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BIOMARKER:

KRAS mutation + TP53 mutation

i
Other names: KRAS, KRAS proto-oncogene GTPase, KRAS1, KRAS2, NS, NS3, OES, CFC2, RALD, K-Ras, RASK2, KI-RAS, C-K-RAS, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, K-Ras 2, C-K-RAS, c-Ki-ras, c-Ki-ras2, Kirsten rat sarcoma viral oncogene homolog, 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:
Associations
Trials
18h
Decoding the Clinical and Molecular Signatures of EGFR Common, Compound, and Uncommon Mutations in Non-Small Cell Lung Cancer. (PubMed, J Thorac Oncol)
This study underscores the clinical and molecular heterogeneity of EGFR mutation classes in LUAD, highlighting the unique profile of uncommon mutations, particularly their association with smoking and co-mutations in KRAS and TP53. Comprehensive molecular testing, including next-generation sequencing, is crucial to identify these uncommon mutations and inform therapeutic decisions. Further investigation into the role of immunotherapy in patients with uncommon EGFR mutations is warranted given the tobacco-related molecular signatures and high TMB associated with this subgroup.
Journal • Tumor mutational burden • IO biomarker
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden)
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TP53 mutation • KRAS mutation • EGFR mutation • TMB-H • EGFR L858R • EGFR exon 19 deletion • EGFR amplification • KRAS amplification • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
3d
Mixed pancreatic ductal adenocarcinoma and well-differentiated neuroendocrine tumor: A case report. (PubMed, World J Gastrointest Oncol)
Mixed NET/non-NET tumors with distinct histology and molecular profiles might be better classified as collision tumors rather than MiNENs.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
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TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
10d
Prevalence of HER3 Expression in Pancreatic Cancer Patients Treated With Systemic Chemotherapy. (PubMed, Cancer Med)
A high prevalence of HER3 expression was observed in pancreatic cancer patients after chemotherapy. Our findings indicate that HER3 is a potential therapeutic target for pancreatic cancer, deserving further clinical investigation.
Retrospective data • Journal
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3)
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TP53 mutation • KRAS mutation • ERBB3 expression • ERBB3 mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
13d
The role of epigenetic regulation in pancreatic ductal adenocarcinoma progression and drug response: an integrative genomic and pharmacological prognostic prediction model. (PubMed, Front Pharmacol)
The integration of epigenetic features with mutation profiles, immune microenvironment, and drug sensitivity offers new insights into PDAC heterogeneity and potential therapeutic strategies. These findings pave the way for personalized medicine in PDAC management and highlight the importance of epigenetic regulation in cancer research.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CD8 (cluster of differentiation 8)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
16d
Analysis of Methylation of Tumor-suppressive miRNAs and KRAS/TP53 Mutations in Pancreatic Juice. (PubMed, Anticancer Res)
Analyzing the methylation of miR-1247 in addition to KRAS and TP53 mutations in pancreatic juice may be useful to distinguish PC from PanIN/IPMN.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MIR200A (MicroRNA 200a) • MIR1247 (MicroRNA 1247)
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TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
1m
Lfng-expressing centroacinar cell is a unique cell-of-origin for p53 deficient pancreatic cancer. (PubMed, Oncogene)
Finally, high LFNG expression is associated with high grade and poor survival in human patients. Taken together, Lfng marks a centroacinar subpopulation that is uniquely susceptible to oncogenic transformation when p53 is lost, and Lfng functions as an oncogene in all three lineages of the exocrine pancreas.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • NOTCH3 (Notch Receptor 3)
|
TP53 mutation • KRAS mutation • TP53 deletion • KRAS deletion • KRAS mutation + TP53 mutation
1m
A Rare Case of Primary Hepatic Undifferentiated Pleomorphic Sarcoma: Exploring Cancer-related Gene Mutations. (PubMed, Intern Med)
Despite initiating hepatic arterial infusion chemotherapy, the tumor continued to grow, and the patient's poor performance status complicated the transition to a phase I KRAS mutation drug trial, leading to death eight months after the symptom onset. A timely genetic mutation analysis may facilitate effective treatment transitions in hepatic UPS despite the lack of established treatments.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
3ms
Combined KRAS and TP53 mutation in patients with colorectal cancer enhance chemoresistance to promote postoperative recurrence and metastasis. (PubMed, BMC Cancer)
Furthermore, advanced-stage patients with concurrent KRAS and TP53 mutations are susceptible to developing cancer-associated cachexia due to chemotherapy resistance or forced cessation of treatment. Our findings underscore the urgent need for the development of innovative and novel chemotherapeutic strategies to effectively manage colorectal cancer patients harboring combined KRAS and TP53 mutations.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CEACAM5 (CEA Cell Adhesion Molecule 5)
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TP53 mutation • KRAS mutation • PIK3CA mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
3ms
Camrelizumab combined with chemotherapy for stage IV pulmonary sarcomatoid cancer with pancreatic metastases. (PubMed, Respir Med Case Rep)
Camrelizumab and chemotherapy were administered, and the metastasis disappeared. Immunotherapy combined with platinum-based chemotherapy is effective in treating PSC with pancreatic metastases.
