ascitic Cancer Research Results
ascitic, ascitic fluid: Click to Expand ⟱
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Ascitic fluid is a type of fluid that accumulates in the abdominal cavity.
In cancer patients, ascitic fluid can be a sign of advanced disease. Cancer cells can spread to the abdominal cavity and produce fluid, leading to an accumulation of ascitic fluid.
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Scientific Papers found: Click to Expand⟱
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vitro+vivo, |
lymphoma, |
NA |
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OS↑, up 50%
ascitic↓, down 65%
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in-vitro, |
Nor, |
HUVECs |
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in-vivo, |
NA, |
NA |
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*VEGF↓,
*angioG↓,
*ascitic↓,
*Sp1/3/4↓, Studies at molecular level revealed that withaferin A inhibits binding of Sp1 transcription factor
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2
pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma
concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer
TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31↓,
NF-kB↓,
COX2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1/CCND1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
GBM, |
U251 |
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in-vivo, |
Ovarian, |
SKOV3 |
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VEGF↓,
Hif1a↓, inhibit expression and phosphorylation of STAT3 and AKT, which are key factors in the regulation of HIF-1α expression
p‑STAT3↓,
p‑Akt↓,
angioG↓,
TumCG↓,
TumW↓,
ascitic↓, reduction in tumor burden and ascites volume
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
lipid-P?, 1,
Metal & Cofactor Biology ⓘ
Tf↓, 1,
Core Metabolism/Glycolysis ⓘ
PPARα↓, 1,
Cell Death ⓘ
p‑Akt↓, 1, Bcl-2↓, 1, Bcl-xL↓, 1, Casp3↑, 1, Casp8↑, 1, DR4↑, 1, DR5↑, 1, IAP1↓, 1, survivin↓, 1,
DNA Damage & Repair ⓘ
cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 2, cycE/CCNE↓, 1, p‑RB1↓, 1,
Proliferation, Differentiation & Cell State ⓘ
p‑ERK↓, 1, Let-7↑, 1, STAT3↓, 1, p‑STAT3↓, 1, TOP1↓, 1, TOP2↑, 1, TumCG↓, 2, Wnt↓, 1,
Migration ⓘ
CD31↓, 1, Ki-67↓, 1, miR-200b↑, 1, MMP1↓, 1, MMP2↓, 1, MMP9↓, 2, PDGF↓, 1, TumCI↓, 1, TumMeta↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, Hif1a↓, 1, p‑PDGFR-BB↓, 1, VEGF↓, 4,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CXCR4↓, 2, ICAM-1↓, 1, IKKα↓, 1, IL1α↓, 1, MCP1↓, 1, MIP2↓, 1, NF-kB↓, 2,
Synaptic & Neurotransmission ⓘ
5HT↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, ChemoSen↑, 1, Dose↑, 1, eff↑, 4, Half-Life↓, 1,
Clinical Biomarkers ⓘ
AR↓, 1, ascitic↓, 4, Ki-67↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, chemoPv↑, 1, OS↑, 1, toxicity↓, 1, TumVol↓, 1, TumW↓, 1, Weight∅, 1,
Total Targets: 66
Pathway results for Effect on Normal Cells:
Cell Death ⓘ
MAPK↑, 1,
Kinase & Signal Transduction ⓘ
Sp1/3/4↓, 1,
Migration ⓘ
Ca+2↝, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Clinical Biomarkers ⓘ
ascitic↓, 1,
Total Targets: 9
Scientific Paper Hit Count for: ascitic, ascitic fluid
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#:622 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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