Q-omics provides the consensus-scored TLN2 profile across patient tissues and cancer cell-line models. TLN2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TLN2 is differentially expressed in 15, with the highest sampling consensus in KIRP. Additionally, TLN2 protein abundance shows 33,106 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, KIRP, and HNSC as cancer lineages where TLN2 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 TLN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TLN2 survival associations across molecular data types. TLN2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (13) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TLN2 RNA expression–survival associations across cancer types. High TLN2 expression shows unfavorable associations in MESO and ESCA, but favorable associations in KIRC, BRCA, KIRP and READ. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for TLN2 RNA expression.
This table summarizes TLN2 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 KIRP for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for TLN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TLN2 shows lower tumor expression in KIRP, KICH, THCA, COAD and BLCA and higher tumor expression in HNSC. The KIRP box plot shows higher TLN2 RNA expression in normal versus tumor tissue (log2 FC = −1.793, t-test p < 0.001).
This table shows molecular features associated with TLN2 in patient tissues and cancer cell lines. In patient samples, TLN2 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, TLN2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BONE.