Journal • PD(L)-1 Biomarker • IO biomarker • Metastases
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
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TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
AiRuiKa (camrelizumab)
7ms
LLS 2024 ELN-REFINED RISK STRATIFICATION IN OLDER ADULTS WITH NEWLY DIAGNOSED ACUTE MYELOID LEUKEMIA TREATED WITH LOW-INTENSITY THERAPY (EHA 2024)
Among patients ≥60 yrs with ND AML given LIT, the current 2022 ELN risk system classifies most (79%)patients as adverse risk and does not reliably distinguish favorable from intermediate-risk, highlighting thelimitations of the model in this patient population. We propose a refined LLS classification using a "mutationscore" incorporating IDH2, MLL2, KRAS and TP53 mutations for those previously assigned ELN 2022 adverserisk, as well as redefining the definition of LLS-favorable risk.
Clinical
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • KMT2D (Lysine Methyltransferase 2D) • MLL2 (Myeloid/lymphoid or mixed-lineage leukemia 2)
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TP53 mutation • KRAS mutation • FLT3-ITD mutation • IDH2 mutation • FLT3 mutation • KMT2D mutation • TP53 mutation + KRAS mutation • MLL2 mutation • KRAS mutation + TP53 mutation
|
FoundationOne® Heme CDx • LeukoStrat® CDx FLT3 Mutation Assay
10ms
TGFβ-induced long non-coding RNA LINC00313 activates Wnt signaling and promotes cholangiocarcinoma. (PubMed, EMBO Rep)
We propose a model whereby TGFβ induces LINC00313 in order to regulate the expression of hallmark Wnt pathway genes, in co-operation with SWI/SNF. By modulating key genes of the Wnt pathway, LINC00313 fine-tunes Wnt/TCF/LEF-dependent transcriptional responses and promotes cholangiocarcinogenesis.
Journal
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • TGFB1 (Transforming Growth Factor Beta 1) • SULF2 (Sulfatase 2) • TCF7 (Transcription Factor 7)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
1year
Prognostic risk signature in patients with acute myeloid leukemia treated with hypomethylating agents and venetoclax. (PubMed, Blood Adv)
The mPRS classification accurately segregated groups of AML patients treated with HMA plus Ven. In these patients, N/KRAS and TP53 mutations appear to negatively impact outcomes and therefore new treatment approaches are warranted.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3)
|
TP53 mutation • KRAS mutation • FLT3-ITD mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
Venclexta (venetoclax)
1year
Outcome of first-line treatment with pembrolizumab according to KRAS/TP53 mutational status for non-squamous PD-L1 high (≥50%) NSCLC in the German National Network Genomic Medicine Lung Cancer (nNGM). (PubMed, J Thorac Oncol)
G12C/TP53 co-mutations identify a subset of patients with a very favorable long-term survival with ICI monotherapy, mediated by highly active IFNγ signaling in a pro-inflammatory TME.
Journal • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • IFNG (Interferon, gamma)
|
PD-L1 expression • TP53 mutation • KRAS mutation • KRAS G12C • KRAS wild-type • KRAS G12 • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
Keytruda (pembrolizumab)
1year
Correlation analysis of clinical, pathological, imaging and genetic features of ground-glass nodule featured lung adenocarcinomas between high-risk and non-high-risk individuals. (PubMed, Eur J Med Res)
GGN-featured lung adenocarcinoma is dominated by non-high-risk female patients. Shorter preoperative follow-up in the non-high-risk group and no statistical difference in GGN detection way suggests the existing screening criteria for high-risk population may not suit GGN-featured lung cancer. In addition, the incidences of KRAS and TP53 mutations are higher in the high-risk group.
