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Cancer Immunoprevention—The Next Frontier

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Cancer Immunoprevention—The Next Frontier Published OnlineFirst September 22, 2014; DOI: 10.1158/1940-6207.CAPR-14-0178 Cancer Prevention Cancer Immunoprevention Series Research Cancer Immunoprevention—The Next Frontier Marie-Anne D. Smit1,2, Elizabeth M. Jaffee1,2,3,4, and Eric R. Lutz1,2,3,4 Abstract Cancer immunotherapy is a rapidly developing field, but limited in its success by a high tumor burden and immune tolerance. In contrast, immunoprevention has the potential to prevent cancer before the development of immune tolerance, and to prevent cancer recurrence in the setting of minimal residual disease. Although immunoprevention for viral-induced cancers has been successful in the setting of hepatitis B and human papillomavirus vaccination, primary prevention of nonviral-induced cancers is in its infancy. In contrast, prevention of cancer recurrence after adjuvant treatment (secondary prevention) is gaining steam. This review provides an overview of the scope of research in cancer immunoprevention over the last three years and directions for future research. See all articles in this Cancer Prevention Research collection, "Cancer Immunoprevention Series." Cancer Prev Res; 7(11); 1072–80. Ó2014 AACR. Introduction many years and drive the transition from normal tissue Cancer immunotherapy is currently undergoing exponen- through programmed stages of premalignant transforma- tial growth. The FDA has recently approved the dendritic cell tion, and eventual development of the full malignancy. This (DC)–based vaccine Sipuleucel-T and the checkpoint inhib- provides a window of time for primary preventive interven- itor ipilimumab for the treatment of metastatic castrate- tion, especially for high-risk patients. Currently, chemo- resistant prostate cancer and metastatic melanoma, respec- preventive agents for breast cancer (tamoxifen) and colon tively. Several other agents, including programmed cell death cancer (aspirin) are the only clinically proven methods of 1 (PD-1) pathway blocking agents (1–3), are currently under primary prevention of non–virus-associated cancers. These clinical investigation, and are showing promising results for interventions have limited utility for several reasons, includ- the treatment of some advanced cancers. However, the ing lack of patient interest due to an unclear benefit, unwant- success of immunotherapy for most patients with progres- ed toxicities experienced by otherwise healthy individuals, sing cancers has been limited because of the established need for daily dosing, and lack of physician comfort in immunosuppressive milieu and a large tumor burden that prescribing these agents. In contrast to chemoprevention prevent optimal immune activation and antitumor efficacy. agents, vaccines induce memory T cells that are active for Cancer immunoprevention has the potential to circumvent years and are nontoxic in most cases. Thus, immunization of these problems, and is feasible if applied in the right setting. otherwise healthy individuals for primary prevention of Primary cancer immunoprevention is gaining attention cancer offers advantages over drug-based approaches, with because vaccines against hepatitis B and human papilloma- low toxicity and no need for daily dosing. virus (HPV) are successfully preventing viral-induced can- Although the role of immunotherapy in the treatment of cers. These vaccines are effective due to their ability to prevent cancer is rapidly increasing, the transition to a preventive primary infection following exposure to these viruses, there- paradigm has been slower. This review provides an overview by eliminating their oncogenic potential. Unlike cancers that of the scope of research in cancer immunoprevention over are induced by viruses, the development of nonviral cancers the last 3 years (Table 1) as well as directions for future involves progressive genetic alterations that accumulate over research (Figure 1). Primary Prevention 1 The Sidney Kimmel Cancer Center, Johns Hopkins University School of Vaccination as primary prevention is well established for Medicine, Baltimore, Maryland. 2Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 3Sol Goldman Pan- both hepatitis B–associated hepatocellular carcinoma (4) creatic Cancer Center, Johns Hopkins University School of Medicine, and for HPV-associated cancers (5). Both the HPV-16/18 Baltimore, Maryland. 