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TP53 and leukemia are reported together in 10 articles.

Gene

TP53

HGNC
HGNC:11998
219articles
219mentions
7variants with confirmed gene link
Most co-reported phenotypes (articles)
Reported variants (articles · ClinVar status)
Phenotype

Leukemia

652articles
652mentions
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

10 records shown · first 60

Biomarkers and advances in AML-MRC: from bench to bedside.

PMID 41711916 | PMCID PMC12920406 | DOI 10.1007/s00277-026-06805-8 · Annals of hematology · 2026 · 5 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“This review provides a comprehensive overview of the pathogenesis, key biomarkers, and diagnostic innovations in AML-MRC, highlighting the role of genetic mutations (e.g., TP53, RUNX1, and splicing factors), cytogenetic abnormalities, and immune microenvironment alterations.”0.98hgnc_dict_v1
phenotypeleukemia“Acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) represents a high-risk subtype of AML, characterized by poor prognosis and limited therapeutic options.”0.98phenotype_alias_lexicon_v2
geneRUNX1“This review provides a comprehensive overview of the pathogenesis, key biomarkers, and diagnostic innovations in AML-MRC, highlighting the role of genetic mutations (e.g., TP53, RUNX1, and splicing factors), cytogenetic abnormalities, and immune microenvironment alterations.”0.98hgnc_dict_v1
geneFLT3“Additionally, we discuss emerging therapies, including CPX-351, hypomethylating agents (HMAs), targeted inhibitors (e.g., FLT3 and IDH1/2 inhibitors), and immunotherapies, while addressing the challenges of treatment resistance and relapse.”0.98hgnc_dict_v1
TypeEntitySource evidenceConfidenceExtractor
geneTP53“Despite the use of antiviral therapies and targeted monoclonal antibodies, therapeutic failure is common due to genomic instability-specifically TP53 mutations compromising Zidovudine/Interferon efficacy and CCR4 antigenic variations leading to mogamulizumab resistance.”0.98hgnc_dict_v1
phenotypeleukemia“HTLV-1-Driven Clonal Evolution and Immune Escape in Adult T-Cell Leukaemia: From Viral Persistence to Therapeutic Failure.”0.93phenotype_alias_lexicon_v2
geneCCR4“Despite the use of antiviral therapies and targeted monoclonal antibodies, therapeutic failure is common due to genomic instability-specifically TP53 mutations compromising Zidovudine/Interferon efficacy and CCR4 antigenic variations leading to mogamulizumab resistance.”0.98hgnc_dict_v1
phenotypelymphoma“Adult T-cell leukaemia/lymphoma (ATL) is an aggressive CD4 +T-cell malignancy caused by the human T-cell leukaemia virus type 1 (HTLV-1).”0.98phenotype_alias_lexicon_v2

Chronic lymphocytic leukaemia in the Middle East: a subgroup analysis from the CREEK study on treatment patterns and outcomes.

PMID 41175395 | DOI 10.1080/14737140.2025.2582649 · Expert review of anticancer therapy · 2026 · 2 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“TP53 aberrations were found in 9.0% of CLL-treated and 9.8% of TN cohorts.”0.98hgnc_dict_v1
phenotypeleukemia“Chronic lymphocytic leukaemia in the Middle East: a subgroup analysis from the CREEK study on treatment patterns and outcomes.”0.93phenotype_alias_lexicon_v2

Omics and artificial intelligence integration for stratifying blast crisis CML using COSMIC signatures and pan-cancer precision drug repurposing.

