ALK-positive Diffuse Large B-cell Lymphoma With the t(2;17)(p23;q23)

2009 ◽  
Vol 17 (2) ◽  
pp. 172-177 ◽  
Author(s):  
Da Zhang ◽  
Ryan C. Denley ◽  
Daniel A. Filippa ◽  
Julie Teruya-Feldstein
2018 ◽  
Vol 101 ◽  
pp. S25
Author(s):  
Werner Kempf ◽  
Rocco Torricelli ◽  
Andreas Zettl ◽  
Michele Ghielmini

Pathology ◽  
2019 ◽  
Vol 51 ◽  
pp. S81
Author(s):  
Samuel Foong ◽  
Sonu Nigam ◽  
Tara Cochrane

2009 ◽  
Vol 40 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Shuji Momose ◽  
Jun-ichi Tamaru ◽  
Hirohisa Kishi ◽  
Ittaku Mikata ◽  
Masaya Mori ◽  
...  

2009 ◽  
Vol 2 (1) ◽  
pp. 11 ◽  
Author(s):  
Brady Beltran ◽  
Jorge Castillo ◽  
Renzo Salas ◽  
Pilar Quiñones ◽  
Domingo Morales ◽  
...  

Blood ◽  
2003 ◽  
Vol 102 (7) ◽  
pp. 2638-2641 ◽  
Author(s):  
Pascale De Paepe ◽  
Mathijs Baens ◽  
Han van Krieken ◽  
Bruno Verhasselt ◽  
Michel Stul ◽  
...  

Abstract We present 3 cases of large B-cell lymphoma (LBCL) with a granular cytoplasmic staining for anaplastic lymphoma kinase (ALK). All of the cases showed striking similarities in morphology and immunohistochemical profile characterized by a massive monomorphic proliferation of CD20-/CD138+ plasmablast-like cells. In one of the cases, initially diagnosed as a null-type anaplastic large cell lymphoma (ALCL), the B-cell phenotype became evident only at recurrence. Fluorescent in situ hybridization (FISH) and molecular studies led to the detection of a CLTC-ALK rearrangement in all 3 cases, without any evidence of full-length ALK receptor expression. The associated t(2;17)(p23;q23) was demonstrated in the karyotype of 2 cases. Although a similar CLTC-ALK aberration was previously identified in ALK-positive T-/null cell ALCL and inflammatory myofibroblastic tumor, its association with ALK-positive LBCL seems to be specific and intriguing. (Blood. 2003;102:2638-2641)


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