A team of Australian scientists have discovered how some cancers are able to mutate into more aggressive and potentially fatal cancers in the human body.
The scientists from Monash University have found that a family of enzymes play a role in changing benign or less aggressive tumours into more deadly cancers.
The discovery provides a important clue into how cancer cells develop and mutate, and could ultimately lead to different treatment options for cancer victims.
The team of scientists led by Associate Professor Tony Tiganis, from the Department of Biochemistry and Molecular Biology, say the enzymes known as protein tyrosine kinases (PTKs) had a greater role than previously thought in the rate of growth and tumour change over time.
Professor Tiganis says it was already know that PTKs are linked with several types of aggressive cancers, including colon, breast and lung cancers, but they have now discovered that PTKs also have an important role to play as cancer cells grow and mutate to become potentially more aggressive tumours.
Tiganis says the more there is known about how tumours develop will mean the more able we are to prevent their growth in the future.
The researchers say there are already drugs that inhibit particular PTKs in the late stages of treatment and their discovery could change the timing of when and how those or similar drugs are administered.
Professor Tiganis says all cells routinely divide and duplicate during growth and an entire genome is replicated and divides equally into two daughter cells - but sometimes things go awry.
In an attempt to prevent this, Tiganis says nature has installed key cell checkpoints where molecular 'wardens' slow down DNA replication to try and correct mistakes and get the cell duplication back on track.
As a rule PTKs are turned off in the face of compromised DNA replication, but when PTK pathways remain on, unscheduled cell division can take place where cells distribute their DNA unevenly between the two resulting daughter cells and as a result, tumour cells can accumulate or lose genes and chromosomes, and gain a growth and survival advantage.
Professor Tiganis says their research has shown that PTK pathways are intimately associated with the regulation of checkpoint responses during DNA replication and they have identified one mechanism by which PTKs may remain activated and allow cancer cells to bypass the molecular warden of DNA replication.
Professor Tiganis says they may lack a key enzyme called TCPTP.
The Monash team now intend to apply their laboratory findings to human cancer samples to see if they contain low levels of TCPTP and hopefully cement the role of this protein in cancer formation and development.
The research is published in the international journal Cancer Cell.