^
Contact us  to learn more about
our Premium Content:  News alerts, weekly reports and conference planners
BIOMARKER:

TP53 wild-type

i
Other names: TP53, Tumor Protein P53, Cellular Tumor Antigen P53, Phosphoprotein P53, Tumor Protein P53, Antigen NY-CO-13, Transformation-Related Protein 53, Mutant Tumor Protein 53, P53 Tumor Suppressor, Tumor Suppressor P53, Tumor Protein 53, BMFS5, TRP53, BCC7, LFS1
Entrez ID:
1d
Expression of CK17 and SOX2 in Vulvar Intraepithelial Neoplasia: A Comprehensive Analysis of 150 Vulvar Lesions. (PubMed, Cancers (Basel))
To conclude, aside from p53, both CK17 and SOX2 can be of value for reaching an accurate diagnosis of HPV-independent VIN.
Journal
|
TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • SOX2 • KRT17 (Keratin 17)
|
TP53 mutation • TP53 wild-type
6d
Identifying Anti-Cancer Effects and Exploring the Mechanism of an MPS1/TTK Inhibitor in Gastric Cancer. (PubMed, Cancer Res Treat)
The TP53MUT-resistant line can tolerate aneuploidy or polyploidy and exhibits drug resistance. Our study explores the potential of an MPS1/TTK inhibitor, compound-9, as a targeted therapy in gastric cancer cells and investigates its mechanism of action.
Journal • MSi-H Biomarker
|
MSI (Microsatellite instability)
|
MSI-H/dMMR • TP53 wild-type
9d
Phase 1/2 trial of XPO1 inhibitor selinexor plus docetaxel in previously treated, advanced KRAS mutant non-small cell lung cancer. (PubMed, Clin Cancer Res)
Selinexor plus docetaxel was relatively well tolerated in patients with advanced KRAS mutant NSCLC. The regimen has promising efficacy in TP53 wild type cases, where selinexor monotherapy may also have activity.
P1/2 data • Journal • IO biomarker • Metastases
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
TP53 mutation • KRAS mutation • TP53 wild-type
|
docetaxel • Xpovio (selinexor)
10d
Enrollment closed • Combination therapy
|
TP53 (Tumor protein P53)
|
TP53 wild-type
|
brigimadlin (BI 907828)
11d
A Phase II Study of Acalabrutinib, Venetoclax, and Obinutuzumab (AVO) in a Treatment-Naive CLL Population Enriched for High-Risk Disease. (PubMed, J Clin Oncol)
AVO was highly active and well-tolerated in patients with previously untreated CLL with high-risk CLL, supporting its use as a new standard of care treatment option.
P2 data • Journal
|
TP53 (Tumor protein P53)
|
TP53 wild-type
|
Venclexta (venetoclax) • Gazyva (obinutuzumab) • Calquence (acalabrutinib)
12d
Interpretation of p16 and p53 in the Classification of Squamous Cell Carcinoma of the Vulva-An Interobserver Agreement Study. (PubMed, Am J Surg Pathol)
Pathologists without gynecologic subspecialty expertise benefited the most from a brief educational module, which fostered a better understanding and improved comfort level with the p16/p53 stain interpretation and tumor pathway designation in the diagnosis of vSCC. Some interpretative challenges remain, particularly in regard to select p53 patterns and high-risk HPV-in situ hybridization utilization, warranting additional research.
Clinical • Journal
|
CDKN2A (Cyclin Dependent Kinase Inhibitor 2A)
|
TP53 mutation • TP53 wild-type • TP53 expression
13d
p53 induces circFRMD4A to suppress cancer development through glycolytic reprogramming and cuproptosis. (PubMed, Mol Cell)
Finally, p53 agonists and elesclomol coordinately suppress the growth of cancer in a xenograft mouse model. Altogether, our study uncovers that p53 promotes glycolytic reprogramming and cuproptosis via circFRMD4A and suggests a potential combination strategy against cancers with wild-type p53.
