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BIOMARKER:

CREBBP mutation

i
Other names: CREBBP, CBP, KAT3A, RSTS, RTS, CREB binding protein
Entrez ID:
Related biomarkers:
17d
Phase classification
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CREBBP (CREB binding protein)
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CREBBP mutation • EP300 mutation
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mocetinostat (MGCD0103)
2ms
Feasibility of Circulating Tumor DNA Analysis in Patients with Follicular Lymphoma. (PubMed, Cancer Res Treat)
Forty samples from patients receiving rituximab-containing immunochemotherapy were analyzed...Analysis of ctDNA mutations in plasma at diagnosis might help predict outcome of disease, while analysis during follow-up may help to monitor disease status of patients with advanced FL. However, the feasibility of ctDNA measurement must be improved in order for it to become an appropriate and clinically relevant test in FL patients.
Journal • Tumor mutational burden • Circulating tumor DNA
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TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • KMT2D (Lysine Methyltransferase 2D) • KMT2C (Lysine Methyltransferase 2C) • CREBBP (CREB binding protein)
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TP53 mutation • KMT2D mutation • CREBBP mutation • KMT2C mutation
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Rituxan (rituximab)
5ms
Molecular and immunological landscape of sex-based differences in breast cancer: a distinct disease in men. (SABCS 2023)
These data indicate that MaBC has a differential mutational frequency, copy number alteration, immune gene expression and immune cell infiltration and overall survival compared to their FeBC counterparts. A better understanding of these sex-based differences with additional research may help inform disease outcomes, provide a rationale for tailored therapeutic approaches and design future treatments. Table 1.
Tumor mutational burden • BRCA Biomarker • MSi-H Biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • STK11 (Serine/threonine kinase 11) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • ASXL1 (ASXL Transcriptional Regulator 1) • BCL6 (B-cell CLL/lymphoma 6) • KMT2D (Lysine Methyltransferase 2D) • RARA (Retinoic Acid Receptor Alpha) • WT1 (WT1 Transcription Factor) • FGF3 (Fibroblast growth factor 3) • CHEK2 (Checkpoint kinase 2) • CREBBP (CREB binding protein) • RAD51B (RAD51 Paralog B) • TSC1 (TSC complex subunit 1) • HLA-DQB1 (Major Histocompatibility Complex, Class II, DQ Beta 1) • FOXA1 (Forkhead Box A1) • MRE11A (MRE11 homolog, double strand break repair nuclease) • CHD1 (Chromodomain Helicase DNA Binding Protein 1) • PPM1D (Protein Phosphatase Mg2+/Mn2+ Dependent 1D) • FLCN (Folliculin) • IL1A (Interleukin 1, alpha) • AMER1 (APC Membrane Recruitment Protein 1) • DAXX (Death-domain associated protein) • HLA-DQB2 (Major Histocompatibility Complex, Class II, DQ Beta 2)
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TP53 mutation • MSI-H/dMMR • HER-2 negative • HER-2 mutation • STK11 mutation • ASXL1 mutation • ESR1 mutation • CREBBP mutation • AKT1 mutation • TSC1 mutation • MHC-II expression • FLCN mutation • RAD51 mutation
5ms
Crebbp Mutations Are Associated with Slow Minimal Residual Response to Upfront Induction Chemotherapy in Pediatric High-Hyperdiploid B-Cell Precursor Acute Lymphoblastic Leukemia Treated in the AIEOP-BFM ALL 2009 Protocol (ASH 2023)
Therefore, the inclusion of CREBBP mutated patients in very low risk protocols should be carefully evaluated. The validation of these findings is ongoing through the analysis of patients treated by other international study groups adopting different chemotherapy backbones.
