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BIOMARKER:

APOBEC mutagenesis

22d
APOBEC Mutational Signatures in Hormone Receptor-Positive Human Epidermal Growth Factor Receptor 2-Negative Breast Cancers Are Associated With Poor Outcomes on CDK4/6 Inhibitors and Endocrine Therapy. (PubMed, JCO Precis Oncol)
APOBEC+ HR+ HER2- patients had shorter TTD on first-line ET plus CDK4/6i relative to APOBEC- patients. Further research is needed to optimize the treatment of APOBEC+ HR+ HER2- BC and to investigate the efficacy of immunotherapeutic strategies in this population.
Journal • Tumor Mutational Burden • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • TMB (Tumor Mutational Burden)
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TMB-H • HR positive • HER-2 negative • HER-2 mutation • EGFR positive • APOBEC mutagenesis
25d
Mutational Mechanisms in Pediatric Acute Lymphoblastic Leukemia with Multiple Relapses (ASH 2022)
The etiology of SBS17 is as yet not established, but it has been proposed to be caused by reactive oxygen species. To conclude, ALL patients with multiple relapses showed an increased prevalence and large variety of interplaying mutational processes at diagnosis (36%) and final relapse (61%), with intrinsic or therapy induced origins.
Clinical • Tumor Mutational Burden
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TMB (Tumor Mutational Burden) • MME (Membrane Metalloendopeptidase)
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APOBEC mutagenesis
2ms
Ultra-high Tumor Mutation Burden in Metastatic/Clinically Advanced Breast Cancer (MBC) (SABCS 2022)
UHTMB MBC is a rare but clinically important subset in breast cancer that could have high response rates to single agent pembrolizumab. This phenotype is driven by APOBEC mutagenesis, more often seen in ER+ lobular cancers, and have higher frequencies of MSI-high status and mutations in CDH1 and PIK3CA.
Clinical • Tumor Mutational Burden • MSi-H Biomarker • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • PGR (Progesterone receptor) • MSI (Microsatellite instability) • CDKN2A (Cyclin-dependent kinase inhibitor 2A) • ARID1A (AT-rich interaction domain 1A) • NF1 (Neurofibromin 1) • CDH1 (Cadherin 1)
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TMB-H • MSI-H/dMMR • PIK3CA mutation • HER-2 expression • APOBEC mutagenesis • PGR expression • CDH1 mutation
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FoundationOne® CDx • VENTANA PD-L1 (SP142) Assay
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Keytruda (pembrolizumab)
3ms
APOBEC mutagenesis and selection for NFE2L2 contribute to the origin of lung squamous-cell carcinoma. (PubMed, Lung Cancer)
We demonstrate that APOBEC effectively deaminates NFE2L2 at the locations that confer high cancer effect. Overall, we demonstrate that APOBEC activity can lead to mutations in NFE2L2 that have large contributions to cancer cell growth and survival, and that NFE2L2 is an attractive potential target for therapeutic intervention.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NFE2L2 (Nuclear Factor, Erythroid 2 Like 2) • APOBEC3B (Apolipoprotein B MRNA Editing Enzyme Catalytic Subunit 3B)
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PIK3CA mutation • APOBEC mutagenesis
6ms
APOBEC-mediated mutagenesis is a favorable predictor of prognosis and immunotherapy for bladder cancer patients: evidence from pan-cancer analysis and multiple databases. (PubMed, Theranostics)
Furthermore, using machine learning approaches, a prognostic APOBEC mutagenesis-related model was established and validated in different BLCA cohorts. Our study illustrates the characterization of APOBECs and APOBEC mutagenesis in multiple cancer types and highlights its potential value as a promising biomarker for prognosis and immunotherapy in BLCA.
Journal • IO biomarker • Pan tumor
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APOB (Apolipoprotein B)
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APOBEC mutagenesis
6ms
Combined exome and transcriptome sequencing of non-muscle-invasive bladder cancer: associations between genomic changes, expression subtypes, and clinical outcomes. (PubMed, Genome Med)
Multi-omic data may facilitate better prognostication and selection of therapeutic interventions in patients with G3pT1 NMIBC. These findings demonstrate the potential for improving the management of high-risk NMIBC patients and warrant further prospective validation.
