Margaret Tyson was an honorary researcher at the Institute of Cancer Sciences, The University of Manchester and now researches epigenetics particularly in cancer and mental illness. She also runs Manchester Amputee Fitnesss Initiative and Karen's Page.
   

Margaret has been studying the effects of metformin on cancer risk. Metformin is used as a treatment for type 2 diabetes (T2D) but has other effects as well. It has been found that people with T2D are less likely to develop various cancers than those on other treatments.

Metformin works by inhibiting respiration thereby increasing energy requirement which is detected by AMPK (5'-adenosine monophosphate activated protein kinase) which acts to inhibit energy requiring actions such as cell growth and proliferation hence cancer growth is inhibited. There may be other mechanisms involved in metformin's effects.

Metformin has been shown to inhibit cancer stem cells which are low-metabolising and therefore difficult to target using other drugs. There are several trials underway to test metformin's efficacy and an anti-cancer drug.

Metformin reduces insulin resistance, increases glucose sensitivity and hence reduces diabetic morbidity and mortality. Although metformin's actions mainly depend on AMPK activation, AMPK independent actions have also been demonstrated. For instance, one of these is direct or indirect activation of the tumour suppressor LKB1 (serine–threonine kinase - liver kinase B1).

The puported mechanisms and actions of metformin are detailed here in this referenced text which is still in the process of being written and edited.

The text contains references to diagrams showing how metformin affects the mTOR and associated pathways. The diagrams and a more detailed description of these pathways is included on the next webpage.