Evidence map›Paper›PMID 30348057›Full record

ArticleTechnology in cancer research & treatment2018

Image-Based Profiling of Patient-Derived Pancreatic Tumor-Stromal Cell Interactions Within a Micropatterned Tumor Model.

Shilpaa Mukundan, Kriti Sharma, Kim Honselmann, Amy Singleton, Andrew Liss, Biju Parekkadan

Open access · goldAbstract read
In one paragraph

Article in Technology in cancer research & treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 2 institutions in 1 country.

Shilpaa Mukundan1 Department of Biomedical Engineering, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Kriti Sharma1 Department of Biomedical Engineering, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Kim Honselmann2 Department of Surgery, Andrew L. Warshaw Institute for Pancreatic Cancer Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Amy Singleton3 Center for Surgery, Bioengineering, and Innovation, Department of Surgery, Massachusetts General Hospital, Harvard Medical School and the Shriners Hospitals for Children, Boston, MA, USA.
Andrew Liss2 Department of Surgery, Andrew L. Warshaw Institute for Pancreatic Cancer Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Biju Parekkadan1 Department of Biomedical Engineering, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.ORCID 0000-0002-3408-8085
Harvard University · USRutgers, The State University of New Jersey · US

Funding

Artificial, Humanized Stem Cell NichesR01EB012521 · NIBIB · RUTGERS, THE STATE UNIV OF N.J. · PI PAREKKADAN, BIJU · 2011 to 2021
$6.0M
NIBIB NIH HHS R01 EB012521
6 · The paper itself

Abstract

Pancreatic cancer is one of the most aggressive cancers with a 5-year patient survival rate of 8.2% and limited availability of therapeutic agents to target metastatic disease. Pancreatic cancer is characterized by a dense stromal cell population with unknown contribution to the progression or suppression of tumor growth. In this study, we describe a microengineered tumor stromal assay of patient-derived pancreatic cancer cells to study the heterotypic interactions of patient pancreatic cancer cells with different types of stromal fibroblasts under basal and drug-treated conditions. The population dynamics of tumor cells in terms of migration and viability were visualized as a functional end point. Coculture with cancer-associated fibroblasts increased the migration of cancer cells when compared to dermal fibroblasts. Finally, we imaged the response of a bromodomain and extraterminal inhibitor on the viability of pancreatic cancer clusters surrounding by stroma in microengineered tumor stromal assay. We visualized a codynamic reduction in both cancer and stromal cells with bromodomain and extraterminal treatment compared to the dimethyl sulfoxide-treated group. This study demonstrates the ability to engineer tumor-stromal assays with patient-derived cells, study the role of diverse types of stromal cells on cancer progression, and precisely visualize a coculture during the screening of therapeutic compounds.

Indexed as

Cell CommunicationDiagnostic ImagingModels, BiologicalTumor MicroenvironmentCancer-Associated FibroblastsCell Line, TumorCell MovementCoculture TechniquesDisease ProgressionHumansNeoplasm InvasivenessPancreatic NeoplasmsStromal CellsBETmicroengineered tumor stromal assay (µTSA)pancreatic cancerstromatumor microenvironment

Identifiers

PMID30348057
PMCPMC6201185
OpenAlexW2896672806

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.