Clinical data • Journal • Tumor Mutational Burden
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HER-2 (Human epidermal growth factor receptor 2) • TMB (Tumor Mutational Burden)
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TMB-H • HER-2 amplification • APOBEC mutagenesis
8ms
Journal
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HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ARID1A (AT-rich interaction domain 1A) • NF1 (Neurofibromin 1) • KMT2C (Lysine Methyltransferase 2C) • CDH1 (Cadherin 1) • ZFHX3 (Zinc Finger Homeobox 3) • MAP3K1 (Mitogen-Activated Protein Kinase Kinase Kinase 1) • APOB (Apolipoprotein B)
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TP53 mutation • ER positive • PIK3CA mutation • HER-2 negative • PIK3CA E545K • PIK3CA E542K • EGFR positive • APOBEC mutagenesis • PIK3CA E545 • PIK3CA E542
9ms
APOBEC3 promotes tumor progression, squamous differentiation and metastasis in bladder cancer mouse model (AACR 2022)
Approximately 60% of cells sequenced were annotated as T-cells and natural killer T-cells by SingleR. We treated mice bearing UPPA primary bladder tumors with anti-PD-1 antibody and observed significant tumor growth inhibition.
Preclinical • Tumor Mutational Burden • PD(L)-1 Biomarker • IO biomarker
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TMB (Tumor Mutational Burden) • PTEN (Phosphatase and tensin homolog) • APOB (Apolipoprotein B)
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APOBEC mutagenesis
9ms
Genomic evolutionary patterns in matched pre-invasive and invasive lung disease in TRACERx (AACR 2022)
We demonstrate that matched pre-invasive and invasive lesions fall in two distinct phylogenetic evolutionary groups: those that have a shared somatic common ancestor and those that do not. SCA pre-invasive lesions exhibit elevated APOBEC mutagenesis and chromosomal instability, shedding some light on the process of malignant transformation.
Tumor Mutational Burden
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • FGFR3 (Fibroblast growth factor receptor 3) • STK11 (Serine/threonine kinase 11) • KEAP1 (Kelch Like ECH Associated Protein 1) • SOX2
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TP53 mutation • KRAS mutation • STK11 mutation • KEAP1 mutation • APOBEC mutagenesis
11ms
APOBEC mediated mutagenesis drives genomic heterogeneity in endometriosis. (PubMed, J Hum Genet)
Further, the relative risk of enriched APOBEC signature mutations was higher in endometriosis patients who were carriers of APOBEC3A/3B germline deletion, a common polymorphism in East Asians which involves the complete loss of APOBEC3B coding region. Our results illustrate the significance of APOBEC induced mutagenesis in driving the genomic heterogeneity of endometriosis.
Journal • Tumor Mutational Burden
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • APOB (Apolipoprotein B)
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PIK3CA mutation • APOBEC mutagenesis
12ms
Analysis of Mutations and Dysregulated Pathways Unravels Carcinogenic Effect and Clinical Actionability of Mutational Processes. (PubMed, Front Cell Dev Biol)
In addition, APOBEC mutational process destroys DNA double-strand break repair pathway, and bladder cancer patients with high APOBEC activity, though with homologous recombination proficient, show a significantly longer overall survival with platinum regimens. These findings help to understand how mutational processes act on the genome to promote carcinogenesis, and further, presents novel insights for cancer prevention and treatment, as our results showing, APOBEC mutagenesis and HRD synergistically contributed to the clinical benefits of platinum-based treatment.
Clinical • Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
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IDH1 R132H • APOBEC mutagenesis • IDH1 R132
1year
APOBEC mutagenesis inhibits breast cancer growth through induction of T cell-mediated antitumor immune responses. (PubMed, Cancer Immunol Res)
In human breast cancers, the relationship between APOBEC mutagenesis and immunogenicity varied by breast cancer subtype and the frequency of subclonal mutations. This work provides a mechanistic basis for the sensitivity of APOBEC tumors to checkpoint inhibitors and suggests a rationale for using APOBEC mutational signatures and clonality as biomarkers predicting immunotherapy response in HER2-positive breast cancers.
Journal • IO biomarker
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CD4 (CD4 Molecule)
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HER-2 positive • APOBEC mutagenesis
1year
APOBEC signature, clinical characteristics, and outcome in hormone receptor-positive (HR+) HER2-negative (HER2-) breast cancer (BC) patients (pts) in real-world data (RWD) (SABCS 2021)
APOBEC+ occurs in ~7% of BC and is more common in ILC and metastatic lesions. APOBEC+ HR+HER2- pts had shorter TTD and OS on SOC ET+CDK4/6i relative to APOBEC- pts. However, TTD on ICI tended to be longer in APOBEC+ pts, but our data is limited, and more research is needed.
