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Michael Goldstein

Researcher at Beth Israel Deaconess Medical Center

Publications -  78
Citations -  4324

Michael Goldstein is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Polysomnography & Cancer. The author has an hindex of 28, co-authored 67 publications receiving 3651 citations. Previous affiliations of Michael Goldstein include Hamilton College & Duke University.

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Platelet Transfusion for Patients With Cancer: Clinical Practice Guidelines of the American Society of Clinical Oncology*

TL;DR: The possible consequences of different approaches to the use of platelet transfusion were considered in evaluating a preference for one or another technique producing similar outcomes and cost alone was not a determining factor.
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Future Supply and Demand for Oncologists : Challenges to Assuring Access to Oncology Services

TL;DR: A multifaceted strategy will be needed to ensure that Americans have access to oncology services in 2020, as no single action will fill the likely gap between supply and demand.
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The DNA Damage Response: Implications for Tumor Responses to Radiation and Chemotherapy

TL;DR: The DDR pathways that are activated after treatment with radiation and different classes of chemotherapeutic drugs are highlighted and mechanisms determining tumor sensitivity and resistance to these agents are described.
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The RET/PTC3 oncogene : Metastatic solid-type papillary carcinomas in murine thyroids

TL;DR: A new member of this fusion oncogene family, RET/PTC3, which has been implicated in more cases of solid tumor carcinoma than PTC1 or PTC2 and predominates in radiation-induced thyroid cancer of children, was investigated in this study.
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Inactivation of the Human Papillomavirus E6 or E7 Gene in Cervical Carcinoma Cells by Using a Bacterial CRISPR/Cas RNA-Guided Endonuclease

TL;DR: It is demonstrated that the recently described bacterial CRISPR/Cas RNA-guided endonuclease can be reprogrammed to target and destroy the E6 or E7 gene in cervical carcinoma cells transformed by HPV, resulting in cell cycle arrest and eventual cell death.