Journal
|
EWSR1 (EWS RNA Binding Protein 1) • PKM (Pyruvate Kinase M1/2)
|
TP53 wild-type
|
elesclomol (STA-4783)
14d
Enrollment closed • Metastases
|
TP53 (Tumor protein P53) • MDM2 (E3 ubiquitin protein ligase)
|
TP53 wild-type • MDM2 amplification
|
brigimadlin (BI 907828)
14d
Dysregulation of the p53 pathway provides a therapeutic target in aggressive pediatric sarcomas with stem-like traits. (PubMed, Cell Oncol (Dordr))
Our results indicate that restoring canonical p53 activity provides a promising strategy for developing improved therapies for pediatric sarcomas with unfavorable stem-like traits.
Journal
|
KLF4 (Kruppel-like factor 4) • SOX2
|
TP53 mutation • TP53 wild-type
15d
Better pre-transplant treatment options for TP53-mutated MDS: cytoreductive or non-cytoreductive therapy? (PubMed, Bone Marrow Transplant)
Multivariate analyses showed that pre-HSCT cytoreduction was not associated with post-transplant survival (all P > 0.05). In conclusion, TP53-mutated MDS patients have poor post-HSCT outcomes; compared to BSC, pre-HSCT cytoreduction doesn't improve prognosis, even in those with MRD negative before transplantation.
Journal • Pre-transplantation
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type
15d
Inhibition of PSF activity overcomes resistance to treatment in cancers harboring mutant p53. (PubMed, Mol Cancer Ther)
We further demonstrated that C-30 impaired tumor growth and increased the expression of p53-target genes in vivo. These results suggested that C-30 produces tumor-suppressive effects similar to the functional reactivation of p53, providing a rationale for the inhibition of PSF activity as a promising therapy against treatment-resistant cancer.
Journal
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type • TP53 expression
16d
Prognostic effect of immunohistochemically determined molecular subtypes in gastric cancer. (PubMed, BMC Cancer)
Immunohistochemical analysis can identify prognostically different molecular subtypes of gastric cancer. The method is inexpensive and fast, yet reveals significant information for clinical decision-making. However, our study did not find that either molecular subtyping performed better than the other classification. Thus, further development of the most optimal grouping of different molecular subtypes is still needed.
Journal
|
MSI (Microsatellite instability) • MLH1 (MutL homolog 1) • MSH6 (MutS homolog 6) • MSH2 (MutS Homolog 2) • PMS2 (PMS1 protein homolog 2) • CDH1 (Cadherin 1)
|
TP53 wild-type
16d
RELAY: Final Overall Survival for Erlotinib + Ramucirumab or Placebo in Untreated, EGFR-Mutated Metastatic NSCLC. (PubMed, J Thorac Oncol)
In RELAY, OS was not significantly improved with similar long OS durations in both treatment arms.
Journal • Metastases
|
EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53)
|
TP53 mutation • EGFR mutation • EGFR L858R • EGFR exon 19 deletion • EGFR T790M • TP53 wild-type
|
Tagrisso (osimertinib) • erlotinib • Cyramza (ramucirumab)
19d
Rotenone adaptation promotes migration and invasion of p53-wild-type colon cancer through lipid metabolism. (PubMed, Clin Transl Oncol)
Our study provides a novel understanding of the role of complex I in lipid reprogramming facilitating colon cancer invasion and metastasis.
Journal
|
CPT1A (Carnitine Palmitoyltransferase 1A)
|
TP53 wild-type • TP53 expression
|
etomoxir (MIQ-001)
26d
Cancer cells restrict immunogenicity of retrotransposon expression via distinct mechanisms. (PubMed, Immunity)
Depletion of either LINE-1 ORF1p or ADAR1 reduced tumor growth in vitro. The fact that tumors utilize multiple pathways to mitigate immunostimulatory repeats implies the stress from their expression is a fundamental phenomenon to which PDAC, and likely other tumors, adapt.
Journal
|
TP53 (Tumor protein P53) • ADAR (Adenosine Deaminase RNA Specific)
|
TP53 mutation • TP53 wild-type
27d
Integrated molecular and functional characterization of the intrinsic apoptotic machinery identifies therapeutic vulnerabilities in glioma. (PubMed, Nat Commun)
Accordingly, a machine-learning approach identifies a composite molecular and functional signature that best predicts responses of diverse intracranial glioma models to standard-of-care therapies combined with ABBV-155, a clinical drug targeting intrinsic apoptosis. This work demonstrates how complementary functional and molecular data can robustly predict therapy-induced cell death.
