Evidence map›Paper›PMID 35159234›Full record

ReviewCells2022

Autophagy Contributes to Metabolic Reprogramming and Therapeutic Resistance in Pancreatic Tumors.

Gabriela Reyes-Castellanos, Nadine Abdel Hadi, Alice Carrier

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.5field-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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. The impact of the PI3K/AKT/mTOR signaling pathway on trastuzumab resistance in HER2-positive gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  16. Modulating Glycolysis to Improve Cancer Therapy.International journal of molecular sciences · 2023
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  19. Mechanisms of cancer cell death induction by paclitaxel: an updated review.Apoptosis : an international journal on programmed cell death · 2022
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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

3 authors at 1 institution in 1 country.

Gabriela Reyes-CastellanosCentre de Recherche en Cancérologie de Marseille (CRCM), CNRS, INSERM, Institut Paoli-Calmettes, Aix Marseille Université, F-13009 Marseille, France.
Nadine Abdel HadiCentre de Recherche en Cancérologie de Marseille (CRCM), CNRS, INSERM, Institut Paoli-Calmettes, Aix Marseille Université, F-13009 Marseille, France.
Alice CarrierCentre de Recherche en Cancérologie de Marseille (CRCM), CNRS, INSERM, Institut Paoli-Calmettes, Aix Marseille Université, F-13009 Marseille, France.ORCID 0000-0001-6599-9642
Centre National de la Recherche Scientifique · FR

Funding

Fondation ARC pour la Recherche sur le Cancer PJA 20151203544Fondation ARC pour la Recherche sur le Cancer PJA 20181208207French National Centre for Scientific Research N/AInserm N/A
6 · The paper itself

Abstract

Metabolic reprogramming is a feature of cancers for which recent research has been particularly active, providing numerous insights into the mechanisms involved. It occurs across the entire cancer process, from development to resistance to therapies. Established tumors exhibit dependencies for metabolic pathways, constituting vulnerabilities that can be targeted in the clinic. This knowledge is of particular importance for cancers that are refractory to any therapeutic approach, such as Pancreatic Ductal Adenocarcinoma (PDAC). One of the metabolic pathways dysregulated in PDAC is autophagy, a survival process that feeds the tumor with recycled intracellular components, through both cell-autonomous (in tumor cells) and nonautonomous (from the local and distant environment) mechanisms. Autophagy is elevated in established PDAC tumors, contributing to aberrant proliferation and growth even in a nutrient-poor context. Critical elements link autophagy to PDAC including genetic alterations, mitochondrial metabolism, the tumor microenvironment (TME), and the immune system. Moreover, high autophagic activity in PDAC is markedly related to resistance to current therapies. In this context, combining autophagy inhibition with standard chemotherapy, and/or drugs targeting other vulnerabilities such as metabolic pathways or the immune response, is an ongoing clinical strategy for which there is still much to do through translational and multidisciplinary research.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAutophagyDrug Resistance, NeoplasmHumansTumor Microenvironmentautophagycancer metabolismmitochondrial metabolismpancreatic ductal adenocarcinomatherapeutic resistance

Identifiers

PMID35159234
PMCPMC8834004
OpenAlexW4210712781

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.