B16 melanoma in C57BL/6J mice: Kinetics and effects of heterologous serum

Hill, George J.; Littlejohn, Brent

doi:10.1002/jso.2930030104

Cited by 12 publications

(4 citation statements)

References 6 publications

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“…This represents a 77% inhibition in tumor size by glycine. The sizes of tumors in mice fed control diet were similar to those reported previously where the time for the tumor volume to increase 10-fold was~10 days (13). After 14 days, mice were killed and the tumors excised.…”

Section: Resultssupporting

confidence: 71%

Dietary glycine inhibits the growth of B16 melanoma tumors in mice

Rose¹,

Madren²,

Bunzendahl³

et al. 1999

Carcinogenesis

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Dietary glycine inhibited hepatocyte proliferation in response to the carcinogen WY-14,643. Since increased cell replication is associated with hepatic cancer caused by WY-14,643, glycine may have anti-cancer properties. Therefore, these experiments were designed to test the hypothesis that dietary glycine would inhibit the growth of tumors arising from B16 melanoma cells implanted subcutaneously in mice. C57BL/6 mice were fed diet supplemented with 5% glycine and 15% casein or control diet (20% casein) for 3 days prior to subcutaneous implantation of B16 tumor cells. Tumor volume was estimated from tumor diameter for 14 days. Tumors were excised, weighed and sectioned for histology post-mortem. B16 cells and endothelial cells were cultured in vitro to assess effects of glycine on cell growth. Statistical tests were two-sided and a P-value of 0.05 was defined as a significant difference between groups. Weight gain did not differ between mice fed control and glycine-containing diets. B16 tumors grew rapidly in mice fed control diet; however, in mice fed glycine diet, tumor size was 50-75% less. At the time of death, tumors from glycine-fed mice weighed nearly 65% less than tumors from mice fed control diet (P < 0.05). Glycine (0.01-10 mM) did not effect growth rates of B16 cells in vitro. Moreover, tumor volume and mitotic index of B16 tumors in vivo did not differ 2 days after implantation when tumors were small enough to be independent of vascularization. After 14 days, tumors from mice fed dietary glycine had 70% fewer arteries (P < 0.05). Furthermore, glycine (0.01-10 mM) inhibited the growth of endothelial cells in vitro in a dose-dependent manner (P < 0.05; IC 50 ⍧ 0.05 mM). These data support the hypothesis that dietary glycine prevents tumor growth in vivo by inhibiting angiogenesis through mechanisms involving inhibition of endothelial cell proliferation.

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Section: Resultssupporting

confidence: 71%

Dietary glycine inhibits the growth of B16 melanoma tumors in mice

Rose¹,

Madren²,

Bunzendahl³

et al. 1999

Carcinogenesis

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“…The C57BL/6 strain is reputed to be relatively resistant to some chemical carcinogenesis protocols [41-43] and relatively susceptible to spontaneous and chemically induced melanomas [44], radiation-induced leukemia [45], and chemically induced urinary bladder carcinomas [46]. Regarding mammary tumorigenesis, the C57BL/6 strain is considered to be resistant to MMTV [7], urethane [47], and γ radiation [20,21].…”

Section: Discussionmentioning

confidence: 99%

Association of estrogen receptor-α and progesterone receptor A expression with hormonal mammary carcinogenesis: role of the host microenvironment

et al. 2007

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Introduction Medroxyprogesterone acetate (MPA) induces estrogen receptor (ER)-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice. We sought to reproduce this MPA cancer model in C57BL/6 mice because of their widespread use in genetic engineering. Within this experimental setting, we studied the carcinogenic effects of MPA, the morphologic changes in mammary glands that are induced by MPA and progesterone, and the levels of ER and PR expression in MPA-treated and progesterone-treated mammary glands. Finally, we evaluated whether the differences found between BALB/c and C57BL/6 mouse strains were due to intrinsic differences in epithelial cells.

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“…B16 tumor cells from S.C. tumors were injected i.p at lo6 cells per mouse into C57BL/6 female mice as previously described [7,13,18,20]. The CY was injected i.p.…”

Section: In Vivo Experimentsmentioning

confidence: 99%

In vitro activation of cyclophosphamide for an in vitro chemosensitivity assay

Hill

1984

Journal of Surgical Oncology

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The problem of activation of cyclophosphamide (CY) for an in vitro chemosensitivity assay was studied using the B16 melanoma. The efficacy of the S9 hepatic microsomal fraction in vitro was compared with activation by passage of drug in vivo. The effect of CY was assayed by inhibition of tritiated thymidine (3HdThd) uptake by B16 tumor cells in vitro, and by its effect in single dose in vivo on the life span of syngeneic C57BL/6 mice injected with B16 tumor cells. In vivo activation of CY that was achieved by injecting 20 mg of CY intraperitoneally (i.p.) into mice and obtaining plasma 20 minutes later was more rapid and more reproducible, while in vitro activation provided a more potent preparation and a better quantitative correlation with the in vivo effect of CY. The activation activity of different preparations of S9 microsomal fractions was found to be directly related to the activity of aminopyrine demethylase, a mixed function oxidase enzyme, in the S9 fraction, rather than to total protein concentration. The S9-activated drug required 2 1/2 to 3 hours to achieve maximum inhibition of subsequent tumor cell tritiated thymidine (3HdThd) incorporation compared with 20 minutes to achieve maximum inhibition by in vivo activated drug. We conclude that rapid qualitative screening for effectiveness of CY may best be done with in vivo activated drug, whereas quantitative prediction of effective concentration appears to be best achieved with drug activated in vitro by the hepatic S9 fraction.

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B16 melanoma in C57BL/6J mice: Kinetics and effects of heterologous serum

Cited by 12 publications

References 6 publications

Dietary glycine inhibits the growth of B16 melanoma tumors in mice

Dietary glycine inhibits the growth of B16 melanoma tumors in mice

Association of estrogen receptor-α and progesterone receptor A expression with hormonal mammary carcinogenesis: role of the host microenvironment

In vitro activation of cyclophosphamide for an in vitro chemosensitivity assay

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