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1.
Figure 3

Figure 3. Survival of SCID, NOD-SCID and NSG mice following resection of the primary tumour.. From: Differential Post-Surgical Metastasis and Survival in SCID, NOD-SCID and NOD-SCID-IL-2Rγnull Mice with Parental and Subline Variants of Human Breast Cancer: Implications for Host Defense Mechanisms Regulating Metastasis.

Metastatic spread and survival were monitored after resection of the primary tumour. Each graph shows the differences in survival of SCID, NOD-SCID and NSG mice for each cell line. Numbers represent the difference in median survival from the median survival of SCID mice (first row) and NSG mice (second row). Dashed line shows 50% survival. Statistical analysis was assessed by ANOVA.

Chloe C. Milsom, et al. PLoS One. 2013;8(8):e71270.
2.
Figure 5

Figure 5. The effect of luciferase on metastatic burden in SCID, NOD-SCID and NSG mice.. From: Differential Post-Surgical Metastasis and Survival in SCID, NOD-SCID and NOD-SCID-IL-2Rγnull Mice with Parental and Subline Variants of Human Breast Cancer: Implications for Host Defense Mechanisms Regulating Metastasis.

(A) Histograms showing the number of mice with metastases in various organs following implantation and resection of the parental MDA-MB-231 cell line or the luciferase-tagged parental cell line (231P/luc+). A greater metastatic burden was observed in NSG mice compared to either SCID or NOD-SCID mice, in which multiple organs were affected. (B) Whole body bioluminescence images of the emerging metastases in SCID, NOD-SCID and NSG mice following resection of a primary orthotopic tumour generated by implantation of the 231P/luc+ cell line.

Chloe C. Milsom, et al. PLoS One. 2013;8(8):e71270.
3.
Figure 2

Figure 2. Variation in primary tumour growth in the different strains of immune-deficient mice.. From: Differential Post-Surgical Metastasis and Survival in SCID, NOD-SCID and NOD-SCID-IL-2Rγnull Mice with Parental and Subline Variants of Human Breast Cancer: Implications for Host Defense Mechanisms Regulating Metastasis.

The parental MDA-MB-231 (A) or the luciferase-tagged parental cell line (231P/luc+) (B) were injected into the right inguinal mammary fat pad of female SCID, NOD-SCID or NSG mice (2×106 cells). Tumour growth was monitored twice weekly and the values for all 8 mice were plotted to show the amount of variation in tumour volume at each time point. Line represents the median value.

Chloe C. Milsom, et al. PLoS One. 2013;8(8):e71270.
4.
Figure 4

Figure 4. Comparison of survival of SCID, NOD-SCID and NSG mice after primary tumour resection.. From: Differential Post-Surgical Metastasis and Survival in SCID, NOD-SCID and NOD-SCID-IL-2Rγnull Mice with Parental and Subline Variants of Human Breast Cancer: Implications for Host Defense Mechanisms Regulating Metastasis.

Following resection of the primary tumour, metastatic spread and survival were monitored. (A) Comparison of survival of each mouse strain after removal of MDA-MB-231, 231P/luc+, LM2-4/luc+ or 164/8-1B/luc+ primary tumours. Dashed line shows 50% survival. Numbers represent median survival and significance (P<0.05) was assessed by ANOVA. (B) Upon sacrifice, the lung and liver weights were recorded and calculated as a percentage of the total body weight. The relative lung and liver weights of NSG mice were significantly higher than those of NOD-SCID and SCID mice (**p = 0.001 and ***p<0.0001, respectively). Statistical analysis was assessed by ANOVA.

Chloe C. Milsom, et al. PLoS One. 2013;8(8):e71270.
5.
Figure 1

Figure 1. Primary tumour growth of human breast cancer cell lines in different immune-deficient mice.. From: Differential Post-Surgical Metastasis and Survival in SCID, NOD-SCID and NOD-SCID-IL-2Rγnull Mice with Parental and Subline Variants of Human Breast Cancer: Implications for Host Defense Mechanisms Regulating Metastasis.

Two million human breast cancer MDA-MB-231 parental or luciferase-tagged parental cells (231P/luc+), or the luciferase-tagged lung (LM2-4/luc+) and brain (164/8-1B/luc+) metastatic variants, were injected into the right inguinal mammary fat pad of female SCID, NOD-SCID or NSG mice. Tumour growth was monitored twice weekly and plotted as tumour volume against time. (A) Comparison of primary tumour growth rate in the various strains of immunocompromised mice. (B) Comparison of the different cell lines’ growth within the three strains of immunocompromised mice. Each group contained 8 mice. Statistical analysis was assessed by ANOVA. Significance was set at P<0.05. There was no statistical difference between any of the tumour growth curves.

Chloe C. Milsom, et al. PLoS One. 2013;8(8):e71270.

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