidants
2 doxorubicin
1 Apigenin (mainly Parsley)
1 Magnetic Fields
1 Radiotherapy/Radiation
1 Selenium
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1106  State#:%  Dir#:6
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