Endothelial-monocyte activating polypeptide II, a novel antitumor cytokine that suppresses primary and metastatic tumor growth and induces apoptosis in growing endothelial cells

Margaret Schwarz, Jessica Kandel, Jerald Brett, Jun Li, Joanne Hayward, Roderich E. Schwarz, Olivier Chappey, Jean Luc Wautier, John Chabot, Paul Lo Gerfo, David Stern

Research output: Contribution to journalArticle

108 Citations (Scopus)

Abstract

Neovascularization is essential for growth and spread of primary and metastatic tumors. We have identified a novel cytokine, endothelial-monocyte activating polypeptide (EMAP) II, that potently inhibits tumor growth, and appears to have antiangiogenic activity. Mice implanted with Matrigel showed an intense local angiogenic response, which EMAP II blocked by 76% (P <0.001). Neovascularization of the mouse cornea was similarly prevented by EMAP II (P <0.003). Intraperitoneally administered EMAP II suppressed the growth of primary Lewis lung carcinomas, with a reduction in tumor volume of 65% versus controls (P <0.003). Tumors from human breast carcinoma-derived MDA-MB 468 cells were suppressed by >80% in EMAP II-treated animals (P <0.005). In a lung metastasis model, EMAP II blocked outgrowth of Lewis lung carcinoma macrometastases; total surface metastases were diminished by 65%, and of the 35% metastases present, ~80% were inhibited with maximum diameter

Original languageEnglish (US)
Pages (from-to)341-353
Number of pages13
JournalJournal of Experimental Medicine
Volume190
Issue number3
DOIs
StatePublished - Aug 2 1999
Externally publishedYes

Fingerprint

Endothelial Cells
Apoptosis
Cytokines
Growth
Neoplasm Metastasis
Neoplasms
Lewis Lung Carcinoma
Lung
small inducible cytokine subfamily E, member 1

Keywords

  • Blood vessels
  • Capillary endothelium
  • Cell growth inhibitors
  • Programmed cell death
  • Tumor

ASJC Scopus subject areas

  • Immunology

Cite this

Endothelial-monocyte activating polypeptide II, a novel antitumor cytokine that suppresses primary and metastatic tumor growth and induces apoptosis in growing endothelial cells. / Schwarz, Margaret; Kandel, Jessica; Brett, Jerald; Li, Jun; Hayward, Joanne; Schwarz, Roderich E.; Chappey, Olivier; Wautier, Jean Luc; Chabot, John; Lo Gerfo, Paul; Stern, David.

In: Journal of Experimental Medicine, Vol. 190, No. 3, 02.08.1999, p. 341-353.

Research output: Contribution to journalArticle

Schwarz, Margaret ; Kandel, Jessica ; Brett, Jerald ; Li, Jun ; Hayward, Joanne ; Schwarz, Roderich E. ; Chappey, Olivier ; Wautier, Jean Luc ; Chabot, John ; Lo Gerfo, Paul ; Stern, David. / Endothelial-monocyte activating polypeptide II, a novel antitumor cytokine that suppresses primary and metastatic tumor growth and induces apoptosis in growing endothelial cells. In: Journal of Experimental Medicine. 1999 ; Vol. 190, No. 3. pp. 341-353.
@article{30d6d48ac76646a483d7bc79ecfbff65,
title = "Endothelial-monocyte activating polypeptide II, a novel antitumor cytokine that suppresses primary and metastatic tumor growth and induces apoptosis in growing endothelial cells",
abstract = "Neovascularization is essential for growth and spread of primary and metastatic tumors. We have identified a novel cytokine, endothelial-monocyte activating polypeptide (EMAP) II, that potently inhibits tumor growth, and appears to have antiangiogenic activity. Mice implanted with Matrigel showed an intense local angiogenic response, which EMAP II blocked by 76{\%} (P <0.001). Neovascularization of the mouse cornea was similarly prevented by EMAP II (P <0.003). Intraperitoneally administered EMAP II suppressed the growth of primary Lewis lung carcinomas, with a reduction in tumor volume of 65{\%} versus controls (P <0.003). Tumors from human breast carcinoma-derived MDA-MB 468 cells were suppressed by >80{\%} in EMAP II-treated animals (P <0.005). In a lung metastasis model, EMAP II blocked outgrowth of Lewis lung carcinoma macrometastases; total surface metastases were diminished by 65{\%}, and of the 35{\%} metastases present, ~80{\%} were inhibited with maximum diameter",
keywords = "Blood vessels, Capillary endothelium, Cell growth inhibitors, Programmed cell death, Tumor",
author = "Margaret Schwarz and Jessica Kandel and Jerald Brett and Jun Li and Joanne Hayward and Schwarz, {Roderich E.} and Olivier Chappey and Wautier, {Jean Luc} and John Chabot and {Lo Gerfo}, Paul and David Stern",
year = "1999",
month = "8",
day = "2",
doi = "10.1084/jem.190.3.341",
language = "English (US)",
volume = "190",
pages = "341--353",
journal = "Journal of Experimental Medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "3",

