Q-omics provides the consensus-scored TPM3 profile across patient tissues and cancer cell-line models. TPM3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TPM3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, TPM3 protein abundance shows 22,520 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRP, KIRC, and HNSC as cancer lineages where TPM3 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 TPM3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPM3 survival associations across molecular data types. TPM3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) 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 TPM3 RNA expression–survival associations across cancer types. High TPM3 expression shows unfavorable associations in KIRP, ACC, LIHC, MESO, UVM and HNSC. The KIRP 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 KIRP as the clearest survival context for TPM3 RNA expression.
This table summarizes TPM3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for TPM3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPM3 shows lower tumor expression in KICH and higher tumor expression in KIRC, BLCA, KIRP, LIHC and STAD. The KIRC box plot shows higher TPM3 RNA expression in tumor versus normal tissue (log2 FC = +0.705, t-test p < 0.001).
This table shows molecular features associated with TPM3 in patient tissues and cancer cell lines. In patient samples, TPM3 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, TPM3 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_Lymphoma and BONE.
