Evidence map›Paper›PMID 24950733›Full record

ArticleTargeted oncology2015

Side population cells of pancreatic cancer show characteristics of cancer stem cells responsible for resistance and metastasis.

Hanno Niess, Peter Camaj, Andrea Renner, Ivan Ischenko, Yue Zhao, Stefan Krebs, Josef Mysliwietz, Carsten Jäckel, Peter J Nelson, Helmut Blum and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Targeted oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. PGC1α-Mediated Metabolic Reprogramming Drives the Stemness of Pancreatic Precursor Lesions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. microRNA-21 Regulates Stemness in Pancreatic Ductal Adenocarcinoma Cells.International journal of molecular sciences · 2022
    Article
  7. Article
  8. Review
  9. The key roles of cancer stem cell-derived extracellular vesicles.Signal transduction and targeted therapy · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. lncRNA SLC7A11-AS1 Promotes Chemoresistance by Blocking SCFMolecular therapy. Nucleic acids · 2020
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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.

Hanno NiessDepartment of Surgery, University of Munich, Campus Großhadern, Munich, Germany.
Peter Camaj
Andrea Renner
Ivan Ischenko
Yue Zhao
Stefan Krebs
Josef Mysliwietz
Carsten Jäckel
Peter J Nelson
Helmut Blum
Karl-Walter Jauch
Joachim W Ellwart
Christiane J Bruns
Institut für Urheber- und Medienrecht · DELudwig-Maximilians-Universität München · DEOtto-von-Guericke University Magdeburg · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) have been proposed to underlie the initiation and maintenance of tumor growth and the development of chemoresistance in solid tumors. The identification and role of these important cells in pancreatic cancer remains controversial. Here, we isolate side population (SP) cells from the highly aggressive and metastatic human pancreatic cancer cell line L3.6pl and evaluate their potential role as models for CSCs. SP cells were isolated following Hoechst 33342 staining of L3.6pl cells. SP, non-SP, and unsorted L3.6pl cells were orthotopically xenografted into the pancreas of nude mice and tumor growth observed. RNA was analyzed by whole genome array and pathway mapping was performed. Drug resistant variants of L3.6pl were developed and examined for SP proportions and evaluated for surface expression of known CSC markers. A distinct SP with the ability to self-renew and differentiate into non-SP cells was isolated from L3.6pl (0.9 % ± 0.22). SP cells showed highly tumorigenic and metastatic characteristics after orthotopic injection. Transcriptomic analysis identified modulation of gene networks linked to tumorigenesis, differentiation, and metastasization in SP cells relative to non-SP cells. Wnt, NOTCH, and EGFR signaling pathways associated with tumor stem cells were altered in SP cells. When cultured with increasing concentrations of gemcitabine, the proportion of SP cells, ABCG2(+), and CD24(+) cells were significantly enriched, whereas 5-fluorouracil (5-FU) treatment lowered the percentage of SP cells. SP cells were distinct from cells positive for previously postulated pancreatic CSC markers. The Hoechst-induced side population in L3.6pl cells comprises a subset of tumor cells displaying aggressive growth and metastasization, increased gemcitabine-, but not 5-FU resistance. The cells may act as a partial model for CSC biology.

Indexed as

Drug Resistance, NeoplasmAdenocarcinomaAnimalsAntimetabolites, AntineoplasticBiomarkers, TumorCell Line, TumorCell ProliferationCell SeparationDeoxycytidineFluorouracilGemcitabineGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMaleAntimetabolites, AntineoplasticBiomarkers, TumorDeoxycytidineFluorouracilGemcitabine

Identifiers

PMID24950733
OpenAlexW2004312364

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.