Clinical
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • NF1 (Neurofibromin 1) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • IKZF1 (IKAROS Family Zinc Finger 1) • CREBBP (CREB binding protein) • AFF1 (AF4/FMR2 Family Member 1)
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KRAS mutation • BRAF mutation • NRAS mutation • NF1 mutation • RAS mutation • CREBBP mutation • IKZF1 deletion • IKZF1 mutation
5ms
Combination Epigenetic Therapy Using YF2, a First-in-Class Histone Acetyltransferase Activator, Restores Immunogenicity in Diffuse Large B-Cell Lymphoma (ASH 2023)
Other epigenetic therapies, such as tazemetostat and belinostat, are approved for use in follicular and T-cell lymphoma, respectively, but have limited single agent activity in DLBCL. In summary, these data propose YF2 combination epigenetic therapy as a means to increase immunogenicity in CBP/p300- and EZH2-mutated DLBCL. While our preliminary mouse experiment provided promising initial results, an expanded study is underway to statistically confirm the exciting trends that we observed.
Epigenetic controller
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CD8 (cluster of differentiation 8) • B2M (Beta-2-microglobulin) • CREBBP (CREB binding protein) • CD4 (CD4 Molecule)
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EZH2 mutation • CREBBP mutation • EZH2 wild-type
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Tazverik (tazemetostat) • YF2 • Beleodaq (belinostat)
5ms
Ibrutinib and Rituximab Versus Fludarabine, Cyclophosphamide, and Rituximab for Patients in NCRI FLAIR Study with Previously Untreated CLL: Assessment of Mutational Landscape of Patients at Baseline and Prognostic Impact (ASH 2023)
Our study confirms that TP53 mutations result in shorter PFS and OS in CLL. We demonstrate improved PFS when patients with ATM or RPS15 mutations are treated with IR compared to FCR. Mutations in the CREBBP gene have recently been described as a novel candidate driver in CLL.
Clinical
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BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • ATM (ATM serine/threonine kinase) • NOTCH1 (Notch 1) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • SF3B1 (Splicing Factor 3b Subunit 1) • IGH (Immunoglobulin Heavy Locus) • CREBBP (CREB binding protein) • POT1 (Protection of telomeres 1)
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TP53 mutation • BRAF mutation • Chr del(17p) • ATM mutation • SF3B1 mutation • IGH mutation • CREBBP mutation
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Imbruvica (ibrutinib) • Rituxan (rituximab) • cyclophosphamide • fludarabine IV
5ms
A Personalized Whole Genome-Informed Assay Targeting Single Mutant in Circulating Tumor DNA Can Identify MRD and Predict Relapse in DLBCL (ASH 2023)
Fifty-nine plasma specimens from 9 patients with relapsed/refractory (R/R) DLBCL treated on a phase II trial (NCT02362997) of post-autologous stem cell transplant (ASCT) pembrolizumab maintenance were tested... In this pilot study, MAESTRO-Pool enabled ultrasensitive detection and quantification of MRD with superior sensitivity compared to IgHTS. Complementary targeted sequencing also characterized genetic evolution, including detection of treatment-emergent mutations. Our results support the incorporation of ctDNA testing using MAESTRO-Pool in future prospective trials in DLBCL.
PD(L)-1 Biomarker • Circulating tumor DNA
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CREBBP (CREB binding protein)
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CREBBP mutation
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Keytruda (pembrolizumab)
5ms
Longitudinal Noninvasive Surveillance & Fragmentomic Characterization of Follicular Lymphoma (ASH 2023)
Depth of response was similar between rituximab monotherapy and cytotoxic regimens, with median -2.2 log10 fold change from baseline...Frequent detectable MRD in radiographic remission suggests that integrating molecular surveillance may augment serial imaging in the long-term management of FL. Simultaneous inferred gene expression from FL cfDNA appears to hold promise, including for noninvasive detection of transformation.
IO biomarker
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TP53 (Tumor protein P53) • BCL2 (B-cell CLL/lymphoma 2) • BCL6 (B-cell CLL/lymphoma 6) • KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein)
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TP53 mutation • KMT2D mutation • CREBBP mutation
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Rituxan (rituximab)
5ms
Concurrent Testing of Spatially Separated Tissue Samples and Circulating Tumor DNA Reveals Substantial Intra-Patient Genetic Heterogeneity in Relapsed/Refractory Follicular Lymphoma (ASH 2023)
Based on our results, R/R FL is characterized by remarkable intra-patient genetic heterogeneity. Although the founder clone harboring pathogenic KMT2D and CREBBP mutations can be identified in majority of the samples, expansion of tumor subclones between lymphoma sites confers divergent evolution, leaving genetic alterations unidentified during single-site based genetic testing. We also provide preliminary evidence, that multitarget high-throughput sequencing of cfDNA can uncover spatially restricted subclones that play a role in disease progression in R/R FL and that pretreatment ctDNA level might have a predictive value in the relapsed setting of FL.
