Variant ALK-fusion positive anaplastic large cell lymphoma (ALCL): A population-based paediatric study of the NHL-BFM study group
Language English Country England, Great Britain Media print-electronic
Document type Journal Article
Grant support
Hamburger Stiftung zur Foerderung der Krebsbekaempfung
Juli Harnack scholarship of the Foerdergemeinschaft Kinderkrebszentrum Hamburg e.V.
KinderkrebsInitiative Buchholz, Holm-Seppensen
Deutsche Kinderkrebsstiftung
PubMed
38279625
DOI
10.1111/bjh.19308
Knihovny.cz E-resources
- Keywords
- ALK positive ALCL, non‐Hodgkin's lymphoma, variant ALK,
- MeSH
- Anaplastic Lymphoma Kinase * genetics analysis MeSH
- Lymphoma, Large-Cell, Anaplastic * genetics pathology MeSH
- Child MeSH
- Oncogene Proteins, Fusion genetics MeSH
- Nuclear Proteins genetics metabolism MeSH
- Infant MeSH
- Humans MeSH
- Adolescent MeSH
- Nucleophosmin * MeSH
- Child, Preschool MeSH
- Prognosis MeSH
- Tropomyosin MeSH
- Check Tag
- Child MeSH
- Infant MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Child, Preschool MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- ALK protein, human MeSH Browser
- Anaplastic Lymphoma Kinase * MeSH
- Oncogene Proteins, Fusion MeSH
- Nuclear Proteins MeSH
- NPM1 protein, human MeSH Browser
- Nucleophosmin * MeSH
- TPM3 protein, human MeSH Browser
- Tropomyosin MeSH
Frequency, distribution and prognostic meaning of ALK-partner genes other than NPM1 in ALK-positive anaplastic large-cell lymphoma (ALCL) are unknown. Forty-nine of 316 ALCL diagnosed in the NHL-BFM study group showed no nuclear ALK expression suggestive of a variant ALK-partner; 41 were analysed by genomic capture high-throughput sequencing or specific RT-PCRs. NPM1::ALK was detected in 13 cases. Among the 28 patients with a non-NPM1::ALK-fusion partner, ATIC (n = 8; 29%) and TPM3 (n = 9; 32%) were the most common. Five of eight patients with ATIC::ALK-positive ALCL relapsed, none of nine with TPM3::ALK. Variant ALK-partners are rare and potentially associated with different prognoses.
Bioinformatics Core University Medical Centre Hamburg Eppendorf Hamburg Germany
Department of Pathology Medical University of Vienna Vienna Austria
Department of Pathology University of Wuerzburg Wuerzburg Germany
Faculty of Health Science and Medicine University of Lucerne Lucerne Switzerland
Institute of Human Genetics Ulm University and Ulm University Medical Centre Ulm Germany
See more in PubMed
Alaggio R, Amador C, Anagnostopoulos I, Attygalle AD, Araujo IBO, Berti E, et al. The 5th edition of the World Health Organization classification of haematolymphoid tumours: lymphoid neoplasms. Leukemia. 2022;36(7):1720–1748.
Elenitoba‐Johnson KS, Ott G, Takeuchi K, Klapper W, Lamant‐Rochaix L, d'Amore ESG, et al. ALK‐positive anaplastic large cell lymphoma. WHO classification of tumours editorial board Haematolymphoid tumours. Volume 11. 5th ed. Lyon (France): WHO Classification of Tumours Series, International Agency for Research on Cancer; 2022 [cited 2023 Oct 20]. Available from: https://tumourclassification.iarc.who.int/chapters/63
Falini B, Pulford K, Pucciarini A, Carbone A, De Wolf‐Peeters C, Cordell J, et al. Lymphomas expressing ALK fusion protein(s) other than NPM‐ALK. Blood. 1999;94(10):3509–3515.
Stein H, Foss HD, Durkop H, Marafioti T, Delsol G, Pulford K, et al. CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features. Blood. 2000;96(12):3681–3695.
Benharroch D, Meguerian‐Bedoyan Z, Lamant L, Amin C, Brugieres L, Terrier‐Lacombe MJ, et al. ALK‐positive lymphoma: a single disease with a broad spectrum of morphology. Blood. 1998;91(6):2076–2084.
Falini B, Bigerna B, Fizzotti M, Pulford K, Pileri SA, Delsol G, et al. ALK expression defines a distinct group of T/null lymphomas ("ALK lymphomas") with a wide morphological spectrum. Am J Pathol. 1998;153(3):875–886.
Perkins SL, Pickering D, Lowe EJ, Zwick D, Abromowitch M, Davenport G, et al. Childhood anaplastic large cell lymphoma has a high incidence of ALK gene rearrangement as determined by immunohistochemical staining and fluorescent in situ hybridisation: a genetic and pathological correlation. Br J Haematol. 2005;131(5):624–627.
Damm‐Welk C, Klapper W, Oschlies I, Gesk S, Rottgers S, Bradtke J, et al. Distribution of NPM1‐ALK and X‐ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular‐histological correlation. Br J Haematol. 2009;146(3):306–309.
Lamant L, McCarthy K, D'Amore E, Klapper W, Nakagawa A, Fraga M, et al. Prognostic impact of morphologic and phenotypic features of childhood ALK‐positive anaplastic large‐cell lymphoma: results of the ALCL99 study. J Clin Oncol. 2011;29(35):4669–4676.
Armstrong F, Duplantier MM, Trempat P, Hieblot C, Lamant L, Espinos E, et al. Differential effects of X‐ALK fusion proteins on proliferation, transformation, and invasion properties of NIH3T3 cells. Oncogene. 2004;23(36):6071–6082.
Armstrong F, Lamant L, Hieblot C, Delsol G, Touriol C. TPM3‐ALK expression induces changes in cytoskeleton organisation and confers higher metastatic capacities than other ALK fusion proteins. Eur J Cancer. 2007;43(4):640–646.
van der Krogt JA, Bempt MV, Ferreiro JF, Mentens N, Jacobs K, Pluys U, et al. Anaplastic lymphoma kinase‐positive anaplastic large cell lymphoma with the variant RNF213‐, ATIC‐ and TPM3‐ALK fusions is characterized by copy number gain of the rearranged ALK gene. Haematologica. 2017;102(9):1605–1616.
Ma Z, Hill DA, Collins MH, Morris SW, Sumegi J, Zhou M, et al. Fusion of ALK to the ran‐binding protein 2 (RANBP2) gene in inflammatory myofibroblastic tumor. Genes Chromosomes Cancer. 2003;37(1):98–105.
Pulford K, Lamant L, Espinos E, Jiang Q, Xue L, Turturro F, et al. The emerging normal and disease‐related roles of anaplastic lymphoma kinase. Cell Mol Life Sci. 2004;61(23):2939–2953.
Wehkamp U, Oschlies I, Nagel I, Brasch J, Kneba M, Gunther A, et al. ALK‐positive primary cutaneous T‐cell‐lymphoma (CTCL) with unusual clinical presentation and aggressive course. J Cutan Pathol. 2015;42(11):870–877.