Evidence map›Paper›PMID 32219902›Full record

ReviewMolecular carcinogenesis2020

Polyomavirus-driven Merkel cell carcinoma: Prospects for therapeutic vaccine development.

Shira Tabachnick-Cherny, Thomas Pulliam, Candice Church, David M Koelle, Paul Nghiem

Abstract readReview
In one paragraph

Review in Molecular carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

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  10. Insights into anti-tumor immunityFrontiers in immunology · 2023
    Review
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  13. Article
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  15. CD8Nature reviews. Immunology · 2022
    Review
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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

5 authors.

Shira Tabachnick-ChernyDepartment of Medicine, Division of Dermatology, University of Washington, Seattle, Washington.ORCID 0000-0003-1595-4619
Thomas PulliamDepartment of Medicine, Division of Dermatology, University of Washington, Seattle, Washington.ORCID 0000-0003-3511-6348
Candice ChurchDepartment of Medicine, Division of Dermatology, University of Washington, Seattle, Washington.ORCID 0000-0003-1582-8292
David M KoelleDepartment of Medicine, Division of Allergy and Infectious Diseases, University of Washington, Seattle, Washington.ORCID 0000-0003-1255-9023
Paul NghiemDepartment of Medicine, Division of Dermatology, University of Washington, Seattle, Washington.ORCID 0000-0003-2784-963X

Funding

Understand & overcome resistance to PD-1P01CA225517 · NCI · UNIVERSITY OF WASHINGTON · PI Cecilia C Yeung · 2019 to 2026
$22.7M
Interdisciplinary Tranining in Cancer ResearchT32CA080416 · NCI · UNIVERSITY OF WASHINGTON · PI STODDARD, BARRY L. · 1998 to 2023
$9.7M
Mechanisms of UV-Induced DNA Damage Responses and Carcinogenesis in SkinR01AR067722 · NIAMS · UNIVERSITY OF WASHINGTON · PI NGHIEM, PAUL · 2015 to 2020
$2.0M
NCI NIH HHS P01 CA225517NCI NIH HHS T32 CA080416NIAMS NIH HHS R01 AR067722
6 · The paper itself

Abstract

Great strides have been made in cancer immunotherapy including the breakthrough successes of anti-PD-(L)1 checkpoint inhibitors. In Merkel cell carcinoma (MCC), a rare and aggressive skin cancer, PD-(L)1 blockade is highly effective. Yet, ~50% of patients either do not respond to therapy or develop PD-(L)1 refractory disease and, thus, do not experience long-term benefit. For these patients, additional or combination therapies are needed to augment immune responses that target and eliminate cancer cells. Therapeutic vaccines targeting tumor-associated antigens, mutated self-antigens, or immunogenic viral oncoproteins are currently being developed to augment T-cell responses. Approximately 80% of MCC cases in the United States are driven by the ongoing expression of viral T-antigen (T-Ag) oncoproteins from genomically integrated Merkel cell polyomavirus (MCPyV). Since T-Ag elicits specific B- and T-cell immune responses in most persons with virus-positive MCC (VP-MCC), and ongoing T-Ag expression is required to drive VP-MCC cell proliferation, therapeutic vaccination with T-Ag is a rational potential component of immunotherapy. Failure of the endogenous T-cell response to clear VP-MCC (allowing clinically evident tumors to arise) implies that therapeutic vaccination will need to be potent anśd synergize with other mechanisms to enhance T-cell activity against tumor cells. Here, we review the relevant underlying biology of VP-MCC, potentially applicable therapeutic vaccine platforms, and antigen delivery formats. We also describe early successes in the field of therapeutic cancer vaccines and address several clinical scenarios in which VP-MCC patients could potentially benefit from a therapeutic vaccine.

Indexed as

AnimalsAntigens, Viral, TumorCarcinoma, Merkel CellHumansImmunotherapyMerkel cell polyomavirusSkin NeoplasmsT-LymphocytesVaccinesAntigens, Viral, TumorVaccinescancer therapeutic vaccineimmunotherapyMCPyVMerkel cell carcinoma

Identifiers

PMID32219902
PMCPMC8238237

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Registered trials

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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.