One of medical science’s biggest mysteries is why cancer treatments work in one patient but not another. Researchers from Australia seem to be one step closer to solving the mystery. Their research delved deep into the smallest elements of a particular form of treatment-resistant ovarian cancer where they discovered these cancer cells use several means of fighting back against the chemotherapy that’s been used for the past few decades.
The study involved researchers from several research facilities in Australia:
- Professor Sean Grimmond, now at the University of Glasgow in Glasgow, Scotland, United Kingdom, was at the University of Queensland when the study was conducted.
- Professor David Bowtell, of the Peter MacCallum (Peter Mac) Cancer Centre in Melbourne.
- Professor Anna deFazio, of the Westmead Millennium Institute for Medical Research in Sydney.
- Dr. Ann-Marie Patch, of the QIMR Berghofer Medical Research Institute in Herston, Queensland.
These research team leaders and their colleagues examined tumors at the DNA level from 91 patients diagnosed with high-grade serous ovarian cancer (HGSC). This form of ovarian cancer, the most deadly, affects more than 1,300 Australian women each year.
Grimmond describes HGSC as a recurrent form of cancer that often develops resistance to the standard treatment being widely used today. During initial treatment, the tumor may shrink as desired but it often returns months, maybe years, later with such aggression that it cannot be destroyed. The standard treatment, a chemotherapy that relies on the use of platinum, targets the tumor, with the expectation it will damage the tumor’s DNA so badly it cannot survive. Although this has been the standard treatment for HGSC for 30 years, the survival rate hasn’t improved over time.
The research team discovered at least four ways the HGSC cells evade destruction, including the rearrangement of the cancer cell’s chromosomes. Grimmond describes this method of evasion as “fundamentally different to other cancers” where cancer treatments produce smaller, more gradual changes that eventually destroy individual genes within the cancer cell’s chromosomes.
Grimmond borrows computer lingo to describe how the rearrangement of the chromosomes escapes chemotherapy: “It is essentially shattering big chunks of the cell’s hard drive and moving them around, rather than just changing bits in the files.”
The 91 study participants allowed the researchers to extract tissue samples from their tumors at various stages of the disease, allowing the research team to document its evolution. Chromosomal changes were identified as treatment progressed.
“We now know that not only are there many sub-types of this disease (ovarian cancer), but there are also different sub-types of resistant disease, which has huge implications for designing future treatments,” said Grimmond.