LymphedemaV1, PascalFrancis, Corpus, bibRecord, 000663

Lymphangiogenic growth factors, receptors and therapies

Identifieur interne : 000663 ( PascalFrancis/Corpus ); précédent : 000662; suivant : 000664

Lymphangiogenic growth factors, receptors and therapies

Auteurs : Marja Lohela ; Anne Saaristo ; Tanja Veikkola ; Kari Alitalo

Source :

Thrombosis and haemostasis [ 0340-6245 ] ; 2003.

RBID : Pascal:04-0045510

Descripteurs français

Pascal (Inist)
- Angiogenèse, Lymphatique, Cellule endothéliale, Facteur croissance endothélium vasculaire, Récepteur biologique, Récepteur facteur croissance, Lymphoedème, Traitement, Homme, Animal, Article synthèse, Lymphangiogenèse.

English descriptors

KwdEn :
- Angiogenesis, Animal, Biological receptor, Endothelial cell, Growth factor receptor, Human, Lymphangiogenesis, Lymphatic, Lymphedema, Review, Treatment, Vascular endothelium growth factor.

Abstract

The lymphatic vasculature is essential for the maintenance of normal fluid balance and for the immune responses, but it is also involved in a variety of diseases. Hypoplasia or dysfuction of the lymphatic vessels can lead to lymphedema, whereas hyperplasia or abnormal growth of these vessels are associated with lymphangiomas and lymphangiosarcomas. Lymphatic vessels are also involved in lymph node and systemic metastasis of cancer cells. Recent novel findings on the molecular mechanisms involved in lymphatic vessel development and regulation allow the modulation of the lymphangiogenic process and specific targeting of the lymphatic endothelium. Recent results show that the homeodomain transcription factor Prox-I is an important lymphatic endothelial cell (LEC) fate-determining factor which can induce LEC-specific gene transcription even in blood vascular endothelial cells (BECs). This suggests that the distinct phenotypes of cells in the adult vascular endothelium are plastic and sensitive to transcriptional reprogramming, which might be useful for future therapeutic applications involving endothelial cells Vascular endothelial growth factor-C (VEGF-C) and VEGF-D are peptide growth factors capable of inducing the growth of new lymphatic vessels in vivo in a process called lymphangiogenesis.They belong to the larger family which also includesVEGF, placenta growth factor (PIGF) and VEGF.B.VEGF-C and VEGF-D are ligands for the endothelial cell specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. In adult human as well as mouse tissuesVEGFR-3 is expressed predominantly in lymphatic endothelial cells which line the inner surface of lymphatic vessels. While VEGFR-2 is thought to be the main mediator of angiogenesis,VEGFR-3 signaling is crucial for the development of the lymphatic vessels. Heterozygous inactivation of the VEGFR-3 tyrosine kinase leads to primary lymphedema due to defective lymphatic drainage in the limbs. Other factors that seem to be involved in lymphangiogenesis include the Tie/angiopoietin system, neuropilin-2 and integrin a9. VEGF-C induces lymphatic vessel growth, but high levels of VEGF-C also resulted in blood vessel leakiness and growth.The VEGFR-3-specific mutant form of VEGF-C called VEGF-C I 56S lacks blood vascular side effects but is sufficient for therapeutic lymphangiogenesis in a mouse model of lymphedema. As VEGF-C 156S is a specific lymphatic endothelial growth factor in the skin, it provides an attractive molecule for pro-lymphangiogenic therapy.