Q-omics provides the consensus-scored NECAB3 profile across patient tissues and cancer cell-line models. NECAB3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, NECAB3 is differentially expressed in 13, with the highest sampling consensus in KICH. Additionally, NECAB3 RNA expression shows 18,036 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, KICH, and ACC as cancer lineages where NECAB3 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 NECAB3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NECAB3 survival associations across molecular data types. NECAB3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (2) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible NECAB3 RNA expression–survival associations across cancer types. High NECAB3 expression shows unfavorable associations in KIRC, UCEC, KICH, THYM, LIHC and COAD. The KIRC 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 KIRC as the clearest survival context for NECAB3 RNA expression.
This table summarizes NECAB3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 1. The strongest signals are observed in KICH for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for NECAB3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NECAB3 shows lower tumor expression in LUAD and higher tumor expression in KICH, LIHC, KIRP, BRCA and COAD. The KICH box plot shows higher NECAB3 RNA expression in tumor versus normal tissue (log2 FC = +1.415, t-test p < 0.001).
This table shows molecular features associated with NECAB3 in patient tissues and cancer cell lines. In patient samples, NECAB3 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, NECAB3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and SOFT_TISSUE.