4The Skip Viragh Pancreatic Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland. AS04-adjuvant vaccine (Cervarix) and the HPV-6/11/16/18 vaccine (Gardasil) are approved by the FDA for the preven- Corresponding Author: Elizabeth M. Jaffee, Johns Hopkins University School of Medicine, Rm 4M07, Bunting Blaustein Cancer Research Build- tion of cervical cancer. In addition to preventing cervical ing, 1650 Orleans Street, Baltimore, MD 21231. Phone: 410-955-2957; Fax: cancer and its precursors cervical intraepithelial neoplasia 410-614-8216; E-mail: [email protected] and adenocarcinoma in situ (6), vaccination against HPV doi: 10.1158/1940-6207.CAPR-14-0178 also decreases the incidence of penile intraepithelial neo- Ó2014 American Association for Cancer Research. plasia (7) and anal intraepithelial neoplasia (8). 1072 Cancer Prev Res; 7(11) November 2014 Downloaded from cancerpreventionresearch.aacrjournals.org on September 26, 2021. © 2014 American Association for Cancer Research. Published OnlineFirst September 22, 2014; DOI: 10.1158/1940-6207.CAPR-14-0178 Immunoprevention: Past, Present, and Future Table 1. Overview of recent nonviral cancer immunoprevention studies Cancer Vaccine type Adjuvant Target Treatment effect Reference Primary prevention Colon cancer Peptide Toll-like MUC1 * 44% MUC1-specific antibody 9 prevention vaccine receptor 3 response for patients agonist * Vaccine induces long-term with (poly-ICLC) memory colorectal adenomas * Nonresponders showed higher percentage of immunesuppressive mediators * No clinical endpoints Secondary prevention Melanoma DC vaccine KLH Melanoma-associated * 3-year DFS 40.9% vs. 14.5% 10 antigens (tyrosinase, (historical controls, P ¼ 0.1083) Melan-A/MART-1, * 3-year OS 68.2% vs. 25.7% gp100, MAGE-1, and (historical controls, P ¼ 0.0290) MAGE-3) or autologous tumor cell lysate Melanoma Ipilimumab Æ Montanide Tyrosinase, gp100, * 23% stopped treatment due to 11 peptide ISA 51 VG MART-1 toxicity related to ipilimumab vaccination * Median RFS and OS not reached at 29.5 months. Breast cancer Peptide GM-CSF HER2 peptide E75 * 2-year DFS 94.3% vs. 86.6% 12 vaccine (controls, P ¼ 0.08) * Subset analysis: improved DFS in node-positive, low HER2- expressing and low grade tumors. * Improved DFS in HER2-high– expressing patients receiving vaccine plus trastuzumab compared with vaccine alone Follicular Protein KLH Tumor isotype matched * Median DFS 44.2 vs. 30.6 months 15 lymphoma vaccine Id (IgM and IgG) (controls, P ¼ 0.047) * Median OS not reached * Subset analysis: improved DFS with IgM isotype vaccine * Trial done pre-rituximab NSCLC Protein AS02B MAGE-A3 * 44-month recurrence rate 35% vs. 21 vaccine 43% (controls, not significant). * DFS or OS not significantly improved Melanoma Peptide KLH plus GM2 ganglioside * Trial stopped after median follow 22 vaccine QS-21 up of 18 months due to increased survival in control group (HR, 1.66; P ¼ 0.02) Colorectal Viral vector vs. GM-CSF (viral CEA, MUC1, CD80, * RFS 22.9 vs. 28.9 months (DC vs. 16 cancer DC vaccine vector) CD54, and CD58 viral vector) * Median OS not reached in either group vs. 44.1 months (historic controls, P < 0.0001) Pancreatic Whole cell GM-CSF Allogeneic pancreatic * OS 24.8 vs. 20.3 months 17 cancer vaccine cancer cell line (historical controls, not significant) (GVAX) antigens (incl. * Induction of mesothelin-specific mutated k-ras, CD8 T cells correlated with mesothelin) increased DFS www.aacrjournals.org Cancer Prev Res; 7(11) November 2014 1073 Downloaded from cancerpreventionresearch.aacrjournals.org on September 26, 2021. © 2014 American Association for Cancer Research. Published OnlineFirst September 22, 2014; DOI: 10.1158/1940-6207.CAPR-14-0178 Smit et al. Vaccination as primary prevention for nonviral cancers In one clinical trial, 22 patients with stage III melanoma and is in the very early stages of development, with only a few an unfavorable prognosis received a vaccine consisting of clinical trials that have been initiated in patients. One bone marrow and peripheral blood mononuclear cell recent trial targeted MUC1 in patients with premalignant (PBMC)–derived DC loaded with melanoma-associated colorectal adenomas and evaluated its immunogenicity, peptides (tyrosinase, Melan A/MART-1, gp100, MAGE-1, though no clinical endpoints were included in the study and/or MAGE-3) or autologous tumor cell lysate, and (9). MUC1 is a tumor-associated antigen that is highly keyhole limpet hemocyanin (KLH; ref. 10). Although expressed by both colon cancer and premalignant colo- 3-year disease-free survival (DFS) showed a trend toward rectal adenomas. A 100-amino acid–long synthetic improvement compared with pair-matched historical con- MUC1 peptide with the adjuvant Toll-like receptor 3 trols (40.9% vs. 14.5% in historical controls), only 3-year agonist poly-ICLC was given to 39 patients with advanced OS was significantly improved (68.2% vs. 25.7%). Mela- colorectal adenomas. The vaccine was administered at noma antigen-specific interferon-g (IFNg) producing CD8- week 0, 2, and 10 and a booster was given at 52 weeks. positive T lymphocytes were detected in peripheral blood Seventeen patients (44%) had
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