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 The lymphatic vasculature is essential for the maintenance of normal fluid balance and for the immune responses, but it is also involved in a variety of diseases. Hypoplasia or dysfuction of the lymphatic vessels can lead to lymphedema, whereas hyperplasia or abnormal growth of these vessels are associated with lymphangiomas and lymphangiosarcomas. Lymphatic vessels are also involved in lymph node and systemic metastasis of cancer cells. Recent novel findings on the molecular mechanisms involved in lymphatic vessel development and regulation allow the modulation of the lymphangiogenic process and specific targeting of the lymphatic endothelium. Recent results show that the homeodomain transcription factor Prox-I is an important lymphatic endothelial cell (LEC) fate-determining factor which can induce LEC-specific gene transcription even in blood vascular endothelial cells (BECs). This suggests that the distinct phenotypes of cells in the adult vascular endothelium are plastic and sensitive to transcriptional reprogramming, which might be useful for future therapeutic applications involving endothelial cells Vascular endothelial growth factor-C (VEGF-C) and VEGF-D are peptide growth factors capable of inducing the growth of new lymphatic vessels in vivo in a process called lymphangiogenesis.They belong to the larger family which also includesVEGF, placenta growth factor (PIGF) and VEGF.B.VEGF-C and VEGF-D are ligands for the endothelial cell specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. In adult human as well as mouse tissuesVEGFR-3 is expressed predominantly in lymphatic endothelial cells which line the inner surface of lymphatic vessels. While VEGFR-2 is thought to be the main mediator of angiogenesis,VEGFR-3 signaling is crucial for the development of the lymphatic vessels. Heterozygous inactivation of the VEGFR-3 tyrosine kinase leads to primary lymphedema due to defective lymphatic drainage in the limbs. Other factors that seem to be involved in lymphangiogenesis include the Tie/angiopoietin system, neuropilin-2 and integrin a9. VEGF-C induces lymphatic vessel growth, but high levels of VEGF-C also resulted in blood vessel leakiness and growth.The VEGFR-3-specific mutant form of VEGF-C called VEGF-C I 56S lacks blood vascular side effects but is sufficient for therapeutic lymphangiogenesis in a mouse model of lymphedema. As VEGF-C 156S is a specific lymphatic endothelial growth factor in the skin, it provides an attractive molecule for pro-lymphangiogenic therapy.
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C03	`02`	`X`	`ENG`	`@0 Lymphatic @5 02`
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C03	`05`	`X`	`FRE`	`@0 Récepteur biologique @5 05`
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C03	`06`	`X`	`FRE`	`@0 Récepteur facteur croissance @5 06`
C03	`06`	`X`	`ENG`	`@0 Growth factor receptor @5 06`
C03	`06`	`X`	`SPA`	`@0 Receptor factor crecimiento @5 06`
C03	`07`	`X`	`FRE`	`@0 Lymphoedème @5 07`
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Format Inist (serveur)