Journal
|
TP53 (Tumor protein P53)
|
TP53 wild-type
|
mirzotamab clezutoclax (ABBV-155)
29d
Misincorporations of amino acids in p53 in human cells at artificially constructed termination codons in the presence of the aminoglycoside Gentamicin. (PubMed, Front Genet)
The incorporation of amino acids at codons 127, 128, or 129 generally result in a p53 protein that is predicted to be 'unfolded' or inactive as defined by molecular dynamic simulations presumably because the production of mixed wild-type p53 and mutant oligomers are known to be inactive through dominant negative effects of the mutation. The data highlight the need to not only produce novel small molecules that can readthrough PTCs or C-terminal termination codons, but also the need to design methods to insert the required amino acid at the position that could result in a 'wild-type' functional protein.
Journal
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type • TP53 expression
1m
p53 pathway genes’ mutations (muts) as prognostic factors in patients (pts) with metastatic Pancreatic Ductal Adenocarcinoma (mPDAC): a single center study (AIOM 2024)
Our study suggests an important prognostic role of p53 signaling muts in mPDAC pts; wt pts resulted in a longer OS than mutated pts, although some muts, in particular tp53 exon4 mut, seem to be associated with longer survival. Further studies are needed to investigate these findings, including an in-depth analysis of structural proteomics.
Clinical • Metastases
|
KRAS (KRAS proto-oncogene GTPase) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • CHEK2 (Checkpoint kinase 2) • MDM4 (The mouse double minute 4) • CHEK1 (Checkpoint kinase 1) • TP53BP1 (Tumor Protein P53 Binding Protein 1)
|
TP53 mutation • KRAS mutation • TP53 wild-type • TP53 exon 4 mutation
|
TruSight Oncology 500 Assay
1m
PIK3CA mutations in endometrial cancer: a pre-planned biomarker analysis from the phase II MITO END-3 study of carboplatin and paclitaxel with or without avelumab in advanced or recurrent endometrial cancer (AIOM 2024)
The frequent alterations of the PI3K pathway in gynecological cancers could emerge as new treatment target. Our data confirm the high frequency of PIK3CA mutations establishing EC as an ideal candidate for testing of PI3K inhibitors regardless of the TCGA classification. Moreover, these data confirm that other targetable mutations are present also in MSS EC group thus suggesting that new target agents should be explored.
P2 data • MSi-H Biomarker • PD(L)-1 Biomarker • IO biomarker • Metastases
|
TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MSI (Microsatellite instability) • PTEN (Phosphatase and tensin homolog) • ARID1A (AT-rich interaction domain 1A) • POLE (DNA Polymerase Epsilon)
|
TP53 mutation • MSI-H/dMMR • PIK3CA mutation • TP53 wild-type • PIK3CA H1047R • PTEN mutation • ARID1A mutation • POLE mutation • PIK3CA E545K • PIK3CA E545 • PIK3CA E542 • PIK3CA H1047L • PIK3CA mutation + PTEN mutation • PIK3CA C420R • PIK3CA E545A • PIK3CA E545G • PIK3CA Q546 • PIK3CA Q546R
|
FoundationOne® CDx
|
carboplatin • paclitaxel • Bavencio (avelumab)
1m
A line in shifting sand: Can we define and target TP53 mutated MDS? (PubMed, Semin Hematol)
Our current understanding is that TP53 mutated MDS and AML are globally quite similar, but as a group have unique features compared to TP53 wildtype (WT) disease. Optimizing immunotherapy and targeting vulnerabilities due to co-mutations and/or chromosome abnormalities should be the focus of future research.
Journal • IO biomarker
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type
1m
Therapy-relevant MDM2 amplification in cholangiocarcinomas in Caucasian patients. (PubMed, Ther Adv Med Oncol)
Real-world evidence in our Caucasian patient population confirmed that a significant number of intrahepatic CCAs showcase MDM2 amplification, qualifying for a personalized therapy option with Brigimadlin. MDM2 amplification must therefore be considered in the context of personalized molecular testing in CCA.
