Evidence map›Paper›PMID 24194908›Full record

ArticlePloS one2013

Reversing the intractable nature of pancreatic cancer by selectively targeting ALDH-high, therapy-resistant cancer cells.

Sang Kyum Kim, Honsoul Kim, Da-Hye Lee, Tae-shin Kim, Tackhoon Kim, Chaeuk Chung, Gou Young Koh, Hoguen Kim, Dae-Sik Lim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Co‑expression ofOncology letters · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Cancer stem cell impact on clinical oncology.World journal of stem cells · 2018
    Review
  13. Article
  14. Review
  15. Cytokines, breast cancer stem cells (BCSCs) and chemoresistance.Clinical and translational medicine · 2018
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

9 authors at 2 institutions in 1 country.

Sang Kyum KimGraduate School of Medical Science and Engineering, South Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea.
Honsoul Kim
Da-Hye Lee
Tae-shin Kim
Tackhoon Kim
Chaeuk Chung
Gou Young Koh
Hoguen Kim
Dae-Sik Lim
Korea Advanced Institute of Science and Technology · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human pancreatic ductal adenocarcinoma (PDAC) is a cancer with a dismal prognosis. The efficacy of PDAC anticancer therapies is often short-lived; however, there is little information on how this disease entity so frequently gains resistance to treatment. We adopted the concept of cancer stem cells (CSCs) to explain the mechanism of resistance and evaluated the efficacy of a candidate anticancer drug to target these therapy-resistant CSCs. We identified a subpopulation of cells in PDAC with CSC features that were enriched for aldehyde dehydrogenase (ALDH), a marker expressed in certain stem/progenitor cells. These cells were also highly resistant to, and were further enriched by, treatment with gemcitabine. Similarly, surgical specimens from PDAC patients showed that those who had undergone preoperative chemo-radiation therapy more frequently displayed cancers with ALDH strongly positive subpopulations compared with untreated patients. Importantly, these ALDH-high cancer cells were sensitive to disulfiram, an ALDH inhibitor, when tested in vitro. Furthermore, in vivo xenograft studies showed that the effect of disulfiram was additive to that of low-dose gemcitabine when applied in combination. In conclusion, human PDAC-derived cells that express high levels of ALDH show CSC features and have a key role in the development of resistance to anticancer therapies. Disulfiram can be used to suppress this therapy-resistant subpopulation.

Indexed as

Aldehyde DehydrogenaseAnalysis of VarianceAnimalsBlotting, WesternCarcinoma, Pancreatic DuctalCell Line, TumorDeoxycytidineDisulfiramDrug Delivery SystemsDrug Resistance, NeoplasmFlow CytometryGemcitabineHumansImmunohistochemistryMiceNeoplastic Stem CellsAldehyde DehydrogenaseDeoxycytidineDisulfiramGemcitabine

Identifiers

PMID24194908
PMCPMC3806801
OpenAlexW2143675498

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.