NO :	PASCAL 04-0045510 INIST
ET :	Lymphangiogenic growth factors, receptors and therapies
AU :	LOHELA (Marja); SAARISTO (Anne); VEIKKOLA (Tanja); ALITALO (Kari)
AF :	Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute and Helsinki University Central Hospital, Biomedicum Helsinki, University of Helsinki/Helsinki/Finlande (1 aut., 2 aut., 3 aut., 4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Thrombosis and haemostasis; ISSN 0340-6245; Coden THHADQ; Allemagne; Da. 2003; Vol. 90; No. 2; Pp. 167-184; Bibl. 226 ref.
LA :	Anglais
EA :	The lymphatic vasculature is essential for the maintenance of normal fluid balance and for the immune responses, but it is also involved in a variety of diseases. Hypoplasia or dysfuction of the lymphatic vessels can lead to lymphedema, whereas hyperplasia or abnormal growth of these vessels are associated with lymphangiomas and lymphangiosarcomas. Lymphatic vessels are also involved in lymph node and systemic metastasis of cancer cells. Recent novel findings on the molecular mechanisms involved in lymphatic vessel development and regulation allow the modulation of the lymphangiogenic process and specific targeting of the lymphatic endothelium. Recent results show that the homeodomain transcription factor Prox-I is an important lymphatic endothelial cell (LEC) fate-determining factor which can induce LEC-specific gene transcription even in blood vascular endothelial cells (BECs). This suggests that the distinct phenotypes of cells in the adult vascular endothelium are plastic and sensitive to transcriptional reprogramming, which might be useful for future therapeutic applications involving endothelial cells Vascular endothelial growth factor-C (VEGF-C) and VEGF-D are peptide growth factors capable of inducing the growth of new lymphatic vessels in vivo in a process called lymphangiogenesis.They belong to the larger family which also includesVEGF, placenta growth factor (PIGF) and VEGF.B.VEGF-C and VEGF-D are ligands for the endothelial cell specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. In adult human as well as mouse tissuesVEGFR-3 is expressed predominantly in lymphatic endothelial cells which line the inner surface of lymphatic vessels. While VEGFR-2 is thought to be the main mediator of angiogenesis,VEGFR-3 signaling is crucial for the development of the lymphatic vessels. Heterozygous inactivation of the VEGFR-3 tyrosine kinase leads to primary lymphedema due to defective lymphatic drainage in the limbs. Other factors that seem to be involved in lymphangiogenesis include the Tie/angiopoietin system, neuropilin-2 and integrin a9. VEGF-C induces lymphatic vessel growth, but high levels of VEGF-C also resulted in blood vessel leakiness and growth.The VEGFR-3-specific mutant form of VEGF-C called VEGF-C I 56S lacks blood vascular side effects but is sufficient for therapeutic lymphangiogenesis in a mouse model of lymphedema. As VEGF-C 156S is a specific lymphatic endothelial growth factor in the skin, it provides an attractive molecule for pro-lymphangiogenic therapy.
CC :	002A22E
FD :	Angiogenèse; Lymphatique; Cellule endothéliale; Facteur croissance endothélium vasculaire; Récepteur biologique; Récepteur facteur croissance; Lymphoedème; Traitement; Homme; Animal; Article synthèse; Lymphangiogenèse
FG :	Appareil circulatoire pathologie; Lymphatique pathologie
ED :	Angiogenesis; Lymphatic; Endothelial cell; Vascular endothelium growth factor; Biological receptor; Growth factor receptor; Lymphedema; Treatment; Human; Animal; Review; Lymphangiogenesis
EG :	Cardiovascular disease; Lymphatic vessel disease
SD :	Angiogénesis; Linfático; Célula endotelial; Factor crecimiento endotelio vascular; Receptor biológico; Receptor factor crecimiento; Linfedema; Tratamiento; Hombre; Animal; Artículo síntesis
LO :	INIST-10255.354000112277180030
ID :	04-0045510

