Joseph Weygand1,2, Prasanta Dutta1, Jessica Molkentine3, Yeonju Lee4,5, Travis Salzillo1,2, Meifang Yu3, Jaehyuk Lee1, Eugene Koay4, Cullen Taniguchi4, and Pratip Bhattacharya1
1Cancer Systems Imaging, University of Texas MD Anderson Cancer Center, Houston, TX, United States, 2Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, TX, United States, 3Experimental Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, United States, 4Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, United States, 5Five Prime Therapeutics, Inc, San Francisco, CA, United States
Synopsis
Although immunotherapy presents an attractive
new treatment option for patients with pancreatic cancer, its implementation
has been underwhelming. As a critical first step in understanding this failure,
we have applied hyperpolarized pyruvate spectroscopic imaging and NMR
spectroscopy to interrogate the metabolic properties of pancreatic tumors
cultivated in the presence of different immune environments. We observed that the
immune environment in which a pancreatic tumor is harvested significantly
alters metabolic function and that these metabolic differences exhibit a
temporal dependence with respect to tumor development.
Purpose
Despite its relatively low incidence, pancreatic
cancer was the fourth leading cause of cancer-related death1 in the
US in 2015. This is due in part to pancreatic cancer’s natural resistance to
both chemotherapy and radiotherapy2. Immunotherapy presents an
attractive potential treatment approach, but initial trials in mice have proved
ineffective3. Because cancer
cells exhibit a significant increase in metabolic activity relative to normal
tissue, an understanding of the metabolic function of tumors in systems with
different levels of immunocompetence is a critical first step to develop an
understanding of the immune-related metabolic properties of the tumor, which
have potential application in assessing a tumor’s response to immunotherapy.
This study intends to identify clear biomarkers that can facilitate the
assessment of metabolic changes between immunocompromised and immunocompetent
pancreatic tumors. Methods
This tumor model system employed the K8484
pancreatic tumor line which is syngeneic to C57BL/6 background and is derived
from mouse tumors with an oncogenic KRAS mutation (G12D) and a homozygous null
mutation in p53. These cells were then
transplanted into the flanks of both immunocompetent C57BL/6 mice and
immunocompromised nude (nu/nu, Jackson labs) mice. Tumors were then allowed to
grow until they reached sizes of 0.75 and 1.5 cm so that the immune-related
metabolic properties of pancreatic cancer could be assessed at different time
points in tumor progression. Hyperpolarized 13C-labeled pyruvate (80
mM) was injected into both cohorts of mice at both time points in tumor
progression (n=2, n=4 and n=3, n=3), and real-time pyruvate-to-lactate
conversion was observed in vivo. The metric nLac, calculated as the lactate pool size normalized by the total pool size (lactate + pyruvate), was employed in the hyperpolarized imaging experiment to assess how glycolytic a given tumor is.In addition, the 1.5 cm flank tumors (n=5,
n=5) were resected then subjected to high-resolution 1H nuclear
magnetic resonance (1H-NMR) metabolomics for both cohorts of mice.
The samples were homogenized (methanol:water 2:1), lyophilized, and immersed in
D2O, and NMR
spectroscopy was implemented to characterize the water-soluble portion of the
metabolome using a Bruker 500 MHz NMR spectrometer coupled with a
cryo-probe.Results
At the earlier time point in tumor progression,
the nude mice were more glycolytic than the immunocompetent mice by a factor of
2.0 (p = 0.026). However, at the later point in tumor progression, we observe
that the immunocompetent mice were more glycolytic by a factor of 1.9. In
addition, higher baseline metabolic activity was observed in the ex vivo tissue samples taken from the
immunocompetent C57BL/6 mice than the immunocompromised nude mice. In particular, we observed statistically
significant upregulation of lactate (p=0.020), alanine (p=0.014), creatine
(p=0.00013), total choline (p=0.046), glutamate (p=0.018), glutathione
(p=0.12), taurine (p=0.012), glycine (p=0.015), methionine (p=0.0015), and
aspartate (p=0.0033).Discussion
The immune cells located in the tumor
microenvironment, present in the immunocompetent mice but missing in the nude
mice, may contribute in some way to the metabolic function of the tumor. A hematoxylin
and eosin stain of the tumor tissue samples taken at the later time point in
tumor progression exhibits that the immune cells readily infiltrate the tumor
in the immunocompetent mouse but stay restricted to the periphery in the
immunocompromised mouse. Further imaging studies are currently underway to
validate these data. In addition, high-resolution 1H NMR
metabolomics and hematoxylin and eosin staining are being performed on the tumors
from the earlier time point in tumor progression to see if the ex vivo data at this earlier time point
corroborates the in vivo data. Conclusion
We see that the immune environment in which a
pancreatic tumor is harvested significantly alters the metabolic function of
that tumor. In particular, higher baseline metabolic activity and higher
glycolytic dependence is observed in 1.5 cm tumors grown in immunocompetent
mice than from 1.5 cm tumors grown in immunocompromised mice, but this trend is
not observed in earlier stages of tumor progression. Further study is underway
so that this phenomenon is understood in a more mechanistic way. Acknowledgements
No acknowledgement found.References
1. American
Cancer Society. Cancer Facts & Figures, 2015. Atlanta, Georgia: American
Cancer Society; 2015.
2.
Laheru D, Jaffee EM. Immunotherapy for Pancreatic Cancer – Science Driving
Clinical Progress. Nature Reviews Cancer. 2005; 5: 459-467.
3. Feig C, Jones JO, Kraman M, et al. Targeting CXCL12 from FAP-expressing
Carcinoma-associated Fibroblasts Synergizes with Anti–PD-L1 Immunotherapy in
Pancreatic Cancer. Proceedings of the National Academy of Sciences of
the United States of America. 2013; 110(50): 20212-20217.