Santosh K Bharti1, Paul T Winnard1, Raj Kumar Sharma1, Marie-France Penet1,2, Balaji Krishnamachary1, and Zaver M. Bhujwalla1,2,3
1Div. of Cancer Imaging Research, The Russell H. Morgan Dept of Radiology and Radiological Science, The Johns Hopkins University School of Medicine,, Baltimore, MD, United States, 2Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, 33Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States
Synopsis
Cancer induced cachexia is a
multifactorial syndrome that results in unexplained weight loss in cancer
patients. A major cause of morbidity and
mortality, the syndrome is most prevalent in pancreatic cancer. Here we have identified changes in brain
choline metabolites and plasma choline in human pancreatic cancer xenografts
that induce cachexia (Pa04C) as well as noncachexia inducing pancreatic cancer
xenografts (Panc1), compared to normal mice.
These results highlight the systemic changes in choline metabolism that
occur with cancer and with cancer induced cachexia that may lead to the
development of early biomarkers as well to metabolic treatment strategies.
Introduction
Cancer-induced cachexia is an under explored
problem with lethal consequences. To
date specialized nutritional supplements have failed as anti-cachexia
treatments. There are no known cures for
this condition, and the multi-faceted nature of cachexia makes it difficult to
investigate. Most prevalent in pancreatic
cancer where resection is not possible for a majority of patients, palliation
with chemotherapy is the only option of prolonging life. Cachexia results in
lower tolerance to chemotherapy [1-3]. Cachectic patients experience a wide range of
symptoms affecting the function of organs such as muscle, liver, brain, and
heart, causing significant morbidity [4]. An altered choline metabolism is one of the
hallmarks of cancer. Changes in choline
metabolism in other organs induced by cancers have not been previously
investigated. Here, for the first time,
we have characterized changes in brain choline metabolism induced by pancreatic
cancer xenografts and related these changes to plasma choline levels. Methods
Cancer-induced cachexia is an under explored
problem with lethal consequences. To
date specialized nutritional supplements have failed as anti-cachexia
treatments. There are no known cures for
this condition, and the multi-faceted nature of cachexia makes it difficult to
investigate. Most prevalent in pancreatic
cancer where resection is not possible for a majority of patients, palliation
with chemotherapy is the only option of prolonging life. Cachexia results in
lower tolerance to chemotherapy [1-3]. Cachectic patients experience a wide range of
symptoms affecting the function of organs such as muscle, liver, brain, and
heart, causing significant morbidity [4]. An altered choline metabolism is one of the
hallmarks of cancer. Changes in choline
metabolism in other organs induced by cancers have not been previously
investigated. Here, for the first time,
we have characterized changes in brain choline metabolism induced by pancreatic
cancer xenografts and related these changes to plasma choline levels. Results and Discussion
Cachexia-inducing Pa04C tumors induced a significant weight loss in
mice compared to Panc1 tumor bearing mice or normal mice as shown in Figure
1. Representative spectra showing the
choline metabolite region of high resolution 1H MRS spectra of brain
extracts are shown in Figure 2A.
Quantitative analyses of choline, phosphocholine (PC) and
glycerophosphocholine (GPC) are summarized in Figures 2B, C and D respectively. A significant decrease of brain choline was
observed in Pa04C tumor bearing mice compared to control mice as well as to
Panc1 tumor bearing mice, whereas brain PC levels were significantly lower
compared to normal mice. Brain GPC was
significantly lower in both tumor bearing groups compared to normal mice. We observed a profound decrease of plasma
choline in Pa04C tumor bearing mice as shown in Figure 3. Plasma choline in Panc1 tumor bearing mice
also decreased but not as drastically.
The changes in plasma choline levels most likely contributed to the reduction
of brain choline, PC and GPC. Causes of
the decrease of plasma choline levels are currently under investigation. Disturbances in the choline/cholinergic pathways may be one underlying
cause of the morbidity associated with cancer and cancer-induced cachexia. Reduced plasma choline may represent a risk
factor for cancer as choline deficiency is known to result in lymphocyte
apoptosis and DNA damage [6] that may compromise the immune response.
Normalization of plasma choline using metabolic supplements merits
investigation in reducing cancer morbidity and the onset of cachexia. Acknowledgements
This work was supported by NIH R35CA209960 and R01CA193365. References
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