Evidence map›Paper›PMID 23404329›Full record

ArticleOncology reports2013

The molecular mechanism of action of aspirin, curcumin and sulforaphane combinations in the chemoprevention of pancreatic cancer.

Arvind Thakkar, Dhruvitkumar Sutaria, B Karthik Grandhi, Jeffrey Wang, Sunil Prabhu

Abstract read
In one paragraph

Article in Oncology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. A randomized clinical trial of nerve block to manage end-stage pancreatic cancerous pain.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Trial
  2. Review
  3. Article
  4. Review
  5. Is Curcumin the Answer to Future Chemotherapy Cocktail?Molecules (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Molecular targets of isothiocyanates in cancer: recent advances.Molecular nutrition & food research · 2014
    Review
  15. Selective killing effect of oxytetracycline, propafenone and metamizole on A549 or Hela cells.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    Article
  16. Article
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Arvind ThakkarDepartment of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, CA 91766, USA.
Dhruvitkumar Sutaria
B Karthik Grandhi
Jeffrey Wang
Sunil Prabhu

Funding

Chemoprevention of pancreatic cancer using a combinatorial nano-drug systemR03CA153812 · NCI · WESTERN UNIVERSITY OF HEALTH SCIENCES · PI PRABHU, SUNIL · 2011 to 2012
$149k
NCI NIH HHS 1R03CA153812-01A1NCI NIH HHS R03 CA153812
6 · The paper itself

Abstract

Pancreatic cancer ranks as the fourth most deadly form of cancer in the United States with ~37,000 deaths each year. The present study evaluated the chemopreventive potential of a combination of aspirin (ASP), curcumin (CUR) and sulforaphane (SFN) in low doses to human pancreatic cancer cells, MIA PaCa-2 and Panc-1. Results demonstrated that low doses of ASP (1 mM), CUR (10 µM) and SFN (5 µM) (ACS) combination reduced cell viability by ~70% (P<0.001), and also induced cell apoptosis by ~51% (P<0.001) accompanied by activation of caspase-3 and Poly(ADP-ribose) polymerase (PARP) proteins. The NF-κB DNA binding activity was inhi-bited by ~45% (P<0.01) and ~75% (P<0.001) in MIA PaCa-2 and Panc-1 cells, respectively. Mechanistic studies revealed that ACS promoted increase expression of phospho extracellular signal-regulated kinase 1/2 (P-ERK1/2), c-Jun, p38 MAPK and p53 proteins. Furthermore, the cells pretreated with U0126 (ERK1/2 inhibitor) partially abolished the effect of ACS on cell viability. Data from this study demonstrate that a low-dose ACS combination inhibits cell growth by inducing cell apoptosis, and proposes sustained activation of the ERK1/2 signaling pathway as one of the possible mechanisms.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsAspirinCell Line, TumorCell SurvivalCurcuminDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansIsothiocyanatesMAP Kinase Signaling SystemNF-kappa BPancreatic NeoplasmsSulfoxidesThiocyanatesAspirinCurcuminDNA-Binding ProteinsIsothiocyanatesNF-kappa BsulforaphaneSulfoxidesThiocyanates

Identifiers

PMID23404329
PMCPMC3621734

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.