Journal
|
FGFR2 (Fibroblast growth factor receptor 2) • MDM2 (E3 ubiquitin protein ligase)
|
TP53 wild-type • MDM2 amplification
|
brigimadlin (BI 907828)
1m
Sodium arsenite-induced DNA methylation alterations exacerbated by p53 knockout in MCF7 cells. (PubMed, Heliyon)
Reconstitution of wild-type p53 only partially restored p53-mutant-specific differential methylation states in response to sodium arsenite exposure, which may be due to the insufficient reconstitution of p53 function, or suggestive of a potential exposure-specific epigenetic memory. Together, our results revealed wide-spread epigenetic alterations associated with p53 mutation that influence cellular response to sodium arsenite exposure, which may constate an important epigenetic mechanism by which tumour promoting agents synergize with driver mutations in cancer promotion.
Journal • Epigenetic controller
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type
1m
HPV and p53 status as precision determinants of head and neck cancer response to DNA-PKcs inhibition in combination with irradiation. (PubMed, Mol Cancer Ther)
This is also recapitulated in-vivo, where HPV+ UD-SCC-2 xenografts display stronger and more durable responses to the combined treatment as compared to p53 wild-type UM-SCC-74A tumors. In conclusion, DNA-PKcs inhibitor peposertib should be further studied as a potential radiosensitizer for HNSCCs, taking into consideration the genetic background and the HPV status of a particular tumor.
Journal • Combination therapy
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type
|
peposertib (M3814)
1m
MGAT4A/Galectin9-Driven N-Glycosylation Aberration as a Promoting Mechanism for Poor Prognosis of Endometrial Cancer with TP53 Mutation. (PubMed, Adv Sci (Weinh))
In addition, oncogenic mutations of TP53 gene in EC cells upregulate MGAT4A expression by disrupting the regulatory oversight exerted by wild-type p53 on tumor-suppressive miRNAs, including miR-34a and miR-449a/b. The findings highlight a new molecular mechanism involving MGAT4A-regulated N-glycosylation on the key regulator of glucose metabolism in p53 mutants-driven EC aggressiveness, which may provide a strategic avenue to combat advanced EC.
Journal
|
TP53 (Tumor protein P53) • MIR34A (MicroRNA 34a-5p) • LGALS9 (Galectin 9) • MIR449A (MicroRNA 449a) • SLC2A1 (Solute Carrier Family 2 Member 1)
|
TP53 mutation • TP53 wild-type
1m
Integrated multiomics analysis identified comprehensive crosstalk between diverse programmed cell death patterns and novel molecular subtypes in Hepatocellular Carcinoma. (PubMed, Sci Rep)
Finally, to explore the prognostic value, we also validated the frequent upregulation of DLAT in a real-world cohort of human HCC specimens by qPCR, western blot, and immunohistochemical staining (IHC). Together, our work herein comprehensively emphasized PCD-related patterns and key regulators, such as DLAT, contributed to the evolution and prognosis of tumor foci in HCC patients, and strengthened our understanding of PCD characteristics and promoted more effective risk stratification strategies.
Journal
|
TP53 (Tumor protein P53) • DLAT (Dihydrolipoamide S-Acetyltransferase) • SLC2A1 (Solute Carrier Family 2 Member 1)
|
TP53 mutation • TP53 wild-type
1m
Case report: The first known case of male retroperitoneal mesonephric-like adenocarcinoma. (PubMed, Front Oncol)
MLA in the retroperitoneum of men has not been reported yet. The diverse morphology and unclear molecular characteristics of this tumor mandate careful diagnosis for good clinical outcomes.
Journal
|
KIT (KIT proto-oncogene, receptor tyrosine kinase) • AR (Androgen receptor) • WT1 (WT1 Transcription Factor) • CD34 (CD34 molecule) • NKX2-1 (NK2 Homeobox 1) • VIM (Vimentin) • MME (Membrane Metalloendopeptidase) • ANO1 (Anoctamin 1) • GATA3 (GATA binding protein 3) • PAX8 (Paired box 8)
|
TP53 wild-type
1m
A novel ITGB8 transcript variant sustains ovarian cancer cell survival through genomic instability and altered ploidy on a mutant p53 background. (PubMed, J Ovarian Res)
pITGB8-205-overexpressing clones sustain ovarian tumor cell survival, achieve homeostasis and are formidable opponents of therapy.
