U-HO1, a new cell line derived from a primary refractory classical Hodgkin lymphomaMader A.a · Brüderlein S.b · Wegener S.b · Melzner I.b · Popov S.b · Müller-Hermelink H.K.d · Barth T.F.b · Viardot A.c · Möller P.b
aHappareute, Röthenbach; bInstitute of Pathology and cDepartment of Hematology and Oncology, University of Ulm, Ulm; dInstitute of Pathology, University of Würzburg, Würzburg (Germany)
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The Hodgkin cell line U-HO1 was established from a malignant pleural effusion of a 23-year-old male patient during the end stage of refractory nodular sclerosing classical Hodgkin lymphoma (cHL). Since its establishment in 2005, U-HO1 has maintained stable characteristics in vitro and has a doubling time of about 4 days under standard culture conditions. U-HO1 forms typical Reed-Sternberg cells in suspension, is EBV negative, lacks HLA-A, -B, -C but expresses HLA-D proteins/CD74 and exposes CD15 together with CD30 in the absence of CD19 and CD20 on the cell surface. Karyotype analysis of U-HO1 revealed a hyperdiploid karyotype with multiple clonal aberrations. Most significant is an elongated chromosome 2, der(2)t(2;10)(q35; q16.1)add(2)(p13). CGH analysis revealed the following imbalances: ish cgh dim(1)(p13p31)(p12q21), enh(2)(p13p23), dim(4)(q31.3qter), enh(6)(q22q27), enh(12), enh(18), enh(20) (q13.1pter). FISH analysis showed about six-fold amplification of REL and BCL11A, thus, U-HO1 is prototypical for cHL in every aspect tested so far. As an outstanding feature compared to the existing HL cell lines, U-HO1 has high levels of microRNA transcripts of MIRN216 and MIRN217 located in the amplicon 2p16. Compared to other HL cell lines, U-HO1 proved far less genetically aberrant suggesting that U-HO1’s imbalances suffice to cause the full-blown phenotype of primary refractory cHL.
© 2008 S. Karger AG, Basel
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