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See detailAnti-tumor effect of caveolin gene delivery are mediated through the inhibition of the pro-angiogenic and vasodilatating effect of nitric oxide
Brouet, A.; DeWever, Julie; MARTINIVE, Philippe ULiege et al

in FASEB Journal (2005)

In tumors, caveolin-1, the structural protein of caveolae, constitutes a key switch through its function as a tumor suppressor and a promoter of metastases. In endothelial cells (EC), caveolin is also ... [more ▼]

In tumors, caveolin-1, the structural protein of caveolae, constitutes a key switch through its function as a tumor suppressor and a promoter of metastases. In endothelial cells (EC), caveolin is also known to directly interact with the endothelial nitric oxide synthase (eNOS) and thereby to modulate nitric oxide (NO)-mediated processes including vasodilation and angiogenesis. In this study, we examined whether the modulation of the stoichiometry of the caveolin/eNOS complex in EC lining tumor blood vessels could affect the tumor vasculature and consecutively tumor growth. For this purpose, we used cationic lipids, which are delivery systems effective at targeting tumor vs. normal vascular networks. We first documented that in vitro caveolin transfection led to the inhibition of both VEGF-induced EC migration and tube formation on Matrigel. The DNA-lipocomplex was then administered through the tail vein of tumor-bearing mice. The direct interaction between recombinant caveolin and native eNOS was validated in coimmunoprecipitation experiments from tumor extracts. A dramatic tumor growth delay was observed in mice transfected with caveolin- vs. sham-transfected animals. Using laser Doppler imaging and microprobes, we found that in the early time after lipofection (e.g., when macroscopic effects on the integrity of the tumor vasculature were not detectable), caveolin expression impaired NO-dependent tumor blood flow. At later stages post-transfection, a decrease in tumor microvessel density in the central core of caveolin-transfected tumors was also documented. In conclusion, our study reveals that by exploiting the exquisite regulatory interaction between eNOS and caveolin and the propensity of cationic lipids to target EC lining tumor blood vessels, caveolin plasmid delivery appears to be a safe and efficient way to block neoangiogenesis and vascular function in solid tumors, independently of any direct effects on tumor cells. [less ▲]

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See detailThe Anti-Tumor Effect of HDAC Inhibition in a Human Pancreas Cancer Model Is Significantly Improved by the Simultaneous Inhibition of Cyclooxygenase 2
Peulen, Olivier ULiege; Gonzalez, Arnaud ULiege; Peixoto, Paul ULiege et al

in PLoS ONE (2013), 8(9), 75102

Pancreatic ductal adenocarcinoma is the fourth leading cause of cancer death worldwide, with no satisfactory treatment to date. In this study, we tested whether the combined inhibition of cyclooxygenase-2 ... [more ▼]

Pancreatic ductal adenocarcinoma is the fourth leading cause of cancer death worldwide, with no satisfactory treatment to date. In this study, we tested whether the combined inhibition of cyclooxygenase-2 (COX-2) and class I histone deacetylase (HDAC) may results in a better control of pancreatic ductal adenocarcinoma. The impact of the concomitant HDAC and COX-2 inhibition on cell growth, apoptosis and cell cycle was assessed first in vitro on human pancreas BxPC-3, PANC-1 or CFPAC-1 cells treated with chemical inhibitors (SAHA, MS-275 and celecoxib) or HDAC1/2/3/7 siRNA. To test the potential antitumoral activity of this combination in vivo, we have developed and characterized, a refined chick chorioallantoic membrane tumor model that histologically and proteomically mimics human pancreatic ductal adenocarcinoma. The combination of HDAC1/3 and COX-2 inhibition significantly impaired proliferation of BxPC-3 cells in vitro and stalled entirely the BxPC-3 cells tumor growth onto the chorioallantoic membrane in vivo. The combination was more effective than either drug used alone. Consistently, we showed that both HDAC1 and HDAC3 inhibition induced the expression of COX-2 via the NF-kB pathway. Our data demonstrate, for the first time in a Pancreatic Ductal Adenocarcinoma (PDAC) model, a significant action of HDAC and COX-2 inhibitors on cancer cell growth, which sets the basis for the development of potentially effective new combinatory therapies for pancreatic ductal adenocarcinoma patients. [less ▲]

