Evidence map›Paper›PMID 42742095›Full record

ArticleFEBS open bio2026

Type I interferons modulate autophagy to shape gemcitabine response in pancreatic cancer cells.

Lucy E Bonilla, Martín M Ledesma, Santiago A Behr, Matías A Pibuel, María L Palanek, Daniel H Grasso, Maria N Garcia, Juan Garona, Silvina L Lompardía, Elida Álvarez and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS open bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Lucy E BonillaCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Martín M LedesmaUnidad de Conocimiento Traslacional, Hospital de Alta Complejidad del Bicentenario Esteban Echeverría, Buenos Aires, Argentina.
Santiago A BehrCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Matías A PibuelCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
María L PalanekUnidad de Conocimiento Traslacional, Hospital de Alta Complejidad del Bicentenario Esteban Echeverría, Buenos Aires, Argentina.
Daniel H GrassoInstituto de Estudios de la Inmunidad Humoral (IDEHU), UBA - CONICET, Buenos Aires, Argentina.
Maria N GarciaCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Juan GaronaCentro de Medicina Traslacional (CEMET), Unidad de Investigaciones Biomédicas en Cáncer (IBioCAN, Unidad N°6), Hospital de Alta Complejidad en Red El Cruce "Dr. Néstor Carlos Kirchner" S.A.M.I.C. Florencio Varela, Buenos Aires, Argentina.
Silvina L LompardíaCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Elida ÁlvarezCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Daniela L PapademetrioCátedra de Inmunología, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.ORCID https://orcid.org/0000-0002-3419-5614

Funding

National Agency for Science and Technology Promotion PICT-2019-00736National Agency for Science and Technology Promotion PICT-2021-0051National Agency for Science and Technology Promotion PICTO-2021-0018Secretaría de Ciencia y Técnica, Universidad de Buenos Aires 20020220400220BA
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by poor prognosis and limited response to gemcitabine, the standard first-line chemotherapy. One major contributor to chemoresistance is autophagy, a process frequently upregulated in PDAC. In this study, we examined the ability of type I interferons (IFNα2b and IFNβ1a) to modulate autophagy and disturb tumor cell resistance to gemcitabine. PDAC cells were treated with increasing concentrations of IFNα2b or IFNβ1a, and cell proliferation was assessed by [

Indexed as

autophagychemoresistancegemcitabineIFNα2bIFNβ1apancreatic cancer

Identifiers

PMID42742095
PMCPMC13576371

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.