PMID 41355924 | PMCID PMC12678951 | DOI 10.5306/wjco.v16.i11.111983 · World journal of clinical oncology · 2025 · 4 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“ML identified three BC-CML clusters: (1) Cluster 1 [breast cancer susceptibility gene 2 (BRCA2), TP53]; (2) Cluster 2 [isocitrate dehydrogenase (IDH) 1/2, ten-eleven translocation 2]; and (3) Cluster 3 [Janus kinase (JAK) 2, colony-stimulating factor 3 receptor], with distinct COSMIC signatures.”0.98hgnc_dict_v1
phenotypeleukemia“BACKGROUND: Although chronic-phase chronic myeloid leukemia (CP-CML) is treatable and nearly curable in about 50% of patients, accelerated-phase chronic myeloid leukemia (AP-CML) shows concerning drug resistance, while blast crisis chronic myeloid leukemia (BC-CML) is highly lethal.”0.98phenotype_alias_lexicon_v2
geneBRCA2“ML identified three BC-CML clusters: (1) Cluster 1 [breast cancer susceptibility gene 2 (BRCA2), TP53]; (2) Cluster 2 [isocitrate dehydrogenase (IDH) 1/2, ten-eleven translocation 2]; and (3) Cluster 3 [Janus kinase (JAK) 2, colony-stimulating factor 3 receptor], with distinct COSMIC signatures.”0.98hgnc_dict_v1
phenotypebreast cancer“ML identified three BC-CML clusters: (1) Cluster 1 [breast cancer susceptibility gene 2 (BRCA2), TP53]; (2) Cluster 2 [isocitrate dehydrogenase (IDH) 1/2, ten-eleven translocation 2]; and (3) Cluster 3 [Janus kinase (JAK) 2, colony-stimulating factor 3 receptor], with distinct COSMIC signatures.”0.98phenotype_alias_lexicon_v2

TP53-mutated MDS and AML: immune dysregulation, tumor microenvironment, and emerging therapeutic strategies.

PMID 40909943 | PMCID PMC12405186 | DOI 10.3389/fonc.2025.1655486 · Frontiers in oncology · 2025 · 3 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“TP53 mutations drive oncogenesis and therapeutic resistance in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML), impairing p53-regulated functions such as apoptosis, immune surveillance, and genomic stability, leading to immune evasion and metabolic reprogramming.”0.98hgnc_dict_v1
phenotypeleukemia“TP53-mutated MDS and AML: immune dysregulation, tumor microenvironment, and emerging therapeutic strategies.”0.93phenotype_alias_lexicon_v2
geneMDM2“However, novel therapeutic approaches provide promising avenues, including MDM2 inhibitors, p53-reactivating agents, pathway-targeted inhibitors (Hedgehog, Wnt, NF-κB), immune modulation (checkpoint inhibitors, CAR-T therapy), metabolic interventions (fatty acid metabolism, glycolysis), and gene-editing technologies (CRISPR/Cas9, base editing).”0.98hgnc_dict_v1

Application of Newly Customized Myeloid NGS Panel in the Diagnosis of Myeloid Malignancies.

PMID 38204493 | PMCID PMC10777859 | DOI 10.2147/IJGM.S437327 · International journal of general medicine · 2024 · 13 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“This panel was designed to sequence the complete genome of CALR, IDH1, IDH2, JAK2, FLT3, NPM1, MPL, TET2, SF3B1, TP53, and MLL.”0.98hgnc_dict_v1
phenotypeleukemia“PURPOSE: Genetic mutations are major factors in the diagnosis and prognosis of leukemia, and it is difficult to assess these variants using single-gene analysis.”0.98phenotype_alias_lexicon_v2
geneCALR“This panel was designed to sequence the complete genome of CALR, IDH1, IDH2, JAK2, FLT3, NPM1, MPL, TET2, SF3B1, TP53, and MLL.”0.98hgnc_dict_v1
geneIDH1“This panel was designed to sequence the complete genome of CALR, IDH1, IDH2, JAK2, FLT3, NPM1, MPL, TET2, SF3B1, TP53, and MLL.”0.98hgnc_dict_v1

Li-Fraumeni Syndrome with Unusual Synchronous Malignancies: A Case Report.

PMID 38188481 | PMCID PMC10769503 | DOI 10.1159/000535099 · Case reports in oncology · 2024 · 3 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“INTRODUCTION: Li-Fraumeni syndrome (LFS) is a rare autosomal dominant disorder brought on by pathogenic mutations in the TP53 tumor suppressor gene.”0.98hgnc_dict_v1
phenotypeleukemia“CASE PRESENTATION: We are presenting a 48-year-old male with a diagnosis of LFS that was confirmed by a genetic test triggered by the patient's son's diagnosis of LFS and leukemia.”0.98phenotype_alias_lexicon_v2
phenotypegastric cancer“CONCLUSION: Gastric cancer and neuroendocrine tumors are not usually associated with LFS.”0.98phenotype_alias_lexicon_v2

TP53 Expression and Mutational Analysis in Hematological Malignancy in Jeddah, Saudi Arabia.