Journal
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type
1m
Preliminary Efficacy and Safety of a Phase 1/2 Study of Acalabrutinib, Venetoclax, and Obinutuzumab in Patients with Relapsed/Refractory and Previously Untreated Mantle Cell Lymphoma (MAVO) (ASH 2024)
The combination of the Bruton tyrosine kinase inhibitor (BTKi) ibrutinib, the BCL-2 inhibitor venetoclax (V), and the anti-CD20 monoclonal antibody (mAb) obinutuzumab (O) has demonstrated safety and efficacy in R/R and TN MCL (Le Gouill, Blood 2021). Conclusions : AVO is safe and active in pts with R/R and TP53-aberrant/transplant ineligible TN MCL. Preliminary efficacy and feasibility of an MRD-guided treatment approach is encouraging in this high-risk TN cohort B. Our data supports further investigation of a targeted triplet approach, and the phase II TN transplant eligible and TP53 wild type cohort is enrolling based on demonstrated safety and efficacy in cohort B. Updated results will be presented at the meeting.
Clinical • P1/2 data • IO biomarker
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type • TP53 expression
|
clonoSEQ
|
Venclexta (venetoclax) • Imbruvica (ibrutinib) • Gazyva (obinutuzumab) • Calquence (acalabrutinib)
1m
Impact of TP53 Mutation on Survival Outcomes in Acute Lymphoblastic Leukemia at a Tertiary Center (ASH 2024)
Because of the above, further research is needed to explore whether using upfront immunotherapy like inotuzumab ozogamicin or blinatumomab in the upfront setting, as well as administering allogeneic transplant early in the treatment course of muTP53-ALL would decrease the risk of relapse and improve long-term survival. Although muTP53 ALL achieved a higher MRD-FC negative response compared to wtTP53 ALL, this did not translate into long-term survival in the muTP53 ALL. Whether using NGS for B-cell and T-cell receptors as a method for MRD testing, like clonoSEQ®, would provide a better prognostic tool is currently unknown.
IO biomarker
|
TP53 (Tumor protein P53) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
|
TP53 mutation • TP53 wild-type • BCR-ABL1 mutation
|
clonoSEQ
|
Blincyto (blinatumomab) • Besponsa (inotuzumab ozogamicin)
1m
MRD-Driven Time-Limited Therapy of Acalabrutinib and Lenalidomide Plus Rituximab (ALR) or Obinutuzumab (ALO) in Patients with Treatment-Naïve Mantle Cell Lymphoma: Phase 2 Trial Outcomes with MRD and cfDNA Analyses (ASH 2024)
The ALO regimen is feasible with encouraging initial safety and efficacy. MRD and cfDNA analyses provide real-time and non-invasive monitoring of molecular response and mutational evolution, which warrants further evaluation in response-adapted strategy (ClinicalTrials.gov - NCT03863184).
Clinical • P2 data • Cell-free DNA
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type • LDH elevation
|
clonoSEQ
|
Rituxan (rituximab) • lenalidomide • Gazyva (obinutuzumab) • Calquence (acalabrutinib)
1m
Precancerous Lesions of HPV-independent Vulvar Squamous Cell Carcinoma: Clinicopathologic Consideration of an Evolving Spectrum. (PubMed, Adv Anat Pathol)
Regarding the latter, some authors consider TP53/p53 aberration to be a diagnostic requirement for dVIN, although this is controversial, as discussed further herein. Also included in the spectrum of lesions that are considered in this review are possibly related HPV-independent, p53-wild type lesions that have historically been reported as "vulvar acanthosis with altered differentiation" (VAAD), "differentiated exophytic vulvar intraepithelial lesion" (DEVIL), "verruciform lichen simplex chronicus" (vLSC), and which more recently, have collectively been described as "verruciform acanthotic vulvar intraepithelial neoplasia (vaVIN)" or "vulvar aberrant maturation (VAM)." In this review, we perform a comprehensive clinicopathologic review of putative precancerous lesions of HPV-independent squamous cell carcinomas of the vulva, with an emphasis on recent developments in terminology, practical diagnostic issues, biomarkers, and pathogenesis.
