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Hepatocellular carcinoma arises in a liver that is usually already diseased, and liver function constrains treatment as much as tumour stage does. It can be diagnosed on imaging characteristics alone, which means tissue is often not available, and this is the main reason genomic profiling is less established here than in other solid tumours.
Also called HCC, Primary liver cancer.
Start here
Hepatocellular carcinoma is one of the few cancers usually diagnosed without a biopsy, and it is managed as two conditions at once: the tumour and the underlying liver disease.
Hepatocellular carcinoma arises in a liver that is usually already diseased, and liver function constrains treatment as much as tumour stage does. It can be diagnosed on imaging characteristics alone, which means tissue is often not available, and this is the main reason genomic profiling is less established here than in other solid tumours.
01Before any molecular question
Usually established first: the underlying liver condition and its severity, tumour burden and vascular involvement, and performance status. Staging systems for this disease incorporate liver function directly, which is unusual and reflects how much it constrains treatment.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
Very early and early stage
Where curative approaches including resection, ablation and transplantation are discussed.
Intermediate stage
Where locoregional approaches such as arterial therapies organise the discussion.
Advanced stage
Where systemic treatment leads, and where immune and antiangiogenic approaches dominate.
Decompensated liver disease
Where liver function rather than tumour stage becomes the limiting factor for any treatment.
03What is discussed
The commonly altered genes include TERT promoter, CTNNB1, TP53, ARID1A and AXIN1. None of these is currently a routine treatment target, which is the central point: comprehensive profiling in hepatocellular carcinoma less often changes management than in lung, breast or colorectal cancer. CTNNB1 alteration and Wnt pathway activation are of interest in relation to immune response. FGFR4 and MET pathways are research areas. Where profiling is done, an unexpected finding sometimes prompts reconsideration of whether the diagnosis is actually a different liver cancer, such as an intrahepatic cholangiocarcinoma or a mixed tumour.
TERT promoter
The most frequently altered region. Descriptive rather than actionable.
CTNNB1
Wnt pathway activation, of interest in relation to immune response.
TP53
Frequent and characteristic.
PD-L1
Assessed in some settings, though its predictive role here is less clear than in other cancers.
AFP
A serum protein, not a genomic marker, but part of the standard discussion.
This is not an exhaustive list, and which markers are relevant depends on the individual case. Not every marker listed is assessed in every patient.
04What is tested, and from what
The practical barrier is that a tissue diagnosis often does not exist, because imaging criteria are sufficient to diagnose the disease. Where profiling is being considered, the first question is whether obtaining tissue is justified by what would change. Profiling is more often discussed for trial access, or where the diagnosis itself is uncertain, than as a route to an approved targeted therapy.
Inherited risk is not usually prominent, though inherited conditions affecting the liver such as haemochromatosis and certain metabolic disorders raise risk indirectly. The dominant risk factors are acquired: chronic viral hepatitis, alcohol and metabolic liver disease.
Cancer genetics and hereditary riskctDNA is under study in hepatocellular carcinoma, and is of particular interest precisely because tissue is so often unavailable. Circulating markers are also studied for early detection in populations under surveillance for chronic liver disease.
More on ctDNA monitoring05The timing question
Testing that arrives after the decision it was meant to inform has already been made is a common and avoidable problem. This is the sequence in which molecular information tends to become relevant.
06Take these to your team
When a decision is being made
Questions worth raising with a treating team.
At progression, recurrence or resistance
The molecular picture at diagnosis is not always the molecular picture later.
07What shapes eligibility
Eligibility in hepatocellular carcinoma almost always specifies liver function grade and performance status alongside prior therapy. These non-molecular criteria exclude more patients than molecular ones do.
| Term | What it means |
|---|---|
| Cirrhosis | Advanced scarring of the liver. The setting in which most hepatocellular carcinoma arises. |
| Locoregional therapy | Treatment directed at the tumour within the liver rather than through the bloodstream. |
| Imaging diagnosis | Diagnosing this cancer from its appearance on scans, without a biopsy. Standard practice in the right clinical setting. |
| Child-Pugh and ALBI | Grading systems for liver function, used to decide what treatment is feasible. |
These are the services most often relevant to this cancer. Which of them applies is a clinical question, not an automatic one.
This entry is educational. It describes what is commonly discussed in this cancer, not what should happen for any individual. Which of it applies depends on the specific diagnosis, stage, prior treatment and the person themselves. Nothing here is a recommendation, and no list of biomarkers here is exhaustive. Decisions belong with a treating team who know the whole case.
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