Evidence map›Paper›PMID 40860798›Full record

ArticleFrontiers in oncology2025

Transcriptomic analysis on pancreatic adenocarcinoma patients uncovers KRAS-mediated PPAR pathway alteration.

Giuseppe Defazio, Federico Scolari, Sara Fancelli, Simone Polvani, Daniele Lavacchi, Lucia Picariello, Alessandro Tubita, Michaela Luconi, Lorenzo Antonuzzo, Andrea Galli and 1 more

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Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Giuseppe Defazio *Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Federico Scolari *Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Sara FancelliClinical Oncology Unit, Careggi University Hospital, Florence, Italy.
Simone PolvaniDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Daniele LavacchiClinical Oncology Unit, Careggi University Hospital, Florence, Italy.
Lucia PicarielloDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Alessandro TubitaDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Michaela LuconiDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Lorenzo AntonuzzoClinical Oncology Unit, Careggi University Hospital, Florence, Italy.
Andrea Galli *Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Serena Pillozzi *Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence and mortality of pancreatic adenocarcinoma (PC) are expected to increase in the coming years, with survival rates remaining poor due to limited treatment options. KRAS mutations, present in over 70% of PC cases, drive aggressive tumor behavior through metabolic reprogramming and immune evasion; however, clinically effective inhibitors for the most common mutations are still lacking. In this study, we analyzed RNA sequencing data from TCGA datasets, comparing tumor versus normal pancreatic tissues and stratifying samples based on KRAS mutation status. Our findings reveal significant dysregulation of the peroxisome proliferator-activated receptor (PPAR) signaling pathway in PC, particularly in the context of KRAS mutations. These findings were validated through RT-qPCR in an independent cohort of primary samples. Key genes, including

Indexed as

KRAS mutationslipid metabolismmolecular profilingpancreatic cancerPPAR signaling pathwaytranscriptomic analysis

Identifiers

PMID40860798
PMCPMC12375456

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