For patients with advanced cancer, the most difficult point in treatment often comes when standard options have been exhausted. At that stage, the challenge is no longer simply identifying what treatments exist, but determining which of them might still have a realistic chance of working.

That is the problem Cancer Commons is trying to address, according to its CEO, Clifford Reid.

The US nonprofit works with patients with advanced cancer to review treatment histories, interpret scientific evidence and identify potential next steps. Those can include clinical trials, further diagnostic testing or, in some cases, therapies that sit outside standard treatment guidelines.

“Cancer Commons helps cancer patients navigate to new options,” Reid said.

The organisation has also launched a clinical study aimed at patients who have exhausted treatments recommended under National Comprehensive Cancer Network guidelines, with the goal of exploring whether existing drugs used in other cancer settings could provide additional options.

For Reid, who has spent more than 30 years leading technology and life-sciences companies including Complete Genomics and Travera, the question is closely tied to the evolution of precision oncology itself.

The limits of the genomic revolution

The rise of genomic sequencing transformed oncology by allowing doctors to identify mutations that could make a tumour susceptible to a particular targeted drug.

Some of the field’s best-known successes have demonstrated the power of that approach. Reid points to Gleevec in chronic myeloid leukaemia as an early example of what precision medicine could achieve when a strong biological target is paired with an effective therapy.

But replicating that success across all cancers has proved far more difficult.

“The biggest challenge is more biomarkers,” Reid said.

While researchers have identified a number of clinically important genomic targets, Reid believes the simplest relationships between single mutations and highly effective drugs may already have been found.

The next advances, he argues, are likely to be more complicated, involving combinations of mutations, biological pathways and therapies rather than a single genetic alteration matched neatly to a single drug.

That complexity is one reason he sees growing potential in an approach known as functional precision medicine.

From predicting response to measuring it

Functional precision medicine takes a different route to treatment selection.

Instead of relying only on a tumour’s molecular profile to predict how it might respond, clinicians or researchers take living cancer cells from a patient and expose them to different drugs in the laboratory. The aim is to observe which therapies the cells appear most sensitive to.

Reid shifted much of his own work from genomics towards live-cell testing around a decade ago.

The attraction, he says, is particularly strong for patients who have already run through standard treatment pathways and may have little time to wait for new biomarkers or drugs to be developed.

He does not see functional testing as a replacement for genomic profiling. Rather, he argues that the two approaches could be used together.

“We think the combination of the two is going to be much stronger than either one individually,” he said.

That combination could become especially relevant when considering drugs that are already approved for one cancer type but are not routinely recommended for another.

In theory, a functional test could offer additional evidence that a particular tumour is sensitive to one of those medicines, helping clinicians decide whether an off-guideline treatment is worth considering.

A broader definition of a biomarker

The wider significance of functional testing may lie in the kind of information it produces.

Traditional precision oncology has focused heavily on molecular biomarkers: genetic mutations, proteins or other biological characteristics associated with response to a therapy.

Functional testing instead produces what Reid describes as a phenotypic or response biomarker — evidence based on what cancer cells actually do when exposed to a drug.

He believes combining those two forms of information could open a new phase in personalised cancer treatment.

The field still faces substantial barriers. Functional testing has historically received less funding and institutional support than genomic approaches, and wider clinical adoption will depend on stronger evidence, standardisation and support from major cancer organisations and healthcare systems.

But Reid believes momentum is beginning to shift.

Over the next five to ten years, he expects advances in molecular profiling to continue while functional precision medicine develops more rapidly alongside it.

If that happens, precision oncology may become less about finding a single mutation that dictates treatment and more about integrating multiple sources of evidence — genomic, biological and functional — to answer a more practical question for each patient: what is most likely to work now?

For patients who have reached the limits of standard care, that distinction could be critical.