Asset Details
Do you wish to reserve the book?
Glioblastoma, IDH-wildtype: A New Association with IgM Paraproteinaemic Neuropathy?
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Glioblastoma, IDH-wildtype: A New Association with IgM Paraproteinaemic Neuropathy?
Do you wish to request the book?
Glioblastoma, IDH-wildtype: A New Association with IgM Paraproteinaemic Neuropathy?
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Glioblastoma, IDH-wildtype: A New Association with IgM Paraproteinaemic Neuropathy?
2022
Overview
It is well recognized that B-cell clonal disorders such as Waldenstrom’s macroglobulinaemia may affect the central nervous system by direct infiltration of malignant B cells (Bing-Neel syndrome). However, there is no recognition in the current literature of a clear link between paraproteinaemia and primary brain tumours such as glioma. We present 3 cases of classical IgM paraproteinaemic neuropathy who developed glioblastoma in the course of their illness following treatment with chemoimmunotherapy (CIT). Due to the progressive symptomatic nature of their neuropathy, all 3 patients were treated with CIT. The patients presented with glioblastoma, IDH-wildtype at 9 months, 5 years, and 6 years following treatment completion. None of the patients had unequivocal evidence of known predisposing factors for glioblastoma. Both disorders are exceedingly rare and the chance of random association is less than one in a million. Potential common pathogenic mechanisms include the influence of paraproteins and circulating lymphoplasmacytic cells on blood-brain permeability and CNS immune micro-environment as well as raised circulating angiogenic cytokines such as vascular endothelial growth factor. In cases with anti-myelin-associated glycoprotein (MAG) antibodies, surface MAG on glial cells may act as a target releasing cells from growth inhibition. We suggest that all glioblastoma cases be screened at diagnosis for serum paraproteins and that such cases be reported to central registries to establish the frequency of the association more accurately.
Publisher
S. Karger AG,Karger Publishers
Subject
