APA (7th ed.) Citation

S, S., M, I., S, T., Y, H., H, M., S, K., . . . JM, C. (2016). Production of truncated MBD4 protein by frameshift mutation in DNA mismatch repair-deficient cells enhances 5-fluorouracil sensitivity that is independent of hMLH1 status. Cancer biology & therapy, 17(7), 760. https://doi.org/10.1080/15384047.2016.1178430

Chicago Style (17th ed.) Citation

S, Suzuki, Iwaizumi M, Tseng-Rogenski S, Hamaya Y, Miyajima H, Kanaoka S, Sugimoto K, and Carethers JM. "Production of Truncated MBD4 Protein by Frameshift Mutation in DNA Mismatch Repair-deficient Cells Enhances 5-fluorouracil Sensitivity That Is Independent of HMLH1 Status." Cancer Biology & Therapy 17, no. 7 (2016): 760. https://doi.org/10.1080/15384047.2016.1178430.

MLA (9th ed.) Citation

S, Suzuki, et al. "Production of Truncated MBD4 Protein by Frameshift Mutation in DNA Mismatch Repair-deficient Cells Enhances 5-fluorouracil Sensitivity That Is Independent of HMLH1 Status." Cancer Biology & Therapy, vol. 17, no. 7, 2016, p. 760, https://doi.org/10.1080/15384047.2016.1178430.