Tumor growth kinetics of human LM2-4LUC+ triple negative breast carcinoma cells

Cell culture and data set

Tumor growth data used in this study were obtained from experiments involving the use of a LM2-4^LUC+ cells (or LM2-4), a metastatic variant of the  human triple-negative breast carcinoma MDA-MB-231 cells. Animal studies were performed as described previously under Roswell Park Comprehensive Cancer Center (RPCCC) Institutional Animal Care and Use Committee (IACUC) protocol number 1227M [1-7]. Tumor growth data were pooled from eight separate experiments conducted with a total of 581 observations, and represent control (vehicle-treated) animals from published studies [1-7]. Vehicle formulation was carboxymethylcellulose sodium (USP, 0.5% w/v), NaCl (USP, 1.8% w/v), Tween-80 (NF, 0.4% w/v), benzyl alcohol (NF, 0.9% w/v), and reverse osmosis deionized water (added to final volume) and adjusted to pH 6 (see [3]) and was given at 10ml/kg/day for 7-14 days prior after tumor implantation and before tumor resection [1-7].

Tumor injections

LM2-4^LUC+ cells were orthotopically implanted (10⁶ cells per injection) into the right inguinal mammary fat pads of 6- to 8-week-old female severe combined immunodeficient (SCID) mice.

Tumor measurements

Tumor size was measured regularly with calipers to a maximum volume of  2 cm³, calculated by the formula 

\(V = \frac{\pi}{6} w^2 L\)

(ellipsoid) where L is the largest and w is the smallest tumor diameter.

Please cite: Vaghi C, Rodallec A, Fanciullino R, Ciccolini J, Mochel JP, et al. (2020) Population modeling of tumor growth curves and the reduced Gompertz model improve prediction of the age of experimental tumors, PLoS Comput Biol, 16, p. e1007178. https://doi.org/10.1371/journal.pcbi.1007178

In the file, the columns correspond to:

• ID: identifier of the animal
• Time: day of the tumor measurement after implantation
• Observation: tumor measurement (in mm³)

References

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[2] Benzekry S, Tracz A, Mastri M, Corbelli R, Barbolosi D, Ebos JML. (2016) Modeling Spontaneous Metastasis Following Surgery: An In Vivo-In Silico Approach. Cancer Res.;76(3):535–547. doi:10.1158/0008-5472.CAN-15-1389.

[3] Ebos JML, Lee CR, Bogdanovic E, Alami J, Van Slyke P, Francia G, et al. (2008) Vascular Endothelial Growth Factor-Mediated Decrease in Plasma Soluble Vascular Endothelial Growth Factor Receptor-2 Levels as a Surrogate Biomarker for Tumor Growth. Cancer Res.;68(2):521–529. doi:10.1158/0008-5472.CAN-07-3217.

[4] Ebos JML, Mastri M, Lee CR, Tracz A, Hudson JM, Attwood K, et al. (2014) Neoadjuvant antiangiogenic therapy reveals contrasts in primary and metastatic tumor efficacy. EMBO Mol Med;6:1561–76. https://doi.org/10.15252/emmm.201403989

[5] Ebos JML, Lee CR, Cruz-Munoz W, Bjarnason GA, Christensen JG, Kerbel RS. (2009) Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis. Cancer Cell;15:232–9. https://doi.org/10.1016/j.ccr.2009.01.021

[6] Mastri M, Tracz A, Lee CR, Dolan M, Attwood K, Christensen JG, et al. (2018) A Transient Pseudosenescent Secretome Promotes Tumor Growth after Antiangiogenic Therapy Withdrawal. Cell Rep.; 25 (13):3706–20 e8. Epub 2018/12/28. https://doi.org/10.1016/j.celrep.2018.12.017

[7] Vaghi C, Rodallec A, Fanciullino R, Ciccolini J, Mochel JP, et al. (2020) Population modeling of tumor growth curves and the reduced Gompertz model improve prediction of the age of experimental tumors, PLoS Comput Biol, 16, p. e1007178. https://doi.org/10.1371/journal.pcbi.1007178