Neoadjuvant Vaccination Provides Superior Protection against
Tumor Relapse following Surgery Compared with
Adjuvant Vaccination
Natalie Grinshtein, Byram Bridle, Yonghong Wan, and Jonathan L. Bramson
Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
Abstract
Tumors that recur following surgical resection of melanoma
are typically metastatic and associated with poor prognosis.
Using the murine B16F10 melanoma and a robust antimela-
noma vaccine, we evaluated immunization as a tool to
improve tumor-free survival following surgery. We investigat-
ed the utility of vaccination in both neoadjuvant and adjuvant
settings. Surprisingly, neoadjuvant vaccination was far supe-
rior and provided f100% protection against tumor relapse.
Neoadjuvant vaccination was associated with enhanced
frequencies of tumor-specific T cells within the tumor and
the tumor-draining lymph nodes following resection. We also
observed increased infiltration of antigen-specific T cells into
the area of surgery. This method should be amenable to any
vaccine platform and can be readily extended to the clinic.
[Cancer Res 2009;69(9):3979–85]
Introduction
Surgery is the leading treatment modality for melanoma and
most solid tumors. More than 90% of primary melanomas can be
cured by surgical resection if diagnosed early. However, resection
alone is rarely curative for advanced tumors due to either local
tumor recurrence or outgrowth of micrometastases. In that regard,
patients with stage II melanoma are at high risk for recurrent
disease and are reported to have only 40% to 60% chance of
survival 5 years after the surgery (1).
Cancer vaccines offer an appealing strategy to improve disease-
free survival following surgical resection. Preclinical studies have
shown that cancer vaccines can routinely confer protection in
prophylactic settings, but the same vaccines usually exhibit only
limited therapeutic efficacy (2, 3). We have observed that existing
tumors can suppress immunity against tumor-associated antigens,
limiting the activity of cancer vaccines (4). Furthermore, in patients
with advanced-stage disease, tumor progression can occur within
the window of time required for induction of an immune response
following vaccination. Based on these data, it seems logical that
cancer vaccines would be most useful as an adjuvant treatment in
the setting of minimal residual disease. Alternatively, cancer
vaccines could be employed in the neoadjuvant setting. Under
these circumstances, surgical resection could be timed to coincide
with the peak of the immune response. Indeed, such a strategy has
been evaluated in the clinic (5, 6). These reports showed evidence
of vaccine immunogenicity, but these studies were not sufficiently
powered to make conclusion regarding efficacy. To date, however,
the issue of whether neoadjuvant immunization provides an
advantage over adjuvant immunization has not been addressed.
Thus, the optimal vaccination schedule remains unknown.
With regards to melanoma, a limited number of randomized
clinical trials have tested the efficacy of adjuvant vaccination (7–9).
All of those trials were halted early because vaccination did not
affect improve either disease-free or overall survival. It was unclear
from those studies whether the lack of clinical benefit was due to
the strategy (adjuvant vaccination) or the vaccine. We have found
that replication-defective adenovirus (rAd)-based cancer vaccines
produce robust antitumor immunity. In particular, a rAd vector
expressing human dopachrome tautomerase (AdhDCT) provided
superior protection against the murine B16F10 melanoma
compared with rAd vectors expressing other melanoma-associated
antigens (10–13).
1
DCT (also called tyrosinase-related protein 2) is
a promising candidate for the development of melanoma vaccines,
as it is widely expressed in melanoma and is naturally recognized
by melanoma-specific CTLs (14, 15). Despite the robust activity of
AdhDCT in prophylactic models (10, 11), we have observed that
vaccination with AdhDCT was ineffective even when the vaccine
was administered as little as 1 day after seeding the tumor (4),
suggesting that AdhDCT may only be useful in the setting of
minimal tumor burden. Given the robust protective immunity
provided by AdhDCT in prophylactic, but not therapeutic, settings,
we reasoned that this vaccine would provide a stringent test for our
hypothesis that immunization against tumor antigen(s) may
improve disease-free survival following surgery. To this end, we
investigated the effect of neoadjuvant and adjuvant immuniza-
tion with AdhDCT on tumor relapse in the B16F10 melanoma
model.
Materials and Methods
Mice. Six- to 8-week-old female C57BL/6 mice were obtained from
Charles River Breeding Laboratories. All of our investigations have been
approved by the McMaster Animal Research Ethics Board.
rAd and immunizations. All rAd vectors employed in this study contain
deletions of E1 and E3 regions (16). The expression cassettes were inserted
into the E1 region under the control of the murine cytomegalovirus (CMV)
promoter and the SV40 polyadenylation sequence. The rAd vectors were
propagated using 293 cells and purified using CsCl gradient centrifugation
as described previously (17). AdhDCT encodes the full-length human DCT
(11). AdLCMV GP expresses the sequence corresponding to residues 33 to
Note: Supplementary data for this article are available at Cancer Research Online
(http://cancerres.aacrjournals.org/).
Requests for reprints: Jonathan L. Bramson, Department of Pathology and
Molecular Medicine, McMaster University, Room MDCL-5025, 1200 Main Street West,
Hamilton, Ontario, Canada L8N 3Z5. Phone: 905-525-9140; Fax: 905-522-6750; E-mail:
bramsonj@mcmaster.ca.
I2009 American Association for Cancer Research.
doi:10.1158/0008-5472.CAN-08-3385
1
Unpublished data.
www.aacrjournals.org 3979 CancerRes2009;69:(9).May1,2009
Research Article
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Published OnlineFirst April 21, 2009; DOI: 10.1158/0008-5472.CAN-08-3385