Johannes Riegler1, Vincent Javinal2, Maj Hedehus1, Jill Schartner2, and Richard A.D. Carano1
1Biomedical Imaging, Genentech, South San Francisco, CA, United States, 2Genentech, South San Francisco, CA, United States
Synopsis
Checkpoint
inhibitors, adoptive T-cell transfer and tumor vaccination are different cancer
immunotherapies which have demonstrated clinical efficacy in certain patients1-3. All of these therapies require sufficient
infiltration of cytotoxic T-cells into the tumor and direct contact with cancer
cells. However, the reasons why certain tumors present with high T-cell infiltration
while others do not are poorly understood. We therefore set out to assess if
imaging vascular adhesion molecule 1 (VCAM-1) expression in the tumor
vasculature could explain some of the observed differences in T-cell
infiltration.
Purpose
To
assess if imaging of VCAM-1 density could predict T-cell infiltration in murine
tumor models.Methods
C57BL/6
mice (n=4) were inoculated with 5E5 EL4-GFP cells and NOD/SCID mice (n=4) with 5E5 E.G7-OVA-GFP
cells s.c. on the hind leg. Once tumors had reached a volume > 400 mm3,
baseline MRI was performed followed by i.v. infusion of 1E7 tdTomato positive
OTI T-cells (these cells recognize OVA) and follow up MRI 2 or 3 days
thereafter. MRI was performed on a 7T horizontal bore scanner (Bruker, Ettlingen,
Germany) with a 86 mm volume transmit and a 4-channel phased array receive only
cryoprobe. Tumors were embedded in dental paste to reduce susceptibility
artifacts from the tumor/air boundary. Pre-contrast imaging included T2,
ADC, T2* mapping as well as T2*-w acquisitions and DCE.
Following pre-contrast imaging, animals were removed from the magnet and 4.5 mg
Fe/kg micron sized iron oxide particles (MPIO) conjugated to either VCAM-1
(VCAM-MPIO) or Rat-IgG (IgG-MPIO) were infused via a tail vein catheter similar
to a previously published protocol4. Mice were kept anesthetized outside of the
magnet for 40 minutes after which T2* mapping and T2*-weighted
acquisitions were repeated. The following imaging parameters were used: T2-mapping:
RARE: TR 3000 ms, TE 14, 28, 42, 56, 70, 84 ms, NSA 1, 25.6x25.6 mm2
0.5 mm slice thickness, 20 slices, Matrix 128x128; Stimulated-echo diffusion: TR
3000 ms, TE 8.7 ms, maximum diffusion gradient 37 G/cm, δ/Δ 1/140
ms, b-values (100, 300, 600, 900, 1200) NSA 1; T2* Multi-gradient-echo;
TR 900, TE 3, 7, 11, 15, 19, 23, 27, 31 ms, FA 60°, Matrix 196x196, NSA 1. T2*-w
GE: TR 50 ms, TE 6 ms, FA 15°, 25.6x25.6x20 mm3, Matrix 213x213x83
(120 µm isotropic), NSA1.Results
The
administration of VCAM-MPIO led to a significant drop in T2* and the
appearance of hypointense spots throughout the tumor tissue on T2*-weighted
images. In contrast, IgG-MPIO administration led to a small change in T2*
and few hypointense spots (Figure 1). To assess if repeated imaging with MPIOs
in tumors would be feasible, we repeated VCAM-MPIO and IgG-MPIO imaging 2 days
after the first imaging session. Pre-contrast images were not significantly
different between imaging sessions. Furthermore, the VCAM-MPIO induced change
in T2* was similar between imaging sessions (Figure 2). We next conducted
the same experiments in NOD/SCID mice with E.G7-OVA-GFP tumors and administered
T-cells that can recognize this tumor line after the first imaging session.
Imaging was repeated 3 days later and tumors were excised for histology. We
observed a good correspondence between VCAM-MPIO contrast, VCAM-1 density and
T-cell density (Figure 3). However, T-cell density decreased towards the center
of the tumor while VCAM density remained constant particularly for slices in
the middle of tumors. Analysis of confocal microscopy data showed T-cells were
always found in close proximity to VCAM positive blood vessels at this time
point (Figure 4). Finally, we also observed signs of cytotoxic activity
indicated by clearance of GFP positive tumor cells in areas of T-cell
accumulation.Discussion
The
feasibility of MPIO-based VCAM-1 expression imaging has been demonstrated previously
for the brain4 and cardiovascular system5. However, its suitability for tumor imaging and
the role of VCAM-1 as potential biomarker for T-cell extravasation has not been
evaluated. We have demonstrated that VCAM-MPIO administration generates strong
T2* changes in inflamed tumor models. We also show that bound MPIOs
are cleared within 2 days enabling repeated assessment of VCAM-1 expression in
the same tumor. Finally, T-cells were generally found in close proximity to
VCAM-1 positive vessels 3 days after adoptive transfer indicating the relevance
of VCAM-1 as a marker for T-cell extravasation. Nonetheless, areas with high
VCAM-1 expression lacking T-cells were also detected, particularly in tumor
centers. This indicates that either perfusion or other parameters such as
chemokine gradients or additional adhesion molecules are required to predict
T-cell extravasation. Ongoing experiments will validate the role of VCAM-1
expression in other tumor models as well as during immune checkpoint blockade.Conclusion
Imaging
VCAM-1 expression might be a suitable biomarker for T-cell extravasation.Acknowledgements
We
would like to thank Luke Xie and Cecile Chalouni for helpful
discussions.References
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M. E. et al. Cancer regression and
autoimmunity in patients after clonal repopulation with antitumor lymphocytes. Science 298:850-854 (2002).
2 Hodi, F. S. et al. Improved survival with ipilimumab in patients with
metastatic melanoma. N Engl J Med 363:11-723 (2010).
3 Michael, A., Relph, K., Annels, N.
& Pandha, H. Prostate cancer vaccines. Expert
Rev Vaccines 12:253-262 (2013).
4 McAteer, M. A. et al. In vivo magnetic resonance imaging of acute brain
inflammation using microparticles of iron oxide. Nat Med 13:1253-1258 (2007).
5 Kelly, K. A. et al. Detection of vascular adhesion molecule-1 expression using
a novel multimodal nanoparticle. Circ Res
96:327-336 (2005).