However what has been under investigation in this instance is the role of a particular HSP, Hsp90 in the Fanconi Anaemia pathway (Yamashita et al. 2007). Fanconi Anaemia (FA) is a recessive genetic disease characterised by congenital abnormalities, progressive bone marrow failure and susceptibility to leukaemia and solid tumours.
The FA pathway forms a core complex of proteins which are members of the body’s DNA damage response team. Hsp90 uses its chaperoning abilities to bring the protein FANCA to the core complex. If Hsp90 is inhibited the complex doesn’t form, leading to symptoms similar to those experienced by FA patients.
Since all cells, especially stem cells and tumour cells rely on DNA damage response pathways to continue their growth and survival, compromising the FA pathway for long periods could lead to the failure of tissues that depend on cell replication, as with bone marrow failure in FA patients. Research shows that tumour cells show increased expression and activity of Hsp90 to help them survive under high replicative stress. The paper thus implicates the use of Hsp90 inhibitors, such as 17-allylamino-17-demethoxygeldanamycin (17-AAG), to assist in the treatment of cancer by removing one of the main defences used by tumour cells making them more vulnerable to existing anti-tumour drugs.
References:
Primary source-
Yamashita, T., & Oda, T., & Sekimoto, T. (2007) Hsp90 and the Fanconi Anemia Pathway: A molecular link between protein quality control and the DNA damage response. Cell Cycle, 6(18), 2232-2235
https://www.landesbioscience.com/journals/cc/article/4653
Secondary source-
Pigliucci, M. (2002). Developmental genetics: Buffer zone. Nature, 417, 598-599
http://www.nature.com/nature/journal/v417/n6889/full/417598a.html
Also see
Wikipedia:
http://en.wikipedia.org/wiki/Fanconi_anemia
http://en.wikipedia.org/wiki/Heat_shock_protein
http://en.wikipedia.org/wiki/Chaperone
