Q-omics provides the consensus-scored TPM4 profile across patient tissues and cancer cell-line models. TPM4 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TPM4 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, TPM4 protein abundance shows 26,170 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, HNSC, and GBM as cancer lineages where TPM4 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 TPM4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPM4 survival associations across molecular data types. TPM4 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TPM4 RNA expression–survival associations across cancer types. High TPM4 expression shows unfavorable associations in KIRP, UVM, MESO, ACC, LGG and OV. 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 TPM4 RNA expression.
This table summarizes TPM4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TPM4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPM4 shows lower tumor expression in KICH and UCEC and higher tumor expression in HNSC, LIHC, COAD and STAD. The HNSC box plot shows higher TPM4 RNA expression in tumor versus normal tissue (log2 FC = +0.918, t-test p < 0.001).
This table shows molecular features associated with TPM4 in patient tissues and cancer cell lines. In patient samples, TPM4 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TPM4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BONE.
