Evidence map›Paper›PMID 27374084›Full record

ArticleOncotarget2016

The pancreatic niche inhibits the effectiveness of sunitinib treatment of pancreatic cancer.

Neus Martínez-Bosch, Pedro Enrique Guerrero, Mireia Moreno, Anabel José, Mar Iglesias, Jessica Munné-Collado, Héctor Anta, Joan Gibert, Carlos Alberto Orozco, Judith Vinaixa and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Targeting galectin-1 inhibits pancreatic cancer progression by modulating tumor-stroma crosstalk.Proceedings of the National Academy of Sciences of the United States of America · 2018
    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 4 institutions in 1 country.

Neus Martínez-BoschHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Pedro Enrique GuerreroHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Mireia MorenoHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Anabel JoséBiomedical Research Institute August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Mar IglesiasPathology Service, Hospital del Mar, Barcelona, Spain.
Jessica Munné-ColladoPathology Service, Hospital del Mar, Barcelona, Spain.
Héctor AntaHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Joan GibertHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Carlos Alberto OrozcoHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Judith VinaixaHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Cristina FillatBiomedical Research Institute August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Francesc ViñalsCatalan Institute of Oncology-IDIBELL, Barcelona University, Barcelona, Spain.
Pilar NavarroHospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Hospital del Mar Research Institute · ESCentro de Investigación Biomédica en Red · ESHospital Del Mar · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current treatments for pancreatic ductal adenocarcinoma (PDA) are ineffective, making this the 4th leading cause of cancer deaths. Sunitinib is a broad-spectrum inhibitor of tyrosine kinase receptors mostly known for its anti-angiogenic effects. We tested the therapeutic effects of sunitinib in pancreatic cancer using the Ela-myc transgenic mouse model. We showed that Ela-myc pancreatic tumors express PDGFR and VEGFR in blood vessels and epithelial cells, rendering these tumors sensitive to sunitinib by more than only its anti-angiogenic activity. However, sunitinib treatment of Ela-myc mice with either early or advanced tumor progression had no impact on either survival or tumor burden. Further histopathological characterization of these tumors did not reveal differences in necrosis, cell differentiation, angiogenesis, apoptosis or proliferation. In stark contrast, in vitro sunitinib treatment of Ela-myc- derived cell lines showed high sensitivity to the drug, with increased apoptosis and reduced proliferation. Correspondingly, subcutaneous tumors generated from these cell lines completely regressed in vivo after sunitinib treatments. These data point at the pancreatic tumor microenvironment as the most likely barrier preventing sunitinib treatment efficiency in vivo. Combined treatments with drugs that disrupt tumor fibrosis may enhance sunitinib therapeutic effectiveness in pancreatic cancer treatment.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic AgentsCarcinoma, Pancreatic DuctalCell Line, TumorIndolesMiceNeovascularization, PathologicPancreatic NeoplasmsPyrrolesSunitinibAngiogenesis InhibitorsAntineoplastic AgentsIndolesPyrrolesSunitinibacinar carcinomafibrosispancreatic cancerPDAsunitinib

Identifiers

PMID27374084
PMCPMC5217016
OpenAlexW2467909253

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.