selectivity Cancer Research Results

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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⟱
5271- 3BP,    The anticancer agent 3-bromopyruvate: a simple but powerful molecule taken from the lab to the bedside
- Review, Var, NA
selectivity↑, 3-bromopyruvate (3BP), a simple alkylating chemical compound was presented to the scientific community as a potent anticancer agent, able to cause rapid toxicity to cancer cells without bystander effects on normal tissues.
selectivity↑, results obtained in cancer research with this small molecule have contradicted the just noted general fear. Indeed, a promising drug has been revealed with an effective mechanism of action and an outstanding selectivity towards cancer cells
ATP↓, once inside cancer cells 3BP can then inhibit both of their energy (ATP) producing systems, i.e., glycolysis, likely by inhibiting hexokinase-2 (hk-2) and mitochondrial oxidative phosphorylation
Glycolysis↓,
HK2↓,
mt-OXPHOS↓,
GAPDH↓, Different reports have shown that 3BP is able to inhibit GAPDH activity leading to the loss of the ATP-producing steps that occur downstream of this enzyme
mtDam↑, Mitochondria related cell death has also been reported following 3BP treatment.
GSH↓, Ehrke and co-workers have demonstrated that 3BP inhibits glycolysis and deplete the glutathione levels in primary rat astrocytes
ROS↑, Others have also observed an increase in ROS levels following 3BP treatment that induces endoplasmic reticulum stress
ER Stress↑,
TumAuto↑, Autophagy has been associated with 3BP activity in breast cancer cell lines (Zhang et al., 2014),
LC3‑Ⅱ/LC3‑Ⅰ↑, 3BP leads to aggressive autophagy involving a decrease in the ratio of LC3I/LC3II and the levels of p62 as well as dephosphorylation of Akt and p53.
p62↓,
Akt↓,
HDAC↓, 3BP’s, it has been reported to be involved in suppressing epigenetic events as it inhibits histone deacetylase (HDAC) isoforms 1 and 3 in MCF-7 breast cancer cells leading to apoptosis
TumCA↑, Proliferation inhibition by 3BP treatment has also been related with the induction of S-phase and G2/M- phase arrest (Liu et al. 2009)
Bcl-2↓, downregulation of the expression of Bcl-2, c-Myc and mutant p53, the upregulation of Bax, activation of caspase-3 and mitochondrial leakage of cytochrome c
cMyc↓,
Casp3↑,
Cyt‑c↑,
Mcl-1↓, mitochondria mediated apoptosis triggered by 3BP was found to be associated with the downregulation of Mcl-1 through the phosphoinositide-3-kinase/Akt pathway (Liu et al. 2014).
PARP↓, 3BP treatment decreases the levels of poly(ADP-ribose) polymerase (PARP) and cleaved PARP.
ChemoSen↑, it might be a good adjuvant for commonly used chemotherapy agents, or a replacement for such agents.

5281- 3BP,    A translational study “case report” on the small molecule “energy blocker” 3-bromopyruvate (3BP) as a potent anticancer agent: from bench side to bedside
- Case Report, Var, NA
Glycolysis↓, 3BP targets cancer cells’ energy metabolism, both its high glycolysis (“Warburg Effect”) and mitochondrial oxidative phosphorylation.
mt-OXPHOS↓,
ATP↓, This inhibits/ blocks total energy production leading to a depletion of energy reserves. Moreover, 3BP as an “Energy Blocker”, is very rapid in killing such cells.
selectivity↑, 3BP at its effective concentrations that kill cancer cells has little or no effect on normal cells.
toxicity↝, The results obtained hold promise for 3BP as a future cancer therapeutic without apparent cyto-toxicity when formulated properly.
OS↑, The patient (Fig. 5) was able to survive a much longer period than expected with an improved quality of life, which is clearly attributable to the treatment with 3BP.
QoL↑,

5280- 3BP,    Anticancer Efficacy of the Metabolic Blocker 3-Bromopyruvate: Specific Molecular Targeting
- in-vitro, PC, NA
mtDam↑, 3-BromoPyruvate severely damaged mitochondrial integrity which might have severely affected ATP generation in cancer cells.
HK2↓, 3-BP inhibits hexokinase II (HK2) and TGFbeta1 and enhanced active caspase-3 expression in tumor tissues as compared to untreated control.
TGF-β↓,
Casp3↑,
selectivity↑,

5278- 3BP,    The effect of 3-bromopyruvate on human colorectal cancer cells is dependent on glucose concentration but not hexokinase II expression
- in-vitro, CRC, HCT116 - in-vitro, CRC, Caco-2 - in-vitro, CRC, SW48
ATP↓, 3-Bromopyruvate (3BP) is a pyruvate analogue with alkylating properties that depletes cellular ATP levels and induces rapid cell death in neoplastic cells with limited cytotoxic effects against normal cells.
TumCD↑,
selectivity↑,
toxicity↓, 3BP treatment led to eradication of tumours of hepatocellular carcinoma cell origin in rats without apparent cytotoxic effects [19]
OS↑, first human case report suggested that 3BP was able to prolong survival in a cancer patient diagnosed with hepatocellular carcinoma in 2012 [19,20].
HK2?, 3BP is able to dissociate and inhibit mitochondrial HKII function, thereby reducing ATP production. 3BP binding also frees up binding sites previously occupied by HKII
Cyt‑c↑, llowing pro-apoptotic molecules (such as BAX and BAD) to promote the release of cytochrome c into the cytosol and induce eventual cell death
eff↑, Raji lymphoma cells grown under hypoxic conditions were more sensitive to 3BP than in normoxia
p‑Akt↑, 3BP induces rapid AKT phosphorylation at residue Thr-308

5277- 3BP,    3-Bromopyruvate inhibits pancreatic tumor growth by stalling glycolysis, and dismantling mitochondria in a syngeneic mouse model
- in-vivo, PC, Panc02
HK2↓, It exerts potent anticancer effects by inhibiting hexokinase II enzyme (HK2) of the glycolytic pathway in cancer cells while not affecting the normal cells.
selectivity↑, it doesn’t affect the normal cells but strongly toxic to cancer cells
ATP↓, 3-BP killed 95% of Panc-2 cells at 15 μM concentration and severely inhibited ATP production by disrupting the interaction between HK2 and mitochondrial Voltage Dependent Anion Channel-1 (VDAC1) protein.
mtDam↑, Electron microscopy data revealed that 3-BP severely damaged mitochondrial membrane in cancer cells.
Dose↝, We further examined therapeutic effect of 3-BP in syngeneic mouse pancreatic cancer model by treating animals with 10, 15 and 20 mg/kg dose. 3-BP at 15 & 20 mg/kg dose level significantly reduced tumor growth by approximately 75-80% in C57BL/6 female
TumCG↓, 3-BP inhibit in vivo pancreatic tumor growth in C57BL/6 mouse model
Casp3↑, observed enhanced expression of active caspase-3 in tumor tissues exhibited apoptotic death.
Glycolysis↓, Notably, metabolomic data also revealed severe inhibition in glycolysis, NADP, ATP and lactic acid production in cancer cells treated with 40 μM 3-BP.
NADPH↓,
ATP↓,
ROS↑, 3-BP treatment produces increased levels of reactive oxygen species (ROS), which causes DNA damage with reduction of free glutathione levels [11].
DNAdam↑,
GSH↓,
Bcl-2↓, Further, treatment with 40 µM of 3-BP suppressed BCL2L1 expression and causing activation of mitochondrial caspases
Casp↑,
lactateProd↓, Metabolic inhibition of glucose consumption and lactic acid production in cancer cells treated with 3-BP

