C-type lectin domain family 1 member AGenealiases: CLEC-1 · CLEC1
Q-omics provides the consensus-scored CLEC1A profile across patient tissues and cancer cell-line models. CLEC1A expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CLEC1A is differentially expressed in 13, with the highest sampling consensus in LUAD. Additionally, CLEC1A RNA expression shows 23,171 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, LUAD, and LSCC as cancer lineages where CLEC1A 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 CLEC1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CLEC1A survival associations across molecular data types. CLEC1A RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CLEC1A RNA expression–survival associations across cancer types. High CLEC1A expression shows unfavorable associations in KIRP and SCLC, but favorable associations in KIRC, HNSC, THCA and SKCM. 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 CLEC1A RNA expression.
This table summarizes CLEC1A 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 KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CLEC1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CLEC1A shows lower tumor expression in LUAD, KICH, KIRP, BLCA and LUSC and higher tumor expression in KIRC. The LUAD box plot shows higher CLEC1A RNA expression in normal versus tumor tissue (log2 FC = −2.343, t-test p < 0.001).
This table shows molecular features associated with CLEC1A in patient tissues and cancer cell lines. In patient samples, CLEC1A shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CLEC1A 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 BREAST and LARGE_INTESTINE.