Clinical • Real-world evidence • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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HR positive • HER-2 negative • APOBEC mutagenesis • HR positive + HER-2 negative
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5-fluorouracil
1year
Apobec mutagenesis is a pervasive feature of poor prognosis breast cancer associating with ESR1 wild type, endocrine resistant disease (SABCS 2021)
Evidence for APOBEC mutagenesis is present in >30% of metastatic breast cancers and associated with resistance to ET. Unlike ESR1 mutations, which are acquired as a late event in metastatic HR+ BCs, APOBEC mutagenesis is commonly present in paired primary and metastatic BCs, indicating its relatively early onset and potential role in driving the poor prognosis of these cancers.
ER (Estrogen receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDH1 (Cadherin 1) • APOB (Apolipoprotein B) • GATA3 (GATA binding protein 3)
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HR positive • PIK3CA mutation • ER mutation • APOBEC mutagenesis
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MSK-IMPACT
1year
Concurrent predictors of an immune responsive tumor microenvironment within tumor mutational burden-high breast cancer (SABCS 2021)
High TMB alone does not strongly correlate with immune infiltrate or immune response gene signatures in MBC. Within TMB-H MBC, concurrent mutations in MSI-H and KMT2D are associated with an immune responsive TME while mutations in PIK3CA, CHEK2, CBFB, amplifications of CCND1, FGF19, FGF4, and MMLT6, and expression of IHC-AR are associated with an immune non-responsive TME. Co-occurring biomarkers within TMB-H breast cancer warrant evaluation in prospective cohorts for response or resistance to ICI to help develop composite biomarkers in breast cancer.
Tumor Mutational Burden • MSi-H Biomarker • PD(L)-1 Biomarker • IO biomarker
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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) • MSI (Microsatellite instability) • CD8 (cluster of differentiation 8) • CCND1 (Cyclin D1) • KMT2D (Lysine Methyltransferase 2D) • FGF19 (Fibroblast growth factor 19) • B2M (Beta-2-microglobulin) • CDH1 (Cadherin 1) • CHEK2 (Checkpoint kinase 2) • FGF4 (Fibroblast growth factor 4) • CD4 (CD4 Molecule)
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TMB-H • MSI-H/dMMR • PIK3CA mutation • TMB-L • CCND1 amplification • CHEK2 mutation • APOBEC mutagenesis
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VENTANA PD-L1 (SP142) Assay • MI Tumor Seek™
1year
APOBEC Mutagenesis Is Concordant between Tumor and Viral Genomes in HPV-Positive Head and Neck Squamous Cell Carcinoma. (PubMed, Viruses)
Using paired sequencing of host somatic exomes, transcriptomes, and viral genomes, we demonstrated for the first-time definitive evidence of concordance between tumor and viral APOBEC mutagenesis. This finding provides a missing link connecting APOBEC mutagenesis in host and virus and supports a common mechanism driving APOBEC dysregulation.
Journal • Tumor Mutational Burden
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TMB (Tumor Mutational Burden)
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APOBEC mutagenesis
over1year
[VIRTUAL] APOBEC Mutagenesis is Concordant Between Tumor and Viral Genomes in HPV Positive Head and Neck Squamous Cell Carcinoma (AHNS 2021)
Using paired sequencing of somatic exomes, transcriptomes, and viral genomes of HPV+ HNSCC samples, here, we demonstrate for the first time concordance between tumor and viral APOBEC mutagenesis in HPV+ HNSCC, supporting existing hypotheses regarding the role of APOBEC in viral restriction and resultant off-target host-genome mutagenesis.
Tumor Mutational Burden
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • IFNG (Interferon, gamma) • APOB (Apolipoprotein B)
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PIK3CA mutation • APOBEC mutagenesis
over1year
Journal • Checkpoint inhibition • Tumor Mutational Burden • PD(L)-1 Biomarker • IO biomarker
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TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • RB1 (RB Transcriptional Corepressor 1) • CD8 (cluster of differentiation 8)
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TP53 mutation • TMB-H • APOBEC mutagenesis
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Tecentriq (atezolizumab)
over1year
Genomic profile of advanced breast cancer in circulating tumour DNA. (PubMed, Nat Commun)
We demonstrate diverse subclonal resistance mutations, including enrichment of HER2 mutations in HER2 positive disease, co-occurring ESR1 and MAP kinase pathway mutations in HR + HER2- disease that associate with poor overall survival (p = 0.0092), and multiple PIK3CA mutations in HR + disease that associate with short progression free survival on fulvestrant (p = 0.0036)...In ER-positive breast cancer subclonal mutations were enriched in an APOBEC mutational signature, with second hit PIK3CA mutations acquired subclonally and at sites characteristic of APOBEC mutagenesis. This study utilises circulating tumour DNA analysis in a large clinical trial to demonstrate the subclonal diversification of pre-treated advanced breast cancer, identifying distinct mutational processes in advanced ER-positive breast cancer, and novel therapeutic opportunities.