5461- AF,    Dual inhibition of thioredoxin reductase and proteasome is required for auranofin-induced paraptosis in breast cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
Paraptosis↑, We show here that 4~5 µM AF induces paraptosis, a non-apoptotic cell death mode characterized by dilation of the endoplasmic reticulum (ER) and mitochondria, in breast cancer cells.
ER Stress↑,
TrxR↓, covalent inhibition of thioredoxin reductase (TrxR)
selectivity↑, subtoxic doses of AF and Bz induced paraptosis selectively in breast cancer cells, sparing non-transformed MCF10A cells
toxicity↝, whereas 4~5 μM AF killed both cancer and MCF10A cells
ROS↑, We found that treatment with 5 μM AF very weakly and transiently increased ROS levels at 2~4 h and then again at 24 h
mt-TrxR1↓, AF inhibits cytosolic and mitochondrial TrxR (TrxR1 and TrxR2), two selenoenzymes for the Trx pathway [3]
mt-TrxR2↓,

5236- AgNPs,    Adaptive regulations of Nrf2 alleviates silver nanoparticles-induced oxidative stress-related liver cells injury
- in-vitro, Liver, HepG2 - in-vitro, Nor, L02
tumCV↓, AgNPs induced a concentration-dependent decline in HepG2 and L02 cells viability.
ROS↑, • AgNPs induced ROS increase and apoptosis in HepG2 and L02 cells.
*ROS↑,
DNAdam↑, AgNPs induced DNA damage, autophagy and cell cycle arrest in HepG2 and L02 cells.
*DNAdam↑,
eff↓, N-acetylcysteine (NAC)alleviated AgNPs-induced cytotoxicity in HepG2 and L02 cells.
selectivity↑, Interestingly, HepG2 cells were more sensitive to AgNPs than L02 cells, and this may be related to the different ROS generation and responses to AgNPs by cancer cells and normal cells.

5977- AgNPs,  CDT,    Silver Nitroprusside as an Efficient Chemodynamic Therapeutic Agent and a Peroxynitrite nanogenerator for Targeted Cancer Therapy
- in-vivo, Ovarian, A2780S - NA, Ovarian, SKOV3
Fenton↑, Chemodynamic therapy (CDT) holds great promise in achieving cancer therapy through Fenton and Fenton-like reactions, which generate highly toxic reactive species
ROS↑, can decompose already existing intracellular H2O2 and produce reactive oxygen species (ROS) to attain a therapeutic outcome.
eff↑, Ag+, Fe2+) based silver pentacyanonitrosylferrate or silver nitroprusside (AgNP) were developed for Fenton like reactions that can specifically kills cancer cells by taking advantage of tumor acidic environment without used of any external stimuli
angioG↓, been reported that Ag-based materials are involved in angiogenesis inhibition by blocking Akt phosphorylation
p‑Akt↓,
EPR↑, These results indicate thatin cancer cell lines internalized AgNP, which partially localized inysosomes and could be relocalized to cytoplasm avoiding degradation due to lysosomal acidic pH, which produce ROS.
selectivity↑, While, in normal fibroblast cells over time AgNP colocalization in lysosomes increased due to the difference in lysosomal pH between cancer and normal cells
selectivity↑, results suggest that AgNP specifically produces ROS in cancer cell lines due to high acidity in comparison to the normal cells.
eff↑, This specific ROS production is probably due to tumor acidic environment in which AgNP act as a Fenton reagent
Cyt‑c↑, Cytochrome c release after AgNP treatment
HO-1↑, In A2780 cell line, HO-1 expression levels increased 8.1-fold when treated with AgNP

4403- AgNPs,    Silver Nanoparticles Decorated UiO-66-NH2 Metal-Organic Framework for Combination Therapy in Cancer Treatment
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vitro, GBM, GL26 - in-vitro, Cerv, HeLa - in-vitro, CRC, RKO
AntiCan↑, Among the various NPs, silver nanoparticles (AgNPs) have garnered attention due to their cytotoxic and genotoxic properties in cancer cells.
eff↑, Our results demonstrate that UiO-66-NH2@AgNPs@Cis-Pt and its combinations exhibit enhanced cytotoxicity compared to individual components such as AgNPs and Cis-Pt.
EPR↑, Their nanometric structure allows them to easily penetrate and accumulate in tumour tissues either actively, via targeting systems [6,7,8], or passively, by taking advantage of tumour angiogenesis and the enhanced permeation and retention (EPR) effe
selectivity↑,
ROS↑, Once inside, AgNPs induce an increase in the production of reactive oxygen species (ROS) and cause mitochondrial dysfunctions, caspases activation, apoptosis, autophagy, and DNA damage
Casp↑,
Apoptosis↑,
DNAdam↑,
tumCV↓, figure 8
eff↑, One of the primary characteristics of AgNPs is their ability to release Ag+ ions from their surface in response to low pH or oxidation.

4402- AgNPs,    Enhancement of Triple-Negative Breast Cancer-Specific Induction of Cell Death by Silver Nanoparticles by Combined Treatment with Proteotoxic Stress Response Inhibitors
- in-vitro, BC, BT549 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumCD↑, Our findings provide additional support for proteotoxic stress as a mechanism by which AgNPs selectively kill TNBCs
selectivity↑,
*toxicity↝, Failure to separate dissolved silver cations (Ag+) from AgNPs before toxicity testing likely contributes to the lack of a definitive answer. Ag+ is highly toxic and has a distinct cytotoxic mechanism of action compared to AgNPs;
Dose↝, doses in the range of 4–6 mg/kg delivered systemically for multiple weeks induced therapeutic responses
OS↑, 40 patients were injected intravenously with 1.8 mg of AgNPs for 3 consecutive days (combined with standard COVID-19 treatments), and the group receiving AgNPs had significantly greater survival rate

4400- AgNPs,  Rad,    Differential cytotoxic and radiosensitizing effects of silver nanoparticles on triple-negative breast cancer and non-triple-negative breast cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, BC, MDA-MB-231
ROS↑, AgNPs is known to cause dose-dependent toxicities, including induction of oxidative stress and DNA damage, which can lead to cell death.
DNAdam↑,
selectivity↑, We show that AgNPs are highly cytotoxic toward TNBC cells at doses that have little effect on nontumorigenic breast cells or cells derived from liver, kidney, and monocyte lineages.
TumCG↓, reduce TNBC growth and improve radiation therapy.
RadioS↑,
Dose↝, s 23±14 nm: particles were diluted to 40 μg/mL. 25 μg/mL AgNP dilution for 24 hours. zeta potential of AgNPs in water at pH 7 was approximately −36 mV, indicating good colloidal stability.
selectivity↑, Depending on AgNP dose, all three TNBC cell lines were 5- to 10-fold more sensitive to AgNP exposure than the nontumorigenic breast cells.
other↝, this study demonstrate that the cytotoxicity was dependent on exposure of cells to intact AgNPs and not due to Ag+ ions
eff↓, toxicity of AgNPs was significantly reduced in MDA-MB-231, MCF-7, and MCF-10A cells following pretreatment with GSH
eff↑, Selective depletion of GSH by BSO resulted in increased AgNP toxicity in all cell lines.
γH2AX↑, AgNPs significantly increased γH2AX in these cells compared to radiation alone.
Dose↓, Strikingly, an AgNP dose of as little as 1 μg/mL resulted in a dose enhancement of IR treatment (approximately 2-fold at the 2 Gy dose) f
eff↑, Moreover, intratumoral injection of AgNPs with or without radiation treatment can inhibit the growth of TNBC xenografts in mice

4397- AgNPs,    Synthesis and Characterization of Silver Nanoparticles from Rhizophora apiculata and Studies on Their Wound Healing, Antioxidant, Anti-Inflammatory, and Cytotoxic Activity
- NA, Wounds, NA
selectivity↑, The cytotoxicity cell viability assay revealed that the AgNPs were less toxic (IC50 105.5 µg/mL) compared to the R. apiculata extract (IC50 47.47 µg/mL) against the non-cancerous fibroblast L929 cell line.
tumCV↓, AgNPs showed considerable cytotoxic effect, and the percentage of cell viability against skin cancer, lung cancer, and oral cancer cell lines was 31.84%, 56.09% and 22.59%, respectively.
antiOx↑, AgNPs exhibited potential antioxidant, anti-inflammatory, wound healing, and cytotoxic properties
Inflam↓,

4388- AgNPs,    Differential Cytotoxic Potential of Silver Nanoparticles in Human Ovarian Cancer Cells and Ovarian Cancer Stem Cells
- in-vitro, Cerv, NA
tumCV↓, the numbers of A2780 (bulk cells) and ALDH+/CD133+ colonies were significantly reduced
CSCs↓,
selectivity↑, induced apoptosis in pancreatic CSCs and cancer cell lines, but had no effect on human normal pancreatic epithelial cells
Apoptosis↑,
ROS↑, figure 5, AgNPs induces apoptosis by oxidative stress
LDH↓, figure 5 (leakage outside the cell increases)
Casp3↑, AgNPs treated cells shows up-regulation of caspase-3, bax, bak, and c-myc, genes
BAX↑,
Bak↑,
cMyc↑,
MMP↓, and loss of mitochondrial membrane potential.