PMID 35328276 | PMCID PMC8946951 | DOI 10.3390/diagnostics12030724 · Diagnostics (Basel, Switzerland) · 2022 · 4 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“TP53 Expression and Mutational Analysis in Hematological Malignancy in Jeddah, Saudi Arabia.”0.98hgnc_dict_v1
phenotypeleukemia“Most of the 6 patients with TP53 deletion had acute lymphoblastic leukemia (ALL), and majority of them were child.”0.98phenotype_alias_lexicon_v2
populationSaudi Arabia, Jeddah“TP53 Expression and Mutational Analysis in Hematological Malignancy in Jeddah, Saudi Arabia. Nevertheless, the prevalence and prognostic role of TP53 mutations in hematological malignancy in Saudi patients are not well reported. We, therefore, aim to assess the frequency of TP53 mutations in hematological malignancies in Saudi Arabia. Most of the 6 patients with TP53 deletion had acute lymphoblastic leukemia (ALL), and majority of them were child.”0.95saudi_context_rules_v1
variantp.H175R“G9963A, p.H175R).”0.95hgvs_regex_v1
TypeEntitySource evidenceConfidenceExtractor
geneTP53“Three patients with B-ALL had heterozygous pathogenic mutations in TP53, BRCA1, and BRCA2; one patient with B-ALL had homozygous pathogenic mutation in PMS2; and one patient with T-ALL had LP homozygous mutation in AK2 that was associated with reticular dysgenesis.”0.98hgnc_dict_v1
phenotypeleukemia“Frequency of pathogenic/likely pathogenic germline variants in cancer-related genes among children with acute leukemia in Saudi Arabia.”0.98phenotype_alias_lexicon_v2
geneBRCA1“Three patients with B-ALL had heterozygous pathogenic mutations in TP53, BRCA1, and BRCA2; one patient with B-ALL had homozygous pathogenic mutation in PMS2; and one patient with T-ALL had LP homozygous mutation in AK2 that was associated with reticular dysgenesis.”0.98hgnc_dict_v1
geneBRCA2“Three patients with B-ALL had heterozygous pathogenic mutations in TP53, BRCA1, and BRCA2; one patient with B-ALL had homozygous pathogenic mutation in PMS2; and one patient with T-ALL had LP homozygous mutation in AK2 that was associated with reticular dysgenesis.”0.98hgnc_dict_v1

Increased TNF α, IL-6 and ErbB2 mRNA expression in peripheral blood leukocytes from breast cancer patients.

PMID 24961464 | DOI 10.1007/s12032-014-0038-0 · Medical oncology (Northwood, London, England) · 2014 · 7 validated mentions
TypeEntitySource evidenceConfidenceExtractor
geneTP53“Therefore, have investigated whether or not the expression levels, of selected genes [tumor necrosis factor-α (TNFα), interleukin 6 (IL-6), adiponectin, leptin, C-reactive protein (CRP), parathyroid hormone (PTH), tumor protein 53 (TP53) and erythroblastic leukemia viral oncogene 2 (ErbB2)] were altered in blood samples of lean, overweight/obese and breast cancer subjects.”0.98hgnc_dict_v1
phenotypeleukemia“Therefore, have investigated whether or not the expression levels, of selected genes [tumor necrosis factor-α (TNFα), interleukin 6 (IL-6), adiponectin, leptin, C-reactive protein (CRP), parathyroid hormone (PTH), tumor protein 53 (TP53) and erythroblastic leukemia viral oncogene 2 (ErbB2)] were altered in blood samples of lean, overweight/obese and breast cancer subjects.”0.98phenotype_alias_lexicon_v2
geneTNF“Increased TNF α, IL-6 and ErbB2 mRNA expression in peripheral blood leukocytes from breast cancer patients.”0.98hgnc_dict_v1
geneCRP“Therefore, have investigated whether or not the expression levels, of selected genes [tumor necrosis factor-α (TNFα), interleukin 6 (IL-6), adiponectin, leptin, C-reactive protein (CRP), parathyroid hormone (PTH), tumor protein 53 (TP53) and erythroblastic leukemia viral oncogene 2 (ErbB2)] were altered in blood samples of lean, overweight/obese and breast cancer subjects.”0.98hgnc_dict_v1