Usted buscó: microenvironment (Inglés - Maltés)

additional effects on the tumour microenvironment including osteoblasts and osteoclasts also contribute to the in vivo efficacy.
effetti addizzjonali fuq il-mikro-ambjent tat-tumur inklużi osteoblasts u osteoklasts ukoll jikkontribwixxu għall-effikaċja in vivo.

microenvironment, making it less conducive to tumour cell growth, anti-angiogenic activity and anti-pain activity.
ambjent tal- mudullun u allura titnaqqaslu l- ħila li jkattar iċ- ċelloli tat- tumur, għandu effett kontra t- tkattir mill- ġdid tal- provvista ta ’ demm lit- tumur u effett kontra l- uġigħ.

in vivo: inhibition of osteoclastic bone resorption, which alters the bone marrow microenvironment, making it less conducive to tumour cell growth and anti-angiogenic activity.
in vivo: impediment tar-risorbiment tal-għadam minn osteoklasts, biex b’hekk ibiddlu l-mikro- ambjent tal-mudullun u allura titnaqqaslu l-ħila li jkattar iċ-ċelloli tat-tumur, għandu effett kontra t-tkattir mill-ġdid tal-provvista ta’ demm lit-tumur u effett kontra l-uġigħ.

the anti-tumour effect of temsirolimus, therefore, may also in part stem from its ability to depress levels of hif and vegf in the tumour or tumour microenvironment, thereby impairing vessel development.
l-effett ta’ kontra t-tumur ta’ temsirolimus, għalhekk, jista’ wkoll jirriżulta parzjalment mill-ħila tiegħu li jnaqqas il-livelli ta’ hif u vegf fit-tumur jew fil-mikro-ambjent tat-tumur, u b’hekk itellef l-iżvilupp tal-vini.

through inhibition of chemokine receptors cxcr4 and cxcr5 signalling induced by the chemokines cxcl12 and cxcl13, respectively, idelalisib inhibits homing and retention of malignant b-cells in the tumour microenvironment including lymphoid tissues and the bone marrow.
permezz tal-inibizzjoni ta’ sinjalazzjoni tar-riċetturi chemokine cxcr4 u cxcr5 indotta minn chemokines cxcl12 u cxcl13, rispettivament, idelalisib jinibixxi homing u żamma ta’ ċelluli b malinni fil-mikro-ambjent tat-tumur inklużi t-tessuti limfatiċi u l-mudullun.

these transcription factors regulate the ability of tumours to adapt to hypoxic microenvironments and to produce the angiogenic factor vascular endothelial growth factor (vegf).
dawn il-fatturi tat-traskrizzjoni jirregolaw il-ħila tat-tumuri biex jadattaw għal mikro-ambjenti ipossiċi u biex jipproduċu l-fattur anġjoġeniku, il-fattur tat-tkabbir endoteljali vaskulari (vascular endothelial growth factor - vegf).