Retrospective data • Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
TP53 mutation • KRAS mutation • EGFR mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
1year
Tumor-specific GPX4 degradation enhances ferroptosis-initiated antitumor immune response in mouse models of pancreatic cancer. (PubMed, Sci Transl Med)
N6F11 also sensitized immune checkpoint blockade that targeted CD274/PD-L1 in advanced cancer models, including genetically engineered mouse models of pancreatic cancer driven by KRAS and TP53 mutations. These findings may establish a safe and efficient strategy to boost ferroptosis-driven antitumor immunity.
Preclinical • Journal • PD(L)-1 Biomarker • IO biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CD8 (cluster of differentiation 8) • GPX4 (Glutathione Peroxidase 4) • HMGB1 (High Mobility Group Box 1)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
1year
3rd-Generation Tyrosine Kinase-Inhibitors and Azacitidine Are Safe and Effective in Myeloid Blast-Phase Chronic Myeloid Leukaemia and Result in a High Proportion of Subjects in 2nd Chronic Phase Able to Receive a Transplant (ASH 2023)
Purposes Study safety and efficacy of olverembatinib or ponatinib and azacitidine (AZA) in this setting. KRAS and TP53 mutations and PFKFB3::LINC02649 fusions had predictive impact on outcomes. Determining whether adding azacitidine to a 3rd-generation TKI requires a randomized controlled trial.
Clinical • IO biomarker
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PFKFB3 (6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3)
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TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
Iclusig (ponatinib) • azacitidine • Nailike (olverembatinib)
1year
Targeted Protein Degradation for c-MYC Overcomes Therapy Resistance in T-Cell Acute Lymphoblastic Leukemias (ASH 2023)
GT19715 also enhanced cell death induced by dexamethasone. Targeted protein degradation of c-MYC induces promising anti-leukemia efficacy in T-ALL cells in vitro and in vivo. Further mechanistic and in vivo studies are ongoing.
IO biomarker
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • CD8 (cluster of differentiation 8) • CRBN (Cereblon) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • CD33 (CD33 Molecule) • CD34 (CD34 molecule) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD5 (CD5 Molecule) • BRD4 (Bromodomain Containing 4) • CD7 (CD7 Molecule)
|
TP53 mutation • KRAS mutation • PTEN mutation • MYC overexpression • BCL2 expression • CD8 expression • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
dexamethasone
1year
Local Control Following Stereotactic Body Radiation Therapy for Liver Oligometastases: Lessons from a Quarter Century. (PubMed, Curr Oncol)
However, several predictive factors play a crucial role in the efficacy of stereotactic body radiation therapy, such as the number and size (volume) of metastatic liver lesions, the primary tumor site (histology), molecular biomarkers (e.g., KRAS and TP53 mutation), the use of systemic therapy prior to SBRT, the radiation dose, and the use of advanced technology and organ motion management during SBRT. These prognostic factors need to be considered when clinical trials are designed to evaluate the efficacy of SBRT for liver metastases.
Review • Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
1year
TFEB activation in mediastinal lymph nodes: a potential modulator of immune response in NSCLC (SITC 2023)
Notably, overexpressing TFEB in CD11c+ dendritic cells augmented tumor-specific CD4 T-cell responses, yet reduced CD8 T-cell activities, suggesting a potential shift towards a tolerogenic immune environment in NSCLC. Conclusions Conclusively, our insights into TFEB’s function in NSCLC highlight the complex relationship between tissue-specific elements and tumor immunogenicity, offering avenues for refining immunotherapeutic strategies.
IO biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD4 (CD4 Molecule) • ITGAX (Integrin Subunit Alpha X) • TFEB (Transcription Factor EB 2)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over1year
Pancreatic ductal adenocarcinoma with a high expression of alcohol dehydrogenase 1B is associated with less aggressive features and a favorable prognosis. (PubMed, Am J Cancer Res)
PDAC patients with a high ADH1B expression had better disease-specific survival (DSS) and overall survival (OS) and ADH1B was an independent prognostic biomarker for both DSS (HR = 0.89, 95% CI = 0.80-0.99, P = 0.045) and OS (HR = 0.90, 95% CI = 0.82-0.99, P = 0.044) in multivariate analysis. In conclusion, PDAC with high ADH1B expression had less cell proliferation and malignant features, along with higher immune cell infiltration, and had a better prognosis.
