Duodenal and nodal follicular lymphomas are distinct: the former lacks activation-induced cytidine deaminase and follicular dendritic cells despite ongoing somatic hypermutations.
Although most follicular lymphomas are believed to be of nodal origin, they sometimes originate from the duodenum. We have reported that the latter differ from nodal follicular lymphomas in having lower clinical stages and uniformly low histological grades, along with variable region of immunoglobulin heavy chain gene (VH) usage that is more similar to mucosa-associated lymphoid tissue (MALT) lymphomas. Little is known, however, about whether they possess other characteristics of nodal follicular lymphomas, particularly ongoing mutations with follicular dendritic cells. We examined 17 cases for which PCR identified the monoclonal bands of the immunoglobulin gene. The duodenal cases showed ongoing mutations, but they lacked activation-induced cytidine deaminase (AID) expression, a statistically significant difference from the nodal cases (P<0.001), and their follicular dendritic cell networks were disrupted. Moreover, not only were VH deviations observed but also they used very restricted VH genes. Although the mechanisms of ongoing mutation without AID and follicular dendritic cell were not clarified, restricted VH usage strongly suggested that antigen stimulation was involved, and that was similar to MALT lymphomas. In conclusion, duodenal follicular lymphomas were shown to be unique, in that they had ongoing hypermutations such as nodal cases, but the mechanisms involved in the hypermutation were quite different; furthermore, restricted VH usage suggested a strong similarity to the antigen-dependent origin of MALT lymphomas.
Takata
Katsuyoshi
K
Department of Pathology, Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Sato
Yasuharu
Y
Nakamura
Naoya
N
Kikuti
Yara Yukie
YY
Ichimura
Koichi
K
Tanaka
Takehiro
T
Morito
Toshiaki
T
Tamura
Maiko
M
Oka
Takashi
T
Kondo
Eisaku
E
Okada
Hiroyuki
H
Tari
Akira
A
Yoshino
Tadashi
T
D000368:Aged; D014408:Biomarkers, Tumor / Q000378:metabolism; D003564:Cytidine Deaminase / Q000378:metabolism*; D004273:DNA, Neoplasm / Q000032:analysis; D020566:Dendritic Cells, Follicular / Q000201:enzymology / Q000473:pathology*; D004379:Duodenal Neoplasms / Q000201:enzymology / Q000235:genetics / Q000473:pathology*; D005260:Female; D050438:Genes, Immunoglobulin Heavy Chain; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D019394:Ki-67 Antigen / Q000378:metabolism; D008198:Lymph Nodes / Q000196:embryology / Q000473:pathology*; D008224:Lymphoma, Follicular / Q000201:enzymology / Q000235:genetics / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D027041:Somatic Hypermutation, Immunoglobulin; D014178:Translocation, Genetic
D014408:Biomarkers, Tumor; D004273:DNA, Neoplasm; D019394:Ki-67 Antigen; D003564:Cytidine Deaminase