Evidence map›Paper›PMID 36399952›Full record

ReviewESMO open2022

Are targeted therapies or immunotherapies effective in metastatic pancreatic adenocarcinoma?

M S Rémond, A Pellat, C Brezault, M Dhooge, R Coriat

Open access · goldAbstract readReview
In one paragraph

Review in ESMO open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Chemotherapy-associated mutational process signature and genomic alterations associated with outcome in metastatic pancreatic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  4. Review
  5. Review
  6. Observational
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Recent advances in drug delivery and targeting for the treatment of pancreatic cancer.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Review
  13. Article
  14. Genes · 2023
    Article
  15. Review
  16. Review
  17. Article
  18. The Landscape and Therapeutic Targeting ofCurrent issues in molecular biology · 2023
    Review
  19. Review
  20. Crosstalk of nervous and immune systems in pancreatic cancer.Frontiers in cell and developmental biology · 2023
    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

5 authors at 1 institution in 1 country.

M S RémondDepartment of Gastroenterology, Cochin Hospital, Université de Paris, Assistance Publique-Hôpitaux de Paris, Paris, France. Electronic address: maxime.remond@aphp.fr.
A PellatDepartment of Gastroenterology, Cochin Hospital, Université de Paris, Assistance Publique-Hôpitaux de Paris, Paris, France.
C BrezaultDepartment of Gastroenterology, Cochin Hospital, Université de Paris, Assistance Publique-Hôpitaux de Paris, Paris, France.
M DhoogeDepartment of Gastroenterology, Cochin Hospital, Université de Paris, Assistance Publique-Hôpitaux de Paris, Paris, France.
R CoriatDepartment of Gastroenterology, Cochin Hospital, Université de Paris, Assistance Publique-Hôpitaux de Paris, Paris, France.
Hôpital Cochin · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastatic pancreatic ductal adenocarcinoma (PDAC) is a major health burden due to its increasing incidence and poor prognosis. PDAC is characterized by a low tumor mutational burden, and its molecular pathogenesis is driven by Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations. Response to DNA damage through homologous repair is defective in 15% of tumors. Chemotherapy using FOLFIRINOX (folinic acid, fluorouracil, irinotecan, oxaliplatin) or gemcitabine-nab-paclitaxel significantly improves life expectancy, but the median overall survival remains <1 year. Targeted therapies are not efficient in the overall population of patients with metastatic PDAC. Improvements in overall survival or progression-free survival, however, have been demonstrated in subgroups carrying certain mutations. Maintenance therapy with poly-ADP-ribose polymerase (PARP) inhibitors increases progression-free survival in patients with germline mutations in BRCA1/2. Sotorasib shows signs of efficacy against tumors carrying the KRAS G12C mutation, and targeted therapies may also benefit patients with KRAS-wild-type PDAC. Combining targeted therapies with chemotherapy holds promise because of potential synergistic effects. These associations, however, have not yet demonstrated clinical benefit. Checkpoint inhibitors are not effective against metastatic PDAC. Combined immunotherapies attempt to restore their efficacy but have not succeeded yet. Other immunotherapies are emerging such as therapeutic vaccines or chimeric antigen receptor (CAR) T cells, but these strategies remain to be evaluated in large trials. In the future, treatment personalization based on tumor-derived organoids could potentially further improve treatment efficiency.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalPancreatic NeoplasmsAntineoplastic Combined Chemotherapy ProtocolsHumansImmunotherapyNeoplasm MetastasisProto-Oncogene Proteins p21(ras)Proto-Oncogene Proteins p21(ras)immunotherapypancreatic adenocarcinomaprecision oncologytargeted therapies

Identifiers

PMID36399952
PMCPMC9674888
OpenAlexW4309341723

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.