Wednesday, 11 March 2015

Cancer and its cocktail future

The health industry is moving toward a future in personalised medicine; one where a cocktail of different immunotherapies targeted at different pathways may be combined and tailored to suit an individual’s needs.
The health industry is moving toward a future in personalised medicine; one where a cocktail of different immunotherapies targeted at different pathways may be combined and tailored to suit an individual’s needs.
Immunotherapy is hot, and most of the players with promising products in the pipeline are big pharma companies.
This much was evident at the American Society of Clinical Oncology (Asco) Conference last year.
One of the biggest cancer research conferences, the event hosted a population the size of a small town, with over 25,000 oncologists in attendance.
A good number of the big announcements related to specific pathways, such as PD 1 (programmed cell death ligand 1) Merck, AstraZeneca, Roche and Bristol Myers Squibb are active in this space, with a number moving into late-stage Phase III trials for its use in a variety of tumour types, including advanced non-small cell lung cancer.
Some of the excitement for these PD 1 drugs stems from the fact that the drugs (a type of immune checkpoint inhibitor, which means that they thwart the cancer’s ability to mask itself from the host immune system) may apply to a broad range of cancer types. When the conference took place in late May, Bioven wasn’t ready to go public.
“Asco is the world’s most obvious, prominent cancer congress in the world. In terms of scope, you have to be at the top of your game to be on the agenda,” says its CEO Steve Drew.
He explains how EGF therapy – which targets a very specific pathway – fits into this bigger picture.
Many of the immunotherapies right now are expected to be used as monotherapies and combination therapies.
In this sense, few of the drugs going to trial will actually be competing head to head, because each is targeted at a different pathway.
“Advances in medicine have led to a much better understanding of the complexities of diseases such as cancers,” says Drew.
“There is a drive toward patient-based treatment, which will require biomarker testing to guide specific treatments.”
(*The word “cancer” describes different sets of diseases characterised by the abnormal and uncontrolled growth of cells; for example, not all cases of non-small cell lung cancer will be caused by the same genetic mutation – there are multiple pathways which can lead to the uncontrolled division of cells.)
Drew offers an example: say a blood sample from a cancer patient shows a specific mutation. “He might be treated with one drug which targets the pathway being disrupted by that particular mutation.
“Now what happens often is, cancers are ‘clever’. In most patients, the pathways develop a resistance to therapy. The cancer switches pathways, (finding) another way to create havoc, to put it very simply.
“So then you would go to the second compound ... perhaps someone using a PD 1 drug as a primary treatment might then go on to use an EGF treatment.”
He says the result could be that instead of living 12 months, the patient may end up living for 24 months as a result of the combination therapy.
A consequence of this trend toward targeted therapies is that the industry will have to focus on smaller patient populations of diseases, such as the trend we see in lung cancer today.
“The challenge here is how to sustain a business model with a patient population of 4% of 490,000 people with a particular mutation requiring a particular treatment.
“This is a growing challenge not only for industry but also governments and healthcare providers.”
Either way, Drew envisions more combination studies where scientists investigate different cancer cell lines, looking at how different types of cancer react, to find optimal drug combination therapies.
“Large pharma companies don’t typically sit down ... and have coffee together. But if large pharma doesn’t do it, then scientists will certainly start asking these questions.”
How does EGF Immunotherapy work?
> For a cancer tumour to grow and proliferate into late-stage disease, it requires nutrients,
oxygen and other components such as growth factors.
> In lung cancer, the specific growth factor for stimulating tumour proliferation is known as
Epidermal Growth Factor (EGF).
> EGF therapy works a bit like a vaccine, except that unlike conventional vaccines which are
designed to induce antibodies towards infectious agents (such as those that cause hepatitis
or influenza), it induces antibodies against the growth factor.
> These antibodies neutralise the growth factor so that they no longer stimulate tumour
How is this therapy different?
> Many emerging immunotherapy drugs undermine the evasion tactics used by tumours.
> They either “unmask” tumours, allowing the body’s disease-fighting cells to attack them
or reinforce the immune system’s weaponry (e.g. programming its killer T-cells to be more
> EGF therapy, instead of trying to attack the tumour itself, cuts off the driver for further
tumour proliferation and metastatic spread. 
(Source: The Star Online, 12 February 2015,

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