4422- AgNPs,    Bioengineering of Piper longum L. extract mediated silver nanoparticles and their potential biomedical applications
- in-vitro, Cerv, HeLa
AntiCan↑, Anticancer activity revealed the strong and dose-dependent cytotoxic effect of AgNPs against the HeLa cells showing maximum IC50 value being 5.27 μg/mL after 24 h
selectivity↑, was also found to be non-toxic to normal cells (HEK)

4421- AgNPs,    Effect of Biologically Synthesized Silver Nanoparticles on Human Cancer Cells
- in-vitro, Cerv, NA
selectivity↑, IC50: ≤4.25 μg/ml for normal and ≤32.5 μg/ml cerival cancer cells
eff↝, in vitro cytotoxicity assessment of the AgNPs has significant correlation with the total protein concentration in treated cells.
other↝, In the present study, silver nanoparticles were biologically synthesized using pure enzyme α-amylase and the other one by using soluble proteins of neem leaf extracts.

4413- AgNPs,  Anzaroot,    Green synthesis of silver nanoparticles from plant Astragalus fasciculifolius Bioss and evaluating cytotoxic effects on MCF7 human breast cancer cells
- in-vitro, BC, MCF-7
chemoP↑, These compounds have been shown to effectively treat heart diseases and inhibit cancer cell growth while also alleviating chemotherapy side effects.
TumCG↓,
eff↑, anzroot plant can be effectively used as a reducing agent for AgNPs synthesis, and AgNPs have the potential to be used effectively in cancer therapy methods and to inhibit the growth of cancer cells.
CellMemb↑, As the AgNPs concentration increased, the permeability of the membrane increased
selectivity↑, Cancer cells exhibit higher permeability and retention, allowing for preferential interaction with SNPs due to their nanoscale size
ROS↑, AgNPs respond to intracellular signaling through ROS activation, and p53-mediated apoptosis is notably effective when using AgNPs
P53↑,

4411- AgNPs,    Eco-friendly synthesis of silver nanoparticles using Anemone coronaria bulb extract and their potent anticancer and antibacterial activities
- in-vitro, Lung, A549 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, PC3 - in-vitro, Nor, HEK293
AntiCan↑, (AgNPs) have emerged as promising multifunctional agents in biomedical applications due to their notable antimicrobial and anticancer properties.
selectivity↑, demonstrated significant cytotoxic effects on cancer cells while sparing normal cells
Apoptosis↑, Apoptosis induction, cell cycle arrest, and gene expression analyses further validated their anticancer efficacy.
TumCCA↑,
Bacteria↓, Figure 6a,b show the inhibition zones of 10 µg ampicillin and 10, 50, 100, and 150 μg/mL AgNPs against bacteria on agar for two repeated tests.
tumCV↓, AgNPs at concentrations of 6.3, 6.8, 7.5, 8.3, 9.4, 10.7 and 12.5 µg/mL for 24 h. After treatment, a significant decrease in cell viability was observed in different cancer cell types,
selectivity↑, The toxic effect was weaker in healthy cells than in cancer cells
Apoptosis↑, Fig. 8a–c, a significant increase (p < 0.01; p < 0.001) in the rate of early and late apoptotic cells was observed in A549, MIA PaCa-2 and PC-3 cells.
TumCCA↑, accompanied by arrest in the S phase and, particularly, the G2/M phase.

4410- AgNPs,    Green-synthesized silver nanoparticles: a sustainable nanoplatform for targeted colon cancer therapy
- Review, Colon, NA
AntiCan↑, AgNPs exert potent anticancer effects against colon cancer cell lines primarily by inducing cell death through mechanisms including reactive oxygen species (ROS) generation
ROS↑,
mtDam↑, mitochondrial dysfunction, and apoptosis modulation, leading to significant reductions in cell viability.
tumCV↓,
selectivity↑, effectively targeting cancer cells while sparing healthy counterparts, thereby emphasizing their safety profile and potential for minimizes ng systemic toxicity.

4431- AgNPs,  doxoR,    Oxidative Stress-Induced Silver Nano-Carriers for Chemotherapy
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1 - in-vitro, Nor, 3T3
AntiCan↑, AgNPs have been demonstrated to exhibit anti-tumor effects through cell apoptosis.
ROS↑, ox-carried PA-AgNPs generate reactive oxidation species intensively beside 4T1 cells.
TumVol↓, in vivo study confirms that PA-AgNPs with Dox successfully inhibit tumors, which are about four times smaller than the control group and have high biosafety that can be applied for chemotherapy.
EPR↑, While all normal cells need enough vitamins to survive, cancer cells require a considerable number of vitamins to proliferate rapidly. As a result, the receptors on the cancer cell surface are overexpressed to capture as many vitamins as possible.
selectivity↑, PA-AgNPs (without/with Dox) concentrations ranging from 0 to 100 μg mL−1 did not seem to impair 3T3 cell viability due to poor uptake by normal cells.
ChemoSen↑, These results suggested that Dox-carried PA-AgNPs were both safer and more effective for cancer prevention.

4429- AgNPs,    Comparative proteomic analysis reveals the different hepatotoxic mechanisms of human hepatocytes exposed to silver nanoparticles
- in-vitro, Liver, HepG2
*toxicity↝, As the liver is one of the largest accumulation and deposition sites of circulatory AgNPs, it is important to evaluate the hepatotoxicity induced by AgNPs
selectivity↑, cancerous liver cells were generally more sensitive than the normal liver cells.
mt-ROS↑, mitochondrial ROS has been identified as one of the causes of AgNPs-induced hepatotoxicity

4363- AgNPs,    Immunomodulatory properties of silver nanoparticles contribute to anticancer strategy for murine fibrosarcoma
- in-vivo, fibroS, NA
TumVol↓, incidence and size of fibrosarcoma were reduced or delayed when murine fibrosarcoma groups were treated by AgNP-MSA
TNF-α↓, TNF-α, IL-6 and IL-1β these cytokines were found to be downregulated after treatment with AgNP-MSA
IL6↓,
IL1β↓,
*toxicity↝, liver sections were found to have normal architecture in all treated groups except those treated at the 9 and 10 mg/kg b.w. doses
TumCG↓, treatment with AgNPs, the logistic growth of the tumor incidence was significantly lower (
selectivity↑, MSA-AgNPs aggregated instantly in response to the acidic extracellular pH of solid tumors, leading to greatly enhanced uptake by cancer cells
selectivity↑, Because the particle size in the study was approximately 10 nm, any AgNP that escaped entry into the tumor microenvironment and entered the systemic circulation was effectively cleared from the body.
Weight↑, AgNP-MSA not only inhibited the tumor incidence but also helped to overcome the progressive body weight loss of tumor-bearing mice.
ROS↑, anticancer property demonstrated by AgNP can be attributed to this increase in oxidative stress in the tumor microenvironment.
NO↑, AgNPs significantly increased the oxygen free radical and NO levels in the tumor microenvironment, which oppose hypoxia.

