Oncology

Glomus Tumor

Also known as paraganglioma of the jugular foramen, glomus jugulare, chemodectoma, SDHD mutation

Head and neck paragangliomas (also historically termed glomus tumours or chemodectomas) are rare, hypervascular neuroendocrine tumours arising from paraganglia associated with the jugular foramen (glomus jugulare), middle ear (glomus tympan

ORPHA:99913 ↗Gene SDHBGene SDHDGene SDHCPrevalence Less than 1 in 1,000,000Onset Adult (3rd–7th decade)Sporadic or hereditary (SDH gene mutations); autosomal dominant with parent-of-origin effect (SDHD)

1

studies recruiting now

as of 7 Sept 2026

4

studies registered in total

as of 7 Sept 2026

1

countries with a recruiting site

as of 7 Sept 2026

2 Feb 2024

most recent study posted

among recruiting studies

Recruiting trials

Showing the 1 most recently updated recruiting study, as recorded 7 Sept 2026. Live status on each study page.

Search all Glomus Tumor studies

Where recruiting studies are running

Countries with at least one recruiting site among the studies above, 7 Sept 2026. Tap a country to search trials there.

Keep watching

Get an email when a new Glomus Tumor study opens.

One email a day at most. Unsubscribe with one click.

Used only for these alerts. Privacy.

Support

Patient organisations

Pheo Para AlliancePatient association
Visit website ↗

Registry: ENSAT-CAP Registry · Join ↗. Registries connect patients to researchers and often hear about trials first.

About Glomus Tumor

Head and neck paragangliomas (also historically termed glomus tumours or chemodectomas) are rare, hypervascular neuroendocrine tumours arising from paraganglia associated with the jugular foramen (glomus jugulare), middle ear (glomus tympanicum), carotid bifurcation, or vagal body. Approximately 35–40% are caused by germline mutations in succinate dehydrogenase (SDH) subunit genes — SDHB, SDHC, and SDHD — with SDHD mutations accounting for the majority of hereditary head and neck paragangliomas due to its paternally imprinted expression. SDHB mutations confer the highest risk of malignant behaviour and metastasis among all SDH subtypes.

Common clinical features

Pulsatile tinnitus and conductive hearing loss from middle ear or jugular foramen involvementLower cranial nerve palsies (IX, X, XI, XII) from jugular foramen tumours causing dysphagia, hoarseness, and shoulder weaknessPalpable pulsatile neck mass at the carotid bifurcation in carotid body paragangliomaFacial nerve palsy from temporal bone invasionCatecholamine excess (hypertension, headache, palpitations, sweating) in functionally secreting tumours — less common than in adrenal phaeochromocytomaIntracranial extension causing headache, cerebellar signs, or raised intracranial pressureDistant metastases to bone, lung, and lymph nodes, particularly in SDHB-mutant tumours

From Orphanet’s phenotype annotations (CC BY 4.0). Not a complete list.

Before you apply

Things trial teams commonly ask about for Glomus Tumor. Not eligibility rules; those are set by each study.

  • Germline SDH gene sequencing (SDHB, SDHC, SDHD, SDHA, SDHAF2) is essential — SDHB mutation status is the strongest predictor of malignant potential and is frequently a stratification criterion in systemic therapy trials.
  • Functional imaging with 68Ga-DOTATATE PET-CT (somatostatin receptor scintigraphy) is the preferred staging modality and is often required to document extent of disease before trial enrolment.
  • Catecholamine and metanephrine secretory status must be assessed and, if elevated, managed with alpha-blockade before any surgical or interventional trial procedures to prevent hypertensive crisis.

Related conditions

Information, not medical advice. Trial listings are shown as recorded on ClinicalTrials.gov; whether any study is right for you is a decision for you and your clinicians, and eligibility is decided by each research team. Disease information from Orphanet (CC BY 4.0).