Links to Exploration step

Pascal:04-0045510

Le document en format XML

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<front><div type="abstract" xml:lang="en">The lymphatic vasculature is essential for the maintenance of normal fluid balance and for the immune responses, but it is also involved in a variety of diseases. Hypoplasia or dysfuction of the lymphatic vessels can lead to lymphedema, whereas hyperplasia or abnormal growth of these vessels are associated with lymphangiomas and lymphangiosarcomas. Lymphatic vessels are also involved in lymph node and systemic metastasis of cancer cells. Recent novel findings on the molecular mechanisms involved in lymphatic vessel development and regulation allow the modulation of the lymphangiogenic process and specific targeting of the lymphatic endothelium. Recent results show that the homeodomain transcription factor Prox-I is an important lymphatic endothelial cell (LEC) fate-determining factor which can induce LEC-specific gene transcription even in blood vascular endothelial cells (BECs). This suggests that the distinct phenotypes of cells in the adult vascular endothelium are plastic and sensitive to transcriptional reprogramming, which might be useful for future therapeutic applications involving endothelial cells Vascular endothelial growth factor-C (VEGF-C) and VEGF-D are peptide growth factors capable of inducing the growth of new lymphatic vessels in vivo in a process called lymphangiogenesis.They belong to the larger family which also includesVEGF, placenta growth factor (PIGF) and VEGF.B.VEGF-C and VEGF-D are ligands for the endothelial cell specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. In adult human as well as mouse tissuesVEGFR-3 is expressed predominantly in lymphatic endothelial cells which line the inner surface of lymphatic vessels. While VEGFR-2 is thought to be the main mediator of angiogenesis,VEGFR-3 signaling is crucial for the development of the lymphatic vessels. Heterozygous inactivation of the VEGFR-3 tyrosine kinase leads to primary lymphedema due to defective lymphatic drainage in the limbs. Other factors that seem to be involved in lymphangiogenesis include the Tie/angiopoietin system, neuropilin-2 and integrin a9. VEGF-C induces lymphatic vessel growth, but high levels of VEGF-C also resulted in blood vessel leakiness and growth.The VEGFR-3-specific mutant form of VEGF-C called VEGF-C I 56S lacks blood vascular side effects but is sufficient for therapeutic lymphangiogenesis in a mouse model of lymphedema. As VEGF-C 156S is a specific lymphatic endothelial growth factor in the skin, it provides an attractive molecule for pro-lymphangiogenic therapy.</div>
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<fC01 i1="01" l="ENG"><s0>The lymphatic vasculature is essential for the maintenance of normal fluid balance and for the immune responses, but it is also involved in a variety of diseases. Hypoplasia or dysfuction of the lymphatic vessels can lead to lymphedema, whereas hyperplasia or abnormal growth of these vessels are associated with lymphangiomas and lymphangiosarcomas. Lymphatic vessels are also involved in lymph node and systemic metastasis of cancer cells. Recent novel findings on the molecular mechanisms involved in lymphatic vessel development and regulation allow the modulation of the lymphangiogenic process and specific targeting of the lymphatic endothelium. Recent results show that the homeodomain transcription factor Prox-I is an important lymphatic endothelial cell (LEC) fate-determining factor which can induce LEC-specific gene transcription even in blood vascular endothelial cells (BECs). This suggests that the distinct phenotypes of cells in the adult vascular endothelium are plastic and sensitive to transcriptional reprogramming, which might be useful for future therapeutic applications involving endothelial cells Vascular endothelial growth factor-C (VEGF-C) and VEGF-D are peptide growth factors capable of inducing the growth of new lymphatic vessels in vivo in a process called lymphangiogenesis.They belong to the larger family which also includesVEGF, placenta growth factor (PIGF) and VEGF.B.VEGF-C and VEGF-D are ligands for the endothelial cell specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. In adult human as well as mouse tissuesVEGFR-3 is expressed predominantly in lymphatic endothelial cells which line the inner surface of lymphatic vessels. While VEGFR-2 is thought to be the main mediator of angiogenesis,VEGFR-3 signaling is crucial for the development of the lymphatic vessels. Heterozygous inactivation of the VEGFR-3 tyrosine kinase leads to primary lymphedema due to defective lymphatic drainage in the limbs. Other factors that seem to be involved in lymphangiogenesis include the Tie/angiopoietin system, neuropilin-2 and integrin a9. VEGF-C induces lymphatic vessel growth, but high levels of VEGF-C also resulted in blood vessel leakiness and growth.The VEGFR-3-specific mutant form of VEGF-C called VEGF-C I 56S lacks blood vascular side effects but is sufficient for therapeutic lymphangiogenesis in a mouse model of lymphedema. As VEGF-C 156S is a specific lymphatic endothelial growth factor in the skin, it provides an attractive molecule for pro-lymphangiogenic therapy.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A22E</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Angiogenèse</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Angiogenesis</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Angiogénesis</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Lymphatique</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Lymphatic</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Linfático</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Cellule endothéliale</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Endothelial cell</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Célula endotelial</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Facteur croissance endothélium vasculaire</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Vascular endothelium growth factor</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Factor crecimiento endotelio vascular</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Récepteur