Latent Neuropathy in Colorectal Cancer: Implications for Cancer Survivorship
Caitlyn M. Gaffney, Angela M. Casaril, Iqbal Mahmud, Bo Wei, Yanyan Jiang, Nathan T. Fiore, Marc A. Pina, Karen M. Valadez, Elizabeth A. Kolb, Fisher R. Cherry, Lei Shi, Kenneth Dunner Jr., Philip L. Lorenzi, Steven R. Reiken, Peter M. Grace, Rajasekaran Mahalingam, Theresa A. Guise, Carolyn L. Hodo, Andrew J. Shepherd
Colorectal cancer survivors are at increased risk of developing neurological issues, particularly peripheral neuropathy and chronic pain. Although pre-existing neuropathy is a risk factor for chronic pain, tumor-induced neuropathy has not been firmly established in pre-clinical models. Consistent with clinical observations, we show that mice with colorectal cancer develop peripheral neuropathy, which was associated with subtle locomotor deficits, without overt hypersensitivity.
We detected widespread differences in pro-inflammatory cytokines and lipid metabolites in peripheral nerves from tumor-bearing mice. Macrophage accumulation, myelin decompaction and ryanodine receptor oxidation were associated with dysfunctional calcium homeostasis and reduced spike amplitude in sensory neurons. Similar alterations in plasma inflammatory mediators and lipid metabolites were associated with neuropathy and macrophage accumulation in peripheral nerves of rhesus macaques with colorectal cancer.
Consistently, mice with colorectal cancer exhibit greater pain sensitivity following treatment with oxaliplatin. These findings suggest colorectal cancer is causally linked to a subacute form of chronic inflammatory demyelinating polyneuropathy across species, which may represent an under-reported, yet important risk factor for neurological dysfunction in colorectal cancer survivors.
Caitlyn M. Gaffney, Angela M. Casaril, Iqbal Mahmud, Bo Wei, Yanyan Jiang, Nathan T. Fiore, Marc A. Pina, Karen M. Valadez, Elizabeth A. Kolb, Fisher R. Cherry, Lei Shi, Kenneth Dunner Jr., Philip L. Lorenzi, Steven R. Reiken, Peter M. Grace, Rajasekaran Mahalingam, Theresa A. Guise, Carolyn L. Hodo, Andrew J. Shepherd
Colorectal cancer survivors are at increased risk of developing neurological issues, particularly peripheral neuropathy and chronic pain. Although pre-existing neuropathy is a risk factor for chronic pain, tumor-induced neuropathy has not been firmly established in pre-clinical models. Consistent with clinical observations, we show that mice with colorectal cancer develop peripheral neuropathy, which was associated with subtle locomotor deficits, without overt hypersensitivity.
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We detected widespread differences in pro-inflammatory cytokines and lipid metabolites in peripheral nerves from tumor-bearing mice. Macrophage accumulation, myelin decompaction and ryanodine receptor oxidation were associated with dysfunctional calcium homeostasis and reduced spike amplitude in sensory neurons. Similar alterations in plasma inflammatory mediators and lipid metabolites were associated with neuropathy and macrophage accumulation in peripheral nerves of rhesus macaques with colorectal cancer.
Consistently, mice with colorectal cancer exhibit greater pain sensitivity following treatment with oxaliplatin. These findings suggest colorectal cancer is causally linked to a subacute form of chronic inflammatory demyelinating polyneuropathy across species, which may represent an under-reported, yet important risk factor for neurological dysfunction in colorectal cancer survivors.
Andrew Shepherd
Dr. Andrew Shepherd conducts preclinical research investigating the mechanisms that link inflammation to the pain induced by various forms of injury, including joint damage and chemotherapy-induced neuropathy, with a particular emphasis on signaling related to the renin-angiotensin system. The ultimate goal of the Shepherd Lab in the Department of Symptom Research is to identify interventions that can mitigate or prevent the development of pain associated with these chronic disease states.
Dr. Shepherd earned his bachelor’s degree in molecular cell biology in 2003 and a doctoral degree in neuroimmunomodulation in 2006, both from the University of Manchester in Great Britain. His training and expertise focus on rodent models of pain, behavioral readouts of pain sensitivity, and assays of primary rodent and human sensory-neuron function.
Dr. Shepherd co-chairs MD Anderson’s Pain Research Consortium, a unique platform that brings together clinical and basic science pain experts for interdisciplinary discussion, innovative problem-solving, and shaping the future of pain management.
Dr. Andrew Shepherd conducts preclinical research investigating the mechanisms that link inflammation to the pain induced by various forms of injury, including joint damage and chemotherapy-induced neuropathy, with a particular emphasis on signaling related to the renin-angiotensin system. The ultimate goal of the Shepherd Lab in the Department of Symptom Research is to identify interventions that can mitigate or prevent the development of pain associated with these chronic disease states.
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TBC
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Dr. Shepherd earned his bachelor’s degree in molecular cell biology in 2003 and a doctoral degree in neuroimmunomodulation in 2006, both from the University of Manchester in Great Britain. His training and expertise focus on rodent models of pain, behavioral readouts of pain sensitivity, and assays of primary rodent and human sensory-neuron function.
Dr. Shepherd co-chairs MD Anderson’s Pain Research Consortium, a unique platform that brings together clinical and basic science pain experts for interdisciplinary discussion, innovative problem-solving, and shaping the future of pain management.
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