Evidence map›Paper›PMID 21730821›Full record

ArticleAnti-cancer drugs2011

Extracelluar matrix metalloproteinase as a novel target for pancreatic cancer therapy.

Hyunki Kim, Guihua Zhai, Zhiyong Liu, Sharon Samuel, Nemil Shah, Emily E Helman, Joseph A Knowles, Cecil R Stockard, Naomi S Fineberg, William E Grizzle and 3 more

Abstract read
In one paragraph

Article in Anti-cancer drugs, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. International journal of molecular sciences · 2018
    Article
  4. Nuclear medicine and biology · 2018
    Article
  5. Article
  6. B7-H3-targetedNuclear medicine and biology · 2017
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. HAb18G/CD147 promotes pSTAT3-mediated pancreatic cancer development via CD44s.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  13. Article
  14. Article
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

13 authors at 3 institutions in 1 country.

Hyunki KimDepartment of Radiology, University of Alabama at Birmingham, USA. hyunki@uab.edu
Guihua Zhai
Zhiyong Liu
Sharon Samuel
Nemil Shah
Emily E Helman
Joseph A Knowles
Cecil R Stockard
Naomi S Fineberg
William E Grizzle
Tong Zhou
Kurt R Zinn
Eben L Rosenthal
University of Alabama at Birmingham · USCancer Research And Biostatistics · USUniversity of Alabama at Birmingham Hospital · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
UAB / UMN SPORE in Pancreatic CancerP50CA101955 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BUCHSBAUM, DONALD J · 2010 to 2014
$11.1M
CD147 as a Novel Target in Head and Neck CancerR01CA142637 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROSENTHAL, EBEN L. · 2010 to 2014
$1.3M
Tumor Stromal Interactions in Head and Neck CancerK08CA102154 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROSENTHAL, EBEN L. · 2005 to 2009
$560k
NCI NIH HHS 5K08CA102154NCI NIH HHS 5P30CA013148NCI NIH HHS K08 CA102154NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA142637NCI NIH HHS R01CA142637
6 · The paper itself

Abstract

The objective of this study was to evaluate extracellular matrix metalloproteinase (EMMPRIN) as a novel target in orthotopic pancreatic cancer murine models. MIA PaCa-2 human pancreatic tumor cells were implanted in groups 1 and 3-7, whereas MIA PaCa-2 EMMPRIN knockdown cells were implanted in group 2. Dosing with anti-EMMPRIN antibody started immediately after implantation for groups 1-3 (residual tumor model) and at 21 days after cell implantation for groups 4-7 (established tumor model). Groups 3, 5, and 7 were treated with anti-EMMRPIN antibody (0.2-1.0 mg) twice weekly for 2-3 weeks, whereas the other groups served as the control. In the residual tumor model, tumor growth of anti-EMMPRIN-treated group was successfully arrested for 21 days (15 ± 4 mm(3)), which was significantly lower than that of the EMMPRIN knockdown group (80 ± 15 mm(3); P=0.001) or the control group (240 ± 41 mm(3); P<0.001). In the established tumor model, anti-EMMPRIN therapy lowered tumor volume increase by approximately 40% compared with the control, regardless of the dose amount. Ki67-expressed cell density of group 5 was 939 ± 150 mm(-2), which was significantly lower than that of group 4 (1709 ± 145 mm(-2); P=0.006). Microvessel density of group 5 (30 ± 6 mm(-2)) was also significantly lower than that of group 4 (53 ± 5 mm(-2); P=0.014), whereas the microvessel size of group 5 (191 ± 22 μm(2)) was significantly larger than that of group 4 (113 ± 26 μm(2); P=0.049). These data show the high potential of anti-EMMPRIN therapy for pancreatic cancer and support its clinical translation.

Indexed as

AnimalsAntibodies, Anti-IdiotypicAntibodies, Monoclonal, Murine-DerivedBasiginCell Line, TumorDrug Evaluation, PreclinicalExtracellular MatrixFemaleGene Knockdown TechniquesHumansKi-67 AntigenMatrix MetalloproteinasesMiceMice, Inbred BALB CMice, SCIDMolecular Targeted TherapyAntibodies, Anti-IdiotypicAntibodies, Monoclonal, Murine-DerivedBasiginBSG protein, humanKi-67 AntigenMatrix Metalloproteinases

Identifiers

PMID21730821
PMCPMC3587034
OpenAlexW207210197

What OpenQuestion holds

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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.