4433- AgNPs,    Advancements in metal and metal oxide nanoparticles for targeted cancer therapy and imaging: Mechanisms, applications, and safety concerns
- in-vitro, Liver, HepG2 - in-vitro, Nor, L02
selectivity↑, we evaluated the cytotoxicity of different-sized AgNPs and found that the cancerous liver cells were generally more sensitive than the normal liver cells
selectivity↓, HepG2 cells respond to stresses by adapting energy metabolism, upregulating metallothionein expression and increasing the expression of antioxidants, while L02 cells protect themselves by increasing DNA repair and macro-autophagy.
mt-ROS↑, mitochondrial ROS has been identified as one of the causes of AgNPs-induced hepatotoxicity.

4435- AgNPs,  Gluc,    Glucose-Functionalized Silver Nanoparticles as a Potential New Therapy Agent Targeting Hormone-Resistant Prostate Cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
selectivity↑, Both AgNPs and G-AgNPs were cytotoxic only to CRPC cells and not to hormone-sensitive ones and their effect was higher after functionalization showing the potential of glucose to favor AgNPs’ uptake by cancer cells.
ROS↑, NPs increased the ROS, inducing mitochondrial damage, and arresting cell cycle in S Phase, therefore blocking proliferation, and inducing apoptosis.
mtDam↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
MMP↓, AgNPs were able to depolarize the cells’ mitochondria to 32.74% and 10.36%, respectively

4364- AgNPs,    Selective cytotoxicity of green synthesized silver nanoparticles against the MCF-7 tumor cell line and their enhanced antioxidant and antimicrobial properties
- in-vitro, BC, MCF-7
TumCD↑, AgNPs and the extract exhibited 70% and 40% cytotoxicity against MCF-7 cancerous cells, respectively, while CSN caused 56% cell death (at the concentration of 60 µg/mL)
selectivity↑, It was observed that AgNPs were much less cytotoxic when tested against a noncancerous cell line (L-929)
*antiOx↑, These include antioxidant, antifungal, anti-inflammatory, antiviral, anti-angiogenesis, and antimicrobial effects
*Inflam↓,
AntiTum↑, antitumor properties of AgNPs
ROS↑, AgNPs interact with mitochondria and disrupt the cellular electron transfer chain function leading to an increase in the ROS level. oxidative stress generated by ROS could be considered as a main toxicity mechanism of AgNPs against cells

4376- AgNPs,    Interaction of multi-functional silver nanoparticles with living cells
- in-vitro, Nor, L929 - in-vitro, Lung, A549
eff↑, significant increase in the rate of lactose-modified AgNPs into the A549 cells is observed
selectivity↑,

4371- AgNPs,    Effects of Green Silver Nanoparticles on Apoptosis and Oxidative Stress in Normal and Cancerous Human Hepatic Cells in vitro
- in-vitro, Liver, HUH7
ROS↑, The gAgNPs induced more ROS in the HuH-7 cells than in the CHANG cells.
selectivity↑, HuH-7 cells showed an increased sensitivity to gAgNPs than the CHANG cells.
DNAdam↑, higher concentrations of gAgNPs may induce significant cytotoxicity and cause DNA damage and apoptosis.
Apoptosis↑,
GSH↓, The level of glutathione was decreased (Figure 4B) and lipid peroxide was increased in HuH-7 cells than CHANG cells (Figure 4A).
lipid-P↑,
MMP↓, indicating loss of MMP
DNAdam↑, higher DNA damage was seen in HuH-7 cells than CHANG cells

4365- AgNPs,    Biomedical Applications of Silver Nanoparticles: An Up-to-Date Overview
- Review, Var, NA
ROS↑, the most remarkable mechanistic mode of AgNP-based antimicrobial effects is represented by their adhesion to microbial cells, ROS and free-radical generation, microbial wall piercing and penetration inside cells, and modulation and modification of mi
*toxicity↓, high intrinsic antimicrobial efficiency and non-toxic nature
*Bacteria↓,
*Inf↓, silver-based compounds and materials were used for the unconventional and effective control of distinctive infections
*Diff↑, Previous studies reported that AgNPs naturally improve the differentiation process of MC3T3-1 pre-osteoblast cells and subsequent bone-like tissue mineralization,
*eff↑, studies showed that AgNP-implanted titanium displayed improved antibacterial ability,
RadioS↑, making them suitable candidates for detection and dose-enhancement purposes in X-ray irradiation applications
selectivity↑, selective uptake into cancerous cells, AgNP-derived scattered light can be used for imaging purposes, whereas absorbed light can be used for selective hyperthermia

4561- AgNPs,  VitC,    Cellular Effects Nanosilver on Cancer and Non-cancer Cells: Potential Environmental and Human Health Impacts
- in-vitro, CRC, HCT116 - in-vitro, Nor, HEK293
NRF2↑, Nanosilver increased Nrf2 protein expression and disrupted the cell cycle at the G1 and G2/M phases.
TumCCA↑, AgNPs interact with DNA to stop the cell cycle and lead to apoptosis
ROS↑, Nanosilver induced significant mitochondrial oxidative stress in HCT116, whereas it did not in the non-cancer HIEC-6 and nanosilver/sodium ascorbate co-treatment was preferentially lethal to HCT116 cells,
selectivity↑,
*AntiViral↑, AgNPs are effective antiviral agents against various viruses such as human immunodeficiency virus, hepatitis B virus, and monkey pox virus through interaction with surface glycoproteins on the virus
*toxicity↝, Citrate and PVP-coated AgNPs have been found to be less toxic than non-coated AgNPs
ETC↓, AgNPs affects mitochondrial function through the disruption of the electron transport chain2,24,26,33,39–41
MMP↓, Studies have shown that exposure to AgNPs resulted in a decrease of mitochondrial membrane potential (MMP) in various in vitro and in vivo experiments
DNAdam↑, AgNPs has also been shown to interact with and induce damage to DNA, DNA strand breaks, DNA damage
Apoptosis↑, apoptosis induced by AgNPs were through membrane lipid peroxidation, ROS, and oxidative stress
lipid-P↑,
other↝, Several studies have showed AgNPs interact with various proteins such as haemoglobin, serum albumin, metallothioneins, copper transporters, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), malate dehydrogenase (MDH), and bacterial proteins.
UPR↑, Studies have shown exposure to AgNPs induces activation of the UPR
*GRP78/BiP↑, AgNPs induced increased levels of GRP78, phosphorylated PERK, phosphorylated eIF2-α, and phosphorylated IRE1α, spliced XBP1, cleaved ATF-6, CHOP, JNK and caspase 12
*p‑PERK↑,
*cl‑eIF2α↑,
*CHOP↑,
*JNK↑,
Hif1a↓, One study showed AgNPs inhibits HIF-1 accumulation and suppresses expression of HIF-1 target genes in breast cancer cells (MCF-7) and also found the protein levels of HIF-1α and HIF-1β decreased
AntiCan↑, Many studies have shown that ascorbic acid, on its own, has anti-cancer effects
*toxicity↓, However, when the rats were treated with both ascorbic acid and AgNPs, a decrease in toxic effects was observed in non-cancer parotid glands in rats
eff↑, Studies have shown both AgNPs and ascorbic acid have greater effects and toxicity in cancer cells relative to non-cancer cells

4558- AgNPs,    Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells
- in-vitro, PC, PANC1
ROS↑, it is known that AgNPs may induce an accumulation of ROS and alteration of antioxidant systems in different type of tumors, and they are indicated as promising agents for cancer therapy.
selectivity↑, We found that the increase was lower in noncancer cells.
NO↑, PANC-1 cells with 0.5–5 μg/mL of 2.6 nm AgNPs or 5–100 μg/mL of 18 nm AgNPs caused an increase of NO level in a concentration-dependent manner
SOD↓, We observed a significant reduction in cytosolic and mitochondrial SOD and GPX-4 at protein level
GPx4↓,
Catalase↓, we showed that 2.6 nm AgNPs caused a higher decrease in SOD1, SOD2, and CAT at mRNA level after 24 h incubation than 18 nm AgNPs
TumCCA↑, 2.6 nm and 18 nm AgNPs, we noticed a decrease of G0/G1 phase cell population in a concentration-dependent manner compared with control
MMP↓, increase of the percentage of cells with low mitochondrial membrane potential (Δψm), compared to the untreated cells

4555- AgNPs,    Silver nanoparticles from Dendropanax morbifera Léveille inhibit cell migration, induce apoptosis, and increase generation of reactive oxygen species in A549 lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Liver, HepG2
*Bacteria↓, silver nanoparticles synthesized from Dendropanax morbifera Léveille leaves (D-AgNPs) exhibit antimicrobial activity and reduce the viability of cancer cells without affecting the viability of RAW 264.7 macrophage-like cells
tumCV↓,
selectivity↑,
ROS↑, enhanced the production of ROS in both cell lines.
Apoptosis↑, An increase in cell apoptosis and a reduction in cell migration in A549 cells were also observed after D-AgNP treatment.
TumCMig↓,
AntiCan↑, potential of D-AgNPs as a possible anticancer agent, particularly for the treatment of non-small cell lung carcinoma.