Journal
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • HRD (Homologous Recombination Deficiency) • CD8 (cluster of differentiation 8) • ALDH2 (Aldehyde Dehydrogenase 2 Family Member) • MKI67 (Marker of proliferation Ki-67) • ADH1B (Alcohol Dehydrogenase 1B (Class I), Beta Polypeptide)
|
TP53 mutation • KRAS mutation • HRD • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over1year
Molecular analysis with pancreaseq® in evaluation and management of pancreatic cysts: A cohort of 28 patients. (PubMed, Cytojournal)
It was interpreted as serous cystadenoma and the risk for progression was low. Molecular analysis of pancreatic cysts with PancreaSeq® is useful in accurate diagnosis, especially when cytologic material is non-diagnostic and helps improve patient management.
Journal
|
KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • RNF43 (Ring Finger Protein 43) • VHL (von Hippel-Lindau tumor suppressor) • GNAS (GNAS Complex Locus)
|
TP53 mutation • KRAS mutation • ALK positive • ALK fusion • VHL mutation • RNF43 mutation • TP53 mutation + KRAS mutation • GNAS mutation • KRAS mutation + TP53 mutation
over1year
Genetic alterations of KRAS and TP53 in intrahepatic cholangiocarcinoma associated with poor prognosis. (PubMed, Open Life Sci)
DNA damage repair and homologs recombinant repair deficiencies were significantly associated with high TMB in ICCA cases. In conclusion, we found that certain genetic mutations of TP53 and KRAS could predict poor prognosis in ICCA patients.
Journal • Tumor mutational burden
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden)
|
TP53 mutation • KRAS mutation • TMB-H • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over1year
An amino acid metabolism-based seventeen-gene signature correlates with the clinical outcome and immune features in pancreatic cancer. (PubMed, Front Genet)
Moreover, high-AMRS group was also more sensitive to paclitaxel, cisplatin, and docetaxel. Overall, we constructed an AA-metabolism prognostic model, which provided a powerful prognostic predictor for the clinical treatment of pancreatic cancer.
Clinical data • Journal • Gene Signature • IO biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • CD8 (cluster of differentiation 8)
|
TP53 mutation • KRAS mutation • TMB-H • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
cisplatin • paclitaxel • docetaxel
over1year
Deciphering SWI/SNF complexes role in lung cancer using the Tuba-seq tool in a mouse model of lung adenocarcinoma (EACR 2023)
Barcoding sequencing will allow the determination of tumor number and size and, therefore, the assessment of this SWI/SNF subunits oncogenic potential. Further transcriptional experiments will allow us to identify the molecular pathways altered by SWI/SNF deficiency in our model.ConclusionWe have successfully generated all necessary tools to perform Tuba-seq experiments to study at the molecular level the role of SWI/SNF alteration in a mouse model of LUAD.
Preclinical
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • ARID1A (AT-rich interaction domain 1A) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • ARID1B (AT-Rich Interaction Domain 1B) • ARID2 (AT-Rich Interaction Domain 2) • SMARCA2 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 2)
|
TP53 mutation • KRAS mutation • KRAS G12D • KRAS G12 • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over1year
Genomic landscape and clinical features of rare subtypes of pancreatic cancer: analysis with the national database of Japan. (PubMed, J Gastroenterol)
ACC clearly harbors different genomics compared with PDAC, possibly accounting for differences in treatment efficacy.
Retrospective data • Journal • BRCA Biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • ATM (ATM serine/threonine kinase) • HRD (Homologous Recombination Deficiency)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
5-fluorouracil • albumin-bound paclitaxel • irinotecan • leucovorin calcium
over1year
Safety and efficacy of Sleeping Beauty TCR-T cells targeting shared KRAS and TP53 mutations expressed by solid tumors in first-in-human phase 1 study. (ASCO 2023)
This is the first-in-human experience administering Sleeping Beauty TCR-T cells. Signs of efficacy, safety and persistence of TCR-T cells was observed. Thus, this treatment has promise for patients with solid tumors expressing shared mutations in driver genes.
Clinical • P1 data • IO biomarker
|
EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • HLA-A (Major Histocompatibility Complex, Class I, A)
|
TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12D • KRAS G12V • KRAS G12 • TP53 R175H • TP53 mutation + KRAS mutation • HLA-A*02 • KRAS mutation + TP53 mutation
over1year
The genomic and transcriptomic landscapes of chemotherapy naïve vs post-chemotherapy germ cell tumors. (ASCO 2023)
Background: Cisplatin resistance occurs in up to 30% of patients with advanced germ cell tumors (GCTs)... This study provides evidence that chemo naïve GCTs with mutations in TP53, KRAS, KIT or MDM2 CNA have higher expression of genes associated with resistance to platinum-based chemotherapy. These findings contribute to a better understanding of the molecular characteristics of GCTs and may inform prognosis and treatment.
