ALK‐positive plasmablastic B‐cell lymphoma with the Clathrin‐ALK gene rearrangement

ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature

“…Thus, ALK gene rearrangements, originally thought to be uniquely associated with T-/null cell ALCL, have now been convincingly shown to occur in rare cases of B-cell lymphoma. [2][3][4][5][6][7][8][9][10][11][12][13] Of note, prior to the initial series by Delsol et al, 1 Arber et al 17 in 1996 reported NPM/ALK fusion transcripts (by RT-PCR) in four of 33 cases of large B-cell lymphoma. Interestingly, and in contrast to the cases of ALK-DLBCL reported thus far, these four cases had a conventional B-cell immunophenotype (CD20 þ and CD79a þ ).…”

“…1 Recently however, Clathrin/ALK (CLTC/ALK) and NPM/ALK gene rearrangements have been identified in 16 and three cases of ALK-DLBCL, respectively. [2][3][4][5][6][7][8][9][10][11][12][13] All of these cases display the morphologic and immunophenotypic features of ALK-DLBCL, as originally described by Delsol et al Importantly, ALK positivity and ALK gene rearrangements can be seen in B-cell lymphomas and are now no longer uniquely restricted to the T-cell lymphoma, ALCL. To our knowledge, only 29 cases of ALK-DLBCL have been reported thus far in the literature.…”

ALK+ histiocytosis: a novel type of systemic histiocytic proliferative disorder of early infancy

“…[12][13][14][15] Currently, only 3 other tumor types are known to exhibit ALK translocation and ALK expression-ALK ϩ large B-cell lymphomas, inflammatory myofibroblastic tumors, and less than 5% of non-small cell lung carcinomas. [16][17][18][19][20][21][22][23] This report expands the spectrum to include ALK ϩ histiocytosis. In all these proliferations, the formation of X-ALK homodimers/polymers using dimerization sites at the N-terminus of ALK partners mimics ligand binding, and is responsible for activation of the ALK catalytic domain and oncogenic properties of the fusion protein.…”

Oncogenic Anaplastic Lymphoma Kinase Rearrangements in Lymphoma

“…23 Similar to ALK + ALCL, the aberrant ALK expression in ALK + LBCL is also driven by 2p23/ALK translocations, of which t(2;17)(p23;q23) is the most frequent (65%). This aberration leads to a chimaeric CLTC-ALK protein and manifests as a distinctive granular cytoplasmic expression of ALK [27][28][29][30][31][32][33][34][35] (see Table 1 and Figure 3). Interestingly, only a few ALK + LBCL cases (13%) showed the t(2;5)(p23;q35)/NPM1-ALK rearrangement, commonly occurring in ALK + ALCL 25,[36][37][38] (see Table 1).…”