On average, 53 men and women will be diagnosed with breast cancer every day in Australia, and although that number is rising, fortunately the number of deaths from breast cancer is decreasing. In fact, Australia has one of the best breast cancer survival rates in the world and that’s partly driven by the wide-spread use of targeted and personalised treatment plans.
To understand a little more about how this precision and personalised medicine (PPM) works, we interviewed Medical Oncologist and Clinician Scientist, Dr Sanjeev Kumar, from Chris O’Brien Lifehouse.
To start with, Dr Kumar, could you please explain what targeted and personalised care is?
“Sure, basically, we create a treatment plan based on the specific characteristics of the patient’s cancer, the patient’s underlying medical history and their underlying hereditary precursors for their cancer. So that just means that we’re targeting a patient’s cancer due to its underlying causes, characteristics and quirks. We now have the capacity to really engineer specific treatment for a specific patient.”
When did this kind of treatment start to be used in Australia?
“Well, we’ve known for a long time that in about 75% of cases the female hormone, estrogen has been a driver for breast cancer and also a feeding source for the cancer. So, the staple care in patients, who have estrogen receptors on the surface of their breast cancer cells, is to block the cancer’s supply of estrogen or to alter the interaction between estrogen and the receptors for the breast cancer cells.
Over the last 20 years, though, we’ve gathered a lot more information about the other breast cancer subtypes and how we can specifically target a treatment for them. The big development there has been the release of a drug called Herceptin and other HER2-targeted drugs. HER2 is found on the outside of cancer cells and it stimulates cell growth. So, if we see HER2 positivity, where a patient’s HER2 level is higher than normal, we’ve got a whole other range of treatment available we can use to specifically target that patient’s cancer.”
What have been some of the other major developments in this field?
“I think the big development we’ve seen is the use of immune modulatory therapies with melanoma, kidney cancer, bladder cancer, and lung cancer. These immunotherapies give the immune system a kick up the bum to fight the cancer. Essentially, they take the brakes off the immune system and then harness this activation of the immune system to fight the cancer. So, we’re sort of taking what is otherwise a normal process in the body and putting it on steroids.”
Do immunotherapies work in breast or ovarian cancer?
“Generally, we know that breast cancer is less likely to have immune cells as a part of the cancer, but we’ve got what we call biomarkers as a way of predicting whether women will respond to these immune treatments or not. These include our histopathologists looking under a microscope to see if there are populations of immune cells in a particular breast cancer, as well as doing some gene sequencing to see if there is a higher number of mutations.”
Can these biomarkers be used in some of the rarer cases of breast cancer?
“Yes, by using these predictive markers with the rare subtypes of breast cancer, called triple-negative breast cancers (TNBC), we’ve now actually got a targeted treatment. As these kinds of cancers are negative for estrogen, progesterone and HER2, we never had a treatment for them, but we can now say have a targeted treatment in the fact that in a certain percentage of them we can use immunotherapy, with some effect.”
Are there any downsides to personalised treatment for breast and ovarian cancer?
“The downside of personalised treatment, I guess, is if you’re that piece of the jigsaw puzzle that doesn’t quite fit the characteristics or the biomarkers, we need to predict a response to these targeted treatments; then it can be challenging. However, I think using biomarkers is really important in any case, as it allows us to predict who’s going to benefit from these often quite expensive treatments and who aren’t.”
What can we expect from this kind of treatment in the future?
“So the big thing recently has been understanding that PARP inhibitors – which target DNA damage repair – are particularly important in patients who have hereditary or underlying familial causes for their breast cancer; particularly in women with BRCA1 and BRCA2 mutations. The evidence is very strong for ovarian cancer as well. We have evidence with metastatic (stage IV) breast cancer, when we in the second- or third-line treatment of women with BRCA mutations, that giving these tablet PARP inhibitors is better than physician’s choice chemotherapy. This is really exciting and that’s something that’s fairly new as well.
The other shift we’ve seen more recently is the trend towards using neoadjuvant chemotherapy (before surgery) in women with HER2 positive and triple-negative breast cancer or in women with slightly more aggressive or regionally advanced estrogen receptor positive breast cancer. This gives us the capacity to downgrade the patient’s cancers to make them more surgically operable, and it gives us individual insight into the biology of patient cancers. This allows us to specifically prognosticate patient cancers, so if patients respond really well to neoadjuvant treatment, they’re more likely to be better long-term survivors from their breast cancer, with a lower risk of recurrence.
A patient’s response to neoadjuvant treatment also dictates what we give them in the adjutant setting or the post-surgery setting in both HER2 positive and triple negative breast cancer, which has really, really exciting. So we’re using pre-surgical treatment to personalise treatment and I think that’s pretty cool. That’s pretty much the bread and butter of my clinical practice and I’m very excited about what it means for cancer patients in the future.”
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