Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma

Abstract Merkel cell carcinoma (MCC) is a rare and aggressive neuroendocrine skin cancer that is responsive to immune checkpoint inhibitors (ICI). On rare occasion, MCC spontaneously regresses. It is speculated that this regression occurs when biopsy-induced antigen shedding precipitates an immune r...

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Main Authors: Patrick Hallaert, John W. Roman, Mairead Baker, Natasha T. Hill, Jennifer L. Marte, James L. Gulley, Nicholas Logemann, Courtney W. Hudgens, Alexandre Reuben, Isaac Brownell
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:npj Precision Oncology
Online Access:https://doi.org/10.1038/s41698-025-00987-6
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author Patrick Hallaert
John W. Roman
Mairead Baker
Natasha T. Hill
Jennifer L. Marte
James L. Gulley
Nicholas Logemann
Courtney W. Hudgens
Alexandre Reuben
Isaac Brownell
author_facet Patrick Hallaert
John W. Roman
Mairead Baker
Natasha T. Hill
Jennifer L. Marte
James L. Gulley
Nicholas Logemann
Courtney W. Hudgens
Alexandre Reuben
Isaac Brownell
author_sort Patrick Hallaert
collection DOAJ
description Abstract Merkel cell carcinoma (MCC) is a rare and aggressive neuroendocrine skin cancer that is responsive to immune checkpoint inhibitors (ICI). On rare occasion, MCC spontaneously regresses. It is speculated that this regression occurs when biopsy-induced antigen shedding precipitates an immune response. Here, we demonstrate the activation of an adaptive immune response in a patient whose tumor underwent spontaneous regression after biopsy. To evaluate the tumor immune microenvironment during regression, we performed quantitative immunohistochemical analysis and T-cell receptor (TCR) sequencing. Relative to baseline, the regressing tumor showed evidence of an activated cytotoxic T-cell response together with increased TCR clonality, greater representation of dominant T-cell clones, and the emergence of novel high-frequency T-cell clones. Similar changes in TCR profiles were observed in an MCC tumor undergoing ICI-induced regression. Taken together, our results provide evidence that the expansion of novel and pre-existing adaptive immune responses drives spontaneous MCC regression.
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series npj Precision Oncology
spelling doaj-art-66db3296771c4c5dab8a49dab63fb55c2025-08-20T03:03:20ZengNature Portfolionpj Precision Oncology2397-768X2025-07-01911610.1038/s41698-025-00987-6Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinomaPatrick Hallaert0John W. Roman1Mairead Baker2Natasha T. Hill3Jennifer L. Marte4James L. Gulley5Nicholas Logemann6Courtney W. Hudgens7Alexandre Reuben8Isaac Brownell9Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH)Department of Dermatology, Naval Medical Center Portsmouth (NMCP)Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH)Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH)Center for Immuno-Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH)Center for Immuno-Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH)Department of Dermatology, Walter Reed National Military Medical Center (WRNMMC)Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer CenterDepartment of Thoracic/Head & Neck Medical Oncology, The University of Texas MD Anderson Cancer CenterDermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH)Abstract Merkel cell carcinoma (MCC) is a rare and aggressive neuroendocrine skin cancer that is responsive to immune checkpoint inhibitors (ICI). On rare occasion, MCC spontaneously regresses. It is speculated that this regression occurs when biopsy-induced antigen shedding precipitates an immune response. Here, we demonstrate the activation of an adaptive immune response in a patient whose tumor underwent spontaneous regression after biopsy. To evaluate the tumor immune microenvironment during regression, we performed quantitative immunohistochemical analysis and T-cell receptor (TCR) sequencing. Relative to baseline, the regressing tumor showed evidence of an activated cytotoxic T-cell response together with increased TCR clonality, greater representation of dominant T-cell clones, and the emergence of novel high-frequency T-cell clones. Similar changes in TCR profiles were observed in an MCC tumor undergoing ICI-induced regression. Taken together, our results provide evidence that the expansion of novel and pre-existing adaptive immune responses drives spontaneous MCC regression.https://doi.org/10.1038/s41698-025-00987-6
spellingShingle Patrick Hallaert
John W. Roman
Mairead Baker
Natasha T. Hill
Jennifer L. Marte
James L. Gulley
Nicholas Logemann
Courtney W. Hudgens
Alexandre Reuben
Isaac Brownell
Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma
npj Precision Oncology
title Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma
title_full Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma
title_fullStr Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma
title_full_unstemmed Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma
title_short Spontaneous tumor regression and immunotherapy response demonstrate clonal T-cell expansion in Merkel cell carcinoma
title_sort spontaneous tumor regression and immunotherapy response demonstrate clonal t cell expansion in merkel cell carcinoma
url https://doi.org/10.1038/s41698-025-00987-6
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