Effect of Cancer Treatment on Neural Stem and Progenitor Cells

Dietrich, Jörg; Kesari, Santosh

doi:10.1007/b109924_6

Cited by 7 publications

(3 citation statements)

References 96 publications

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“…In our setting, 10 Gy leads to minimal artifacts and robust chimerism in the periphery (Lampron, Lessard, & Rivest, ). Others have reported radiation effects on neurogenesis, killing neural stem cells or altering their microenvironment (Dietrich & Kesari, ), although we see normal levels of nestin+ neural stem cells in chimeric mice. Thus, we developed a chemotherapy protocol that produces no effect on cell death or on the BBB.…”

Section: Commentarycontrasting

confidence: 65%

Bone Marrow Chimeras to Study Neuroinflammation

et al. 2018

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Bone marrow transplantation is the standard of care for a host of diseases such as leukemia and multiple myeloma, as well as genetically inherited metabolic diseases affecting the central nervous system. In mouse models, bone marrow transplantation has proven a valuable tool for understanding the hematopoietic system and the homing of hematopoietic cells to their target organs. Many techniques have been developed to create chimeric mice, animals with a hematopoietic system derived from a genetic background that differs from the rest of the body. Current genetic tools allow for virtually limitless possibilities in the choice of donor mice. This protocol describes methods of bone marrow transplantation in mouse models for studies of the brain under basal and pathological conditions. Specific points to be addressed include the preparation of recipient mice by irradiation or chemotherapy; the choice, isolation, and injection of donor cells; and analytical methods such as fluorescence-activated cell sorting and immunostaining. © 2018 by John Wiley & Sons, Inc.

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Section: Commentarycontrasting

confidence: 65%

Bone Marrow Chimeras to Study Neuroinflammation

et al. 2018

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“…study raises the possibility that the tumour itself might deplete neurogenic niches in the brain by attracting neural progenitors to support its own development, and suggests that treatment-naive patients with cancer may also develop cognitive impairment 44,45 .…”

Section: Article Researchmentioning

confidence: 99%

Progenitors from the central nervous system drive neurogenesis in cancer

Mauffrey

Tchitchek

Barroca

et al. 2019

Nature

239

186

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“…It is known that neural progenitor cells and mature post-mitotic oligodendrocytes are the most vulnerable cell populations to various chemotherapeutic agents [73,74] . Long-term cognitive decline in cancer survivors may be the result of a combination of decreased proliferation of neural progenitor cells, impaired hippocampal neurogenesis and damage to oligodendroglial cells and white matter tracts [75] . As many different chemotherapeutic agents seem to have similar effects on the CNS, studies are also exploring common indirect mechanisms of neurotoxicity, such as pro-oxidative effects, toxic neurotransmitters/monoamine release, disruption of blood vessel density and supply and inflammation [76] .…”

Section: Cognition In Patients Without Central Nervous System Diseasementioning

confidence: 99%

Monitoring and optimising cognitive function in cancer patients: Present knowledge and future directions

Schagen

Klein

Reijneveld

et al. 2014

European Journal of Cancer Supplements

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The potentially detrimental effects of cancer and related treatments on cognitive functioning are emerging as a key focus of cancer survivorship research. Many patients with central nervous system (CNS) or non-CNS tumours develop cognitive problems during the course of their disease that can result in diminished functional independence. We review the state of knowledge on the cognitive functioning of patients with primary and secondary brain tumours at diagnosis, during and after therapy, and discuss current initiatives to diminish cognitive decline in these patients. Similarly, attention is paid to the cognitive sequelae of cancer and cancer therapies in patients without CNS disease. Disease and treatment effects on cognition are discussed, as well as current insights into the neural substrates and the mechanisms underlying cognitive dysfunction in these patients. In addition, rehabilitation strategies for patients with non-CNS disease confronted with cognitive dysfunction are described. Special attention is given to knowledge gaps in the area of cancer and cognition, in CNS and non-CNS diseases. Finally, we point to the important role for cooperative groups to include cognitive endpoints in clinical trials in order to accelerate our understanding and treatment of cognitive dysfunction related to cancer and cancer therapies.

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Effect of Cancer Treatment on Neural Stem and Progenitor Cells

Cited by 7 publications

References 96 publications

Bone Marrow Chimeras to Study Neuroinflammation

Bone Marrow Chimeras to Study Neuroinflammation

Progenitors from the central nervous system drive neurogenesis in cancer

Monitoring and optimising cognitive function in cancer patients: Present knowledge and future directions

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