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See detailAnti-Tumor Necrosis Factor Therapy Restores Peripheral Blood B-cell Subsets and CD40 Expression in Inflammatory Bowel Diseases.
Li, Zhe; Vermeire, Severine; Bullens, Dominique et al

in Inflammatory Bowel Diseases (2015), 21(12), 2787-96

BACKGROUND: Anti-tumor necrosis factor (TNF) therapy has become a standard therapy for severe inflammatory bowel diseases (IBD), but its effect on B lymphocytes is largely unexplored. In this study we ... [more ▼]

BACKGROUND: Anti-tumor necrosis factor (TNF) therapy has become a standard therapy for severe inflammatory bowel diseases (IBD), but its effect on B lymphocytes is largely unexplored. In this study we investigated peripheral blood B cells, B-cell subsets, and CD40 expression in patients with IBD before and during anti-TNF therapy with infliximab (IFX). METHODS: Blood was taken from healthy controls (n = 52) and patients with active IBD before (n = 46) and/or during anti-TNF therapy (n = 55). B-cell markers were detected by immunofluorescent staining and FACS analysis. Patients were classified as responders or nonresponders to anti-TNF therapy. RESULTS: We found a numerical deficiency of circulating CD19 B cells, a lower activation state (CD40 expression) and lower proportions of CD5 B cells and IgMIgDCD27 preswitched memory cells among B cells in active patients with IBD before IFX therapy compared with healthy controls. IFX treatment increased CD19 B-cell numbers as well as the proportions of named B-cell subsets in responders but not in nonresponders. IFX more effectively upregulated CD40 expression in responders than in nonresponders. Restoration of B cells correlated with the biological response to therapy (C-reactive protein). Trough serum levels of IFX correlated with the number of B cells during therapy. CONCLUSIONS: A lower number of circulating B cells, a low CD40 expression, and a decrease in the proportion of CD5 and in the preswitched memory subset characterize active IBD. Restoration of these abnormalities correlates with the clinical response to anti-TNF therapy. The mechanism for this effect on B cells should be further explored. [less ▲]

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See detailAnti-tumour effect of an aromatic retinoic acid analog in a mouse syngeneic transplantable sarcoma
Deneufbourg, Jean-Marie ULiege

in Biomedicine Express (1979), 31

Anti-tumour activity of an aromatic retinoic acid analog was tested on Sarcoma J. Complete regression and survival time are significantly improved. These results are at variance with observations ... [more ▼]

Anti-tumour activity of an aromatic retinoic acid analog was tested on Sarcoma J. Complete regression and survival time are significantly improved. These results are at variance with observations suggesting the lack of activity of this compound on transplanted murine tumours. Arguments in favour of an immunological stimulation are presented. [less ▲]

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See detailAnti-utopie, dystopie et contre-utopie : quelles traversées de l’utopie ? D’Émile Souvestre à Léon Daudet
Stienon, Valérie ULiege

Conference (2012, November 16)

Les récits anticipant des sociétés futures sous oppression ou sur le déclin sont régulièrement confondus sous les appellations génériques d’« anti-utopie », de « contre-utopie » et de « dystopie » ... [more ▼]

Les récits anticipant des sociétés futures sous oppression ou sur le déclin sont régulièrement confondus sous les appellations génériques d’« anti-utopie », de « contre-utopie » et de « dystopie ». Rarement problématisés en tant que tels, ces appariements dénotent une certaine indécision dans l’appréhension de tout un pan de la tradition littéraire utopique. Réfèrent-ils vraiment à une diversité de représentations des conditions d’accès au bonheur et de réalisation d’un idéal en société ? [less ▲]