Journal
|
TP53 (Tumor protein P53)
|
TP53 wild-type
2ms
Gene expression profiling of brain metastases and matched primary breast tumours with focus on the immune system and tumour microenvironment (SABCS 2024)
We found a downregulation of GE signatures related to the immune system and tumour ME in BM compared with PT. This was validated by the lower levels of TILs, CD4+ and CD8+ T cells in BM. The lower immunogenicity of BM may partly explain the reduced effect by immunotherapy intracranially.
BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker • Gene expression profiling
|
PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CD8 (cluster of differentiation 8) • PD-1 (Programmed cell death 1) • IFNG (Interferon, gamma) • CD276 (CD276 Molecule) • BRCA (Breast cancer early onset) • TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains 2) • IDO1 (Indoleamine 2,3-dioxygenase 1) • CD4 (CD4 Molecule) • SOX2 • CD68 (CD68 Molecule) • TGFB1 (Transforming Growth Factor Beta 1) • FOXP3 (Forkhead Box P3)
|
TP53 mutation • PIK3CA mutation • TP53 wild-type • PIK3CA expression • CD4 expression
|
nCounter® Breast Cancer 360™ Panel
2ms
Cyclin-dependent kinase 7 (CDK7) inhibitor samuraciclib combined with selective estrogen receptor degrader (SERD) elacestrant in advanced HR+ breast cancer after CDK4/6i: dose escalation data from the Phase 1b/2 SUMIT-ELA study (SABCS 2024)
Samuraciclib (CT7001), a once-daily oral CDK7 inhibitor, combined with the SERD fulvestrant had a favorable safety profile and clinical activity in patients with HR+/HER2− advanced breast cancer (BC) previously treated with a CDK4/6i [Coombes, 2023]. The most frequent treatment-related AEs were similar to the known safety profiles from both previous samuraciclib and elacestrant studies. With no drug-drug interactions between the treatments, further study of combination treatment in expansion C4 is supported. Preliminary signs of antitumor activity were observed.
P1/2 data • Metastases
|
HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • CDK4 (Cyclin-dependent kinase 4) • CDK7 (Cyclin Dependent Kinase 7)
|
TP53 mutation • TP53 wild-type
|
Guardant360® CDx
|
fulvestrant • Orserdu (elacestrant) • samuraciclib (CT7001)
2ms
Comprehensive characterization of the androgen receptor in male breast cancer (SABCS 2024)
Our analysis suggests a strong association between AR expression and TP53 mutations, TMB-H, and PD-L1 positivity, immune cell infiltration, immune checkpoint and stem cell-related gene. Also, T cell inflamed and IFNy score were inversely related. Further exploration of specific alterations and immune-oncology markers associated with AR expression may help in clinical trial design for male patients with BC.
Tumor mutational burden • BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • BRCA2 (Breast cancer 2, early onset) • PTEN (Phosphatase and tensin homolog) • AR (Androgen receptor) • IFNG (Interferon, gamma) • LAG3 (Lymphocyte Activating 3) • CHEK2 (Checkpoint kinase 2) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • CD34 (CD34 molecule) • KLF4 (Kruppel-like factor 4) • POU5F1 (POU Class 5 Homeobox 1) • ALDH2 (Aldehyde Dehydrogenase 2 Family Member) • FOXP3 (Forkhead Box P3)
|
TP53 mutation • TMB-H • TP53 wild-type • AR overexpression • AR expression • TP53 expression • FOXP3 expression
|
MI Tumor Seek™
2ms
Advances in Vulvar Cancer Biology and Management. (PubMed, J Clin Oncol)
Like other rare cancers, vulvar cancer lags behind in the identification and optimization of precision medicine strategies. Molecular-based preclinical models and rationally designed clinical trials, incorporating high-quality translational studies, are urgently required. These trials will require international collaboration to ensure feasibility and improvement of outcomes for women diagnosed with this disease.
