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treatment with Herceptin ( trastuzumabresultedHER2 ) receptor positive breast cancer cells with induced overexpression of CCND1 in culture
additional targetis contributingto the overexpression of EGFR in Akt1 impaired breast cancer cells
WA treatmentcausestranscriptional activation of Notch in human breast cancer cells
represses expression 's own inhibitory molecule , BCAR3further leadingto enhanced TGFβ / Smad signaling in breast cancer cells
Loss of the E3 ubiquitin ligase HACE1 results in enhanced RAC1signaling contributingto breast cancer progression while eIF2α - mediated downregulation of RAC1 signaling attenuates malignant phenotypes of breast cancer cells
the combination of Herceptin ( trastuzumab ) and Eloxatin ( oxaliplatinresultedHER2)-positive breast cancer cells in culture ( PMID : 24300914
the molecular basisleadingto the depletion of glutathione by CDDO in breast cancer cells
hypermethylation of its promoter(passive) to be caused byDownregulation of miR-203 in metastatic breast cancer cells appeared
More ) Deregulation of PKBinfluencesantiapoptotic signaling by PKC in breast cancer cells
the eventsleadto increased Notch activity during EMT of breast cancer cells
to cell deathleadingto cell death
in a POL3-driven increase in RN7SL1 ... an endogenous RNA normally shielded by RNA binding proteinsresultsin a POL3-driven increase in RN7SL1 ... an endogenous RNA normally shielded by RNA binding proteins
a transcriptional program associated with a more aggressive tumor phenotype independently of promitogenic effectstriggersa transcriptional program associated with a more aggressive tumor phenotype independently of promitogenic effects
to overgrowths that were sensitive to Jak / Stat signallingledto overgrowths that were sensitive to Jak / Stat signalling
in increased CCL18 secretion , which promoted the invasion and metastasis of breast cancer cells [ 28resultedin increased CCL18 secretion , which promoted the invasion and metastasis of breast cancer cells [ 28
to increased tumor cell migrationleadingto increased tumor cell migration
to their aggressive phenotypecontributesto their aggressive phenotype
induced osteoclast differentiation and bone destructionmay contributeinduced osteoclast differentiation and bone destruction