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Fasting-mimicking diet and hormone therapy induce breast cancer regression
Nature (London), 2020-07, Vol.583 (7817), p.620-624
2020
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Autor(en) / Beteiligte
Titel
Fasting-mimicking diet and hormone therapy induce breast cancer regression
Ist Teil von
  • Nature (London), 2020-07, Vol.583 (7817), p.620-624
Ort / Verlag
England: Nature Publishing Group
Erscheinungsjahr
2020
Quelle
MEDLINE
Beschreibungen/Notizen
  • Approximately 75% of all breast cancers express the oestrogen and/or progesterone receptors. Endocrine therapy is usually effective in these hormone-receptor-positive tumours, but primary and acquired resistance limits its long-term benefit . Here we show that in mouse models of hormone-receptor-positive breast cancer, periodic fasting or a fasting-mimicking diet enhances the activity of the endocrine therapeutics tamoxifen and fulvestrant by lowering circulating IGF1, insulin and leptin and by inhibiting AKT-mTOR signalling via upregulation of EGR1 and PTEN. When fulvestrant is combined with palbociclib (a cyclin-dependent kinase 4/6 inhibitor), adding periodic cycles of a fasting-mimicking diet promotes long-lasting tumour regression and reverts acquired resistance to drug treatment. Moreover, both fasting and a fasting-mimicking diet prevent tamoxifen-induced endometrial hyperplasia. In patients with hormone-receptor-positive breast cancer receiving oestrogen therapy, cycles of a fasting-mimicking diet cause metabolic changes analogous to those observed in mice, including reduced levels of insulin, leptin and IGF1, with the last two remaining low for extended periods. In mice, these long-lasting effects are associated with long-term anti-cancer activity. These results support further clinical studies of a fasting-mimicking diet as an adjuvant to oestrogen therapy in hormone-receptor-positive breast cancer.
Sprache
Englisch
Identifikatoren
ISSN: 0028-0836
eISSN: 1476-4687
DOI: 10.1038/s41586-020-2502-7
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7881940
Format
–
Schlagworte
AKT protein, Animal models, Animals, Anticancer properties, Biological Factors - blood, Breast cancer, Breast Neoplasms - diet therapy, Breast Neoplasms - drug therapy, Breast Neoplasms - pathology, Care and treatment, Cell adhesion & migration, Cell cycle, Cooperation, Cyclin-dependent kinase, Cyclin-dependent kinase 4, Cyclin-dependent kinases, Diet, Diet therapy, Diet Therapy - methods, Diet, Healthy - methods, Disease Models, Animal, Disease Progression, Drug Resistance, Neoplasm - drug effects, Early Growth Response Protein 1 - metabolism, EGR-1 protein, Endocrine therapy, Endometrium, Enzyme inhibitors, Estrogens, Fasting, Fasting - physiology, Female, Fulvestrant, Fulvestrant - administration & dosage, Fulvestrant - therapeutic use, Gene expression, Glucose, Hormone replacement therapy, Hormone therapy, Humans, Hyperplasia, Insulin, Insulin - blood, Insulin-Like Growth Factor I - metabolism, Insulin-like growth factors, Kinases, Leptin, Leptin - blood, MCF-7 Cells, Medical prognosis, Methods, Mice, Inbred NOD, Mice, SCID, Mimicry, Phosphorylation, Piperazines - administration & dosage, Piperazines - therapeutic use, Progesterone, Progesterone receptors, Proteins, PTEN Phosphohydrolase - metabolism, PTEN protein, Pyridines - administration & dosage, Pyridines - therapeutic use, Receptors, Receptors, Estrogen, Receptors, Progesterone, Tamoxifen, Tamoxifen - adverse effects, Tamoxifen - therapeutic use, Therapy, TOR protein, Tumor necrosis factor-TNF, Tumors, Xenograft Model Antitumor Assays

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