Tumour brain: pre-treatment cognitive and affective disorders caused by peripheral cancers

Myrthe Mampay, Melanie Flint, Graham Sheridan

Research output: Contribution to journalArticlepeer-review


People that develop extracranial cancers often display co-morbid neurological disorders, such as anxiety, depression and cognitive impairment, even before commencement of chemotherapy. This suggests bidirectional crosstalk between non-CNS tumours and the brain, which can regulate peripheral tumour growth. However, the reciprocal neurological effects of tumour progression on brain homeostasis are not well understood. Here, we review brain regions involved in regulating peripheral tumour development and how they, in turn, are adversely affected by advancing tumour burden. Tumour-induced activation of the immune system, blood–brain barrier breakdown and chronic neuroinflammation can lead to circadian rhythm dysfunction, sleep disturbances, aberrant glucocorticoid production, decreased hippocampal neurogenesis and dysregulation of neural network activity, resulting in depression and memory impairments. Given that cancer-related cognitive impairment diminishes patient quality of life, reduces adherence to chemotherapy and worsens cancer prognosis, it is essential that more research is focused at understanding how peripheral tumours affect brain homeostasis.

Original languageEnglish
Pages (from-to)3977-3996
Number of pages20
JournalBritish Journal of Pharmacology
Issue number19
Publication statusPublished - 24 May 2021

Bibliographical note

Funding Information: G.K.S. is grateful for support from the Leverhulme Trust Research Project Grant (RPG‐2018‐443).


  • blood–brain barrier
  • cancer-related cognitive impairment
  • circadian rhythms
  • depression
  • hypothalamic–pituitary–adrenal axis
  • inflammation
  • stress
  • tumour brain
  • Pharmacology


Dive into the research topics of 'Tumour brain: pre-treatment cognitive and affective disorders caused by peripheral cancers'. Together they form a unique fingerprint.

Cite this