Evidence map›Paper›PMID 20086170›Full record

ArticleCancer research2010

Combined treatment of pancreatic cancer with mithramycin A and tolfenamic acid promotes Sp1 degradation and synergistic antitumor activity.

Zhiliang Jia, Yong Gao, Liwei Wang, Qiang Li, Jun Zhang, Xiangdong Le, Daoyan Wei, James C Yao, David Z Chang, Suyun Huang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  4. Role of post-translational modifications of Sp1 in cancer: state of the art.Frontiers in cell and developmental biology · 2024
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  10. Targeting the pH Paradigm at the Bedside: A Practical Approach.International journal of molecular sciences · 2020
    Review
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  14. Angiocrine endothelium: from physiology to cancer.Journal of translational medicine · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Zhiliang JiaDepartment of Gastrointestinal Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Yong Gao
Liwei Wang
Qiang Li
Jun Zhang
Xiangdong Le
Daoyan Wei
James C Yao
David Z Chang
Suyun Huang
Keping Xie
Ruijin Hospital · CN

Funding

SPORE in Pancreatic CancerP20CA101936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABBRUZZESE, JAMES L. · 2003 to 2009
$5.4M
Functional Validation of Pancreatic Cancer Progression BiomarkerR01CA152309 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.6M
KLF4 Genetic and Epigenetic Changes in Human Pancreatic CancerR01CA129956 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2008 to 2012
$1.3M
Genetic Approaches to Pancreatic Cancer ProgressionR01CA148954 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.3M
NCI NIH HHS 1P20-CA101936-01-PP4NCI NIH HHS 5R01-CA129956NCI NIH HHS P20 CA101936NCI NIH HHS R01 CA129956NCI NIH HHS R01 CA148954NCI NIH HHS R01 CA152309
6 · The paper itself

Abstract

Mithramycin (MIT) and tolfenamic acid (TA) inhibit the activity of the transcription factor Sp1. In the present study, we investigated whether pancreatic cancer treatment with a combination of these compounds has a synergistic effect on Sp1 activity, tumor growth, and their underlying response mechanisms. Treatment of pancreatic tumor xenografts with MIT and TA produced dose-dependent antitumor activity, and significant antitumor activity of either compound alone was directly associated with systemic side effects. Combination treatment with nontoxic doses of both compounds produced synergistic antitumor activity, whereas treatment with a nontoxic dose of either compound alone lacked a discernible antitumor effect. Synergistic therapeutic effects correlated directly with synergistic antiproliferation and antiangiogenesis in vitro. Moreover, combination treatment resulted in Sp1 protein degradation, drastically downregulating expression of Sp1 and vascular endothelial growth factor. Our findings established that Sp1 is a critical target of TA and MIT in human pancreatic cancer therapy, rationalizing clinical studies to determine the effect of existing pancreatic cancer therapy regimens on Sp1 signaling in tumors and normal pancreatic tissue, and the ability of Sp1-targeting strategies to modify cancer responses.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsBlotting, WesternBody WeightCell Line, TumorChromatin ImmunoprecipitationDose-Response Relationship, DrugDrug SynergismFemaleHumansMiceMice, Inbred BALB CMice, Nudeortho-AminobenzoatesPancreatic NeoplasmsPlicamycinmithramycin Aortho-AminobenzoatesPlicamycinSp1 Transcription Factortolfenamic acidVascular Endothelial Growth Factor A

Identifiers

PMID20086170
PMCPMC2840649
OpenAlexW2132899220

What OpenQuestion holds

Textmetadata
LicenceTDM
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.