Where it comes from
- Made in
- Most cells, highest in the developing brain and in many cancers
- Sent out by
- Intracellular above all; released by injured cells
- Acts on
- Actin
- Tumour and endothelial cells
What it does
- Buffers actin like thymosin beta-4
- Promotes or restrains tumour spread depending on the cancer studied
- One of three peptides the subcommissural organ secretes into the fetal brain to support its development in mice 4
In medicine
- No medicine, and nothing is measured through it in practice
- Studied as a marker in several cancers: in papillary thyroid cancer the gene is amplified in the aggressive, metastatic tumours 2
Beyond the body’s own use
- Not a treatment and not in trials. What is studied is its two faces in cancer: forced into tumour cells it bound Ras, cut off vessel growth and shrank human ovarian tumours in mice, the opposite of what its level in human tumours suggests 3
- Whether it does anything outside the cell in people is unsettled: it has no receptor of its own, and the actin it binds is inside the cell 1
Sources
- Yu et al., Thymosin beta 10 and thymosin beta 4 are both actin monomer sequestering proteins, Journal of Biological Chemistry 1993
- Fehér et al., Amplification of thymosin beta 10 in aggressive papillary thyroid carcinomas, Pathology and Oncology Research 2012
- Lee et al., Thymosin beta-10 inhibits angiogenesis and tumour growth by interfering with Ras, Cancer Research 2005
- Zhang et al., The subcommissural organ regulates brain development via secreted peptides, Nature Neuroscience 2024
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.