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Carlos Cordon-Cardo

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  620
Citations -  91832

Carlos Cordon-Cardo is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Cancer & Prostate cancer. The author has an hindex of 144, co-authored 589 publications receiving 84862 citations. Previous affiliations of Carlos Cordon-Cardo include The Rogosin Institute & Erasmus University Rotterdam.

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Inhibition of the autocrine IL-6–JAK2–STAT3–calprotectin axis as targeted therapy for HR−/HER2+ breast cancers

TL;DR: It is demonstrated that inhibition of the IL-6-Janus kinase 2 (JAK2)-STAT3-calprotectin axis with FDA-approved drugs, alone and in combination with HER2 inhibitors, reduced the tumorigenicity of HR(-)/HER2(+) breast cancers, opening novel targeted therapeutic opportunities.
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ETS rearrangements and prostate cancer initiation

TL;DR: It is shown that ETS genetic rearrangements may in fact represent progression events rather than initiation events in prostate tumorigenesis, and it is demonstrated that the prostate-specific overexpression of ERG does not initiate prostate neoplasia.
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Role of Dok-1 and Dok-2 in leukemia suppression.

TL;DR: The discovery of a family of proteins, Dok, coexpressed in hematopoietic progenitor cells, uncovers the critical and unexpected role of Dok-1 andDok-2 in tumor suppression and control of the hematoplastic compartment homeostasis.
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Contrasting roles for Myc and Mad proteins in cellular growth and differentiation.

TL;DR: Observations support the view that both downregulation of Myc and accumulation of Mad may be necessary for progression of precursor cells to a growth-arrested, terminally differentiated state.
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Molecular genetic alterations of chromosome 17 and p53 nuclear overexpression in human bladder cancer.

TL;DR: A strong correlation was found between the presence of mutation and the loss of heterozygosity of the remaining allele in p53 as detected by immunohistochemistry and the role of p53 nuclear overexpression and 17p deletions as markers of tumor progression in human bladder cancer.