4541- AgNPs,  RosA,    Eco-friendly synthesis of silver nanoparticles: multifaceted antioxidant, antidiabetic, anticancer, and antimicrobial activities
- in-vitro, Nor, WI38 - in-vitro, BC, MDA-MB-231 - in-vitro, PC, PANC1
*antiOx↑, Potent antioxidant activity was observed with an EC₅₀ of 7.81 µg mL⁻1, close to ascorbic acid (3.27 µg mL⁻1).
TumCD↓, Ag-NPs showed selective cytotoxicity against MDA and PANC-1 cells (IC₅₀: 177.2 and 115.3 µg mL⁻1), with lower toxicity toward Vero and Wi38 normal cells (IC₅₀: 233 and 207 µg mL⁻1).
selectivity↑,

4540- AgNPs,  VitC,    Silver nanoparticles from ascorbic acid: Biosynthesis, characterization, in vitro safety profile, antimicrobial activity and phytotoxicity
- in-vitro, Nor, NA
*Bacteria↓, AgNPs showed antibacterial activity against Gram-positive and Gram-negative strains.
*selectivity↑, AgNPs did not show cytotoxicity on VERO cells ranging from 0.5 to 150 μg mL−1 with a good gemoprotection.

4584- AgNPs,    Silver Nanoparticles Synthesized Using Carica papaya Leaf Extract (AgNPs-PLE) Causes Cell Cycle Arrest and Apoptosis in Human Prostate (DU145) Cancer Cells
- in-vitro, Pca, DU145
selectivity↑, AgNPs-PLE when compared with AgNPs-citric acid or PLE showed better efficacy against cancer cells and was also relatively less toxic to normal cells.
ROS↑, ROS production was observed at earlier time points in presence of AgNPs-PLE, suggesting its role behind apoptosis in DU145 cells.
BAX↑, induction of Bax, cleaved caspase-3, and cleaved PARP proteins. G1-S phase cell cycle check point marker, cyclin D1 was down-regulated along with an increase in cip1/p21 and kip1/p27 tumor suppressor proteins by AgNPs-PLE.
cl‑Casp3↑,
p‑PARP↑,
TumCCA↑,
cycD1/CCND1↓,
p27↑,
P21↑,
AntiCan↑, These findings suggest the anti-cancer properties of AgNPs-PLE.

4573- AgNPs,    Bioactive silver nanoparticles derived from Carica papaya floral extract and its dual-functioning biomedical application
- in-vitro, Var, MCF-7 - NA, NA, HEK293
toxicity↓, Using 20% (v/v) KQE, highly stable, spherical KQ-AgNPs (12.3 ± 3.0 nm) were synthesized via in-situ generation of free radicals, such as ortho-quinones, which reduced Ag+ ions.
Bacteria↓, KQ-AgNPs exhibit superior antibacterial activity against both gram-positive and gram-negative bacteria compared to chemically synthesized AgNPs (AgNPs-Chem) and KQE alone
selectivity↑, (MCF-7) with an IC50 of 21.25 ± 1.14 µg/mL, significantly lower than AgNPs-Chem (33.05 ± 3.13 µg/mL), while maintaining high biocompatibility with normal cells (HEK-293) with a greater IC50 of 169.96 ± 2.3 µg/mL.

5147- AgNPs,    Size dependent anti-invasiveness of silver nanoparticles in lung cancer cells
- in-vitro, Lung, A549
TumCMig↓, 13 nm AgNPs significantly inhibit the migration and invasiveness of lung adenocarcinoma A549 cells, induce elevated reactive oxygen species and lead to NF-κB directed cellular apoptosis
TumCI↓,
ROS↑,
p‑NF-kB↑, 13 nm AgNPs was able to significantly upregulate the phosphorylation of NF-κB (p-NF-κB) in A549 cells
selectivity↑, we speculate that, AgNPs, which are pointed out that have a sustained release of Ag+ in an environment with lower pH (such as cancer cells)
eff↝, and this inhibitive effect is most pronounced treated with 13 nm AgNPs, while the effect starts decreasing with the size of 45 nm and completely vanishes for 92 nm AgNPs.

5145- AgNPs,    Silver nanoparticles induce irremediable endoplasmic reticulum stress leading to unfolded protein response dependent apoptosis in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D
Bacteria↓, Nowadays, silver nanoparticles (AgNP) are widely used in the medical field mainly for their antibacterial properties
Apoptosis↑, AgNP of 2 (AgNP2) and 15 nm (AgNP15) induce apoptosis in human MCF-7 and T-47D breast cancer cells.
ER Stress↑, Treatment with AgNP2 and AgNP15 led to accumulation and aggregation of misfolded proteins causing an endoplasmic reticulum (ER) stress and activating the unfolded protein response (UPR).
UPR↑,
PERK↑, The three main ER sensors, PERK, IRE-1α and ATF-6, were rapidly activated in response to AgNP2 and AgNP15
IRE1↑,
ATF6↑,
ATF4↑, AgNP2 and AgNP15 induced upregulation of the transcription factors ATF-4 and GADD153/CHOP
CHOP↑,
Casp9↑, Moreover, the initiating caspase-9 and the effector caspase-7 were activated in response to these NPs.
Casp7↑,
Mcl-1↓, In contrast, a downregulation of Mcl-1 and xIAP protein expression as well as a processing of PARP were observed.
XIAP↓,
PARP↝,
selectivity↑, Of note, the non-cancerous MCF-10A cells were more resistant to both AgNP2 and AgNP15 when compared to MCF-7 and T-47D cell lines.

375- AgNPs,  ALA,    Alpha-Lipoic Acid Prevents Side Effects of Therapeutic Nanosilver without Compromising Cytotoxicity in Experimental Pancreatic Cancer
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vivo, NA, NA
mtDam↑, in cancer cells only. ALA protected normal cells
ROS↑, in cancer cells only. ALA protected normal cells
*toxicity↓, Nonmalignant CRL-4023 and LX-2 cells were treated with α-lipoic acid at concentrations of 0.5 mM, 1 mM, 2 mM and 3 mM, Both cell lines were largely resistant to any concentration
Dose∅, ALA dose: we used α-lipoic acid concentrations of 0.5 and 1 mM
selectivity↑, higher sensitivity of malignant cells to AgNPs.

5340- Ajoene,    Ajoene, a compound of garlic, induces apoptosis in human promyeloleukemic cells, accompanied by generation of reactive oxygen species and activation of nuclear factor kappaB
- in-vitro, AML, NA
Apoptosis↑, The present study demonstrates that ajoene, a major compound of garlic induces apoptosis in human leukemic cells, but not in peripheral mononuclear blood cells of healthy donors.
selectivity↑,
H2O2↑, Ajoene increased the production of intracellular peroxide in a dose- and time-dependent fashion, which could be partially blocked by preincubation of the human leukemic cells with the antioxidant N-acetylcysteine.
NF-kB↑, These results suggested that ajoene might induce apoptosis in human leukemic cells via stimulation of peroxide production and activation of nuclear factor kappaB.

