A family of enzymes that play a crucial role in turning benign or less aggressive tumours into more potentially fatal cancers have been identified by researchers from Monash University.
The team led by associate professor Tony Tiganis, from the Department of Biochemistry and Molecular Biology at Monash University, has shown that enzymes known as protein tyrosine kinases (PTKs) had a greater role than previously thought in the rate of growth and tumour change over time.
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"We already know that PTKs are associated with several types of aggressive cancers, including colon, breast and lung cancers," said Prof Tiganis.
"What we have discovered is that PTKs have an important role to play as cancer cells grow and mutate to become potentially more aggressive tumours.
![Women and Cancer]( "Women and Cancer")
Cancer is one of the frequently talked about and most feared disease that falls under the genre of lifestyle diseases that have evolved, rather rapidly, in the past two decades.
"The more we can learn about how tumours develop, the more we are able to prevent their growth in the future.
"There are already drugs that inhibit particular PTKs in the late stages of treatment. Our discovery could change the timing of when and how those or similar drugs are administered," he added.
Tiganis said all cells routinely divide and duplicate during growth. An entire genome is replicated and divides equally into two daughter cells. Sometimes things go wrong.
To try to prevent this, there are natural cell surveillance checkpoints where molecular 'wardens' slow down DNA replication to try and correct mistakes to get the cell duplication back on track.
Generally, 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.
"Our studies have shown that PTK pathways are intimately associated with the regulation of checkpoint responses during DNA replication," Tiganis said.
"We have identified one mechanism by which PTKs may remain activated and allow cancer cells to bypass the molecular warden of DNA replication. They may lack a key enzyme called TCPTP," he added.
The study is published in international journal Cancer Cell.
Source: ANI
RAS/L
Women and Cancer
Cancer is one of the frequently talked about and most feared disease that falls under the genre of lifestyle diseases that have evolved, rather rapidly, in the past two decades.
Advertisement
"The more we can learn about how tumours develop, the more we are able to prevent their growth in the future.
"There are already drugs that inhibit particular PTKs in the late stages of treatment. Our discovery could change the timing of when and how those or similar drugs are administered," he added.
Tiganis said all cells routinely divide and duplicate during growth. An entire genome is replicated and divides equally into two daughter cells. Sometimes things go wrong.
To try to prevent this, there are natural cell surveillance checkpoints where molecular 'wardens' slow down DNA replication to try and correct mistakes to get the cell duplication back on track.
Generally, 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.
"Our studies have shown that PTK pathways are intimately associated with the regulation of checkpoint responses during DNA replication," Tiganis said.
"We have identified one mechanism by which PTKs may remain activated and allow cancer cells to bypass the molecular warden of DNA replication. They may lack a key enzyme called TCPTP," he added.
The study is published in international journal Cancer Cell.
Source: ANI
RAS/L
Liver Cancer - Animation
Liver is the largest organ inside the human body. It performs 500 different functions and processes 720 liters of blood per day. The important functions of the liver, the development of liver cancer and it's symptoms are presented in this interactive.
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