TY - JOUR
T1 - Molecular epidemiology, cancer-related symptoms, and cytokines pathway
AU - Reyes-Gibby, Cielito C.
AU - Wu, Xifeng
AU - Spitz, Margaret
AU - Kurzrock, Razelle
AU - Fisch, Michael
AU - Bruera, Eduardo
AU - Shete, Sanjay
N1 - Funding Information:
Data for this Review were identified by searches of Pubmed for articles published in the past 10 years with the search terms “pain”, “fatigue”, “depression”, “cancer”, “genes”, “polymorphisms”, “cytokines”, “epidemiology”. References were also identified from the reference lists of relevant articles. Only papers published in English were included. Conflicts of interest The authors declared no conflicts of interest. Acknowledgments The corresponding author is a recipient of KO7CA109043 from the National Institute of Health (NIH/NCI).
PY - 2008/8
Y1 - 2008/8
N2 - The Human Genome Project and HapMap have led to a better appreciation of the importance of common genetic variation in determining cancer risk, created potential for predicting response to therapy, and made possible the development of targeted prevention and therapeutic interventions. Advances in molecular epidemiology can be used to explore the role of genetic variation in modulating the risk for severe and persistent symptoms, such as pain, depression, and fatigue, in patients with cancer. The same genes that are implicated in cancer risk might also be involved in the modulation of therapeutic outcomes. For example, polymorphisms in several cytokine genes are potential markers for genetic susceptibility both for cancer risk and for cancer-related symptoms. These genetic polymorphisms are stable markers and easily and reliably assayed to explore the extent to which genetic variation might prove useful in identifying patients with cancer at high-risk of symptom development. Likewise, they could identify subgroups who might benefit most from symptom intervention, and contribute to developing personalised and more effective therapies for persistent symptoms.
AB - The Human Genome Project and HapMap have led to a better appreciation of the importance of common genetic variation in determining cancer risk, created potential for predicting response to therapy, and made possible the development of targeted prevention and therapeutic interventions. Advances in molecular epidemiology can be used to explore the role of genetic variation in modulating the risk for severe and persistent symptoms, such as pain, depression, and fatigue, in patients with cancer. The same genes that are implicated in cancer risk might also be involved in the modulation of therapeutic outcomes. For example, polymorphisms in several cytokine genes are potential markers for genetic susceptibility both for cancer risk and for cancer-related symptoms. These genetic polymorphisms are stable markers and easily and reliably assayed to explore the extent to which genetic variation might prove useful in identifying patients with cancer at high-risk of symptom development. Likewise, they could identify subgroups who might benefit most from symptom intervention, and contribute to developing personalised and more effective therapies for persistent symptoms.
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U2 - 10.1016/S1470-2045(08)70197-9
DO - 10.1016/S1470-2045(08)70197-9
M3 - Review article
C2 - 18672213
AN - SCOPUS:47849090505
SN - 1470-2045
VL - 9
SP - 777
EP - 785
JO - The lancet oncology
JF - The lancet oncology
IS - 8
ER -