}

TY - JOUR

T1 - Endothelial-monocyte activating polypeptide II, a novel antitumor cytokine that suppresses primary and metastatic tumor growth and induces apoptosis in growing endothelial cells

AU - Schwarz, Margaret

AU - Kandel, Jessica

AU - Brett, Jerald

AU - Li, Jun

AU - Hayward, Joanne

AU - Schwarz, Roderich E.

AU - Chappey, Olivier

AU - Wautier, Jean Luc

AU - Chabot, John

AU - Lo Gerfo, Paul

AU - Stern, David

PY - 1999/8/2

Y1 - 1999/8/2

N2 - Neovascularization is essential for growth and spread of primary and metastatic tumors. We have identified a novel cytokine, endothelial-monocyte activating polypeptide (EMAP) II, that potently inhibits tumor growth, and appears to have antiangiogenic activity. Mice implanted with Matrigel showed an intense local angiogenic response, which EMAP II blocked by 76% (P <0.001). Neovascularization of the mouse cornea was similarly prevented by EMAP II (P <0.003). Intraperitoneally administered EMAP II suppressed the growth of primary Lewis lung carcinomas, with a reduction in tumor volume of 65% versus controls (P <0.003). Tumors from human breast carcinoma-derived MDA-MB 468 cells were suppressed by >80% in EMAP II-treated animals (P <0.005). In a lung metastasis model, EMAP II blocked outgrowth of Lewis lung carcinoma macrometastases; total surface metastases were diminished by 65%, and of the 35% metastases present, ~80% were inhibited with maximum diameter

AB - Neovascularization is essential for growth and spread of primary and metastatic tumors. We have identified a novel cytokine, endothelial-monocyte activating polypeptide (EMAP) II, that potently inhibits tumor growth, and appears to have antiangiogenic activity. Mice implanted with Matrigel showed an intense local angiogenic response, which EMAP II blocked by 76% (P <0.001). Neovascularization of the mouse cornea was similarly prevented by EMAP II (P <0.003). Intraperitoneally administered EMAP II suppressed the growth of primary Lewis lung carcinomas, with a reduction in tumor volume of 65% versus controls (P <0.003). Tumors from human breast carcinoma-derived MDA-MB 468 cells were suppressed by >80% in EMAP II-treated animals (P <0.005). In a lung metastasis model, EMAP II blocked outgrowth of Lewis lung carcinoma macrometastases; total surface metastases were diminished by 65%, and of the 35% metastases present, ~80% were inhibited with maximum diameter

KW - Blood vessels

KW - Capillary endothelium

KW - Cell growth inhibitors

KW - Programmed cell death

KW - Tumor

UR - http://www.scopus.com/inward/record.url?scp=0033517112&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033517112&partnerID=8YFLogxK

U2 - 10.1084/jem.190.3.341

DO - 10.1084/jem.190.3.341

M3 - Article

VL - 190

SP - 341

EP - 353

JO - Journal of Experimental Medicine

JF - Journal of Experimental Medicine

SN - 0022-1007

IS - 3

ER -