selectivity Cancer Research Results

selectivity, selectivity: Click to Expand ⟱
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The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
6185- Cuc,    Cucurbitacin B: A review of its pharmacology, toxicity, and pharmacokinetics
- Review, Var, NA - Review, Arthritis, NA - Review, AD, NA
*Inflam↓, results showed that CuB exhibits potent anti-inflammatory, antioxidant, antiviral, hypoglycemic, hepatoprotective, neuroprotective, and anti-cancer activities
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*AntiCan↑,
*toxicity↝, Studies of its toxicity and pharmacokinetic properties showed that CuB has non-specific toxicity and low bioavailability.
*BioAv↓,
*HO-1↑, CuB can exert its anti-inflammatory effect via the induction of heme oxygenase-1 (HO-1) by the activation Nrf2 [25].
*NRF2↑,
*NLRP3↑, CuB could act as an anti-inflammatory agent to inhibit gouty arthritis in mice [28]. The mechanism of action was mainly attributed to inhibition of the formation and activation of the NOD-like receptor thermal protein domain associated protein 3 (NLR
*SOD↑, Its antioxidant activity may be indirectly realized by increasing the activities of the antioxidant enzymes total SOD and SOD-1, and thereby eliminating excessive ROS and other free radicals in cells
*SOD1↑,
*ROS↓,
*AntiAge↑, this study also confirmed that CuB could exert anti-aging effects by regulating autophagy, ROS, and aging-related genes, which suggested that CuB might be a promising anti-aging drug
*ARE↑, activating the Nrf2/ARE signaling pathway and inhibiting the STAT/NF-κB signaling pathway, and thereby exerting a protective effect on cortical neurons
*STAT↓,
*NF-kB↓,
*neuroG↑, CuB (0.1 mg/kg) could also promote neurogenesis in APP/PS1 mice and alleviate memory deficits associated with enhanced neurogenesis in mice.
*memory↑,
ROS↑, Figure 2
NLRP3↑,
CIP2A↓,
Akt↓,
STAT3↑,
VEGFR2↓,
DNMTs↓, tudies have shown that in H1299 human lung cancer cells CuB (6, 60, 600, and 860 nM) can inhibit DNA methyltransferases (DNMTs)
MAPK↓,
YAP/TEAD↓,
PI3K↓,
Wnt↓,
NOTCH↓,
TumCCA↑,
TumCG↓, Inhibit cell growth and proliferation
TumCP↓,
FAK↑, CuB inhibited the migration, invasion, and adhesion of KKU-452 CCA cells in a dose-dependent manner by suppressing the activation of FAK and down-regulating MMP-9,
MMP9↓,
TumAuto↑, CuB ccould induce autophagy in BEL-7402 hepatocellular carcinoma cells by affecting autophagy-related proteins, such as up-regulating the expression of light chain 3 (LC3)-II
toxicity↝, Most experiments have demonstrated that CuB is moderately cytotoxic, both to human cancer cells and to normal cells
BioAv↓, When Wistar rats were given CuB orally at a dose of 8 mg/kg, the absorption degree was low and the absorption speed was slowest, which was specifically reflected in the fact that the time to peak concentration was longest (180 min, Tmax = 3 h). T
Half-Life↝, When CuB was administered intravenously at 0.1 mg/kg and orally at 1 mg/kg, the clearance rates of CuB in Wistar rats were similar, with a half-life (t1/2) of 5.08 ± 2.87 h and 5.09 ± 2.20 h, respectively [139].
BioAv↑, CuB-loaded mixed micelles with collagen peptides as a carrier, which improved the solubility of CuB and enhanced the absorption of orally administered CuB, and its relative bioavailability increased by a factor of 3.43
selectivity∅, Although CuB displays potent activity against tumor cells, its non-selective toxicity has limited its clinical applications.

2005- PLB,    Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases (MKP1/2)
- in-vivo, Nor, EL4 - in-vitro, AML, Jurkat
JNK↑, Plumbagin induced persistent activation of JNK
Cyt‑c↑, plumbagin induced cytochrome c release, FasL expression and Bax levels via activation of JNK pathway
FasL↑,
BAX↑,
ROS↑, plumbagin has been reported to induce ROS in normal as well as in tumor cells
*ROS↑, induce ROS in normal as well as in tumor cells
MKP1↓, plumbagin induced oxidative stress may suppress MKP activity in lymphoma cells leading to sustained JNK activation resulting in apoptosis.
MKP2↓,
selectivity∅, Plumbagin induced cell death in EL4(normal) cells and Jurkat cells
tumCV↑, cell viability dramatically decreased with increasing concentrations of plumbagin (0.05-2.5uM) when incubated for 24 or 48 h
Cyt‑c↑, Bax dependent cytochrome c release and apoptosome complex formation is followed by the cleavage of pro-caspase-3
Casp3↑,
GSH/GSSG↓, progressive decrease in GSH/GSSG ratio in tumor cells following plumbagin treatment
ROS↑, simultaneous increase in the levels of intracellular ROS was observed in both these cell lines which remained high up to 4 h indicating an increase in oxidative stress in tumor cells
mt-ROS↑, While we observed low basal mtROS levels in untreated cells, plumbagin treatment resulted in a significant increase in mtROS levels
*ROS↑, both cell lines, meaning normal EL4 cells too
eff↓, NAC, GSH and PEG-catalase were able to abrogate plumbagin induced ROS and cell death.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH/GSSG↓, 1,   ROS↑, 3,   mt-ROS↑, 1,  

Cell Death ⓘ

Akt↓, 1,   BAX↑, 1,   Casp3↑, 1,   Cyt‑c↑, 2,   FasL↑, 1,   JNK↑, 1,   MAPK↓, 1,   MKP1↓, 1,   MKP2↓, 1,   YAP/TEAD↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CIP2A↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   STAT3↑, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

FAK↑, 1,   MMP9↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGFR2↓, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   eff↓, 1,   Half-Life↝, 1,   selectivity∅, 2,  

Functional Outcomes ⓘ

toxicity↝, 1,  
Total Targets: 34

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ARE↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 2,   SOD↑, 1,   SOD1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

neuroG↑, 1,   STAT↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   toxicity↝, 1,  
Total Targets: 20

Scientific Paper Hit Count for: selectivity, selectivity
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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