کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2794109 1155252 2015 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Chemobrain: A critical review and causal hypothesis of link between cytokines and epigenetic reprogramming associated with chemotherapy
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی علوم غدد
پیش نمایش صفحه اول مقاله
Chemobrain: A critical review and causal hypothesis of link between cytokines and epigenetic reprogramming associated with chemotherapy
چکیده انگلیسی


• Chemotherapy related cognitive dysfunction becomes an increasing concern.
• The exact biological pathways remain unknown.
• We hypothesize chemotherapy changes cytokine milieu inducing epigenetic alterations.
• Epigenetic changes are responsible for the subjective experience of cognition.
• This hypothesis is critical to identify targets for cancer cognitive dysfunction.

One consequence of modern cancer therapy is chemotherapy related cognitive dysfunction or “chemobrain”, the subjective experience of cognitive deficits at any point during or following chemotherapy. Chemobrain, a well-established clinical syndrome, has become an increasing concern because the number of long-term cancer survivors is growing dramatically. There is strong evidence that correlates changes in peripheral cytokines with the development of chemobrain in commonly used chemotherapeutic drugs for different types of cancer. However, the mechanisms by which these cytokines elicit change in the central nervous system are still unclear. In this review, we hypothesize that the administration of chemotherapy agents initiates a cascade of biological changes, with short-lived alterations in the cytokine milieu inducing persistent epigenetic alterations. These epigenetic changes lead to changes in gene expression, alterations in metabolic activity and neuronal transmission that are responsible for generating the subjective experience of cognition. This speculative but testable hypothesis should help to gain a comprehensive understanding of the mechanism underlying cognitive dysfunction in cancer patients. Such knowledge is critical to identify pharmaceutical targets with the potential to prevent and treat cancer-treatment related cognitive dysfunction and similar disorders.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 72, Issue 1, March 2015, Pages 86–96
نویسندگان
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