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Neoantigen-Targeted Cell Therapy

The strategy of targeting tumor-specific mutations (neoantigens) with engineered T cells — the leading approach for bringing cell therapy to solid epithelial cancers. Championed by Steven Rosenberg (NCI) at Session V.

The Problem

  • Solid epithelial cancers cause ~90% of cancer deaths
  • No antibody recognizes a surface molecule unique to a major solid epithelial cancer (despite 50+ years of monoclonal antibodies)
  • Targeting shared antigens → fatal on-target/off-tumor toxicity
  • Whole TIL (as grown for melanoma) did not work in epithelial cancers

The Approach

  1. Whole-exome and transcriptome sequencing identifies every mutation (~200 in epithelial cancers)
  2. Mutated 25-mer peptides loaded onto patient’s APCs and screened against expanded TIL
  3. ~1 in 70 mutated neoepitopes is genuinely immunogenic
  4. ~75% of patients have TIL recognizing at least one neoantigen
  5. Almost every neoantigen is unique to the individual patient

Three Strategies

StrategyMethodStatus
Selected TILIsolate only neoantigen-reactive TIL subsetNature Medicine 2025
TCR transductionClone reactive TCR, transduce into patient’s normal lymphocytesNature Medicine 2024
Shared-mutation TCRsLibraries against KRAS and p53 hotspot mutationsMost exciting current work

Key Data

  • Selected TIL in chemorefractory pancreatic/colorectal/cholangiocarcinoma: ~24% RECIST response rate (median 4 prior regimens)
  • Proof-of-principle patient (2014): cholangiocarcinoma, disease-free 12 years
  • KRAS G12V–targeted TCR: pancreatic cancer regression
  • p53 R175H–targeted TCR: colorectal liver/lung mets shrinking
  • Visceral disease responds — lung, liver, bone metastases

Why KRAS and p53 Are the Unlock

  • KRAS hotspot mutations in ~30% of all cancers
  • p53 hotspot mutations in ~50% of all cancers
  • Converts a hyper-personalized therapy into a partially shared one — the prerequisite for scaling

Cross-References