microRNA expression profiling identifies molecular signatures associated with anaplastic large cell lymphoma

Liu, Cuiling; Iqbal, Javeed; Teruya‐Feldstein, Julie; Shen, Yulei; Dabrowska, Magdalena; Dybkær, Karen; Lim, Megan S.; Piva, Roberto; Barreca, Antonella; Pellegrino, Elisa; Spaccarotella, Elisa; Lachel, Cynthia M.; Küçük, Can; Jiang, Chong; Hu, Xiaozhou; Bhagavathi, Sharathkumar; Greiner, Timothy C.; Weisenburger, Dennis D.; Aoun, Patricia; Perkins, Sherrie L.; McKeithan, Timothy W.; Inghirami, Giorgio; Chan, Wing C.

doi:10.1182/blood-2012-08-447375

Cited by 84 publications

(79 citation statements)

References 48 publications

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“…Expression profiling of these lymphomas/leukemias provides an important insight into the oncogenic mechanisms triggered by this oncogenic miR cluster. MiR-17∼92 has been linked to multiple cancers, and its expression signature was observed in various lymphomas, including anaplastic large cell lymphomas, by a recent study (12). A study by Fassina et al (13) demonstrated the utility of the miR-17∼92 cluster as a diagnostic tool in large B-cell malignancies.…”

Section: Discussionmentioning

confidence: 99%

B-cell malignancies in microRNA Eμ-miR-17∼92 transgenic mice

Sandhu

Fassan

Volinia

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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miR-17∼92 is a polycistronic microRNA (miR) cluster (consisting of miR-17, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a) which frequently is overexpressed in several solid and lymphoid malignancies. Loss-and gain-of-function studies have revealed the role of miR-17∼92 in heart, lung, and B-cell development and in Mycinduced B-cell lymphomas, respectively. Recent studies indicate that overexpression of this locus leads to lymphoproliferation, but no experimental proof that dysregulation of this cluster causes B-cell lymphomas or leukemias is available. To determine whether miR-17∼92-overexpression induces lymphomagenesis/leukemogenesis, we generated a B-cell-specific transgenic mouse model with targeted overexpression of this cluster in B cells. The miR-17∼92 overexpression was driven by the Eμ-enhancer and Ig heavy-chain promoter, and a 3′ GFP tag was added to the transgene to track the miR expression. Expression analysis using Northern Blot and quantitative RT-PCR confirmed 2.5-to 25-fold overexpression of all six miRs in the transgenic mice spleens as compared with spleens from wild-type mice. Eμ-miR-17∼92 mice developed B-cell malignancy by the age of 12-18 mo with a penetrance of ∼80% (49% splenic B-cell lymphoproliferative disease, 28% lymphoma). At this stage mice exhibited severe splenomegaly with abnormal B-cell-derived white pulp expansion and enlarged lymph nodes. Interestingly, we found three classes of B-cell lymphomas/leukemias at varying grades of differentiation. These included expansion of CD19 + and CD5 + double-positive B cells similar to the aggressive form of human B-cell chronic lymphocytic leukemia, B220 + CD43 + B1-cell proliferation, and a CD19 + aggressive diffuse large B-cell lymphoma-like disease, as assessed by flow cytometry and histopathological analysis. miR-17∼92 cluster | animal model | SLC/ABC transporters M icroRNAs (miRs) are 21-to 22-nucleotide-long noncoding RNA molecules that regulate the expression of multiple cellular genes, and their dysregulation is involved in many human diseases including cancer. The MiR-17∼92 cluster frequently is up-regulated in several different malignancies including diffuse large B-cell lymphoma (DLBCL) (1) and lung cancer (2, 3). The MiR-17∼92 cluster is encoded by the chromosome 13q31 locus in humans and the 14qE4 locus in mice. This genomic region is amplified in DLBCLs and several other tumors (reviewed in ref. 4). The cluster consists of six miRs (miR-17, 18a, 19a, 20a, 19b-1, and 92a-1) and has two paralogs in the genome, miR-106a∼363 and miR-106b∼25, proposed to have arisen through series of duplication and deletion events during vertebrate evolution (5).The first suggestion for its possible role in oncogenesis came from the study in Eμ-Myc mice in which enforced expression of miR-17∼92 was shown to accelerate B-cell tumor development (6). An additional study that investigated the role of miR-17∼92 in mice by driving its overexpression under the human CD2 promoter in both B and T cells found that mice overexpressing the miR-17∼92 clust...

