Evidence map›Paper›PMID 24605027›Full record

ReviewWorld journal of gastroenterology2014

Role of abnormal lipid metabolism in development, progression, diagnosis and therapy of pancreatic cancer.

Julian Swierczynski, Areta Hebanowska, Tomasz Sledzinski

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

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

116 citing papers in PubMed, 194 citations in OpenAlex.

  1. Review
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  4. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
    Review
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  17. The role of tumor-associated macrophages in tumor immune evasion.Journal of cancer research and clinical oncology · 2024
    Review
  18. Review
  19. Article
  20. Review

56 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

3 authors at 1 institution in 1 country.

Julian SwierczynskiJulian Swierczynski, Areta Hebanowska, Department of Biochemistry, Medical University of Gdansk, 80-211 Gdansk, Poland.
Areta HebanowskaJulian Swierczynski, Areta Hebanowska, Department of Biochemistry, Medical University of Gdansk, 80-211 Gdansk, Poland.
Tomasz SledzinskiJulian Swierczynski, Areta Hebanowska, Department of Biochemistry, Medical University of Gdansk, 80-211 Gdansk, Poland.
Gdańsk Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is growing evidence that metabolic alterations play an important role in cancer development and progression. The metabolism of cancer cells is reprogrammed in order to support their rapid proliferation. Elevated fatty acid synthesis is one of the most important aberrations of cancer cell metabolism. An enhancement of fatty acids synthesis is required both for carcinogenesis and cancer cell survival, as inhibition of key lipogenic enzymes slows down the growth of tumor cells and impairs their survival. Based on the data that serum fatty acid synthase (FASN), also known as oncoantigen 519, is elevated in patients with certain types of cancer, its serum level was proposed as a marker of neoplasia. This review aims to demonstrate the changes in lipid metabolism and other metabolic processes associated with lipid metabolism in pancreatic ductal adenocarcinoma (PDAC), the most common pancreatic neoplasm, characterized by high mortality. We also addressed the influence of some oncogenic factors and tumor suppressors on pancreatic cancer cell metabolism. Additionally the review discusses the potential role of elevated lipid synthesis in diagnosis and treatment of pancreatic cancer. In particular, FASN is a viable candidate for indicator of pathologic state, marker of neoplasia, as well as, pharmacological treatment target in pancreatic cancer. Recent research showed that, in addition to lipogenesis, certain cancer cells can use fatty acids from circulation, derived from diet (chylomicrons), synthesized in liver, or released from adipose tissue for their growth. Thus, the interactions between de novo lipogenesis and uptake of fatty acids from circulation by PDAC cells require further investigation.

Indexed as

Energy MetabolismLipogenesisAnimalsAntineoplastic AgentsBiomarkers, TumorCarcinoma, Pancreatic DuctalDisease ProgressionFatty AcidsFatty Acid Synthase, Type IHumansPancreatic NeoplasmsPredictive Value of TestsTreatment OutcomeAntineoplastic AgentsBiomarkers, TumorFASN protein, humanFatty AcidsFatty Acid Synthase, Type ICyclooxygenase-2FarnesylationFatty acid synthaseHypoxia inducible factor 1αLipid metabolismLipogenic enzymes inhibitorsMonounsaturated fatty acidsOncogenesPancreatic cancerTumor suppressors

Identifiers

PMID24605027
PMCPMC3942833
OpenAlexW2021183081

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.