Markers of immune activation and immunotherapy responsiveness are increased in 3D Pancreatic cancer organoids when primed with photodynamic- and chemo-therapy.

Fernanda V Cabral, Jose Quilez-Alburquerque, Madeline J Szoo, Pushpamali de Silva, Mohammad A Saad, Tayyaba Hasan

Abstract read

In one paragraph

Article in Translational oncology, 2026. 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

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

2 citing papers in PubMed.

Photodynamic Priming and Minocycline Overcome Chemoresistance by Reprogramming the Pancreatic Tumor Immune Microenvironment In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
Article
Pancreatic metastases are suppressed by photodynamic therapy and irinotecan through macrophage reprogramming in immunodeficient mice.Neoplasia (New York, N.Y.) · 2026
Article

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.

Fernanda V CabralWellman Center for Photomedicine, Massachusetts General Hospital and Harvard Medical School, 40 Blossom Street, Boston, MA, USA.

Jose Quilez-AlburquerqueWellman Center for Photomedicine, Massachusetts General Hospital and Harvard Medical School, 40 Blossom Street, Boston, MA, USA.

Madeline J SzooDepartments of Chemical Engineering and Biochemistry, Northeastern University, Boston, MA, USA.

Pushpamali de SilvaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.

Mohammad A SaadWellman Center for Photomedicine, Massachusetts General Hospital and Harvard Medical School, 40 Blossom Street, Boston, MA, USA.

Tayyaba HasanWellman Center for Photomedicine, Massachusetts General Hospital and Harvard Medical School, 40 Blossom Street, Boston, MA, USA; Division of Health Sciences and Technology, Harvard University and Massachusetts Institute of Technology, Cambridge, MA, USA. Electronic address: thasan@mgh.harvard.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains highly resistant to chemotherapy and immunotherapy due to a dense tumor stroma and an immunosuppressive tumor microenvironment. In this study, we explored whether the photodynamic priming (PDP) effect, a fallout of Photodynamic therapy (PDT), an approved treatment, could improve the treatment responses in 3D mouse-derived organoids. The organoids reproduced key features of pancreatic tumors and showed strong resistance to chemotherapy (nanoliposomal irinotecan, nal-IRI) and immune checkpoint inhibitor (anti-PD-1) when used alone. PDP overcame this resistance by enhancing the uptake and activation of nal-IRI, thereby increasing tumor cell death. PDP also triggered immunogenic cell death, marked by the release of danger signals that promote immune activation. When organoids were co-cultured with autologous peripheral blood mononuclear cells (PBMCs), PDP enhanced immune-mediated tumor killing. Notably, combining PDP with low doses of chemotherapy and PD-1 blockade resulted in complete tumor eradication. These effects were associated with increased immune activation and improved responsiveness to immunotherapy. Together, these findings show that PDP remodels the pancreatic tumor microenvironment, enhances chemotherapy efficacy, and sensitizes tumors to immune checkpoint inhibitors. This strategy uses clinically approved agents and offers a promising, translatable approach to overcoming treatment resistance in pancreatic cancer.

Indexed as

Immune checkpoint blockadeImmunogenic cell deathNanoliposomal irinotecanPancreatic ductal adenocarcinomaPhotodynamic primingTumor organoids

Identifiers

PMID41762540

DOI10.1016/j.tranon.2026.102716

PMCPMC12954193

What OpenQuestion holds

Textmetadata

LicenceCC BY-NC

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.