Review • Journal
|
HER-2 (Human epidermal growth factor receptor 2)
|
TP53 wild-type
2ms
Trial completion date • Metastases
|
TP53 (Tumor protein P53)
|
TP53 wild-type
|
brigimadlin (BI 907828) • itraconazole • rifampicin
2ms
Trp53 Deletion Promotes Exacerbated Colitis, Facilitates Lgr5+ Cancer Stem Cell Expansion, and Fuels Tumorigenesis in AOM/DSS-Induced Colorectal Cancer. (PubMed, Int J Mol Sci)
This study highlights how Trp53 deletion promotes the perfect storm of inflammation and stemness, driving colon cancer progression. Trp53 deletion dramatically shortened AOM/DSS latency and improved tumor induction efficiency, offering an excellent inflammation-driven CRC model.
Journal • Cancer stem
|
TP53 (Tumor protein P53) • LGR5 (Leucine Rich Repeat Containing G Protein-Coupled Receptor 5)
|
TP53 mutation • TP53 wild-type • TP53 deletion
2ms
Synergistic Dual Targeting of Thioredoxin and Glutathione Systems Irrespective of p53 in Glioblastoma Stem Cells. (PubMed, Antioxidants (Basel))
Intriguingly, Auranofin increased the expression of glutathione S-transferase pi-1 (GSTP-1), a target of PPL. Combining Auranofin with PPL synergistically decreased IC50s to a nanomolar range in GSCs, supporting the potential to repurpose Auranofin and PPL in GBM.
Journal • PARP Biomarker
|
AKT1 (V-akt murine thymoma viral oncogene homolog 1) • GSTP1 (Glutathione S-transferase pi 1) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
|
TP53 mutation • TP53 wild-type • GSTP1 overexpression
2ms
Enhanced Anti-Melanoma Activity of Nutlin-3a Delivered via Ethosomes: Targeting p53-Mediated Apoptosis in HT144 Cells. (PubMed, Cells)
Overall, nutlin-3a delivery using ethosomes appears to be a significantly effective means for upregulating the p53 pathway and downregulating active Notch-1, while also taking advantage of their unexpected ability to reduce cellular migration. The findings of this study could pave the way for the development of specific nutlin-3a-loaded ethosome-based medicinal products for cutaneous use.
Journal
|
NOTCH1 (Notch 1) • NICD (NOTCH1 intracellular domain) • TNFRSF10B (TNF Receptor Superfamily Member 10b)
|
TP53 mutation • TP53 wild-type • NICD expression
|
Nutlin-3
2ms
TP53 mutations in cancer: Molecular features and therapeutic opportunities (Review). (PubMed, Int J Mol Med)
This approach could involve the use of small molecules, gene therapy and other methods to re‑establish wild‑type p53 activity. This review describes the complexity of the biological activities of different p53 mutants and summarizes the current therapeutic approaches to restore p53 function.
Review • Journal
|
TP53 (Tumor protein P53)
|
TP53 mutation • TP53 wild-type
2ms
Prognostic value of the TP53 mutation in patients with pancreatic ductal adenocarcinoma receiving FOLFIRINOX. (PubMed, Ther Adv Med Oncol)
Studies on the clinical significance and treatment response to 5-fluorouracil, leucovorin, irinotecan, and oxaliplatin (FOLFIRINOX) regimen in terms of the presence of these mutations remain inconclusive. PDAC patients with wild-type TP53 demonstrated longer OS than those with TP53 mutation, and this trend was intensified in patients with localized disease. This result may be due to an impaired response to FOLFIRINOX chemotherapy in patients with TP53 mutation.
Journal
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • SMAD4 (SMAD family member 4)
|
TP53 mutation • KRAS mutation • TP53 wild-type
|
5-fluorouracil • oxaliplatin • irinotecan • leucovorin calcium
2ms
TAF15 inhibits p53 nucleus translocation and promotes HCC cell 5-FU resistance via post-transcriptional regulation of UBE2N. (PubMed, J Physiol Biochem)
This study explored the role played by UBE2N in development of 5-fluorouracil (5-FU) resistance in HCC cells...Collectively, our present study identified a novel mechanism by which TAF15/UBE2N regulates p53 distribution to increase 5-FU resistance. Our results also suggest potential therapeutic strategies for treating HCC.
Journal
|
TAF15 (TATA-Box Binding Protein Associated Factor 15) • UBE2N (Ubiquitin Conjugating Enzyme E2 N)
|
TP53 mutation • TP53 wild-type • UBE2N expression
|
5-fluorouracil