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See detailAnti-UVC Irradiation and Metal Chelation Properties of 6-Benzoyl-5,7-dihydroxy-4-phenyl-chromen-2-one: An Implication for Anti-Cataract Agent
Liao, Jiahn-Haur; Wu, Tzu-Hua; Hsu, Feng-Lin et al

in International Journal of Molecular Sciences (2011), 12

Coumarin derivative 1, 5,7-dihydroxy-6-(3-methyl-1-butyryl)-4-phenyl-chromen- 2-one, has been reported to possess radical scavenging activity and DNA protection. We have synthesized a series of coumarins ... [more ▼]

Coumarin derivative 1, 5,7-dihydroxy-6-(3-methyl-1-butyryl)-4-phenyl-chromen- 2-one, has been reported to possess radical scavenging activity and DNA protection. We have synthesized a series of coumarins with structural modifications at positions C4, C5, C6 and C7 and evaluated them for their anti-UVC properties. Coumarin 7, 6-benzoyl-5,6-dihydroxy-4-phenyl-chromen-2-one, was found to have the most potent activity in protecting porcine γ-crystallin against UVC insults. Results of fluorescence assays indicated that compound 7 was capable of decreasing the loss of intensity while lens crystallins and DNA PUC19 were irradiated with UVC. Presence of compound 7 decreased hydroxyl radical levels determined by probe 1b and the free iron concentrations determined by Ferrozine reagent. The chelation assay showed that compound 7 was chelated to metal via 6-CO and 5-OH on the benzopyrone ring. The observed protective effects of compound 7 towards crystallins from insults of UVC and free radicals may be due to its iron-chelating activity and its peak absorption at 254 nm. [less ▲]

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See detailAntiagregants: doit-on les arreter avant un acte invasif?
Maeyns, K.; Legrand, Victor ULiege; Pierard, Luc ULiege et al

in Revue Médicale de Liège (2008), 63(3), 136-40

Antiplatelet therapy is the leading therapy for the primary and secondary prevention for the atherosclerotic arterial disease. The practical question of withdraw alavoiding or continuation of oral ... [more ▼]

Antiplatelet therapy is the leading therapy for the primary and secondary prevention for the atherosclerotic arterial disease. The practical question of withdraw alavoiding or continuation of oral antiplatelet agents accurs currently before any invasive procedure. It is important to compare the relative thrombotic vs hemorrhagic risk. For most interventions, it is recommended to continue antiplatelet therapy. It is particularly important in patients who benefited from drug-eluting stents where the thrombotic risk is major. [less ▲]

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See detailAntiamoebic and Antiplasmodial Activities of Alkaloids Isolated from Strychnos usambarensis
Wright, Colin; Bray, Dorothy; O'Neill, Melanie et al

in Planta Medica (1991), 57

Seven alkaloids isolated from Strychnos usambarensis have been assessed for in vitro activities against Entamoeba histolytica and Plasmodium falciparum and for in vivo activity against Plasmodium berghei ... [more ▼]

Seven alkaloids isolated from Strychnos usambarensis have been assessed for in vitro activities against Entamoeba histolytica and Plasmodium falciparum and for in vivo activity against Plasmodium berghei in mice. Strychnopentamine and 3'-4'-dihydrousambarensine were highly active against P. falciparum in vitro, but were inactve and non-toxic against P.berghei in vivo.Usambarensine, usambarine and 18,19-dihydrousambarine were highly active against E. histolytica in vitro, but were less active against P. falciparum in vitro. Nb-methylusambarensine was less active against both protozoa than was usambarensine, and akagerine possessed little antiprotozoal activity.Structure-activity relationships are discussed in the context of the reported cytotoxic and pharmacological properties of those alkaloids. [less ▲]

Detailed reference viewed: 44 (9 ULiège)
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See detailThe antiangiogenic 16K prolactin disturbs functional tumor neovascularization by affecting vessel maturation
Nguyen, Ngoc-Quynh-Nhu ULiege; Castermans, Karolien; Berndt, Sarah et al