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Section: Discussionmentioning

confidence: 99%

B-cell malignancies in microRNA Eμ-miR-17∼92 transgenic mice

Sandhu

Fassan

Volinia

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…Similarly to miRNA-146a, miRNA-155 has also been implicated in a variety of pathologies 8,9,10 . However, in the case of SS and in relation to the viral differentially expressed microRNA reported in this article, the relation of miRNA-155 to Epstein-Barr virus infection (EBV) 11,12 and the association of this microRNA to lymphomas deserve further evaluation 13,14,15 .…”

Section: Human and Viral Microrna Expression In Sjögren Syndromementioning

confidence: 99%

Human and Viral microRNA Expression in Sjögren Syndrome

Cotrim

Alevizos

2014

J Rheumatol

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“…RT-PCR analysis of TNFRSF8, BATF3, and TMOD1 successfully distinguished ALK-negative ALCL from PTCL, NOS [44]. MicroRNA expression profiling identified molecular signatures that differentiated ALK-negative ALCL from other PTCLs [45]. A balanced translocation that disrupted the DUSP22 phosphatase gene on chromosome 6p25.3 and adjoined the FRA7H fragile site on chromosome 7q32.3 was identified in up to 45 % of ALK-negative ALCL cases [46].…”

Section: Alk-negative Alclmentioning

confidence: 97%

Peripheral T cell lymphoma in Asia

Park

2014

Int J Hematol

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Peripheral T-cell lymphomas (PTCLs) comprise a heterogeneous group of mature T-and NK-cell neoplasms, the incidence of which is higher in Asian countries than in Western countries. Although its etiology is mainly unknown, several risk factors (such as genetic factors, abnormal immunity, environmental factors, and infectious causes) have been proposed. PTCL are classified based on a combination of several parameters, including morphology, site of presentation, viral status, immunophenotype, and specific genetic alterations. Their classification is ongoing, with the emergence of new entities and refinement of existing entities because of the development of diagnostic markers and new genetic alterations. This review presents epidemiologic data for PTCL in Asia, together with recent progress in the pathology of PTCL compared with the WHO 2008 classification.Epidemiology T-and NK-cell lymphomas are uncommon: overall, they represent fewer than 25 % of all non-Hodgkin's lymphoma (NHL) [1][2][3]. The occurrence rates of various subtypes of T-and NK-cell lymphomas in Asia are significantly different from those observed in Western countries, and even among Asian countries. The incidence and distribution of T-and NK-cell lymphomas in several Asian countries is summarized in Fig. 1 and Table 1 [ [4][5][6][7][8][9][10][11][12][13][14][15].The frequencies of T-and NK-cell lymphomas seem to increase from West to East Asia. The occurrence rate of Tand NK-cell lymphomas are relatively low (\20 % of NHL) mainly in West Asia (Turkey 16.2 %, Iraq 19 %, and Kuwait 18 %) and South Asia (Pakistan 11.3 %, and India 20.2 %), but relatively high mainly in East Asia (China 32.5 %, Korea 22 %, and Japan 24.9 %) and Southeast Asia (Thailand 25 %). The proportion of T-and NK-cell lymphomas in Taiwan is very low (13.3 %) compared with that of other East Asian countries. Regarding the subtypes of T-and NK-cell lymphomas, two West (Turkey and Iraq) and one South (Pakistan) Asian countries share similar distribution patterns, presenting T lymphoblastic lymphoma (T-LBL) as the most common subtype, followed by peripheral T-cell lymphoma (PTCL) or anaplastic largecell lymphoma (ALCL). The frequency of mycosis fungoides/sezary syndrome (MF/SS) is very high in Kuwait. The distribution patterns of T-and NK-cell lymphomas in Thailand, Taiwan, and Korea are similar, whereas adult T-cell leukemia/lymphoma (ATLL) represents a high proportion of T-and NK-cell lymphomas in Japan. When ATLL is excluded, four countries (Thailand, Taiwan, Korea, and Japan) exhibit very similar patterns of subtype distribution of T-and NK-cell lymphomas. Extranodal NK/ T-cell lymphoma (ENKL) is frequent in China (48 %) and Korea (28.7 %), but is less frequent in Japan (10.4 %), as reported by a recent study performed by an international T-cell project [2]. In China, the frequency of T-or NK-cell lymphoma varies according to geographic region

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microRNA expression profiling identifies molecular signatures associated with anaplastic large cell lymphoma

Cited by 84 publications

References 48 publications

B-cell malignancies in microRNA Eμ-miR-17∼92 transgenic mice

B-cell malignancies in microRNA Eμ-miR-17∼92 transgenic mice

Human and Viral microRNA Expression in Sjögren Syndrome

Peripheral T cell lymphoma in Asia

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