Evidence map›Paper›PMID 29702208›Full record

ReviewBiochimica et biophysica acta. Reviews on cancer2018

The plasticity of pancreatic cancer metabolism in tumor progression and therapeutic resistance.

Douglas E Biancur, Alec C Kimmelman

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Reviews on cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 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. Article
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  10. Circular RNAs: key regulators in cancer stem cell dynamics.Molecular genetics and genomics : MGG · 2026
    Review
  11. Article
  12. Molecular Imaging: Unveiling Metabolic Abnormalities in Pancreatic Cancer.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Article
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25 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Douglas E BiancurPerlmutter Cancer Center, Department of Radiation Oncology, NYU Medical School, New York 10016, NY, United States.
Alec C KimmelmanPerlmutter Cancer Center, Department of Radiation Oncology, NYU Medical School, New York 10016, NY, United States. Electronic address: Alec.Kimmelman@nyumc.org.
NYU Langone Health · US

Funding

The RAS and P13K Pathways in Pancreatic AdenocarcinomaP01CA117969 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2006 to 2025
$41.7M
Network organization of the human autophagy systemR01GM095567 · NIGMS · HARVARD MEDICAL SCHOOL · PI HARPER, JEFFREY W, KIMMELMAN, ALEC · 2011 to 2018
$3.0M
Investigating the Role of Autophagy in Pancreatic Cancer Radiation ResistanceR01CA157490 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KIMMELMAN, ALEC · 2011 to 2018
$2.5M
Investigating a Novel Glutamine Metabolism Pathway in Pancreatic CancerR01CA188048 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KIMMELMAN, ALEC · 2015 to 2018
$1.5M
NCI NIH HHS P01 CA117969NCI NIH HHS R01 CA157490NCI NIH HHS R01 CA188048NIGMS NIH HHS R01 GM095567
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDA) is an aggressive cancer that is highly refractory to the current standards of care. The difficulty in treating this disease is due to a number of different factors, including altered metabolism. In PDA, the metabolic rewiring favors anabolic reactions which supply the cancer cell with necessary cellular building blocks for unconstrained growth. Furthermore, PDA cells display high levels of basal autophagy and macropinocytosis. KRAS is the driving oncogene in PDA and many of the metabolic changes are downstream of its activation. Together, these unique pathways for nutrient utilization and acquisition result in metabolic plasticity enabling cells to rapidly adapt to nutrient and oxygen fluctuations. This remarkable adaptability has been implicated as a cause of the intense therapeutic resistance. In this review, we discuss metabolic pathways in PDA tumors and highlight how they contribute to the pathogenesis and treatment of the disease.

Indexed as

AutophagyCarcinoma, Pancreatic DuctalCell HypoxiaDisease ProgressionHumansNutrientsPancreatic NeoplasmsReactive Oxygen SpeciesNutrientsReactive Oxygen SpeciesAutophagyMacropinocytosisMetabolismMicroenvironmentPancreatic cancer

Identifiers

PMID29702208
PMCPMC6345383
OpenAlexW2801197016

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.