Evidence map›Paper›PMID 30221051›Full record

ArticleOncoimmunology

Oncolytic vaccines increase the response to PD-L1 blockade in immunogenic and poorly immunogenic tumors.

S Feola, C Capasso, M Fusciello, B Martins, S Tähtinen, M Medeot, S Carpi, F Frascaro, E Ylosmäki, K Peltonen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Multifactoral immune modulation potentiates durable remission in multiple models of aggressive malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

12 authors at 5 institutions in 2 countries.

S FeolaDipartimento di medicina Molecolare e Biotecnologie Mediche, Universitá di Napoli Federico II, Via Pansini 5, Naples, Italy.
C CapassoLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.
M FuscielloLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.
B MartinsLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.
S TähtinenLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.
M MedeotDepartment of pharmaceutical and pharmacological sciences, University of Padova, Via F. Marzolo 5, Padova, Italy.
S CarpiDepartment of Pharmacy, University of Pisa, Lungarno Antonio Pacinotti, Pisa, Italy.
F FrascaroUniversity of Siena, via Aldo Moro 2, Siena, Italy.
E YlosmäkiLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.
K PeltonenLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.ORCID 0000-0002-3063-451X
L PastoreDipartimento di medicina Molecolare e Biotecnologie Mediche, Universitá di Napoli Federico II, Via Pansini 5, Naples, Italy.
V CerulloLaboratory of Immunovirotherapy, Drug Research Doctoral Program, University of Helsinki, Helsinki, Finland.ORCID 0000-0003-4901-3796
University of Helsinki · FIUniversity of Naples Federico II · ITUniversity of Padua · ITUniversity of Pisa · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of immune checkpoint pathways and limited T- cell infiltration result in immunological escape of tumors. Although immune checkpoint inhibitors are currently approved for several types of cancers, the response rate is often limited by the lack of tumor specific T-cells within the malignant tissue. Therefore, new combinatorial strategies are needed to enhance the clinical benefit of immune checkpoint inhibitors. We have previously developed PeptiCRAd, an oncolytic vaccine platform capable of directing the immune response toward tumor epitopes. In this study, we evaluated whether the platform could be used to increase the response rate to checkpoint inhibitors in both highly immunogenic and poorly immunogenic tumors, such as melanoma and triple negative breast cancer (TNBC). We report here that anti-PD-L1 therapy in combination with PeptiCRAd significantly reduced the growth of melanomas and increased the response rate to checkpoint inhibition. In fact, we registered a higher rate of complete responses among mice treated with the combination. This approach promoted the presence of non-exhausted antigen-specific T-cells within the tumor in comparison to anti-PD-L1 monotherapy. Furthermore, we found that targeting both MHC-I and II restricted tumor epitopes was necessary to decrease the growth of the poorly immunogenic TNBC model 4T1 and that combination with PD-L1 blockade increased the number of responders to checkpoint inhibition. Finally, the described strategy was validated in a translational

Indexed as

breast cancercancer epitopescancer vaccinescheckpoint inhibitorsimmunotherapymelanomaoncolytic vaccinesoncolytic virusestherapeutic antibodiestherapeutic vaccination

Identifiers

PMID30221051
PMCPMC6136871
OpenAlexW2796425825

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.