CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth
EHA Learning Center. Jiménez-P R. Oct 1, 2018; 234246
Topic: 3A B-cell neoplasms and B-cell disorders
Raúl Jiménez-P
Raúl Jiménez-P
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Co-Authors: Carla Martín-Cortázar, Omar Kourani, Yuri Chiodo, Raul Cordoba, María Purificación Domínguez-Franjo, Juan Miguel Redondo, Teresa Iglesias, Miguel R. Campanero

Abstract: Tumor formation involves the acquisition of numerous capacities along the progression from a normal cell into a malignant cell, including limitless proliferation (immortalization) and anchorage-independent growth, a capacity that correlates extremely well with tumorigenesis. Great efforts have been made to uncover genes involved in tumor formation, but most genes identified participate in processes related to cell proliferation. Accordingly, therapies targeting these genes also affect the proliferation of normal cells. To identify potential targets for therapeutic intervention more specific to tumor cells, we looked for genes implicated in the acquisition of anchorage-independent growth and in vivo tumorigenesis capacity. A transcriptomic analysis identified CDCA7 as a candidate gene. Indeed, CDCA7 protein was upregulated in Burkitt’s lymphoma cell lines and human tumor biopsy specimens relative to control cell lines and tissues, respectively. CDCA7 levels were also markedly elevated in numerous T and B-lymphoid tumor cell lines. While CDCA7 was not required for anchorage-dependent growth of normal fibroblasts or non-malignant lymphocytes, it was essential but not sufficient for anchorage-independent growth of lymphoid tumor cells and for lymphomagenesis. These data suggest that therapies aimed at inhibiting CDCA7 expression or function might significantly decrease the growth of lymphoid tumors.

Article Number: 1669

Doi: 10.3324/haematol.2018.188961

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