biologique</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Biological receptor</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Receptor biológico</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Récepteur facteur croissance</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Growth factor receptor</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Receptor factor crecimiento</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Lymphoedème</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Lymphedema</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Linfedema</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Traitement</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Treatment</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Tratamiento</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Human</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hombre</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Animal</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Animal</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Animal</s0>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Article synthèse</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Review</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Artículo síntesis</s0>
<s5>11</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Lymphangiogenèse</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Lymphangiogenesis</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Appareil circulatoire pathologie</s0>
<s5>53</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cardiovascular disease</s0>
<s5>53</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0>
<s5>53</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Lymphatique pathologie</s0>
<s5>54</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Lymphatic vessel disease</s0>
<s5>54</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Linfático patología</s0>
<s5>54</s5>
</fC07>
<fN21><s1>026</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
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<server><NO>PASCAL 04-0045510 INIST</NO>
<ET>Lymphangiogenic growth factors, receptors and therapies</ET>
<AU>LOHELA (Marja); SAARISTO (Anne); VEIKKOLA (Tanja); ALITALO (Kari)</AU>
<AF>Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute and Helsinki University Central Hospital, Biomedicum Helsinki, University of Helsinki/Helsinki/Finlande (1 aut., 2 aut., 3 aut., 4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Thrombosis and haemostasis; ISSN 0340-6245; Coden THHADQ; Allemagne; Da. 2003; Vol. 90; No. 2; Pp. 167-184; Bibl. 226 ref.</SO>
<LA>Anglais</LA>
<EA>The lymphatic vasculature is essential for the maintenance of normal fluid balance and for the immune responses, but it is also involved in a variety of diseases. Hypoplasia or dysfuction of the lymphatic vessels can lead to lymphedema, whereas hyperplasia or abnormal growth of these vessels are associated with lymphangiomas and lymphangiosarcomas. Lymphatic vessels are also involved in lymph node and systemic metastasis of cancer cells. Recent novel findings on the molecular mechanisms involved in lymphatic vessel development and regulation allow the modulation of the lymphangiogenic process and specific targeting of the lymphatic endothelium. Recent results show that the homeodomain transcription factor Prox-I is an important lymphatic endothelial cell (LEC) fate-determining factor which can induce LEC-specific gene transcription even in blood vascular endothelial cells (BECs). This suggests that the distinct phenotypes of cells in the adult vascular endothelium are plastic and sensitive to transcriptional reprogramming, which might be useful for future therapeutic applications involving endothelial cells Vascular endothelial growth factor-C (VEGF-C) and VEGF-D are peptide growth factors capable of inducing the growth of new lymphatic vessels in vivo in a process called lymphangiogenesis.They belong to the larger family which also includesVEGF, placenta growth factor (PIGF) and VEGF.B.VEGF-C and VEGF-D are ligands for the endothelial cell specific tyrosine kinase receptors VEGFR-2 and VEGFR-3. In adult human as well as mouse tissuesVEGFR-3 is expressed predominantly in lymphatic endothelial cells which line the inner surface of lymphatic vessels. While VEGFR-2 is thought to be the main mediator of angiogenesis,VEGFR-3 signaling is crucial for the development of the lymphatic vessels. Heterozygous inactivation of the VEGFR-3 tyrosine kinase leads to primary lymphedema due to defective lymphatic drainage in the limbs. Other factors that seem to be involved in lymphangiogenesis include the Tie/angiopoietin system, neuropilin-2 and integrin a9. VEGF-C induces lymphatic vessel growth, but high levels of VEGF-C also resulted in blood vessel leakiness and growth.The VEGFR-3-specific mutant form of VEGF-C called VEGF-C I 56S lacks blood vascular side effects but is sufficient for therapeutic lymphangiogenesis in a mouse model of lymphedema. As VEGF-C 156S is a specific lymphatic endothelial growth factor in the skin, it provides an attractive molecule for pro-lymphangiogenic therapy.</EA>
<CC>002A22E</CC>
<FD>Angiogenèse; Lymphatique; Cellule endothéliale; Facteur croissance endothélium vasculaire; Récepteur biologique; Récepteur facteur croissance; Lymphoedème; Traitement; Homme; Animal; Article synthèse; Lymphangiogenèse</FD>
<FG>Appareil circulatoire pathologie; Lymphatique pathologie</FG>
<ED>Angiogenesis; Lymphatic; Endothelial cell; Vascular endothelium growth factor; Biological receptor; Growth factor receptor; Lymphedema; Treatment; Human; Animal; Review; Lymphangiogenesis</ED>
<EG>Cardiovascular disease; Lymphatic vessel disease</EG>
<SD>Angiogénesis; Linfático; Célula endotelial; Factor crecimiento endotelio vascular; Receptor biológico; Receptor factor crecimiento; Linfedema; Tratamiento; Hombre; Animal; Artículo síntesis</SD>
<LO>INIST-10255.354000112277180030</LO>
<ID>04-0045510</ID>
</server>
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Lymphangiogenic growth factors, receptors and therapies

Lymphangiogenic growth factors, receptors and therapies

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