Cell division leads chromosomes on a merry dance.
Every time a cell divides, its chromosomes go through a country dance. Forming pairs, they line up in a neat row, facing each other, before dramatically shimmying to opposite ends of the room along long ‘spindles’ of protein.
Having split its dancing partners, the cell pinches itself in two and separates them forevermore. The spindle is a crucial part of this dance: without it, the chromosomes never separate and the cell can’t divide.
To try to exploit this, some cancer drugs such as taxanes work by interfering with cancer cells’ spindles, stopping them from dividing. But over time, tumour cells can adapt to become resistant to these drugs.
This can be particularly frustrating in treating ovarian cancers. Often patients fare extremely well after their first round of chemo, only to find their cancer starts growing again. This makes the disease particularly difficult to treat, as patients often need many rounds of chemotherapy.
Recognising this, an international research group led by one of our scientists, Dr Ahmed Ahmed, who has recently moved from the University of Cambridge to Oxford University, and Dr Robert Bast, from the University of Texas M.D. Anderson Cancer Center, has been trying to crack this problem by hunting down the genes responsible for this resistance, with the ultimate aim of developing new drugs to overcome the problem.
Their latest, somewhat surprising discovery was revealed in Cancer Cell this week. The team has found a new player in ovarian cancer drug resistance – a gene previously only known to be involved in helping fat and liver cells recover from starvation. It now turns out this gene also plays a key role in helping the spindle form during cell division, and thus helping cancer’s genetic dancers do their dance.
Here’s a short interview with Dr Ahmed, explaining more about the team’s research and what they found: