ArticleCancer immunology research2023
Antitumor Immune Responses in B2M-Deficient Cancers.
Article in Cancer immunology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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.
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Who cites it
36 citing papers in PubMed, 34 citations in OpenAlex.
- Cellular Neighborhoods Govern Antitumor T-cell Infiltration Following Anti-CTLA-4 in Melanoma with Primary Resistance to Anti-PD-1.Cancer discovery · 2026Trial
- Efficacy of pembrolizumab and vorinostat combination in patients with recurrent and/or metastatic squamous cell carcinomas: a phase 2 basket trial.Nature cancer · 2025Trial
- Tumor microenvironment-mediated resistance to immune checkpoint inhibitors in non-small cell lung cancer: Mechanisms, combination strategies and clinical perspectives (Review).Molecular and clinical oncology · 2026Review
- Targeting cancer-intrinsic protein neddylation bypasses the loss of JAK/STAT signaling and overcomes acquired resistance to immunotherapy.Research square · 2026Article
- A 3D pooled PBMC-organoid co-culture platform for profiling immune susceptibility and PD-1 blockade response in gastric cancer.BMC medicine · 2026Article
- Hallmarks and correlates of effective adoptive cell immunotherapy for cancer.Nature reviews. Immunology · 2026Review
- CXCL16-driven CD4Journal for immunotherapy of cancer · 2026Article
- Harnessing Inflammatory Monocytes to Overcome Resistance to Anti-PD-1 Immunotherapy.bioRxiv : the preprint server for biology · 2026Article
- Characterisation of tumor-infiltrating gamma-delta T cells in human colorectal cancer with MHC-I loss.Clinical & translational immunology · 2026Article
- Resistance mechanisms and reversal strategies of PD-1/PD-L1 inhibitors in melanoma.Frontiers in pharmacology · 2026Review
- Immunotherapy Resistance in dMMR/MSI-H Colorectal Cancer: Unraveling Mechanisms and Exploring Overcoming Strategies.Journal of immunology research · 2026Review
- Beyond the tumor microenvironment: a hierarchical immune-circuit model of immune checkpoint blockade resistance.Frontiers in oncology · 2026Review
- Loss of Ribosomal Protein L22 (RPL22) Expression Identifies a Transcriptional Subset of MLH1-Deficient Endometrial Cancers With Lower Numbers of Tumor-Associated Lymphocytes.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026Article
- A B cell-IgA-epithelial axis enhances antitumor immunity and improves outcome in HPV-associated penile squamous cell carcinoma.Nature communications · 2025Article
- Review
- CRATER tumor niches facilitate CD8Cell · 2025Article
- Ligand-receptor interaction profiling as a predictive biomarker for anti-PD-1 therapy response in melanoma.Clinical and experimental medicine · 2025Article
- From intracellular drivers to immune modulators: emerging paradigms in oncogenic pathway-directed immunotherapy optimization.Cell communication and signaling : CCS · 2025Review
- Palmitoylation modulates antitumor immunity.Molecular biology reports · 2025Review
- The Role of Immune Checkpoint Inhibitors in Cancer Therapy: Mechanism and Therapeutic Advances.MedComm · 2025Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
β2-microglobulin (B2M) is a critical component of the MHC class I molecule and is required to present tumor antigens to T cells. Its loss results in acquired resistance to immune checkpoint blockade (ICB) therapies. However, there have been well-documented cases of B2M-inactivated tumors responding to ICB, justifying investigation of how an antitumor immune response can be generated to tumors without surface MHC class I. We knocked out B2M in three murine models with varying baseline MHC class I expression and sensitivity to anti-programmed death receptor (PD-1) therapy and analyzed the immune responses. MC38 and YUMMER2.1 without B2M responded to anti-PD-1 alone or with an IL2 agonist, and this was mediated by CD4+ T cells and natural killer (NK) cells. The more aggressive B16 without B2M expression only partially responded to the IL2 agonist, and this was dependent on NK cells. When analyzing nearly 300 pretreatment biopsies from patients with melanoma receiving PD-1 blockade-based therapies, we found infrequent B2M mutations or homozygous loss but more frequent LOH or copy-number gains. B2M LOH was enriched in biopsies from patients without response to therapy, and these biopsies were more frequently infiltrated by activated NK cells. We conclude that in the absence of B2M, activation of CD4+ T cells and NK cells can mediate responses to murine models of PD-1 blockade therapy. In addition, in human melanoma, the intratumoral presence of activated NK cells upon partial B2M loss likely selects against tumor escape through low surface MHC class I expression.
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Registered trials
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.