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Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428

ABSTRACT: We identified copy number changes associated with fusion transcripts and breakpoints on chromosomes 15 and 16. Data integration with RNAseq data

ORGANISM(S): Homo sapiens

SUBMITTER: Christian Steidl

PROVIDER: E-GEOD-25989 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Hodgkin lymphoma

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2010-12-11 | E-GEOD-25990 | biostudies-arrayexpress

Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428

Project description:We identified copy number changes associated with fusion transcripts and breakpoints on chromosomes 15 and 16.

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Melittin Increases Cisplatin Sensitivity and Kills KM-H2 and L-428 Hodgkin Lymphoma Cells.

Project description:Hodgkin lymphoma (HL) is neoplasia with high cure rates. However, not all patients can be cured with the current treatment. Chemo-resistance of tumor cells is one factor involved in treatment failure. In addition to its pore-forming activity on lipid bilayer membranes, the toxin melittin from bee venom is an inhibitor of several cancer-related signaling pathways. Moreover, melittin analogs have been shown to inhibit the activity of ATP binding cassette (ABC) transporters which are known to play important roles in the chemo-resistance of tumor cells. Therefore, we tested the toxicity of melittin for HL cell lines KM-H2 and L-428 and whether melittin can increase the chemo-sensitivity of cisplatin-resistant HL cells. We found high toxicity of melittin for KM-H2 and L-428 cells. In co-cultures with normal blood cells, melittin preferentially killed KM-H2 and L-428 cells. In addition, we observed increased cisplatin sensitivity of chemo-resistant L-428 cells after treatment with melittin. ABC transporter activity was not reduced after treatment with melittin. Our data suggest that melittin or melittin analogs might be promising agents for the future development of treatment strategies for HL patients with resistant disease.

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