Udskriv Udskriv
Switch language
Rigshospitalet - en del af Københavns Universitetshospital

Leser–Trélat syndrome in malignant mesothelioma and pulmonary adenocarcinoma: is the EGFR pathway part of the syndrome?

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


  1. Reproducibility of histologic prognostic parameters for mantle cell lymphoma: cytology, Ki67, p53 and SOX11

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Methodological approach to Microscopic Colitis diagnosis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Lymphomas of the head and neck region: an update

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

  4. Prognostic significance of 1p36 locus deletion in adenoid cystic carcinoma of the salivary glands

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Oxidized resorbable cellulose (Gelita-cel) causing foreign body reaction in the mediastinum

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

The syndrome of Leser–Trélat (LT) is characterized by the sudden appearance of multiple seborrhoeic keratoses (SKs) in association with internal occult malignancy. Usually, the syndrome has been associated with adenocarcinoma, most frequently of the gastrointestinal tract and breast. The pathogenesis is unclear but might be explained by circulating tumor-associated growth factors. We present two thoracic malignancies associated with LT: adenocarcinoma of the lung (ACL) and pleural malignant mesothelioma (MM). Both malignant tumors expressed high levels of epidermal growth factor receptors (EGFR) detected by immunohistochemistry (IHC), with membranous staining on the majority of malignant cells corresponding to maximum IHC scores of 290 and 300, respectively, for the MM and the ACL. SKs revealed a universal membranous staining throughout the entire epithelium with no difference in EGFR expression between the two cases and two controls with no malignant history. By fluorescence in situ hybridization, no amplification of the EGFR gene in malignant tumors as well as in SK lesions was observed. Further investigations are needed to see whether tumor-associated EGFR ligands/EGFR autocrine loops in malignant cells expressing high levels of EGFR protein on the surface might play a role for the development of SKs, as well as for the growth of malignant tumors in LT.

TidsskriftVirchows Archiv : an international journal of pathology
Udgave nummer1
Sider (fra-til)117-20
Antal sider4
StatusUdgivet - jan. 2014

ID: 44705391