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JCI table of contents: Dec. 3, 2007
Date:12/3/2007

e: 39-051-636-4009; Fax: 39-051-636-3902; E-mail: massimiliano.bonafe@unibo.it.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32533

RELATED MANUSCRIPT
TITLE: Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas

AUTHOR CONTACT:
Jacqueline F. Bromberg
Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
Phone: (212) 639-2577; Fax: (646) 422-2231; E-mail: bromberj@mskcc.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=31871

ACCOMPANYING COMMENTARY
TITLE: IL-6 involvement in epithelial cancers

AUTHOR CONTACT:
Joan S. Brugge
Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 432-3974; Fax: (617) 432-3969; E-mail: joan_brugge@hms.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34237


HEMATOLOGY: G1ME more platelets: An inflammatory mediator drives maturation of platelet precursor cells

Infection and inflammation are sometimes accompanied by an excess of circulating platelet cells, a condition called thrombocytosis. In a new study, John Crispino and his colleagues at Northwestern University Feinberg School of Medicine, Chicago, have explored this relationship between inflammatory disease and platelet formation in mice.

Cellular differentiation is the process by which cells specialize. For example, megakaryocytic precursor cells differentiate into megakaryocytes, the parent cells of platelets. G1ME cells are mouse megakaryocytic precursors tha
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Journal of Clinical Investigation
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