Open AccessMolecular Significance of Excess Body Weight in Postmenopausal Breast Cancer Patients, in Relation to Expression of Insulin‐like Growth Factor I Receptor and Insulin‐like Growth Factor II Genes
Author(s) -
Suga Kenji,
Imai Kazue,
Eguchi Hidetaka,
Hayashi Shinichi,
Higashi Yasuhiro,
Nakachi Kei
Publication year - 2001
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.2001.tb01074.x
Subject(s) - breast cancer , endocrinology , medicine , mammary gland , insulin like growth factor , cancer , growth factor , body mass index , risk factor , menopause , clinical significance , biology , receptor
A number of epidemiological and clinical studies have revealed that excess body weight increases the risk of postmenopausal breast cancer and also adversely affects subsequent malignant progression. To elucidate the molecular mechanisms underlying these observations, we examined mRNA expression of various genes in normal (non‐cancerous) mammary gland and cancer tissue of Japanese patients with primary breast cancer, in association with their body mass index (BMI). On the basis of analysis of 106 breast cancer patients, we found that mRNA expression of insulin‐like growth factor I receptor (IGF‐IR) and insulin‐like growth factor II (IGF‐II) in the normal mammary gland showed a significant and positive association with increased BMI among postmenopausal patients. Furthermore, the positive association of increased BMI with IGF‐IR mRNA expression was also found in postmenopausal breast cancer tissue, while this association was not observed among premenopausal patients. In addition, increased mRNA expression of cyclin Dl and bcl‐2 was observed in association with increased mRNA levels of IGF‐IR among the patients regardless of menopausal status. These findings suggest that the molecular consequence of the increased BMI is the increased expression of IGF‐II and IGF‐IR, resulting in development of postmenopausal breast cancer and its progression mediated through modulation of the cell cycle and apoptosis.