Advanced search
Combine gene, variant, phenotype, region and year filters
Every result shows the extracted entities next to the sentences that support them; rows for the searched entities come first.
Transparent by designEvery result links extracted entities to its source sentence and publication identifier.
Knowledge-base search
About your search
Phenotype
Prostate cancer
218articles
218mentions
12co-reported genes shown
Most co-reported genes (articles)
Counts are literature co-mentions in SaudiVarKB, not clinical or causal assertions. Gene details: HGNC; variant status: ClinVar via dbSNP.
Publications
2 records shown · first 60Unveiling Ligand-Induced Conformational Changes in Mutant AR-LBD: Molecular Dynamics Insights into the Androgen Receptor-Coactivator Mechanism.
PMID 40841914 | DOI 10.1021/acs.jcim.5c01406 · Journal of chemical information and modeling · 2025 · 4 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| phenotype | prostate cancer | “The androgen receptor (AR) is a nuclear receptor involved in regulating gene expression, maintaining the sexual phenotype, and contributing to the development of prostate cancer (PCa).” | 0.98 | phenotype_alias_lexicon_v2 |
| variant | T877A | “In addition, F876L and T877A mutations in AR-LBD alter the ligand-to-coactivator allosteric pathway involving the coactivator, helix 3 (H3), helix 4 (H4), the loop between H3-H4, and helix 12 (H12), potentially converting the AR-apalutamide complex from an antagonistic to an agonistic state.” | 0.82 | literature_variant_regex_v2 |
| gene | AR | “The androgen receptor (AR) is a nuclear receptor involved in regulating gene expression, maintaining the sexual phenotype, and contributing to the development of prostate cancer (PCa).” | 0.98 | hgnc_dict_v1 |
| variant | F876L | “In addition, F876L and T877A mutations in AR-LBD alter the ligand-to-coactivator allosteric pathway involving the coactivator, helix 3 (H3), helix 4 (H4), the loop between H3-H4, and helix 12 (H12), potentially converting the AR-apalutamide complex from an antagonistic to an agonistic state.” | 0.82 | literature_variant_regex_v2 |
Structural insights into the mechanism of resistance to bicalutamide by the clinical mutations in androgen receptor in chemo-treatment resistant prostate cancer.
PMID 37144757 | DOI 10.1080/07391102.2023.2208203 · Journal of biomolecular structure & dynamics · 2024 · 4 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| phenotype | prostate cancer | “Structural insights into the mechanism of resistance to bicalutamide by the clinical mutations in androgen receptor in chemo-treatment resistant prostate cancer.” | 0.98 | phenotype_alias_lexicon_v2 |
| variant | T877A | “Among several well-studied PCa-specific mutations, T877A, T877S and H874Y are the most common substitutions in the ligand-binding domain (LBD) of the AR.” | 0.82 | literature_variant_regex_v2 |
| variant | T877S | “Among several well-studied PCa-specific mutations, T877A, T877S and H874Y are the most common substitutions in the ligand-binding domain (LBD) of the AR.” | 0.82 | literature_variant_regex_v2 |
| variant | H874Y | “Among several well-studied PCa-specific mutations, T877A, T877S and H874Y are the most common substitutions in the ligand-binding domain (LBD) of the AR.” | 0.82 | literature_variant_regex_v2 |