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Squamous cell carcinoma and adenocarcinoma of the oesophagus differ in risk factors, location, biology and treatment discussion. Adenocarcinoma of the lower oesophagus and gastro-oesophageal junction is usually discussed alongside gastric cancer, while squamous cell carcinoma has more in common with head and neck cancers.
Also called Esophageal cancer, Oesophageal squamous cell carcinoma, Oesophageal adenocarcinoma.
Start here
Oesophageal cancer is really two diseases sharing an organ, and the histological type decides which molecular conversation applies.
Squamous cell carcinoma and adenocarcinoma of the oesophagus differ in risk factors, location, biology and treatment discussion. Adenocarcinoma of the lower oesophagus and gastro-oesophageal junction is usually discussed alongside gastric cancer, while squamous cell carcinoma has more in common with head and neck cancers.
01Before any molecular question
Usually established first: histological type, tumour location within the oesophagus, stage, and whether the disease is resectable. Nutritional status and the ability to swallow are practical considerations that shape treatment sequencing.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
Squamous cell carcinoma
More common in the upper and middle oesophagus. Associated with tobacco and alcohol, and with a distinct molecular profile.
Adenocarcinoma
More common in the lower oesophagus and junction. Associated with reflux and Barrett oesophagus, and discussed largely alongside gastric cancer.
Locally advanced disease
Combined chemoradiation and surgical approaches organise the discussion.
Metastatic disease
Where marker status most directly shapes the systemic treatment discussion.
03What is discussed
PD-L1 expression is the marker most consistently assessed across both histologies. In adenocarcinoma, HER2 status, mismatch repair status and Claudin 18.2 are discussed in line with gastric cancer. In squamous cell carcinoma, TP53 alteration is near-universal, with CCND1 amplification, FGFR1 amplification and NOTCH1 alteration commonly seen but less often directly actionable. The practical consequence is that the histological type determines which panel of questions is relevant.
PD-L1
Assessed in both histologies, though scoring conventions differ between settings.
HER2 (ERBB2)
Relevant in adenocarcinoma, particularly at the junction. Not part of the squamous discussion.
MMR / MSI
Uncommon, but assessed in advanced disease.
Claudin 18.2
Relevant to junctional adenocarcinoma, alongside gastric cancer.
TP53
Near-universal in squamous disease. Descriptive rather than actionable.
FGFR1 and CCND1
Amplifications seen in squamous disease, of research interest.
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 first question is whether the histology is squamous or adenocarcinoma, because it determines which markers are worth requesting. In adenocarcinoma, HER2 and Claudin 18.2 belong in the request; in squamous disease they generally do not. PD-L1 applies to both. Biopsy tissue is often limited, so requesting markers together rather than sequentially is a practical concern.
Inherited risk is not usually a prominent part of the oesophageal cancer discussion. Rare syndromes exist, and a striking family history or very young onset can prompt evaluation, but this is not a routine question in the way it is for colorectal or breast cancer.
Cancer genetics and hereditary riskPlasma testing is used where tissue is limited, and serial ctDNA after curative-intent treatment is under study, particularly in adenocarcinoma where recurrence rates are high.
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
Histological type, PD-L1 score and prior therapy dominate eligibility. Squamous and adenocarcinoma trials are usually separate, so an imprecise histological designation can exclude a patient from the trials that actually apply.
| Term | What it means |
|---|---|
| Barrett oesophagus | A change in the lining of the lower oesophagus caused by long-term reflux, associated with increased adenocarcinoma risk. |
| Squamous cell carcinoma | A cancer arising from the flat lining cells. The predominant type in the upper oesophagus. |
| Junctional | Arising at the point where the oesophagus meets the stomach. Often grouped with gastric cancer. |
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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