Poster (2011, May)

16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Here we investigated the effect of 16K ... [more ▼]

16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Here we investigated the effect of 16K hPRL on tumor vessel maturation and on the related signaling pathways. We show that 16K hPRL treatment leads, in a murine B16-F10 tumor model, to a dysfunctional tumor vasculature with reduced pericyte coverage, and disruption of the PDGF-B/PDGFR-B, Ang/Tie2, and Delta/Notch pathways. In an aortic ring assay, 16K hPRL impairs endothelial cell and pericyte outgrowth from the vascular ring. In addition, 16K hPRL prevents pericyte migration to endothelial cells. This event was independent of a direct inhibitory effect of 16K hPRL on pericyte viability, proliferation, or migration. In endothelial cell-pericyte cocultures, we found 16K hPRL to disturb Notch signaling, this being the first time such an effect is observed with an endogenous antiangiogenic agent. These findings provide new insights into the mechanisms of 16K hPRL action and highlight its potential for use in anticancer therapy. [less ▲]

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See detailThe Antiangiogenic 16K Prolactin Impairs Functional Tumor Neovascularization by Inhibiting Vessel Maturation
Nguyen, Ngoc-Quynh-Nhu ULiege; Castermans, Karolien; Berndt, Sarah et al

in PLoS ONE (2011), 6(11), 27318-27318

Background: Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumor growth, invasion, and metastasis. 16K hPRL, the antiangiogenic 16-kDa N-terminal ... [more ▼]

Background: Angiogenesis, the formation of new blood vessels from existing vasculature, plays an essential role in tumor growth, invasion, and metastasis. 16K hPRL, the antiangiogenic 16-kDa N-terminal fragment of human prolactin was shown to prevent tumor growth and metastasis by modifying tumor vessel morphology. Methodology/Principal Findings: Here we investigated the effect of 16K hPRL on tumor vessel maturation and on the related signaling pathways. We show that 16K hPRL treatment leads, in a murine B16-F10 tumor model, to a dysfunctional tumor vasculature with reduced pericyte coverage, and disruption of the PDGF-B/PDGFR-B, Ang/Tie2, and Delta/Notch pathways. In an aortic ring assay, 16K hPRL impairs endothelial cell and pericyte outgrowth from the vascular ring. In addition, 16K hPRL prevents pericyte migration to endothelial cells. This event was independent of a direct inhibitory effect of 16K hPRL on pericyte viability, proliferation, or migration. In endothelial cell-pericyte cocultures, we found 16K hPRL to disturb Notch signaling. Conclusions/Significance: Taken together, our data show that 16K hPRL impairs functional tumor neovascularization by inhibiting vessel maturation and for the first time that an endogenous antiangiogenic agent disturbs Notch signaling. These findings provide new insights into the mechanisms of 16K hPRL action and highlight its potential for use in anticancer therapy. [less ▲]

Detailed reference viewed: 95 (21 ULiège)
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See detailThe antiangiogenic factor 16K human prolactin induces caspase-dependent apoptosis by a mechanism that requires activation of nuclear factor-kappa B
Tabruyn, Sébastien ULiege; Sorlet, C. M.; Rentier-Delrue, Françoise ULiege et al

in Molecular Endocrinology (2003), 17(9), 1815-1823

We have previously shown that the 16-kDa N-terminal fragment of human prolactin (16K hPRL) has antiangiogenic properties, including the ability to induce apoptosis in vascular endothelial cells. Here, we ... [more ▼]

