Evidence map›Paper›PMID 30273655›Full record

ReviewSeminars in cancer biology2019

Metabolism and epigenetics of pancreatic cancer stem cells.

M Perusina Lanfranca, J K Thompson, F Bednar, C Halbrook, C Lyssiotis, B Levi, T L Frankel

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in cancer biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Molecular Targets for the Diagnosis and Treatment of Pancreatic Cancer.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Role of Diet in Stem and Cancer Stem Cells.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

7 authors at 1 institution in 1 country.

M Perusina LanfrancaDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
J K ThompsonDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
F BednarDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States.
C HalbrookRogel Cancer Center, University of Michigan, Ann Arbor, MI, United States; Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, United States.
C LyssiotisRogel Cancer Center, University of Michigan, Ann Arbor, MI, United States; Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, United States.
B LeviDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
T L FrankelDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States. Electronic address: timofran@med.umich.edu.
University of Michigan · US

Funding

Role of Interleukin-22 and Innate Lymphoid Cells in Pancreas Cancer Initiation and ProgressionK08CA201581 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FRANKEL, TIMOTHY LOUIS · 2016 to 2020
$703k
NCI NIH HHS K08 CA201581
6 · The paper itself

Abstract

Pancreatic Cancer (PDA) is an aggressive malignancy characterized by early spread and a high mortality. Current studies suggest that a subpopulation of cells exist within tumors, cancer stem cell (CSC), which are capable of self-renewal and give rise to unique progeny which form the major neoplastic cellular component of tumors. While CSCs constitute a small cellular subpopulation within the tumor, their resistance to chemotherapy and radiation make them an important therapeutic target for eradication. Along with distinctive phenotypic properties, CSCs possess a unique metabolic plasticity allowing them to rapidly respond and adapt to environmental changes. These cells and their progeny also display a significantly altered epigenetic state with distinctive patterns of DNA methylation. Several mechanisms of cross-talk between epigenetic and metabolic pathways in PDA exist which ultimately contribute to the observed cellular plasticity and enhanced tumorigenesis. In this review we discuss various examples of this metabolic-epigenetic interplay and how it may constitute a new avenue for therapy specifically targeting CSCs in PDA.

Indexed as

Energy MetabolismEpigenesis, GeneticGene Expression Regulation, NeoplasticAnimalsCarcinoma, Pancreatic DuctalCell PlasticityDisease SusceptibilityEpithelial-Mesenchymal TransitionHumansNeoplastic Stem CellsPancreatic NeoplasmsAcinar-ductal-metaplasiaCancer stem cellsEpigeneticsEpithelial-to-mesenchymal transitionMetabolismPancreatic cancerStemness

Identifiers

PMID30273655
PMCPMC6438777
OpenAlexW2893583276

What OpenQuestion holds

Textmetadata
LicenceTDM
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.