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New Cellular Model May Increase Understanding of MCL Pathogenesis

Key clinical point: A novel clinically relevant cellular model may help improve understanding of the molecular and genetic pathogenesis of mantle cell lymphoma (MCL).

Major finding: The novel JeKo-1-spheroid cell line showed similar biological characteristics and enhanced tumorigenic capabilities compared with tumor cells enriched from MCL patients.

Study details: An integrated analysis of clinical and molecular data that included 4 patients with MCL.

Disclosures: The study was funded by the National Natural Science Fund, the Funds for Luzhou Medical College Applied Basic Research Plan, the Key Research Project from Health and Family Planning Commission of Sichuan Province, the National Natural Science Fund, the Key Research Project of Sichuan Education Department, and the Luzhou Science and Technology Project. The authors reported having no conflicts of interest.

Commentary

Mantle cell lymphoma is a uniquely heterogeneous cancer. Some patients die a few months after diagnosis with a highly proliferative blastoid variant that is highly treatment refractory while others may defer initial therapy for over a decade with no ill effects. It is likely that the combination of cell cycle dysregulation and DNA damage repair contribute to the relative aggressiveness of the lymphoma, with the cell cycle being linked to multiple other metabolic and immunological pathways. Studying the heterogeneity of MCL has been a challenging endeavor, owing to the rarity of the disease and its variants. Three-dimensional models that more closely mimic the tumor microenvironment may better support a heterogeneous group of tumor cells compared to standard cell lines in suspension. Models that capture some of the variability of MCL tumors may enable a deeper understanding of subclonal evolution and could help speed up the development of treatment strategies that better balance activity with quality of life for individual patients.—Peter Martin, MD

Citation:

Tang J et al. Genes Dis. 2018 Dec 21. doi: 10.1016/j.gendis.2018.12.002.