5356- AL,    Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects
- Review, GC, NA
Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo

2000- AL,    Exploring the ROS-mediated anti-cancer potential in human triple-negative breast cancer by garlic bulb extract: A source of therapeutically active compounds
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, NA
selectivity↑, The inhibitory effect of ASEE was more pronounced in MDA-MB-231 cells than in MCF-7 cells, however, no substantial cytotoxicity was seen in normal Vero cells.
TumCG?,
*toxicity∅, no substantial cytotoxicity was seen in normal Vero cells
ROS↑, TNBC cells treated with high concentrations of ASEE were found in the late apoptotic stage and exhibited an increase in ROS level and a reduction in MMP
MMP↓,
TumCCA↑, increased the percentage of cells in the G2/M phase
P53↑, ASEE upregulated the p53 and Bax proteins while downregulated the Bcl-2, p-Akt, and p-p38 proteins.
Bcl-2↓,
p‑Akt↓,
p‑p38↓,
*ROS∅, Vero normal cells did not display the unusual morphological alteration and reduction in cell viability. ROS production revealed a 1.21 % ROS level only in control cells that is typically seen in healthy cells.

234- AL,    Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy
- in-vitro, HCC, Hep3B
ROS↑, increased the production of ROS levels at 1, 3, 6 h. I
*toxicity∅, In other study, allicin treatment did not increase the leakage of lactate-dehydrogenase (LDH) of primary rat hepatocytes until 1 mM allicin treated with rat hepatocytes24. For this reason, allicin could be inferred as safe to normal liver cells
MMP↓, Allicin decreased mitochondrial membrane potential
BAX↑,
Bcl-2↓,
AIF↑,
Casp3↑, protein expression levels of caspase-3, -8, -9 increased after allicin treatment
Casp8↑,
Casp9↑,
eff↓, Allicin significantly induced ROS overproduction, whereas NAC pretreatment decreased the ROS induction by allicin exposure in Hep 3B cells
γH2AX↑, significant increase in the expression of γ-H2AX was observed at the initial stages (3, 6 h), but not at the later stages of 12, 24, 48 h
selectivity↑, data suggested that allicin induced apoptosis in p53-deficiency human liver carcinoma cells but caused autophagy in p53-normal function human liver carcinoma cells.
DNA-PK↑, increases production of ROS, triggers DNA damage

3442- ALA,    α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B - in-vitro, Nor, 3T3
tumCV↓, Notably, α‑LA treatment significantly reduced the cell viability, migration, and invasion of PCa cell lines in a dose‑dependent manner.
TumCMig↓,
TumCI↓,
ROS↑, α‑LA supplementation dramatically increased reactive oxygen species (ROS) levels and HIF‑1α expression, which started the downstream molecular cascade and activated JNK/caspase‑3 signaling pathway
Hif1a↑, The expression of HIF-1α significantly increased following α-LA treatment and was comparable with the changes in ROS.
JNK↑,
Casp↑,
TumCCA↑, arrest of the cell cycle in the S‑phase, which has led to apoptosis of PCa cells
Apoptosis↑,
selectivity↑, Also, the treatment of α‑LA improved bone health by reducing PCa‑mediated bone cell modulation.

3454- ALA,    Lipoic acid blocks autophagic flux and impairs cellular bioenergetics in breast cancer and reduces stemness
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
TumCG↑, Lipoic acid inhibits breast cancer cell growth via accumulation of autophagosomes.
Glycolysis↓, Lipoic acid inhibits glycolysis in breast cancer cells.
ROS↑, Lipoic acid induces ROS production in breast cancer cells/BCSC.
CSCs↓, Here, we demonstrate that LA inhibits mammosphere formation and subpopulation of BCSCs
selectivity↑, In contrast, LA at similar doses. had no significant effect on the cell viability of the human embryonic kidney cell line (HEK-293)
LC3B-II↑, LA treatment (0.5 mM and 1.0 mM) increased the expression level of LC3B-I to LC3B-II in both MCF-7 and MDA-MB231cells at 48 h
MMP↓, LA induced mitochondrial ROS levels, decreased mitochondria complex I activity, and MMP in both MCF-7 and MDA-MB231 cells
mitResp↓, In MCF-7 cells, we found a substantial reduction in maximal respiration and ATP production at 0.5 mM and 1 mM of LA treatment after 48 h
ATP↓,
OCR↓, LA at 2.5 mM decreased OCR
NAD↓, we found that LA (0.5 mM and 1 mM) significantly reduced ATP production and NAD levels in MCF-7 and MDA-MB231 cells
p‑AMPK↑, LA treatment (0.5 mM and 1.0 mM) increased p-AMPK levels;
GlucoseCon↓, LA (0.5 mM and 1 mM) significantly decreased glucose uptake and lactate production in MCF-7, whereas LA at 1 mM significantly reduced glucose uptake and lactate production in MDA-MB231 cells but it had no effect at 0.5 mM
lactateProd↓,
HK2↓, LA reduced hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA) expression in MCF-7 and MDA-MB231 cells
PFK↓,
LDHA↓,
eff↓, Moreover, we found that LA-mediated inhibition of cellular bioenergetics including OCR (maximal respiration and ATP production) and glycolysis were restored by NAC treatment (Fig. 6E and F) which indicates that LA-induced ROS production is responsibl
mTOR↓, LA inhibits mTOR signaling and thereby decreased the p-TFEB levels in breast cancer cells
ECAR↓, LA also inhibits glycolysis as evidenced by decreased glucose uptake, lactate production, and ECAR.
ALDH↓, LA decreased ALDH1 activity, CD44+/CD24-subpopulation, and increased accumulation of autophagosomes possibly due to inhibition of autophagic flux of breast cancer.
CD44↓,
CD24↓,

278- ALA,    The Multifaceted Role of Alpha-Lipoic Acid in Cancer Prevention, Occurrence, and Treatment
- Review, NA, NA
ROS↑, direct anticancer effect of the antioxidant ALA is manifested as an increase in intracellular ROS levels in cancer cells
NRF2↑, enhance the activity of the anti-inflammatory protein nuclear factor erythroid 2–related factor 2 (Nrf2), thereby reducing tissue damage
Inflam↓,
frataxin↑,
*BioAv↓, Oral ALA has a bioavailability of approximately 30% due to issues such as poor stability in the stomach, low solubility, and hepatic degradation.
ChemoSen↑, ALA can enhance the functionality of various other anticancer drugs, including 5-fluorouracil in colon cancer cells and cisplatin in MCF-7 breast cancer cells
Hif1a↓, it is inferred that lipoic acid may inhibit the expression of HIF-1α
eff↑, act as a synergistic agent with natural polyphenolic substances such as apigenin and genistein
FAK↓, ALA inhibits FAK activation by downregulating β1-integrin expression and reduces the levels of MMP-9 and MMP-2
ITGB1↓,
MMP2↓,
MMP9↓,
EMT↓, ALA inhibits the expression of EMT markers, including Snail, vimentin, and Zeb1
Snail↓,
Vim↓,
Zeb1↓,
P53↑, ALA also stimulates the mutant p53 protein and depletes MGMT
MGMT↓, depletes MGMT by inhibiting NF-κB signalling, thereby inducing apoptosis
Mcl-1↓,
Bcl-xL↓,
Bcl-2↓,
survivin↓,
Casp3↑,
Casp9↑,
BAX↑,
p‑Akt↓, ALA inhibits the activation of tumour stem cells by reducing Akt phosphorylation.
GSK‐3β↓, phosphorylation and inactivation of GSK3β
*antiOx↑, indirect antioxidant protection through metal chelation (ALA primarily binds Cu2+ and Zn2+, while DHLA can bind Cu2+, Zn2+, Pb2+, Hg2+, and Fe3+) and the regeneration of certain endogenous antioxidants, such as vitamin E, vitamin C, and glutathione
*ROS↓, ALA can directly quench various reactive species, including ROS, reactive nitrogen species, hydroxyl radicals (HO•), hypochlorous acid (HclO), and singlet oxygen (1O2);
selectivity↑, In normal cells, ALA acts as an antioxidant by clearing ROS. However, in cancer cells, it can exert pro-oxidative effects, inducing pathways that restrict cancer progression.
angioG↓, Combining these two hypotheses, it can be hypothesized that ALA may regulate copper and HIF-2α to limit tumor angiogenesis.
MMPs↓, ALA was shown to inhibit invasion by decreasing the mRNA levels of key matrix metalloproteinases (MMPs), specifically MMP2 and MMP9, which are crucial for the metastatic process
NF-kB↓, ALA has been shown to enhance the efficacy of the chemotherapeutic drug paclitaxel in breast and lung cancer cells by inhibiting the NF-κB signalling pathway and the functions of integrin β1/β3 [138,139]
ITGB3↓,
NADPH↓, ALA has been shown to inhibit NADPH oxidase, a key enzyme closely associated with NP, including NOX4