We have previously shown that the 16-kDa N-terminal fragment of human prolactin (16K hPRL) has antiangiogenic properties, including the ability to induce apoptosis in vascular endothelial cells. Here, we examined whether the nuclear factor-kappaB (NF-kappaB) signaling pathway was involved in mediating the apoptotic action of 16K hPRL in bovine adrenal cortex capillary endothelial cells. In a dose-dependent manner, treatment with 16K hPRL induced inhibitor kappaB-alpha degradation permitting translocation of NF-kappaB to the nucleus and reporter gene activation. Inhibition of NF-kappaB activation by overexpression of a nondegradable inhibitor kappaB-alpha mutant or treatment with NF-kappaB inhibitors blocked 16K hPRL-induced apoptosis. Treatment with 16K hPRL activated the initiator caspases-8 and -9 and the effector caspase-3, all of which were essential for stimulation of DNA fragmentation. This activation of the caspase cascade by 16K hPRL was also NF-kappaB dependent. These findings support the conclusion that NF-kappaB signaling plays a central role in 16K hPRL-induced apoptosis in vascular endothelial cells. [less ▲]

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See detailThe antiangiogenic factor 16K PRL induces programmed cell death in endothelial cells by caspase activation
Martini, J. F.; Piot, C.; Humeau, L. M. et al

in Molecular Endocrinology (2000), 14(10), 1536-49

We asked whether the antiangiogenic action of 16K human PRL (hPRL), in addition to blocking mitogen-induced vascular endothelial cell proliferation, involved activation of programmed cell death. Treatment ... [more ▼]

We asked whether the antiangiogenic action of 16K human PRL (hPRL), in addition to blocking mitogen-induced vascular endothelial cell proliferation, involved activation of programmed cell death. Treatment with recombinant 16K hPRL increased DNA fragmentation in cultured bovine brain capillary endothelial (BBE) and human umbilical vein endothelial (HUVE) cells in a time- and dose-dependent fashion, independent of the serum concentration. The activation of apoptosis by 16K hPRL was specific for endothelial cells, and the activity of the peptide could be inhibited by heat denaturation, trypsin digestion, and immunoneutralization, but not by treatment with the endotoxin blocker, polymyxin-B. 16K hPRL-induced apoptosis was correlated with the rapid activation of caspases 1 and 3 and was blocked by pharmacological inhibition of caspase activity. Caspase activation was followed by inactivation of two caspase substrates, poly(ADP-ribose) polymerase (PARP) and the inhibitor of caspase-activated deoxyribonuclease (DNase) (ICAD). Furthermore, 16K hPRL increased the conversion of Bcl-X to its proapoptotic form, suggesting that the Bcl-2 protein family may also be involved in 16K hPRL-induced apoptosis. These findings support the hypothesis that the antiangiogenic action of 16K hPRL includes the activation of programmed cell death of vascular endothelial cells. [less ▲]

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See detailThe antiangiogenic factor, 16-kDa human prolactin, induces endothelial cell cycle arrest by acting at both the G(0)-G(1) and the G(2)-M phases
Tabruyn, Sébastien ULiege; Nguyen, Ngoc-Quynh-Nhu ULiege; Cornet, Anne ULiege et al

in Molecular Endocrinology (2005), 19(7), 1932-1942

The 16-kDa N-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor that has been shown to prevent tumor growth in a xenograph mouse model. In this paper we first demonstrate ... [more ▼]

The 16-kDa N-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor that has been shown to prevent tumor growth in a xenograph mouse model. In this paper we first demonstrate that 16K hPRL inhibits serum-induced DNA synthesis in adult bovine aortic endothelial cells. This inhibition is associated with cell cycle arrest at both the G(0)-G(1) and the G(2)-M phase. Western blot analysis revealed that 16K hPRL strongly decreases levels of cyclin D1 and cyclin B1, but not cyclin E. The effect on cyclin D1 is at least partially transcriptional, because treatment with 16K hPRL both reduces the cyclin D1 mRNA level and down-regulates cyclin D1 promoter activity. This regulation may be due to inhibition of the MAPK pathway, but it is independent of the glycogen synthase kinase-3 beta pathway. Lastly, 16K hPRL induces the expression of negative cell cycle regulators, the cyclin-dependent kinase inhibitors p21(cip1) and p27(kip1). In summary, 16K hPRL inhibits serum-induced proliferation of endothelial cells through combined effects on positive and negative regulators of cell cycle progression. [less ▲]