IO biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MDM2 (E3 ubiquitin protein ligase)
|
TP53 mutation • KIT mutation • MDM2 amplification • TP53 mutation + KRAS mutation • MDM2 mutation • KRAS mutation + TP53 mutation
|
MI Tumor Seek™
|
cisplatin
over1year
p53 protects against formation of extrahepatic biliary precancerous lesions in the context of oncogenic Kras. (PubMed, Oncotarget)
This was also the case in the context of additional activation of the Wnt signaling pathway. Thus, p53 protects against formation of extrahepatic biliary precancerous lesions in the context of oncogenic Kras.
Journal
|
KRAS (KRAS proto-oncogene GTPase)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over1year
LKB1-dependent regulation of TPI1 creates a divergent metabolic liability between human and mouse lung adenocarcinoma. (PubMed, Cancer Discov)
In mice, Ser21 of TPI1 is a Cys residue which can be oxidized to alter TPI1 activity without a need for SIKs or LKB1. Our findings suggest this metabolic flexibility is critical in rapidly growing cells with KRAS and TP53 mutations, explaining why loss of LKB1 creates a liability in these tumors.
Preclinical • Journal
|
KRAS (KRAS proto-oncogene GTPase) • STK11 (Serine/threonine kinase 11)
|
TP53 mutation • KRAS mutation • STK11 mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over1year
Cell-free DNA Predicts Prolonged Response to Multi-agent Chemotherapy in Pancreatic Ductal Adenocarcinoma. (PubMed, Cancer Res Commun)
We report on the association of cfDNA with response durability for patients undergoing treatment with a novel metronomic chemotherapy regimen (gemcitabine, nab-paclitaxel, capecitabine, cisplatin, irinotecan; GAX-CI) for metastatic PDAC. This investigation offers encouraging evidence that cfDNA may prove to be a valuable diagnostic tool to guide clinical management.
Journal
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CA 19-9 (Cancer antigen 19-9)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
cisplatin • gemcitabine • capecitabine • albumin-bound paclitaxel • irinotecan
over1year
SENESCENCE-BASED COLORECTAL CANCER SUBTYPING REVEALS DISTINCT MOLECULAT CHARACTERISTICS AND THERAPEUTIC STRATEGIES (DDW 2023)
We proposed the senescence subtypes of CRC for the first time and demonstrated the characteristics of different subtypes. We also found potential treatment interventions for each subtype, which can promote the precision treatment of CRC patients.
IO biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
almost2years
Concurrent KRAS and TP53 mutations in pancreatic cancer real-world data (RWD) highlight convergent tumor evolutionary patterns (AACR 2023)
Here we describe multiple independent combinations of KRAS and TP53 mutations leading to convergent functional outcomes for tumor cells, in the context of patient-specific gene mutation landscapes. Recurrent patterns of paired mutations with common cellular function dysregulation outcomes highlight core underlying mechanisms of pancreatic tumor evolution.
Clinical • Real-world evidence • Real-world
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • ARID1A (AT-rich interaction domain 1A) • SMAD4 (SMAD family member 4) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
|
TP53 mutation • KRAS mutation • KRAS G12D • ARID1A mutation • KRAS G12V • KRAS G12 • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
almost2years
Spatial and longitudinal tumor heterogeneity in head and neck squamous cell carcinoma patients treated with primary surgery (AACR 2023)
Our study suggests spatial and longitudinal tumor heterogeneity and reports emerging mutations in ctDNA over time in HNSCC. Prognostic significance characterization of the ctDNA dominant clone allele frequency is ongoing.
Clinical • Surgery
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog) • NOTCH1 (Notch 1) • JAK2 (Janus kinase 2) • FAT1 (FAT atypical cadherin 1) • SDHA (Succinate Dehydrogenase Complex Flavoprotein Subunit A)
|
TP53 mutation • KRAS mutation • PIK3CA mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
|
OncoFOLLOW
almost2years
Rectal Carcinoma With a Sarcomatoid Component: A Case Report With Detailed Immunohistochemistry, Molecular Analysis, and Literature Review. (PubMed, Int J Surg Pathol)
Conclusions. Immunohistochemistry and mutation analyses revealed tumorigenesis of rectal carcinoma with sarcomatoid components correlated with EMT and TP53 mutations.