5326- ALC,    L-Carnitine Is an Endogenous HDAC Inhibitor Selectively Inhibiting Cancer Cell Growth In Vivo and In Vitro
- vitro+vivo, Liver, HepG2
TumCG↓, Here we found that (1) LC treatment selectively inhibited cancer cell growth in vivo and in vitro;
P21↑, (2) LC treatment selectively induces the expression of p21cip1 gene, mRNA and protein in cancer cells
ac‑H3↑, (4) LC increases histone acetylation and induces accumulation of acetylated histones both in normal thymocytes and cancer cells
HDAC↓, (5) LC directly inhibits HDAC I/II activities via binding to the active sites of HDAC and induces histone acetylation and lysine-acetylation accumulation in vitro;
*ATP↑, LC is able to generate ATP in normal mouse thymocytes, but not in hepatic HepG2 and SMMC-7721 cancer cells.
selectivity↑,
ac‑H4↑, LC dose-dependently increased acetylation of H3 and H4 (

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.

1548- Api,    A comprehensive view on the apigenin impact on colorectal cancer: Focusing on cellular and molecular mechanisms
- Review, Colon, NA
*BioAv↓, Apigenin is not easily absorbed orally because of its low water solubility, which is only 2.16 g/mL
*Half-Life∅, Apigenin is slowly absorbed and eliminated from the body, as evidenced by its half‐life of 91.8 h in the blood
selectivity↑, selective anticancer effects and effective cell cytotoxic activity while exhibiting negligible toxicity to ordinary cells
*toxicity↓, intentional consumption in higher doses, as the toxicity hazard is low
Wnt/(β-catenin)↓, inhibiting the Wnt/β‐catenin
P53↑,
P21↑,
PI3K↓,
Akt↓,
mTOR↓,
TumCCA↑, G2/M
TumCI↓,
TumCMig↓,
STAT3↓, apigenin can activate p53, which improves catalase and inhibits STAT3,
PKM2↓,
EMT↓, reversing increases in epithelial–mesenchymal transition (EMT)
cl‑PARP↑, apigenin increases the cleavage of poly‐(ADP‐ribose) polymerase (PARP) and rapidly enhances caspase‐3 activity,
Casp3↑,
Bax:Bcl2↑,
VEGF↓, apigenin suppresses VEGF transcription
Hif1a↓, decrease in hypoxia‐inducible factor 1‐alpha (HIF‐1α
Dose∅, effectiveness of apigenin (200 and 300 mg/kg) in treating CC was evaluated by establishing xenografts on Balb/c nude mice.
GLUT1↓, Apigenin has been found to inhibit GLUT1 activity and glucose uptake in human pancreatic cancer cells
GlucoseCon↓,

1559- Api,    Dually Active Apigenin-Loaded Nanostructured Lipid Carriers for Cancer Treatment
- in-vitro, Lung, A549 - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Dose↓, IC50 change from 33ug/mL(APG) to 2.4ug/mL(APG-NLC)
selectivity↑, higher selectivity from cancer to normal cell: see Table 4

1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, Metformin increased cellular ROS levels in AsPC-1 pancreatic cancer cells, with minimal effect in HDF, human primary dermal fibroblasts.
selectivity↑, Metformin reduced cellular ATP levels in HDF, but not in AsPC-1 cells
selectivity↓, Metformin increased AMPK, p-AMPK (Thr172), FOXO3a, p-FOXO3a (Ser413), and MnSOD levels in HDF, but not in AsPC-1 cells
ROS↑,
eff↑, Metformin combined with apigenin increased ROS levels dramatically and decreased cell viability in various cancer cells including AsPC-1 cells, with each drug used singly having a minimal effect.
tumCV↓,
MMP↓, Metformin/apigenin combination synergistically decreased mitochondrial membrane potential in AsPC-1 cells but to a lesser extent in HDF cells
Dose∅, co-treatment with metformin (0.05, 0.5 or 5 mM) and apigenin (20 µM) dramatically increased cellular ROS levels in AsPC-1 cells
eff↓, NAC blocked the metformin/apigenin co-treatment-induced cell death in AsPC-1 cells
DNAdam↑, Combination of metformin and apigenin leads to DNA damage-induced apoptosis, autophagy and necroptosis in AsPC-1 cells but not in HDF cells
Apoptosis↑,
TumAuto↑,
Necroptosis↑,
p‑P53↑, p-p53, Bim, Bid, Bax, cleaved PARP, caspase 3, caspase 8, and caspase 9 were also significantly increased by combination of metformin and apigenin in AsPC-1
BIM↑,
BAX↑,
p‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑, Cytochrome C was also released from mitochondria in AsPC-1 cell
Bcl-2↓,
AIF↑, Interestingly, autophagy-related proteins (AIF, P62 and LC3B) and necroptosis-related proteins (MLKL, p-MLKL, RIP3 and p-RIP3) were also increased by combination of metformin and apigenin
p62↑,
LC3B↑,
MLKL↑,
p‑MLKL↓,
RIP3↑,
p‑RIP3↑,
TumCG↑, in vivo
TumW↓, metformin (125 mg/kg) or apigenin (40 mg/kg) caused a reduction of tumor size compared to the control group (Fig. 7D). However, oral administration of combination of metformin and apigenin decreased tumor weight profoundly

2584- Api,  Chemo,    The versatility of apigenin: Especially as a chemopreventive agent for cancer
- Review, Var, NA
ChemoSen↑, Apigenin has also been studied for its potential as a sensitizer in cancer therapy, improving the efficacy of traditional chemotherapeutic drugs and radiotherapy
RadioS↑, Apigenin enhances radiotherapy effects by sensitizing cancer cells to radiation-induced cell death
eff↝, It works by suppressing the expression of involucrin (hINV), a hallmark of keratinocyte development. Apigenin inhibits the rise in hINV expression caused by differentiating agents
DR5↑, Apigenin also greatly upregulates the expression of death receptor 5 (DR5
selectivity↑, Surprisingly, apigenin-mediated increase of DR5 expression is missing in normal mononuclear cells from human peripheral blood and doesn't subject these cells to TRAIL-induced death.
angioG↓, Apigenin has been found to prevent angiogenesis by targeting critical signaling pathways involved in blood vessel creation.
selectivity↑, Importantly, apigenin has been demonstrated to selectively kill cancer cells while sparing normal ones
chemoP↑, This selective cytotoxicity is beneficial in cancer therapy because it reduces the negative effects frequently associated with traditional treatments like chemotherapy
MAPK↓, Apigenin's ability to suppress MAPK signaling adds to its anticancer properties.
PI3K↓, Apigenin suppresses the PI3K/Akt/mTOR pathway, which is typically dysregulated in cancer.
Akt↓,
mTOR↓,
Wnt↓, Apigenin inhibits Wnt signaling by increasing β-catenin degradation
β-catenin/ZEB1↓,
GLUT1↓, fig 3
radioP↑, while reducing radiation-induced damage to healthy tissues
BioAv↓, obstacles associated with apigenin's low bioavailability and stability
chemoPv↑, Especially as a chemopreventive agent for cancer


