Evidence map›Paper›PMID 31225458›Full record

ReviewCell stress2018

The role of metabolic adaptation to nutrient stress in pancreatic cancer.

Abhishek Derle, Maria Chiara De Santis, Luca Gozzelino, Edoardo Ratto, Miriam Martini

Open access · goldAbstract readReview
In one paragraph

Review in Cell stress, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  18. Frontiers in bioengineering and biotechnology · 2019
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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

5 authors at 1 institution in 1 country.

Abhishek DerleDepartment of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
Maria Chiara De SantisDepartment of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
Luca GozzelinoDepartment of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
Edoardo RattoDepartment of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
Miriam MartiniDepartment of Molecular Biotechnology and Health Science, Molecular Biotechnology Center, University of Torino, Torino, Italy.
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is the fourth most common cause of cancer-related mortality, with a dismal prognosis that has changed little over the past few decades. Despite extensive efforts in understanding the oncogenetics of this pathology, pancreatic cancer remained largely elusive. One of the main characteristics of pancreatic cancer is the reduced level of oxygen and nutrient perfusion, caused by the new matrix formation, through the activation of stromal cells (desmoplasia). This stromal reaction leads to metabolic adaptations in surviving tumor cells in order to cope with these challenging conditions. The oncogenic signaling driven by KRAS mutation is necessary to fuel pancreatic tumors by activating key metabolic processes, including enhanced glycolysis and glutamine consumption. Here we review our current understanding of the pancreatic cancer metabolism as well as discuss recent work pointing to the importance of various metabolic strategies as well as autophagy and macropinocytosis as critical nutrient supply pathways. The elucidation of these metabolic networks may highlight new opportunities to further develop novel therapeutic strategies.

Indexed as

autophagymacropinocytosismetabolic rewiringnutrient stresspancreatic cancer

Identifiers

PMID31225458
PMCPMC6551672
OpenAlexW2902817611

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.