Review • Journal
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDH1 (Cadherin 1) • SNAI2 (Snail Family Transcriptional Repressor 2) • ZEB1 (Zinc Finger E-box Binding Homeobox 1)
|
TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • CDH1 expression • KRAS mutation + TP53 mutation
2years
Analysis of the benefit of anti PD-1s in monotherapy according to genetic alterations diagnosed by NGS in patients with bronchial cancer non-small cells (CPLF 2023)
To our knowledge, there is no study evaluating the mutations of Kras and TP53 in this way in the literature. Co-humations must therefore be taken into account before prescription of immune control point inhibitors.
Clinical • Next-generation sequencing • PD(L)-1 Biomarker • IO biomarker
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
PD-L1 expression • TP53 mutation • KRAS mutation • RAS wild-type • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
2years
Immunotherapy combined with chemotherapy improved clinical outcomes over bevacizumab combined with chemotherapy as first-line therapy in adenocarcinoma patients. (PubMed, Cancer Med)
ICIs combined with ChT improved clinical outcomes over Beva combined with ChT as first-line therapy for adenocarcinoma patients without driver gene alterations, especially in patients with PD-L1 ≥ 1%.
Clinical data • Journal • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
|
PD-L1 expression • TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • TP53 expression • KRAS expression • KRAS mutation + TP53 mutation
|
Avastin (bevacizumab)
over2years
Targeted Next-Generation Sequencing Analysis of 2 Undifferentiated Carcinomas With Osteoclast-like Giant Cells of the Pancreas (CAP 2022)
MED12 mutations have been recently identified in other tumors. Recurrent detection of MED12 mutations in UC-OGC warrants further evaluation of its roles in this unique tumor.
Next-generation sequencing
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • KDM6A (Lysine Demethylase 6A) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD68 (CD68 Molecule)
|
TP53 mutation • KRAS mutation • KRAS G12V • KRAS G12A • KRAS G12 • TP53 mutation + KRAS mutation • TP53 Y220C • KRAS mutation + TP53 mutation
|
FoundationOne® CDx
over2years
Targeted Next-Generation Sequencing Analysis of 2 Undifferentiated Carcinomas With Osteoclast-like Giant Cells of the Pancreas (CAP 2022)
MED12 mutations have been recently identified in other tumors. Recurrent detection of MED12 mutations in UC-OGC warrants further evaluation of its roles in this unique tumor.
Next-generation sequencing
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • KDM6A (Lysine Demethylase 6A) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD68 (CD68 Molecule)
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TP53 mutation • KRAS mutation • KRAS G12V • KRAS G12A • KRAS G12 • TP53 mutation + KRAS mutation • TP53 Y220C • KRAS mutation + TP53 mutation
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FoundationOne® CDx
over2years
Molecular correlates of male germ cell tumors with overgrowth of components resembling somatic malignancies. (PubMed, Mod Pathol)
In conclusion, GCT with SM are characterized by widespread aneuploidy, a distinct epigenetic signature and the presence of mutations that are otherwise rare in testicular GCT without SM. The similarity of the mutational and DNA methylation profiles of different histologic types of SM suggests that the identification of SM components could be more important than their precise histologic subclassification, pending confirmation by further studies.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MDM2 (E3 ubiquitin protein ligase)
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TP53 mutation • KRAS mutation • MDM2 amplification • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
over2years
An immune-related gene prognostic risk index for pancreatic adenocarcinoma. (PubMed, Front Immunol)
In comparison, high IRGPRI was associated with cancer-related pathways, low expression of CTLA4, high KRAS and TP53 mutation rate, more infiltration of M2 macrophages, and less benefit from ICIs therapies. This IRGPRI is an encouraging biomarker to define the prognosis, immune and molecular features, and benefits from ICIs treatments in PAAD.
Journal • IO biomarker
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CD8 (cluster of differentiation 8) • TNFRSF4 (TNF Receptor Superfamily Member 4) • CD40 (CD40 Molecule) • S100A16 (S100 Calcium Binding Protein A16) • TRAF1 (TNF Receptor Associated Factor 1) • VCAM1 (Vascular Cell Adhesion Molecule 1)
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TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • TP53 expression • CTLA4 expression • KRAS expression • KRAS mutation + TP53 mutation