chemoR Cancer Research Results

chemoR, chemoresistance: Click to Expand ⟱
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Chemoresistance refers to the ability of cancer cells to resist the effects of chemotherapy drugs, rendering treatments less effective or even ineffective. This resistance can be intrinsic (present before treatment) or acquired (developing during treatment) and poses a significant challenge in cancer therapy.

Eight recognized mechanisms underlying chemoresistance:
1.tumor heterogeneity;
2.inactivation of drugs (cytochrome P450, glutathione-S-transferase (GST), uridine diphospho-glucuronosyltransferase (UGT) superfamily);
3.overexpression of drug targets (EGFR and its downstream signaling targets);
4.efflux pump overexpression (MDR or P-gp, MRP1, ABCG2);
5.DNA damage repair;
6.evasion of cell death mediated by Bcl-2, Akt, NF-κB and STAT;
7.EMT favored by overexpression of TGF-β, FAK VEGF; and
8.epigenetic changes.
Scientific Papers found: Click to Expand⟱
1744- RosA,    Therapeutic Applications of Rosmarinic Acid in Cancer-Chemotherapy-Associated Resistance and Toxicity
- Review, Var, NA
chemoR↓, Recently, several studies have shown that RA is able to reverse cancer resistance to first-line chemotherapeutics
ChemoSideEff↓, as well as play a protective role against toxicity induced by chemotherapy and radiotherapy
RadioS↑, RA decreased radiation-induced ROS with RA by 21% compared to control
ROS↓, mainly due to its scavenger capacity
ChemoSen↑, recent years, evidence has emerged demonstrating the ability of RA to act as a chemosensitizer
BioAv↑, bioavailability of RA have been studied in animal models, revealing rapid absorption in the stomach and intestine
Half-Life↝, Urine was the primary route of RA excretion, with 83% of the total metabolites excreted during the period from 8 to 18 h after RA administration
antiOx↑, RA, well known for its antioxidant properties,
ROS↑, has recently been identified as a potential pro-oxidant in the presence of superoxide anions.
Fenton↑, Studies indicate that RA can facilitate the reduction of Cu (II) to Cu (I) and Fe (III) to Fe (II) leading to Fenton-type reactions that generate reactive hydroxyl radicals (HO˙)
DNAdam↑, These radicals are implicated in DNA damage and induction of apoptosis in cancer cells
Apoptosis↑,
CSCs↓, RA has demonstrated potential in controlling breast cancer stem cells (CSCs)
HH↓, RA inhibits stem-like breast cancer cells by targeting the hedgehog signaling pathway and modulating the Bcl-2/Bax ratio at concentrations of 270 and 810 μM
Bax:Bcl2↑,
MDR1↓, It has been observed to downregulate P-glycoprotein (P-gp) expression and decrease MDR1 gene transcription, thereby reversing MDR.
P-gp↓,
eff↑, RA has been reported to modulate the ADAM17/EGFR/AKT/GSK3β signaling axis in A375 melanoma cells, potentially enhancing synergy with cisplatin
eff↑, RA has demonstrated effectiveness in enhancing chemosensitivity to 5-FU, a commonly used chemotherapy agent for gastrointestinal cancers.
FOXO4↑, By upregulating FOXO4 expression, RA restored the sensitivity of cells to 5-FU
*eff↑, RA has been shown to reduce DOX-induced apoptosis in H9c2 cardiac muscle cells, and reduce intracellular ROS generation through downregulation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), as well as to restore the
*ROS↓,
*JNK↓,
*ERK↓,
*GSH↑, RA has also shown an antioxidant role, which is evidenced by the ability and recovery of levels of glutathione (GSH), hydrogen peroxide (H2O2), and superoxide radicals (O2·), reducing the expression of malondialdehyde
*H2O2↑,
*MDA↓,
*SOD↑, regulating the expression of antioxidant enzymes such as superoxide dismutase (SOD), as well as upregulating catalase heme oxygenase-1, resulting in significantly improved viability
*HO-1↑,
*CardioT↓, The cardioprotective effect of RA
selectivity↑, RA blocked caspases 3 and 9 activation, cytochrome c release, and ROS generation induced by cisplatin in HEI-OC1(normal)cells

1509- SFN,    Combination therapy in combating cancer
- Review, NA, NA
NRF2↑, chemopreventive properties that are thought to be due to potent upregulation of Nrf2
ChemoSideEff↓, chemopreventive properties
eff↑, combined SFN with taxol in treatment of prostate cancer cell line DU145, and observed that SFN potentiated the effects of low doses of taxol
TumCP↓,
Apoptosis↑,
TumCCA↑, induce G2/M cell cycle arrest in vitro and in vivo
eff↑, SFN positively enhanced bortezomib, lenalidomide, and conventional drugs, such as dexamethasone, doxorubicin, and melphalan in a synergistic manner
PSA↓, SFN has shown to significantly reduce levels of prostate-specific antigen (PSA) (44.4% SFN group vs. 71.8% in placebo)
P53↑, SFN activates various anti-cancer responses such as p53, ARE, IRF-1, Pax-6 and XRE while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
Hif1a↓, while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
CAIX↓,
chemoR↓, SFN has thus shown to reduce chemoresistance and may be a potential agent to be used in conjunction with chemotherapeutics
5HT↓, SFN downregulates 5-HT receptor expression in Caco-2 cells

4741- SSE,    Selenium in Oncological Intervention
- Review, Var, NA
Risk↓, The trace element selenium has a long history as a cancer preventive agent.
*other↝, optimal selenium supply gives serum levels between about 110 µg/L and 130 µg/L [
Risk↓, The incidence of prostate cancer was also reduced in the selenium group (relative risk 0.51; 95% CI: 0.29–0.87) with the greatest effect being seen in the men who initially had the lowest selenium supplies (serum selenium levels <123 µg/L) [
AntiTum↑, findings from this study indicate that sodium selenite might work in three ways against cancer: the antitumor effect by itself, by reversing chemoresistance and by ameliorating toxic effects from chemotherapy.
chemoR↓,
chemoP↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Fenton↑, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   Bax:Bcl2↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   FOXO4↑, 1,   HH↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

PSA↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   chemoR↓, 3,   ChemoSen↑, 1,   eff↑, 4,   Half-Life↝, 1,   MDR1↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

PSA↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,   ChemoSideEff↓, 2,   Risk↓, 2,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   H2O2↑, 1,   HO-1↑, 1,   MDA↓, 1,   ROS↓, 1,   SOD↑, 1,  

Cell Death ⓘ

JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Functional Outcomes ⓘ

CardioT↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: chemoR, chemoresistance
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Selenite (Sodium)
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#:1118  State#:%  Dir#:1
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