Evidence map›Paper›PMID 39902502›Full record

ArticleMolecular oncology2025

Stroma gene signature predicts responsiveness to chemotherapy in pancreatic ductal adenocarcinoma patient-derived xenograft models.

Alessia Anastasia, Laura Formenti, Paola Ostano, Lucia Minoli, Andrea Resovi, Lavinia Morosi, Claudia Fioravanti, Edoardo Micotti, Cristina Matteo, Eugenio Scanziani and 4 more

Abstract read
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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

3 citing papers in PubMed.

  1. Review
  2. KRAS-mediated CCDC6 degradation drives xCT upregulation and ferroptosis evasion.Apoptosis : an international journal on programmed cell death · 2026
    Article
  3. Review
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

14 authors.

Alessia AnastasiaDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Laura FormentiDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Paola OstanoLab of Cancer Genomics, Fondazione "Edo ed Elvo Tempia", Biella, Italy.
Lucia MinoliDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Andrea ResoviDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Lavinia MorosiDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Claudia FioravantiDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Edoardo MicottiDepartment of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
Cristina MatteoDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Eugenio ScanzianiMouse and Animal Pathology Laboratory (MAPLab), Fondazione Unimi, Milan, Italy.
Giovanna ChiorinoLab of Cancer Genomics, Fondazione "Edo ed Elvo Tempia", Biella, Italy.
Raffaella GiavazziDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.
Carmen GhilardiDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.ORCID https://orcid.org/0000-0002-3036-8557
Dorina BelottiDepartment of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo and Milan, Italy.ORCID https://orcid.org/0000-0002-3868-9144

Funding

Associazione Italiana per la Ricerca sul Cancro 23443Associazione Italiana per la Ricerca sul Cancro 23520Italian Ministry of University and Research (MUR) under PNRR M4C2I1.3 Heal Italia PE00000019 CUP B43D22000710006
6 · The paper itself

Abstract

Despite many efforts to understand the molecular mechanisms of pancreatic ductal adenocarcinoma (PDAC) treatment resistance, there is still no reliable method for selecting patients who could benefit from standard pharmacological treatment. Here, four PDAC patient-derived xenografts (PDAC-PDXs) with different responses to gemcitabine plus nab-paclitaxel (nanoparticle albumin-bound paclitaxel) were studied to dissect the contribution of both tumor and host microenvironment to treatment response. PDAC-PDXs transplanted into the pancreas of immunodeficient mice retained the main genetic and histopathological characteristics of the original human tumors, including invasiveness and desmoplastic reaction. Response to chemotherapy was associated with a specific 294 stroma gene signature and was not due to the intrinsic responsiveness of tumor cells or differences in drug delivery. Human dataset analysis validated the expression of the 294 stroma gene signature in PDAC clinical samples, confirming PDAC-PDXs as a useful tool to study the biology of tumor-host interactions and to test drug efficacy. In summary, we identified a stroma gene signature that differentiates PDAC-PDXs that are responsive to gemcitabine plus Nab-paclitaxel treatment from those that are not, confirming the active role of the tumor microenvironment in the drug response.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsStromal CellsTranscriptomeAlbuminsAnimalsDeoxycytidineFemaleGemcitabineGene Expression Regulation, NeoplasticHumansMaleMicePaclitaxelTumor MicroenvironmentXenograft Model Antitumor Assays130-nm albumin-bound paclitaxelAlbuminsDeoxycytidineGemcitabinePaclitaxelpancreatic cancerpatient‐derived xenograftsstroma signaturetreatment response

Identifiers

PMID39902502
PMCPMC11977644

What Socratic 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 Socratic graph.