Brain cancers, particularly glioblastoma and lower-grade glioma, remain major clinical
challenges due to their molecular heterogeneity, invasive behavior, treatment resistance, and
recurrence potential. MEIS1, MEIS2, and MEIS3 are TALE-class homeobox transcription
factors functioning within MEIS–PBX–HOX regulatory networks, yet their roles in brain
cancers remain incompletely understood. This thesis aimed to evaluate the biological
and clinical relevance of MEIS family members in brain cancers by integrating current literature
with exploratory bioinformatics analyses using publicly available platforms, including
GEPIA2, cBioPortal, UALCAN, STRING, TIMER3, and the Human Protein Atlas.
The findings suggest that MEIS family members show member-specific and context-
dependent patterns in glioma biology rather than behaving as a single uniform group. MEIS1
emerged as the most evidence-supported candidate, with associations related to glioma
aggressiveness, survival, and stemness-related features. MEIS2 showed a more limited profile,
suggesting a possible neural-lineage or cell-cycle-associated role without strong prognostic
support. MEIS3 displayed a distinct pattern, indicating a potential progression-related signal
that requires further validation. Overall, this thesis provides a comparative framework for
understanding the possible roles of MEIS1, MEIS2, and MEIS3 in brain cancer and supports
future experimental studies using glioma stem cell models, IDH-stratified cohorts, and MEIS-
directed therapeutic approaches.