Detailed reference viewed: 27 (14 ULiège)
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See detailAntiangiogenic liposomal gene therapy with 16K human prolactin efficiently reduces tumor growth.
Kinet, Virginie ULiege; Nguyen, Ngoc-Quynh-Nhu ULiege; Sabatel, Céline ULiege et al

in Cancer Letters (2009), 284(2), 222-228

Human 16K PRL (16K hPRL) is a potent inhibitor of angiogenesis both in vitro and in vivo. It has been shown to prevent tumor growth in three xenograft mouse models. Here we have used a gene transfer ... [more ▼]

Human 16K PRL (16K hPRL) is a potent inhibitor of angiogenesis both in vitro and in vivo. It has been shown to prevent tumor growth in three xenograft mouse models. Here we have used a gene transfer method based on cationic liposomes to produce 16K hPRL and demonstrate that 16K hPRL inhibits tumor growth in a subcutaneous B16F10 mouse melanoma model. Computer-assisted image analysis shows that 16K hPRL treatment results in the reduction of tumor vessel length and width, leading to a 57% reduction in average vessel size. We thus show, for the first time, that administration of the 16K hPRL gene complexed to cationic liposomes is effective to maintain antiangiogenic activities of 16K hPRL level. [less ▲]

Detailed reference viewed: 115 (36 ULiège)
See detailAntiangiogenic peptides
Martial, Joseph ULiege; Struman, Ingrid ULiege; Nguyen, Ngoc-Quynh-Nhu ULiege et al

Patent (2007)

The present invention refers to antiangiogenic peptides, especially to tilted peptides having antiangiogenic properties and peptides from the prolactin/growth hormone familiy having antiangiogenic ... [more ▼]

The present invention refers to antiangiogenic peptides, especially to tilted peptides having antiangiogenic properties and peptides from the prolactin/growth hormone familiy having antiangiogenic properties. [less ▲]

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See detailAntiangiogenic peptides
Martial, Joseph ULiege; Struman, Ingrid ULiege; Nguyen, Ngoc-Quynh-Nhu ULiege et al

Patent (2008)

The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 ... [more ▼]

The present invention refers to a pharmaceutical composition comprising an isolated antiangiogenic peptide or a recombinant protein comprising the antiangiogenic peptide, wherein the peptide is between 11 and 40 amino acids in length and having antiangiogenic activity, the peptide comprising the amino acid sequence: X1-X2-X3-X4-X5-X6-X7-X8-X9-X10-X11-X12-X13-X14, wherein X1 is any amino acid residue comptabile with forming a helix; X2 is an amino acid redisue of : Leu, Ile, Val; X3 is an amino acid residue of: Arg, Lys, His, Ser, Thr; X4 is an amino acid residue of: Ile, Leu, Val; X5 is any amino acid residue compatible with forming a helix; X6 is an amino acid residue of: Leu, Ile, Val; X7 is an amino acid residue of: Leu, Ile, Val, Ser, Thr; X8 is any amino acid residue compatible with forming a helix; X9 is any amino acid residue compatible with forming a helix; X10 is an amino acid residue of: Gln, Glu, Asp, Arg, His, Lys, Asn; X11 is an amino acid residue of: Ser, Thr; X12 is an amino acid residue of: Trp, Tyr, Phe; X13 is an animo acid residue of Leu, Ile, Val, Asn, Gln; X14 is an amino acid residue of: Glu, Gln, Asp, Asn. [less ▲]

Detailed reference viewed: 63 (16 ULiège)
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See detailAntiapoptotic effect of GM-CSF activated STAT5 signaling pathway in chronic mastitis-affected cows : possible involvement in persistent accumulation of neutrophils in milk
Boutet, Philippe ULiege; Bureau, Fabrice ULiege; Gillet, Laurent ULiege et al

in Congress COST Action 844: “Apoptosis and programmed cell death : molecular mechanisms and applications in Biotechnology and Agriculture” (2004)

Detailed reference viewed: 32 (7 ULiège)