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Obesity enhances melanoma tumor growth independently of circulating leptin
Author(s) -
Brandon Elizabeth Lynn,
Cantwell Lauren,
Gu JianWei,
Hall John E.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a927-a
Subject(s) - leptin , obesity , melanoma , medicine , endocrinology , cancer research
Epidemiological studies indicate that obesity increases the risk of developing several cancers, including melanoma. Once cancer occurs, obese subjects have poorer prognoses than lean subjects. Obesity increases the expression of several proangiogenic factors required for tumor growth, such as leptin. Leptin can stimulate angiogenesis in the chick chorioallantoic membrane assay. Plasma leptin levels correlate with total body fat and actions of leptin, including stimulation of cell migration and enhancement of angiogenesis, suggest that this hormone may promote tumor growth. However, no studies have directly tested whether obesity stimulates tumor growth via increased secretion of leptin. We injected melanoma cells into lean wild type, obese melanocortin receptor 4 knockout (MC4R(−/−), which have very high leptin levels, and obese leptin deficient ( ob/ob ) mice. Mean body weights were 29.7 ± 0.3 g, 46.3 ± 1.9 g, and 63.7 ± 0.9 g for lean wild type, MC4R(−/−), and ob/ob mice, respectively. All mice were on the C57BL6/J background. Mice were injected subcutaneously with 1 x 10 6 B16F10 cells and tumors were harvested and weighed post mortem. Tumors were 2.5 fold larger in obese ob/ob and MC4R(−/−) than lean wild‐type mice (5.1 ± 0.9 g and 5.1 ± 0.7 g vs lean 2.1 ± 0.3 g, respectively). These results indicate that obesity enhances melanoma tumor growth by mechanisms that are independent of circulating leptin levels.