Journal • Circulating tumor DNA
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HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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HER-2 positive • ER positive • PIK3CA mutation • HER-2 negative • ER mutation • APOBEC mutagenesis
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fulvestrant
over1year
Reconstructing tumor history in breast cancer: signatures of mutational processes and response to neoadjuvant chemotherapy. (PubMed, Ann Oncol)
The results of this investigation suggest that the clinical behavior of a tumor, in particular response to neoadjuvant chemotherapy and DFS of therapy-resistant tumors, could be predicted by the composition of mutational signatures as an indicator of the individual genomic history of a tumor. After additional validations, mutational signatures might be used to identify tumors with an increased response rate to neoadjuvant chemotherapy and to define therapy-resistant subgroups for future therapeutic interventions.
Clinical • Journal
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HRD (Homologous Recombination Deficiency)
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HR positive • HRD • APOBEC mutagenesis
over1year
[VIRTUAL] Integrative genomic and transcriptomic characterization of metastatic urothelial carcinoma (AACR 2021)
Based on genomic alterations, potential therapeutic targets were identified in 111/116 mUC patients, of which FGFR3 alterations (18%) and fusions (6%), and CDKN2A (44%), ERBB2 (20%), and TSC1 (14%) alterations were most common. By integrating the genomic and transcriptomic data, we propose potential novel therapeutic options per transcriptomic subtype, like addition of a TGF-β inhibitor to immune checkpoint inhibition for the stroma-rich and basal/squamous subtypes that showed the highest TGF-β pathway activity.Using WGS and RNAseq analyses, we provide a comprehensive overview of the molecular landscape of mUC that may serve as a reference for more subgroup-oriented and patient-specific research on the etiology of mUC and future drug development.
Tumor Mutational Burden • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • FGFR3 (Fibroblast growth factor receptor 3) • CDKN2A (Cyclin-dependent kinase inhibitor 2A) • TSC1 (TSC complex subunit 1) • TGFB1 (Transforming Growth Factor Beta 1)
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TP53 mutation • APOBEC mutagenesis • FGFR3 fusion
over1year
[VIRTUAL] APOBEC3B and TKI resistance in EGFR mutant lung cancer (AACR 2021)
To model APOBEC mutagenesis in lung cancer, we have developed a novel lung cancer mouse model, by crossing the ROSA26LSL-APOBEC3B (A3B) mouse model with several different EGFR mutant mouse models. Using these models, we find that APOBEC3B expression is selected for post-TKI and contributes to resistance to TKI therapy.
Tumor Mutational Burden
|
EGFR (Epidermal growth factor receptor) • TMB (Tumor Mutational Burden)
|
EGFR mutation • APOBEC mutagenesis
over1year
[VIRTUAL] APOBEC mutagenesis is concordant between tumor and viral genomes in HPV positive head and neck squamous cell carcinoma (AACR 2021)
Paired host and viral analyses revealed APOBEC-enriched somatic samples (higher APOBEC mutational burden, A3A expression, and A3A-associated RNA editing) also have higher viral APOBEC mutation rates, strongly supporting a direct link between APOBEC mutations in host and viral genomes. APOBEC-enriched samples also had higher IFN-γ scores, suggesting immune upregulation, possibly in response to viral infection.Using paired sequencing of somatic exomes, transcriptomes, and viral genomes of HPV+ HNSCC samples, here, we demonstrate concordance between tumor and viral APOBEC mutagenesis in HPV+ HNSCC, supporting existing hypotheses regarding the role of APOBEC in viral restriction and resultant off-target host-genome mutagenesis.
Tumor Mutational Burden
|
PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • IFNG (Interferon, gamma) • APOB (Apolipoprotein B)
|
PIK3CA mutation • APOBEC mutagenesis
almost2years
Germline APOBEC3B deletion increases somatic hypermutation in Asian breast cancer that is associated with Her2 subtype, PIK3CA mutations, and immune activation. (PubMed, Int J Cancer)
Taken together, our results suggest that the germline A3B deletion polymorphism, via the A3A-B hybrid isoform, contributes to APOBEC-mutagenesis in a significant proportion of Asian breast cancers. In addition, APOBEC somatic hypermutation, regardless of A3B background, may be an important clinical biomarker for Asian breast cancers.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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PIK3CA mutation • APOBEC mutagenesis
2years
[VIRTUAL] APOBEC driving genomic evolution in ER+/HER2- breast cancer (EBCC-I 2020)
We demonstrate that APOBEC leads to alterations in genes known to be able to act as a driver in early and mBC and further facilitates endocrine resistance in mBC. Our results underscore the importance of APOBEC mutagenesis in the genomic evolution of BC.
HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ARID1A (AT-rich interaction domain 1A) • KMT2C (Lysine Methyltransferase 2C) • CDH1 (Cadherin 1) • APOB (Apolipoprotein B)
|
TP53 mutation • PIK3CA mutation • ARID1A mutation • NF1 mutation • KMT2C mutation • APOBEC mutagenesis
|
MSK-IMPACT
2years
[VIRTUAL] APOBEC driving genomic evolution in ER+/HER2- breast cancer (EBCC-I 2020)
We demonstrate that APOBEC leads to alterations in genes known to be able to act as a driver in early and mBC and further facilitates endocrine resistance in mBC. Our results underscore the importance of APOBEC mutagenesis in the genomic evolution of BC.
HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ARID1A (AT-rich interaction domain 1A) • KMT2C (Lysine Methyltransferase 2C) • CDH1 (Cadherin 1) • APOB (Apolipoprotein B)
|
TP53 mutation • PIK3CA mutation • ARID1A mutation • NF1 mutation • KMT2C mutation • APOBEC mutagenesis
|
MSK-IMPACT
2years
Identification of new driver and passenger mutations within APOBEC-induced hotspot mutations in bladder cancer. (PubMed, Genome Med)
Our study identified novel potential drivers within APOBEC-associated hotspot mutations in BCa reinforcing the importance of APOBEC mutagenesis in BCa. It could allow a better understanding of BCa biology and aetiology and have clinical implications such as AhR as a potential therapeutic target. Our results also challenge the dogma that all hotspot mutations are drivers and mostly gain-of-function mutations affecting oncogenes.
Journal
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FGFR3 (Fibroblast growth factor receptor 3) • AHR (Aryl hydrocarbon receptor)
|
FGFR3 mutation • FGFR3 S249C • APOBEC mutagenesis
over2years
Timing the initiation of multiple myeloma. (PubMed, Nat Commun)
We identify eight processes, including a mutational signature caused by exposure to melphalan...We define four main patterns of activation-induced deaminase (AID) and apolipoprotein B mRNA editing catalytic polypeptide-like (APOBEC) mutagenesis over time, including a subset of patients with evidence of prolonged AID activity during the pre-malignant phase, indicating antigen-responsiveness and germinal center reentry. Our findings provide a framework to study the etiology of multiple myeloma and explore strategies for prevention and early detection.
Journal
|
APOB (Apolipoprotein B)
|
APOBEC mutagenesis
|
melphalan
over2years
APOBEC mutagenesis is tightly linked to the immune landscape and immunotherapy biomarkers in head and neck squamous cell carcinoma. (PubMed, Oral Oncol)
Multiple mechanisms may exist within HNSCC leading to APOBEC mutations including immune upregulation in response to neoantigens and viral infection, via induction of IFNy. These mechanisms may be additive and not mutually exclusive, which could explain higher levels of APOBEC mutations in HPV mediated HNSCC.
Journal • Tumor Mutational Burden
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TMB (Tumor Mutational Burden)
|
APOBEC mutagenesis
over2years
APOBEC Mutagenesis and Copy-Number Alterations Are Drivers of Proteogenomic Tumor Evolution and Heterogeneity in Metastatic Thoracic Tumors. (PubMed, Cell Rep)
CNAs occurring late in tumor evolution correlated with downstream transcriptomic and proteomic heterogeneity, although global proteomic heterogeneity was significantly greater than transcriptomic and CNA heterogeneity. These results illustrate key mechanisms underlying multi-dimensional heterogeneity in metastatic thoracic tumors.
Journal
|
TP53 (Tumor protein P53)
|
TP53 mutation • APOBEC mutagenesis
over2years
[VIRTUAL] Multi-modality sequencing of multiple HPV mediated oropharyngeal squamous cell carcinomas from single patients reveals synchrony in viral genomes yet discordant mutational profiles and signatures (AACR-II 2020)
This suggests that despite infection by a single oncogenic virus, HPVmOPSCCs may develop via multiple, disparate pathways. Of particular interest is the tumor pairs' clear discordance in APOBEC mutational burden, which challenges existing hypotheses on the role of APOBEC mutagenesis in this disease.
Clinical • Tumor Mutational Burden
|
TMB (Tumor Mutational Burden)
|
APOBEC mutagenesis