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Renal cell carcinoma is a family of diseases distinguished by histology. Clear cell renal cell carcinoma is the most common and has the most developed treatment landscape. Genomic profiling is less central here than in lung or colorectal cancer, but inherited syndromes are unusually important and specific subtypes carry specific implications.
Also called Renal cell carcinoma, RCC, Clear cell renal cell carcinoma.
Start here
Kidney cancer is classified by histological subtype rather than by mutation, and the subtype, not a genomic panel, is what most shapes the treatment discussion.
Renal cell carcinoma is a family of diseases distinguished by histology. Clear cell renal cell carcinoma is the most common and has the most developed treatment landscape. Genomic profiling is less central here than in lung or colorectal cancer, but inherited syndromes are unusually important and specific subtypes carry specific implications.
01Before any molecular question
Usually established first: histological subtype, stage, and whether the tumour is localised or metastatic. Many are found incidentally. In metastatic disease a risk classification based on clinical and laboratory features carries substantial weight in the treatment discussion, often more than any molecular finding.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
Clear cell renal cell carcinoma
The most common subtype. Characterised by VHL alteration and consequent hypoxia pathway activation, which underlies the antiangiogenic treatment class.
Papillary renal cell carcinoma
A distinct subtype where MET alterations are relevant, particularly in type 1.
Chromophobe and oncocytic tumours
Different biology again, and generally less responsive to the treatments used in clear cell disease.
Translocation renal cell carcinoma
Defined by TFE3 or TFEB rearrangements. More common in younger patients.
Collecting duct and renal medullary carcinoma
Rare and aggressive. Renal medullary carcinoma is associated with sickle cell trait and is characterised by SMARCB1 loss.
Sarcomatoid features
Can occur within any subtype and changes both prognosis and the treatment discussion.
03What is discussed
VHL alteration is characteristic of clear cell disease and underpins the antiangiogenic approach, though it is not used as a predictive test in routine practice. PBRM1, SETD2 and BAP1 are commonly altered chromatin genes; BAP1 loss is associated with more aggressive behaviour and raises a germline question. MET alterations matter in papillary disease. FH and SDH alterations define specific inherited syndromes with distinctive renal tumours. TFE3 and TFEB rearrangements define translocation carcinomas. The practical point is that in kidney cancer, subtype and inherited syndrome questions carry more weight than a broad mutation panel.
VHL
Characteristic of clear cell disease. Explains the biology rather than predicting response.
MET
Relevant in papillary renal cell carcinoma.
FH
Defines hereditary leiomyomatosis and renal cell cancer. Aggressive tumours, and a consequential inherited diagnosis.
BAP1
Associated with aggressive behaviour and with an inherited predisposition syndrome.
SDHB
Defines a rare inherited renal tumour syndrome.
TFE3 and TFEB
Rearrangements defining translocation renal cell carcinoma.
SMARCB1
Loss defines renal medullary carcinoma, which is associated with sickle cell trait.
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
Comprehensive profiling is less routine in kidney cancer than in several other solid tumours, and the higher-value questions are usually about subtype confirmation and inherited syndromes. Testing is more often discussed where the subtype is unusual, where the patient is young, where there are bilateral or multifocal tumours, or where a family history or associated features suggest a syndrome.
Kidney cancer has an unusually rich set of inherited syndromes: von Hippel-Lindau, hereditary leiomyomatosis and renal cell cancer (FH), Birt-Hogg-Dube (FLCN), hereditary papillary renal carcinoma (MET), succinate dehydrogenase-deficient renal cell carcinoma, tuberous sclerosis and BAP1 tumour predisposition. Prompts include young age, bilateral or multifocal tumours, a suggestive family history, and characteristic skin, uterine or other findings. These syndromes affect surveillance for the patient and for relatives, sometimes substantially.
Cancer genetics and hereditary riskKidney cancer sheds relatively little ctDNA compared with many other solid tumours, which limits how useful plasma testing is here. A negative plasma result carries less weight in this disease than it would in lung or colorectal cancer.
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 is usually written around histological subtype, risk group and prior therapy rather than around specific mutations. Non-clear-cell subtypes have their own distinct and smaller trial landscape, which is a reason to name the subtype precisely.
| Term | What it means |
|---|---|
| Clear cell | The most common kidney cancer subtype, named for how the cells look under a microscope. |
| Sarcomatoid features | A spindle-cell appearance that can occur in any subtype and indicates more aggressive behaviour. |
| Risk group | A classification based on clinical and laboratory features that guides treatment in metastatic kidney cancer. |
| Multifocal | More than one tumour in the same kidney. A prompt to consider an inherited syndrome. |
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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