Skip Navigation

JNCI Journal of the National Cancer Institute 2002 94(11):783; doi:10.1093/jnci/94.11.783-b
© 2002 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Search for Related Content

Journal of the National Cancer Institute, Vol. 94, No. 11, 783, June 5, 2002
© 2002 Oxford University Press

IN THIS ISSUE

VEGF Receptor 3 Signaling and Lymph Node Metastasis

Vascular endothelial growth factor-C (VEGF-C) stimulates tumor lymphangiogenesis (the formation of lymphatic vessels) via VEGF receptor 3 (VEGFR-3), which could facilitate lymphatic tumor spread to regional lymph nodes. He et al. (p. 819) investigated whether inhibition of VEGFR-3 signaling would inhibit tumor lymphangiogenesis and metastasis by using a lung cancer cell line (LNM35) selected for high lymphatic metastasis and abundant VEGF-C and its parental line (N15), which has low metastatic capacity. The authors found that blocking VEGFR-3 signaling suppressed tumor lymphangiogenesis and lymphatic metastasis but not lung metastasis. Overexpression of VEGF-C in N15 cells did . . . [Full Text of this Article]

HER2 Testing in Local and Central Laboratories

Lung Cancer Rates and Improved Household Stoves

Cancer Registry Data and Quality of Breast Cancer Care

BRCA Mutation Estimates Using a Computer Model

LOH in Breast Epithelium and Breast Cancer Risk