Evidence map›Paper›PMID 33804240›Full record

ReviewMolecules (Basel, Switzerland)2021

The Glycolytic Pathway as a Target for Novel Onco-Immunology Therapies in Pancreatic Cancer.

Claudia Curcio, Silvia Brugiapaglia, Sara Bulfamante, Laura Follia, Paola Cappello, Francesco Novelli

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Sperm meet the elevated energy demands to attain fertilization competence by increasing flux through aldolase.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  12. Modulating Glycolysis to Improve Cancer Therapy.International journal of molecular sciences · 2023
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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

6 authors at 2 institutions in 1 country.

Claudia CurcioDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0001-5306-4399
Silvia BrugiapagliaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Sara BulfamanteDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Laura FolliaDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0003-1580-0505
Paola CappelloDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.ORCID 0000-0002-5321-7794
Francesco NovelliDepartment of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy.
Azienda Ospedaliera Citta' della Salute e della Scienza di Torino · ITUniversity of Turin · IT

Funding

Associazione Italiana per la Ricerca sul Cancro 12182Associazione Italiana per la Ricerca sul Cancro 19931Bando CRT Città della Salute e della Scienza di Torino 2019.1887Fondazione Nadia Valsecchi 2020Fondazione Nastro Viola 2020Fondazione Ricerca Molinette Onlus Associazione Ursula e Giorgio CytronFondazione Ricerca Molinette Onlus Fundus CD38University of Turin Progetti Ateneo 2014 Compagnia di San Paolo PANTHERUniversity of Turin Progetti Ateneo 2014 Compagnia di San Paolo PC-METAIMMUN-OTHER
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal forms of human cancer, characterized by unrestrained progression, invasiveness and treatment resistance. To date, there are limited curative options, with surgical resection as the only effective strategy, hence the urgent need to discover novel therapies. A platform of onco-immunology targets is represented by molecules that play a role in the reprogrammed cellular metabolism as one hallmark of cancer. Due to the hypoxic tumor microenvironment (TME), PDA cells display an altered glucose metabolism-resulting in its increased uptake-and a higher glycolytic rate, which leads to lactate accumulation and them acting as fuel for cancer cells. The consequent acidification of the TME results in immunosuppression, which impairs the antitumor immunity. This review analyzes the genetic background and the emerging glycolytic enzymes that are involved in tumor progression, development and metastasis, and how this represents feasible therapeutic targets to counteract PDA. In particular, as the overexpressed or mutated glycolytic enzymes stimulate both humoral and cellular immune responses, we will discuss their possible exploitation as immunological targets in anti-PDA therapeutic strategies.

Indexed as

AnimalsGlycolysisHumansImmunityImmunotherapy, AdoptivePancreatic NeoplasmsSignal TransductionTumor Microenvironmentglycolysisimmunotherapiespancreatic cancer

Identifiers

PMID33804240
PMCPMC7998946
OpenAlexW3137936827

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.