Engineered T cells for pancreatic cancer treatment

HPB (Oxford). 2011 Sep;13(9):643-50. doi: 10.1111/j.1477-2574.2011.00344.x. Epub 2011 Jul 20.

Abstract

Objective: Conventional chemotherapy and radiotherapy produce marginal survival benefits in pancreatic cancer, underscoring the need for novel therapies. The aim of this study is to develop an adoptive T cell transfer approach to target tumours expressing prostate stem cell antigen (PSCA), a tumour-associated antigen that is frequently expressed by pancreatic cancer cells.

Methods: Expression of PSCA on cell lines and primary tumour samples was confirmed by immunohistochemistry. Healthy donor- and patient-derived T cells were isolated, activated in vitro using CD3/CD28, and transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) targeting PSCA. The ability of these cells to kill tumour cells was analysed by chromium-51 (Cr(51)) release.

Results: Prostate stem cell antigen was expressed on >70% of the primary tumour samples screened. Activated, CAR-modified T cells could be readily generated in clinically relevant numbers and were specifically able to kill PSCA-expressing pancreatic cancer cell lines with no non-specific killing of PSCA-negative target cells, thus indicating the potential efficacy and safety of this approach.

Conclusions: Prostate stem cell antigen is frequently expressed on pancreatic cancer cells and can be targeted for immune-mediated destruction using CAR-modified, adoptively transferred T cells. The safety and efficacy of this approach indicate that it deserves further study and may represent a promising novel treatment for patients with pancreatic cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Neoplasm / metabolism*
  • Carcinoma, Pancreatic Ductal / genetics
  • Carcinoma, Pancreatic Ductal / immunology
  • Carcinoma, Pancreatic Ductal / pathology
  • Carcinoma, Pancreatic Ductal / therapy*
  • Cell Line, Tumor
  • Cytotoxicity, Immunologic
  • Feasibility Studies
  • GPI-Linked Proteins / metabolism
  • Genetic Therapy*
  • HEK293 Cells
  • Humans
  • Immunohistochemistry
  • Immunotherapy, Adoptive*
  • Lymphocyte Activation
  • Muromonab-CD3 / pharmacology
  • Neoplasm Proteins / metabolism*
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / immunology
  • Pancreatic Neoplasms / pathology
  • Pancreatic Neoplasms / therapy*
  • Receptors, Antigen, T-Cell / biosynthesis
  • Receptors, Antigen, T-Cell / genetics*
  • Single-Chain Antibodies / biosynthesis
  • Single-Chain Antibodies / genetics*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / transplantation*
  • Time Factors
  • Transduction, Genetic
  • Up-Regulation

Substances

  • Antigens, Neoplasm
  • GPI-Linked Proteins
  • Muromonab-CD3
  • Neoplasm Proteins
  • PSCA protein, human
  • Receptors, Antigen, T-Cell
  • Single-Chain Antibodies