Q-omics provides the consensus-scored NIM1K profile across patient tissues and cancer cell-line models. NIM1K expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, NIM1K is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, NIM1K RNA expression shows 17,162 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and KIRC as cancer lineages where NIM1K 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 NIM1K — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes NIM1K survival associations across molecular data types. NIM1K RNA expression shows survival associations in the most cancer types (20), followed by mutation status (5) 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 NIM1K RNA expression–survival associations across cancer types. High NIM1K expression shows unfavorable associations in UVM, DLBC, THCA and LUSC, but favorable associations in STAD and PAAD. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .004). Together, the overview and detailed table identify UVM as the clearest survival context for NIM1K RNA expression.
This table summarizes NIM1K 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 1. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for NIM1K. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. NIM1K shows lower tumor expression in LUAD, COAD, LUSC and THCA and higher tumor expression in KIRC and HNSC. The KIRC box plot shows higher NIM1K RNA expression in tumor versus normal tissue (log2 FC = +0.582, t-test p < 0.001).
This table shows molecular features associated with NIM1K in patient tissues and cancer cell lines. In patient samples, NIM1K shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, NIM1K RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BONE.
