Abstract:
:Burkitt lymphoma (BL) is classified into 3 clinical subsets: endemic, sporadic, and immunodeficiency-associated BL. So far, possible differences in their gene expression profiles (GEPs) have not been investigated. We studied GEPs of BL subtypes, other B-cell lymphomas, and B lymphocytes; first, we found that BL is a unique molecular entity, distinct from other B-cell malignancies. Indeed, by unsupervised analysis all BLs clearly clustered apart of other lymphomas. Second, we found that BL subtypes presented slight differences in GEPs. Particularly, they differed for genes involved in cell cycle control, B-cell receptor signaling, and tumor necrosis factor/nuclear factor κB pathways. Notably, by reverse engineering, we found that endemic and sporadic BLs diverged for genes dependent on RBL2 activity. Furthermore, we found that all BLs were intimately related to germinal center cells, differing from them for molecules involved in cell proliferation, immune response, and signal transduction. Finally, to validate GEP, we applied immunohistochemistry to a large panel of cases and showed that RBL2 can cooperate with MYC in inducing a neoplastic phenotype in vitro and in vivo. In conclusion, our study provided substantial insights on the pathobiology of BLs, by offering novel evidences that may be relevant for its classification and possibly future treatment.
journal_name
Bloodjournal_title
Bloodauthors
Piccaluga PP,De Falco G,Kustagi M,Gazzola A,Agostinelli C,Tripodo C,Leucci E,Onnis A,Astolfi A,Sapienza MR,Bellan C,Lazzi S,Tumwine L,Mawanda M,Ogwang M,Calbi V,Formica S,Califano A,Pileri SA,Leoncini Ldoi
10.1182/blood-2010-08-301556subject
Has Abstractpub_date
2011-03-31 00:00:00pages
3596-608issue
13eissn
0006-4971issn
1528-0020pii
blood-2010-08-301556journal_volume
117pub_type
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