MYC Amplification in Metastatic Prostate Cancer Associated with Reduced Tumor Immunogenicity
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March 11, 2026“MYC amplification is associated with reduced tumor immunogenicity as assessed by the recovery of IR recombination reads from prostate cancer genomics files.”
BUFFALO, NY — March 11, 2026 — A new research paper was published in Volume 13 of Oncoscience on February 7, 2026, titled “Reduced immunogenicity of MYC amplified, metastatic prostate cancer.”
Led by Sunny Kahlon of the Department of Molecular Medicine, Morsani College of Medicine, University of South Florida — with corresponding author George Blanck (also affiliated with the Department of Immunology, H. Lee Moffitt Cancer Center and Research Institute) — the study uses a genomics-based approach to test whether MYC copy-number amplification in prostate tumors is linked to clinical outcomes and to tumor immunogenicity as inferred from adaptive immune receptor (IR) recombination reads recovered from sequencing files.
Using TCGA-PRAD and multiple metastatic prostate cancer datasets (including WCDT-MCRPC and CMI-MPC), the authors quantified MYC copy numbers and then measured recovery of adaptive IR recombination reads (IGH, IGK, IGL for B cells; TRA, TRB, TRG, TRD for T cells) from tumor RNAseq and whole-genome sequence files. They found that MYC amplification was more frequent in metastatic disease and associated with worse progression-free survival. Importantly, MYC-amplified metastatic tumors yielded significantly fewer recovered adaptive IR recombination reads and showed reduced expression of immune-marker gene sets, consistent with reduced tumor immunogenicity — with the reduction most pronounced for B-cell–related reads.
“The above findings reveal a correlation of increased MYC amplification with metastatic stages of prostate cancer. And, the MYC amplification is associated with poorer PFS outcomes and reduced immunogenicity, particularly in the MYC-amplified metastatic tumors.”
The authors stress that these results derive from computational mining of existing genomics files and that confirmatory immune-repertoire measurements (for example, PCR-based assays) and prospective clinical sampling will strengthen the conclusions. Nevertheless, the pattern reported — MYC amplification linked to both aggressive disease and a quantitatively reduced adaptive immune footprint — suggests that MYC status could be an important biomarker for prognosis and for predicting which metastatic prostate cancers are unlikely to respond to immune checkpoint blockade alone. The authors propose that strategies to restore T-cell (or B-cell) infiltration or function might re-sensitize MYC-amplified tumors to immunotherapy.
DOI: https://doi.org/10.18632/oncoscience.644
Correspondence to: George Blanck – gblanck@usf.edu
Keywords: cancer, prostate cancer, MYC amplification, adaptive immune receptor recombinations, reduced immunogenicity, RNAseq files
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