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Your search keyword '"Gilkes, Daniele M."' showing total 11 results
Start Over Author "Gilkes, Daniele M." Journal cancer research
11 results on '"Gilkes, Daniele M."'

1. Abstract 2130: Uncovering the spatial landscape of tumor-immune interactions using latent spaces from spatial transcriptomics

Author

Deshpande, Atul, primary, Loth, Melanie, additional, Sidiropoulos, Dimitrios, additional, Zhu, QingFeng, additional, Stein-O'Brien, Genevieve, additional, Rao, NIkhil, additional, Uytingco, Cedric, additional, Williams, Stephen, additional, Santa-Maria, Cesar, additional, Gilkes, Daniele M., additional, Zhang, Lei, additional, Jaffee, Elizabeth, additional, Anders, Robert, additional, Danilova, Ludmila, additional, Kagohara, Luciane T., additional, and Fertig, Elana J., additional

Published
2022
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11. RETRACTED: PHGDH Expression Is Required for Mitochondrial Redox Homeostasis, Breast Cancer Stem Cell Maintenance, and Lung Metastasis.

Author

Samanta D, Park Y, Andrabi SA, Shelton LM, Gilkes DM, and Semenza GL

Subjects
Breast Neoplasms pathology, Female, Humans, Neoplasm Metastasis, Neoplastic Stem Cells pathology, Transfection, Breast Neoplasms genetics, Lung Neoplasms secondary, Mitochondria metabolism, Neoplastic Stem Cells metabolism, Phosphoglycerate Dehydrogenase metabolism
Abstract

Intratumoral hypoxia stimulates enrichment of breast cancer stem cells (BCSC), which are critical for metastasis and patient mortality. Here we report a metabolic adaptation that is required for hypoxia-induced BCSC enrichment and metastasis. Hypoxia-inducible factors coordinately regulate expression of genes encoding phosphoglycerate dehydrogenase (PHGDH) and five downstream enzymes in the serine synthesis pathway and mitochondrial one-carbon (folate) cycle. RNAi-mediated silencing of PHGDH expression in both estrogen receptor-positive and negative breast cancer cells led to decreased NADPH levels, disturbed mitochondrial redox homeostasis, and increased apoptosis, which abrogated BCSC enrichment under hypoxic conditions. PHGDH-deficient cells exhibited increased oxidant levels and apoptosis, as well as loss of BCSC enrichment, in response to treatment with carboplatin or doxorubicin. PHGDH-deficient cells were relatively weakly tumorigenic and tumors that did form were deficient in BCSCs, abolishing metastatic capacity. Our findings highlight a role for PHGDH in the formation of secondary (recurrent or metastatic) tumors, with potential implications for therapeutic targeting of advanced cancers. Cancer Res; 76(15); 4430-42. ©2016 AACR., (©2016 American Association for Cancer Research.)

Published
2016
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