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Distribution of NPM1‐ALK and X‐ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular–histological correlation
Author(s) -
DammWelk Christine,
Klapper Wolfram,
Oschlies Ilske,
Gesk Stefan,
Röttgers Silja,
Bradtke Jutta,
Siebert Reiner,
Reiter Alfred,
Woessmann Willi
Publication year - 2009
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2009.07754.x
Subject(s) - anaplastic lymphoma kinase , anaplastic large cell lymphoma , fusion gene , large cell , npm1 , biology , lymphoma , alk inhibitor , cancer research , pathology , gene , medicine , cancer , immunology , genetics , adenocarcinoma , karyotype , lung cancer , malignant pleural effusion , chromosome
Summary Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1‐ALK . The distribution of X‐ALK among 66 childhood ALCLs was analysed. One ALCL was ALK‐negative. Reverse transcription polymerase chain reaction detected NPM1‐ALK in 58 tumours, all showing nuclear and cytoplasmic ALK staining. The remaining seven ALCL stained for ALK in the cytoplasm only: two expressed TPM3‐ALK , one ATIC‐ALK , one MYH9‐ALK ; three no TPM3‐ , TFG‐ , ATIC‐ , CLTC‐ or MYH9‐ALK . Almost 90% of paediatric ALK‐positive ALCLs express NPM1‐ALK . There was complete concordance between ALK staining pattern and the presence of a typical/variant ALK fusion partner.