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Reduced metastasis of transgenic mammary cancer in urokinase‐deficient mice
International journal of cancer, 2005-02, Vol.113 (4), p.525-532
Almholt, Kasper
Lund, Leif R.
Rygaard, Jørgen
Nielsen, Boye S.
Danø, Keld
Rømer, John
Johnsen, Morten
2005
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Almholt, Kasper
Lund, Leif R.
Rygaard, Jørgen
Nielsen, Boye S.
Danø, Keld
Rømer, John
Johnsen, Morten
Titel
Reduced metastasis of transgenic mammary cancer in urokinase‐deficient mice
Ist Teil von
International journal of cancer, 2005-02, Vol.113 (4), p.525-532
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2005
Quelle
Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
Beschreibungen/Notizen
A prominent phenotype of plasmin deficiency in mice is reduced metastasis in the MMTV‐PymT transgenic breast cancer model. Proteolytically active plasmin is generated from inactive plasminogen by one of 2 activators, uPA or tPA. We now find that uPA deficiency alone significantly reduces metastasis >7‐fold in the MMTV‐PymT model. We studied a cohort of 55 MMTV‐PymT transgenic mice, either uPA‐deficient or wild‐type controls. Tumor incidence, latency, growth rate and final primary tumor burden were not significantly affected by uPA deficiency. In contrast, average lung metastasis volume was reduced from 1.58 mm3 in wild‐type controls to 0.21 mm3 in uPA‐deficient mice (p = 0.023). Tumor cell dissemination to brachial lymph nodes was also reduced from 53% (28/53) in wild‐type controls to 31% (17/54) in uPA‐deficient mice (p = 0.032). Mice without plasminogen display a severe pleiotropic phenotype. By comparison, spontaneous phenotypes are modest in uPA‐deficient mice, probably because they still have active tPA. We show that metastasis is strongly and selectively decreased in uPA‐deficient mice, suggesting that uPA‐directed antimetastatic therapy would be efficacious and have limited side effects. © 2004 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0020-7136
eISSN: 1097-0215
DOI: 10.1002/ijc.20631
Titel-ID: cdi_proquest_miscellaneous_67338018
Format
–
Schlagworte
Animal tumors. Experimental tumors
,
Animals
,
Antigens, Polyomavirus Transforming - genetics
,
Biological and medical sciences
,
breast cancer
,
Experimental genital and mammary tumors
,
Female
,
Humans
,
In Situ Hybridization
,
Incidence
,
Lung Neoplasms - enzymology
,
Lung Neoplasms - prevention & control
,
Lung Neoplasms - secondary
,
Lymphatic Metastasis - pathology
,
Lymphatic Metastasis - prevention & control
,
Male
,
Mammary Neoplasms, Experimental - enzymology
,
Mammary Neoplasms, Experimental - pathology
,
Mammary Tumor Virus, Mouse - genetics
,
Medical sciences
,
Mice
,
Mice, Transgenic
,
mouse model
,
plasminogen
,
Plasminogen Activators - deficiency
,
proteolysis
,
Survival Rate
,
Tumors
,
Urokinase-Type Plasminogen Activator - deficiency
,
urokinase‐type plasminogen activator
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