Evidence map›Paper›PMID 20590594›Full record

ArticleBritish journal of pharmacology2010

Cucurbitacin B, a novel in vivo potentiator of gemcitabine with low toxicity in the treatment of pancreatic cancer.

Gabriela B Iwanski, Dhong H Lee, Shlomit En-Gal, Ngan B Doan, Brandon Castor, Marco Vogt, Melvin Toh, Carsten Bokemeyer, Jonathan W Said, Nils H Thoennissen and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
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

34 citing papers in PubMed, 76 citations in OpenAlex.

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  11. Targeting Cancer Metabolism and Current Anti-Cancer Drugs.Advances in experimental medicine and biology · 2021
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  14. Cucurbitacins extracted from Cucumis melo L. (CuEC) exert a hypotensive effect via regulating vascular tone.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
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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

11 authors at 5 institutions in 3 countries.

Gabriela B IwanskiDivision of Hematology and Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA 90048, USA. gabriela.iwanski@cshs.org
Dhong H Lee
Shlomit En-Gal
Ngan B Doan
Brandon Castor
Marco Vogt
Melvin Toh
Carsten Bokemeyer
Jonathan W Said
Nils H Thoennissen
H Phillip Koeffler
Cedars-Sinai Medical Center · USUCLA Medical Center · USAsklepios Klinikum Harburg · DEEppendorf (Germany) · DENational University of Singapore · SG

Funding

REGULATION OF HEMATOPOIETIC CYTOKINESR01CA026038 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOEFFLER, HAROLD PHILLIP · 1985 to 2013
$4.7M
NCI NIH HHS R01 CA026038
6 · The paper itself

Abstract

background and purposePancreatic cancer is a highly aggressive malignancy, and improvement in systemic therapy is necessary to treat this frequently encountered metastatic disease. The current targeted agents used in combination with gemcitabine improved objective response rates, but with little or no improvements in survival and also increased toxicities in pancreatic cancer patients. Recently, we showed that the triterpenoid cucurbitacin B inhibited tumour growth in pancreatic cancer cells by inhibition of the JAK/STAT pathway, and synergistically increased antiproliferative effects of gemcitabine in vitro. EXPERIMENTAL APPROACH: The anti-tumour effects and toxicities of cucurbitacin B in combination with gemcitabine were tested against human pancreatic cancer cells in a murine xenograft model. KEY

resultsCombined therapy with cucurbitacin B and gemcitabine at relatively low doses (0.5 mg x kg(-1) and 25 mg x kg(-1) respectively) resulted in highly significant tumour growth inhibition of pancreatic cancer xenografts (up to 79%). Remarkably, this therapy was well tolerated by the animals, as shown by histology of visceral organs, analysis of serum chemistry, full blood counts and bone marrow colony numbers. Western blot analysis of the tumour samples of mice who received both cucurbitacin B and gemcitabine, revealed stronger inhibition of Bcl-XL, Bcl-2 and c-myc, and higher activation of the caspase cascades, than mice treated with either agent alone. CONCLUSIONS AND IMPLICATIONS: Combination of cucurbitacin B and gemcitabine had profound anti-proliferative effects in vivo against xenografts of human pancreatic cancer cells, without any significant signs of toxicity. This promising combination should be examined in therapeutic trials of pancreatic cancer.

Indexed as

AnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosis Regulatory ProteinsBone Marrow CellsCell Line, TumorCell ProliferationDeoxycytidineDose-Response Relationship, DrugDrug SynergismEnzyme ActivationFemaleGemcitabineHumansMiceMice, NudeAntineoplastic AgentsApoptosis Regulatory Proteinscucurbitacin BDeoxycytidineGemcitabineMYC protein, humanProto-Oncogene Proteins c-mycTriterpenes

Identifiers

PMID20590594
PMCPMC2936004
OpenAlexW1481973004

What OpenQuestion holds

Textmetadata
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.