Q-omics provides the consensus-scored TUBA1C profile across patient tissues and cancer cell-line models. TUBA1C expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, TUBA1C is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, TUBA1C protein abundance shows 29,882 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, KIRC, and PDAC as cancer lineages where TUBA1C shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for TUBA1C — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TUBA1C survival associations across molecular data types. TUBA1C RNA expression shows survival associations in the most cancer types (29), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TUBA1C RNA expression–survival associations across cancer types. High TUBA1C expression shows unfavorable associations in MESO, KICH, LIHC, KIRC, BRCA and SKCM. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify MESO as the clearest survival context for TUBA1C RNA expression.
This table summarizes TUBA1C tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TUBA1C. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TUBA1C shows higher tumor expression in KIRC, KIRP, HNSC, BLCA, COAD and LUSC. The KIRC box plot shows higher TUBA1C RNA expression in tumor versus normal tissue (log2 FC = +0.993, t-test p < 0.001).
This table shows molecular features associated with TUBA1C in patient tissues and cancer cell lines. In patient samples, TUBA1C shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, TUBA1C RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
