Background:　Acute　lymphoblastic　leukemia　is　the　most　prevalent　neoplasia　among　children.　Despite　the　tremendous　achievements　of　state-of-the-art　treatment　strategies,　drug　resistance　is　still　a　major　cause　of　chemotherapy　failure　leading　to　relapse　in　pediatric　acute　lymphoblastic　leukemia.　The　underlying　mechanisms　of　such　phenomenon　are　not　yet　clear　and　subject　to　further　exploration.　Prior　research　has　shown　that　microRNAs　can　act　as　post-transcriptional　regulators　of　many　genes　related　to　drug　resistance.　However,　details　of　microRNA　regulation　mechanisms　in　pediatric　acute　lymphoblastic　leukemia　are　far　from　completely　understood.　Methods:　We　utilized　a　computational　approach　based　upon　emerging　biomedical　and　biological　ontologies　and　semantic　technologies　to　investigate　the　important　roles　of　microRNA:　mRNA　regulation　on　glucocorticoid　resistance　in　pediatric　acute　lymphoblastic　leukemia.　In　particular,　various　filtering　mechanisms　were　designed　based　on　the　user-provided　MeSH　term　to　narrow　down　the　most　promising　microRNAs　in　an　effective　manner.　Results:　During　our　manual　search　on　background　literature,　we　found　a　total　of　18　candidate　microRNAs　that　possibly　regulate　glucocorticoid　resistance　in　pediatric　acute　lymphoblastic　leukemia.　After　the　first-round　filtering　using　the　Broader-Match　option　where　both　the　user-provided　MeSH　term　and　its　direct　parent　term　were　utilized,　the　number　of　targets　for　18　microRNAs　was　reduced　from　232　to　74.　During　the　second-round　filtering　with　the　Exact-Match　option　where　only　the　MeSH　term　itself　was　utilized,　the　number　of　targets　was　further　reduced　to　19.　Finally,　we　conducted　semantic　searches　in　the　OmniSearch　software　tool　on　the　five　likely　regulating　microRNAs　and　identified　two　most　likely　microRNAs.　Conclusions:　We　successfully　identified　two　microRNAs,　hsa-miR-142-3p　and　hsa-miR-17-5p,　which　are　computationally　predicted　to　closely　relate　to　glucocorticoid　resistance,　thus　potentially　serving　as　novel　biomarkers　and　therapeutic　targets　in　pediatric　acute　lymphoblastic　leukemia.