Showing Research Papers: 1 to 50 of 422
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 422

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↓, 1,   Fenton↑, 1,   frataxin↑, 1,   GPx4↓, 1,   GSH↓, 3,   H2O2↑, 1,   HO-1↑, 1,   lipid-P↑, 2,   NRF2↑, 2,   mt-OXPHOS↓, 2,   ROS↑, 30,   mt-ROS↑, 2,   SOD↓, 1,   TrxR↓, 1,   mt-TrxR1↓, 1,   mt-TrxR2↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 3,   ATP↓, 6,   ETC↓, 1,   mitResp↓, 1,   MMP↓, 10,   mtDam↑, 6,   OCR↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

p‑AMPK↑, 1,   cMyc↓, 1,   cMyc↑, 1,   ECAR↓, 1,   GAPDH↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 4,   H2S↑, 1,   HK2?, 1,   HK2↓, 4,   lactateProd↓, 2,   LDH↓, 1,   LDHA↓, 1,   NAD↓, 1,   NADPH↓, 2,   PFK↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 3,   p‑Akt↑, 1,   Apoptosis↑, 14,   Bak↑, 1,   BAX↑, 6,   Bax:Bcl2↑, 1,   Bcl-2↓, 7,   Bcl-xL↓, 1,   BIM↑, 1,   Casp↑, 4,   Casp3↑, 8,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 3,   Casp9↑, 4,   Cyt‑c↑, 5,   DR5↑, 1,   Fas↑, 1,   JNK↑, 1,   MAPK↓, 2,   Mcl-1↓, 3,   MLKL↑, 1,   p‑MLKL↓, 1,   Necroptosis↑, 1,   p27↑, 1,   p‑p38↓, 1,   Paraptosis↑, 1,   survivin↓, 1,   TumCD↓, 1,   TumCD↑, 3,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   other↝, 3,   tumCV↓, 9,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 4,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 2,  

Autophagy & Lysosomes ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3B↑, 1,   LC3B-II↑, 1,   p62↓, 1,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNA-PK↑, 1,   DNAdam↑, 9,   MGMT↓, 1,   P53↑, 4,   p‑P53↑, 2,   PARP↓, 1,   PARP↝, 1,   p‑PARP↑, 2,   cl‑PARP↑, 2,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 4,   TumCCA↑, 10,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CD24↓, 1,   CD44↓, 1,   CSCs↓, 2,   EMT↓, 2,   GSK‐3β↓, 1,   HDAC↓, 2,   mTOR↓, 3,   PI3K↓, 3,   STAT3↓, 1,   TumCG?, 1,   TumCG↓, 5,   TumCG↑, 2,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↑, 1,   FAK↓, 1,   ITGB1↓, 1,   ITGB3↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   RIP3↑, 1,   p‑RIP3↑, 1,   Snail↓, 1,   TGF-β↓, 2,   TumCA↑, 1,   TumCI↓, 3,   TumCMig↓, 4,   TumCP↓, 2,   Vim↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   ATF4↑, 1,   EPR↑, 3,   HIF-1↓, 1,   Hif1a↓, 3,   Hif1a↑, 1,   NO↑, 2,   VEGF↓, 1,  

Barriers & Transport ⓘ

CellMemb↑, 1,   GLUT1↓, 2,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 2,   NF-kB↑, 2,   p‑NF-kB↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 5,   ChemoSen∅, 1,   Dose↓, 2,   Dose↝, 3,   Dose∅, 3,   eff↓, 5,   eff↑, 12,   eff↝, 3,   RadioS↑, 4,   selectivity↓, 2,   selectivity↑, 56,  

Clinical Biomarkers ⓘ

IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 9,   AntiTum↑, 1,   chemoP↑, 3,   chemoPv↑, 1,   neuroP↑, 1,   OS↑, 3,   QoL↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 2,   toxicity↝, 2,   TumVol↓, 2,   TumW↓, 1,   Weight↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 3,  
Total Targets: 186

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 1,   ROS∅, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  

Cell Death ⓘ

JNK↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   cl‑eIF2α↑, 1,   GRP78/BiP↑, 1,   p‑PERK↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   toxicity↓, 5,   toxicity↝, 4,   toxicity∅, 2,  

Infection & Microbiome ⓘ

AntiViral↑, 1,   Bacteria↓, 3,   Inf↓, 1,  
Total Targets: 26

Scientific Paper Hit Count for: selectivity, selectivity
33 Silver-NanoParticles
27 Magnetic Fields
17 Piperlongumine
13 Selenium NanoParticles
13 Thymoquinone
12 Betulinic acid
11 Radiotherapy/Radiation
11 Chemotherapy
10 Phenethyl isothiocyanate
10 Shikonin
9 Vitamin C (Ascorbic Acid)
9 Capsaicin
9 Propolis -bee glue
9 chitosan
9 salinomycin
8 Carvacrol
8 Copper and Cu NanoParticles
8 Dichloroacetate
8 Honokiol
8 Magnetic Field Rotating
8 Quercetin
8 Selenite (Sodium)
7 doxorubicin
7 Artemisinin
7 Berberine
7 Sulforaphane (mainly Broccoli)
6 Apigenin (mainly Parsley)
6 Baicalein
6 EGCG (Epigallocatechin Gallate)
6 Fisetin
6 Hydrogen Gas
5 3-bromopyruvate
5 Rosmarinic acid
5 Ashwagandha(Withaferin A)
5 Melatonin
5 Curcumin
5 Cisplatin
5 Selenium
5 HydroxyTyrosol
4 Alpha-Lipoic-Acid
4 Metformin
4 Phenylbutyrate
4 Boron
4 diet FMD Fasting Mimicking Diet
4 Ellagic acid
4 Lycopene
4 Magnolol
4 VitK3,menadione
3 chemodynamic therapy
3 Allicin (mainly Garlic)
3 Astaxanthin
3 Atorvastatin
3 Caffeic acid
3 Chrysin
3 Citric Acid
3 diet Methionine-Restricted Diet
3 Shilajit/Fulvic Acid
3 γ-linolenic acid (Borage Oil)
3 Parthenolide
3 Urolithin
2 Dipyridamole
2 Berbamine
2 Gold NanoParticles
2 Bifidobacterium
2 immunotherapy
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Coenzyme Q10
2 Hydroxycinnamic-acid
2 Date Fruit Extract
2 Oxygen, Hyperbaric
2 Disulfiram
2 Electrical Pulses
2 Fenbendazole
2 Gambogic Acid
2 Graviola
2 Luteolin
2 SonoDynamic Therapy UltraSound
2 Sulfasalazine
2 polyethylene glycol
2 Silymarin (Milk Thistle) silibinin
2 Aflavin-3,3′-digallate
2 Zerumbone
1 Auranofin
1 Anzaroot, Astragalus fasciculifolius Bioss
1 Glucose
1 Ajoene (compound of Garlic)
1 Acetyl-l-carnitine
1 Sorafenib (brand name Nexavar)
1 5-Aminolevulinic acid
1 Baicalin
1 Bufalin/Huachansu
1 probiotics
1 Brucea javanica
1 Boswellia (frankincense)
1 Butyrate
1 Carnosic acid
1 urea
1 Thymol-Thymus vulgaris
1 Cat’s Claw
1 Cannabidiol
1 Chocolate
1 Calorie Restriction Mimetics
1 diet Ketogenic
1 PXD, phenoxodiol
1 Emodin
1 Juglone
1 Methylene blue
1 Methyl Jasmonate
1 Methylglyoxal
1 Bicarbonate(Sodium)
1 Nimbolide
1 Oleuropein
1 Hyperthermia
1 Propyl gallate
1 temozolomide
1 borneol
1 Plumbagin
1 Psoralidin
1 Pterostilbene
1 Resveratrol
1 irinotecan
1 Ursolic acid
1 Vitamin B1/Thiamine
1 Vitamin K2
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#:1110  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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