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Sumanta Goswami

Researcher at Albert Einstein College of Medicine

Publications -  45
Citations -  6375

Sumanta Goswami is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Metastasis & Breast cancer. The author has an hindex of 29, co-authored 42 publications receiving 5871 citations. Previous affiliations of Sumanta Goswami include All India Institute of Medical Sciences & Yeshiva University.

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Direct Visualization of Macrophage-Assisted Tumor Cell Intravasation in Mammary Tumors

TL;DR: The results show that the interaction between macrophages and tumor cells lying in close proximity defines a microenvironment that is directly involved in the intravasation of cancer cells in mammary tumors.
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Macrophages Promote the Invasion of Breast Carcinoma Cells via a Colony-Stimulating Factor-1/Epidermal Growth Factor Paracrine Loop

TL;DR: It is shown that macrophages and tumor cells are necessary and sufficient for comigration and invasion into collagen I and that this process involves a paracrine loop.
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Identification and Testing of a Gene Expression Signature of Invasive Carcinoma Cells within Primary Mammary Tumors

TL;DR: Reexpression of Z BP1 in metastatic cells with otherwise low levels of ZBP1 reestablished normal patterns of β-actin mRNA targeting and suppressed chemotaxis and invasion in primary tumors, and inhibited metastasis from tumors.
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Cancer stem cells from human breast tumors are involved in spontaneous metastases in orthotopic mouse models

TL;DR: These metastatic cancer models, combined with noninvasive imaging techniques, constitute an integrated approach that could be applied to dissect the molecular mechanisms underlying the dissemination of metastatic CSCs (MCSCs) and to explore therapeutic strategies targeting MCSCs in general or to evaluate individual patient tumor cells and predict response to therapy.
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Impairment of BRCA1-related DNA double-strand break repair leads to ovarian aging in mice and humans

TL;DR: Impaired ATM (ataxia-telangiectasia mutated)–mediated DNA double-strand break repair is identified as a cause of aging in mouse and human oocytes and the efficiency of DNA DSB repair is a crucial determinant of oocyte loss.