AntiTum Cancer Research Results
AntiTum, AntiTumor: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
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vitro+vivo, |
BC, |
T47D |
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in-vitro, |
BC, |
MCF10 |
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AntiTum↓, Carnosic acid (CA) exerts an anti‐tumor effect via generating ROS or activating the mitochondria‐related apoptosis pathway in vitro and in vivo.
ROS↑, CA promoted cancer cell apoptosis via ROS generation, which activated c‐Jun N‐terminal kinase (JNK) and p38 phosphorylation.
cJun↑, CA Activated JNK and p38 in Breast Cancer Cell Lines
p‑p38↑,
Apoptosis↑, CA induced apoptosis of hepatocellular carcinoma cells via the reactive oxygen species (ROS)‐mediated mitochondrial pathway
ROS↑,
eff↑, Furthermore, the combined application of CA and curcumin suppressed the proliferative activity and disrupted the mitochondrial function of metastatic prostate cancer cells compared with their individual uses
TumCP↓, CA Inhibited Breast Cancer Proliferation and Glucose Uptake
glucose↓, Glucose consumption was accelerated by low concentrations of CA, but decreased with increasing time and CA concentration.
BAX↑, up‐regulating Bax and PARP and down‐regulating Bcl‐2.
PARP↑,
Bcl-2↓,
eff↓, We then abrogated the effect of CA‐induced ROS using the antioxidant NAC (5 mM).
Ki-67↓, These findings indicated that CA could accelerate tumor apoptosis by up‐regulating Bax expression and down‐regulating Ki67 and Bcl‐2 in vivo.
toxicity↝, Furthermore, CA did not injure vital organs.
STAT3↓, CA has been reported to suppress the STAT3 signaling pathway through ROS generation and inhibit the phosphoinositide 3‐kinase/Akt/mTOR signaling pathway in colon cancer and lung cancer
PI3K↓,
Akt↓,
mTOR↓,
AntiTum↓, Cyclic fasting–mimicking diet (FMD) is an experimental nutritional intervention with potent antitumor activity in preclinical models of solid malignancies.
Apoptosis↑, murine CLL models had mild cytotoxic effects, which resulted in apoptosis activation mediated in part by lowered insulin and IGF1 concentrations.
IGF-1↓,
eff↑, In CLL cells, fasting conditions promoted an increase in proteasome activity that served as a starvation escape pathway. Pharmacologic inhibition of this escape mechanism with the proteasome inhibitor bortezomib resulted in a strong enhancement
OS↑, combining cyclic fasting/FMD with bortezomib and rituximab, an anti-CD20 antibody, delayed CLL progression and resulted in significant prolongation of mouse survival
eff↑, recent clinical reports have shown that combining cyclic FMD with chemotherapy, endocrine therapies, or immunotherapy improves tumor responses in patients with early-stage neoplasms
HMG-CoA↓, Statins are promising anticancer agents that target the mevalonate pathway
AntiTum↓, dipyridamole inhibits this feedback response and potentiates statin antitumor activity.
eff↑, this combination of 2 FDA-approved drugs has the potential to be fast-tracked to cancer patient care.
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in-vitro, |
NPC, |
TW01 |
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in-vitro, |
NPC, |
TW06 |
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CSCs↓, EGCG potently inhibited sphere formation and can eliminate the stem cell characteristics of NPC and inhibit the epithelial-mesenchymal transition (EMT) signatures.
EMT↓,
TumCMig↓, Inhibition on NPC sphere-derived cell colony formation, migration, and invasion by EGCG
TumCI↓,
OCT4↓, EGCG inhibited the expression of Klf-4 and Oct-4 in sphere-derived cells.
Snail↓, EGCG significantly inhibited the levels of Snail, Vimentin and increased E-Cadherin expression in a dose-dependent manner
Vim↓,
E-cadherin↓,
HSP70/HSPA5↓, EGCG suppresses the expression of HSP70 and HSP90, and exhibits anti-tumor activity in vitro and in vivo
HSP90↓,
AntiTum↓,
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 2,
Core Metabolism/Glycolysis ⓘ
glucose↓, 1, HMG-CoA↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 2, BAX↑, 1, Bcl-2↓, 1, p‑p38↑, 1,
Transcription & Epigenetics ⓘ
cJun↑, 1,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↓, 1, HSP90↓, 1,
DNA Damage & Repair ⓘ
PARP↑, 1,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, EMT↓, 1, IGF-1↓, 1, mTOR↓, 1, OCT4↓, 1, PI3K↓, 1, STAT3↓, 1,
Migration ⓘ
E-cadherin↓, 1, Ki-67↓, 1, Snail↓, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1, Vim↓, 1,
Drug Metabolism & Resistance ⓘ
eff↓, 1, eff↑, 4,
Clinical Biomarkers ⓘ
Ki-67↓, 1,
Functional Outcomes ⓘ
AntiTum↓, 4, OS↑, 1, toxicity↝, 1,
Total Targets: 32
Pathway results for Effect on Normal Cells:
Total Targets: 0
Scientific Paper Hit Count for: AntiTum, AntiTumor
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#:913 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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