Q-omics provides the consensus-scored TPM1 profile across patient tissues and cancer cell-line models. TPM1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, TPM1 is differentially expressed in 14, with the highest sampling consensus in KICH. Additionally, TPM1 protein abundance shows 27,644 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight BLCA, KICH, and LSCC as cancer lineages where TPM1 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 TPM1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TPM1 survival associations across molecular data types. TPM1 RNA expression shows survival associations in the most cancer types (23), 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 TPM1 RNA expression–survival associations across cancer types. High TPM1 expression shows unfavorable associations in BLCA, MESO, KICH, UVM, LUSC and HNSC. The BLCA 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 BLCA as the clearest survival context for TPM1 RNA expression.
This table summarizes TPM1 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 8. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TPM1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TPM1 shows lower tumor expression in KICH, BLCA, COAD and UCEC and higher tumor expression in KIRC and LIHC. The KICH box plot shows higher TPM1 RNA expression in normal versus tumor tissue (log2 FC = −2.409, t-test p < 0.001).
This table shows molecular features associated with TPM1 in patient tissues and cancer cell lines. In patient samples, TPM1 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TPM1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BONE.
