Q-omics provides the consensus-scored LZTS3 profile across patient tissues and cancer cell-line models. LZTS3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, LZTS3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, LZTS3 protein abundance shows 18,320 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight COAD, KIRC, and GBM as cancer lineages where LZTS3 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 LZTS3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes LZTS3 survival associations across molecular data types. LZTS3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (8) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible LZTS3 RNA expression–survival associations across cancer types. High LZTS3 expression shows unfavorable associations in COAD, THCA, MESO and ESCA, but favorable associations in HNSC and LGG. The COAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify COAD as the clearest survival context for LZTS3 RNA expression.
This table summarizes LZTS3 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 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for LZTS3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. LZTS3 shows lower tumor expression in KIRC, KIRP and KICH and higher tumor expression in COAD, LIHC and STAD. The KIRC box plot shows higher LZTS3 RNA expression in normal versus tumor tissue (log2 FC = −2.544, t-test p < 0.001).
This table shows molecular features associated with LZTS3 in patient tissues and cancer cell lines. In patient samples, LZTS3 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, LZTS3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BONE.
