Q-omics provides the consensus-scored C7orf69 profile across patient tissues and cancer cell-line models. C7orf69 expression is associated with patient survival in 17 of 34 cancer types, with the highest sampling consensus in CHOL. Among the 18 cancer types available for tumor–normal comparison, C7orf69 is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, C7orf69 protein abundance shows 8,767 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight CHOL, COAD, and GBM as cancer lineages where C7orf69 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 C7orf69 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes C7orf69 survival associations across molecular data types. C7orf69 RNA expression shows survival associations in the most cancer types (17), followed by 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 C7orf69 RNA expression–survival associations across cancer types. High C7orf69 expression shows unfavorable associations in CHOL, LUSC, STAD and PAAD, but favorable associations in COAD and ESCA. The CHOL Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify CHOL as the clearest survival context for C7orf69 RNA expression.
This table summarizes C7orf69 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 3. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for C7orf69. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. C7orf69 shows lower tumor expression in BRCA and higher tumor expression in COAD, STAD, HNSC, KIRP and READ. The COAD box plot shows higher C7orf69 RNA expression in tumor versus normal tissue (log2 FC = +0.166, t-test p < 0.001).
This table shows molecular features associated with C7orf69 in patient tissues and cancer cell lines. In patient samples, C7orf69 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, C7orf69 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in NCI60_ALL.
