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Saraswati Sukumar

Researcher at Johns Hopkins University School of Medicine

Publications -  262
Citations -  28255

Saraswati Sukumar is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 77, co-authored 248 publications receiving 26027 citations. Previous affiliations of Saraswati Sukumar include Tufts University & Salk Institute for Biological Studies.

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Tumor‐specific changes in mtDNA content in human cancer

TL;DR: The mtDNA alterations have been suggested as a potentially sensitive and specific biomarker for several cancer types, suggesting that the mitochondrial genome may be a critical contributing factor in carcinogenesis as mentioned in this paper.
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Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal.

TL;DR: This work found that insulin-like growth factor-1- and dopamine-stimulated methionine synthase activity and folate-dependent methylation of phospholipids in SH-SY5Y human neuroblastoma cells are regulated through a PI3-kinase- and MAP-kinases-dependent mechanism, which suggests that this pathway may be an important target of neurodevelopmental toxins.
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Epigenomics and breast cancer

TL;DR: A review of the role of epigenetic machinery in the development and recurrence of breast cancer can be found in this paper, where the authors highlight the significance of the epigenetic alterations as predictive biomarkers and as new targets of anticancer therapy.
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Breast cancer cells condition lymphatic endothelial cells within pre-metastatic niches to promote metastasis.

TL;DR: This study demonstrates anti-metastatic activities of multiple repurposed drugs, blocking a self-reinforcing paracrine loop between breast cancer cells and LECs.
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Functional Activation of the Estrogen Receptor-α and Aromatase by the HDAC Inhibitor Entinostat Sensitizes ER-Negative Tumors to Letrozole

TL;DR: The results show that ENT treatment can be used to restore the letrozole responsiveness of ER-negative tumors, and provide a strong rationale for immediate clinical evaluation of combinations of histone deacetylase and aromatase inhibitors to treat ER- negative and endocrine-resistant breast cancers.