Clinical • Circulating tumor DNA
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IGH (Immunoglobulin Heavy Locus) • KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein) • TNFRSF14 (TNF Receptor Superfamily Member 14) • STAT6 (Signal transducer and activator of transcription 6)
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KMT2D mutation • CREBBP mutation
5ms
Clinicopathologic and mutational profiles of primary breast diffuse large B cell lymphoma in a male patient: case report and literature review. (PubMed, World J Surg Oncol)
We reported a relatively rare PB-DLBCL in a male, non-GBC phenotype, dual-expression type. It is worth mentioning that this case had IgH/BCL6 fusion, nonsense mutations in TNFAIP3, frameshift mutations in PRDM1, and missense mutations in CREBBP, DTX1, and FOXO1. To the best of our knowledge, this case is the first report of genomic mutational profiles of PB-DLBCL in males.
Review • Journal • IO biomarker
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • BCL2 (B-cell CLL/lymphoma 2) • CD20 (Membrane Spanning 4-Domains A1) • BCL6 (B-cell CLL/lymphoma 6) • CREBBP (CREB binding protein) • TNFAIP3 (TNF Alpha Induced Protein 3) • IRF4 (Interferon regulatory factor 4) • MME (Membrane Metalloendopeptidase) • PRDM1 (PR/SET Domain 1)
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CD20 positive • BCL2 positive • CREBBP mutation • MYC rearrangement • BCL6 rearrangement • BCL2 rearrangement • PRDM1 mutation • BCL6 positive • BCL6 fusion
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Rituxan (rituximab) • cytarabine • Yinuokai (orelabrutinib)
5ms
NOTCH1 and CREBBP co-mutations negatively affect the benefit of adjuvant therapy in completely resected EGFR-mutated NSCLC: translational research of phase III IMPACT study. (PubMed, Mol Oncol)
The phase III IMPACT study (UMIN000044738) compared adjuvant gefitinib with cisplatin plus vinorelbine (cis/vin) in completely resected epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC). In patients with CREBBP co-mutations, the gefitinib group had a longer DFS than the cis/vin group, with a significant interaction (P for interaction=0.058). In completely resected EGFR-mutated NSCLC, NOTCH1 and CREBBP mutations might predict poor outcome in patients treated with gefitinib and cis/vin, respectively.
P3 data • Journal • Tumor mutational burden
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • NOTCH1 (Notch 1) • CREBBP (CREB binding protein) • CSMD3 (CUB And Sushi Multiple Domains 3)
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TP53 mutation • EGFR mutation • NOTCH1 mutation • CREBBP mutation
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cisplatin • gefitinib • vinorelbine tartrate
6ms
Mutations Associated with Progression in Follicular Lymphoma Predict Inferior Outcomes at Diagnosis (Alliance A151303). (PubMed, Blood Adv)
Patients with dx FL possessing a MAP signature had shorter frontline PFS, revealing a seven-gene set offering insight into FL progression risk potentially more generalizable than the m7-FLIPI, which had modest prognostic value in our cohort. Future studies are warranted to validate the poor prognosis associated with a MAP signature in dx FL, potentially facilitating novel trials specifically in these high-risk patients.
Journal • Tumor mutational burden
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TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • B2M (Beta-2-microglobulin) • CREBBP (CREB binding protein) • SOCS1 (Suppressor Of Cytokine Signaling 1) • STAT6 (Signal transducer and activator of transcription 6) • IGLL5 (Immunoglobulin Lambda Like Polypeptide 5)
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TP53 mutation • CREBBP mutation
8ms
Dermatological findings in Rubinstein-Taybi Syndrome. (PubMed, Ital J Dermatol Venerol)
Both susceptibility to the formation of keloids and pilomatricomas are the most often associated cutaneous features. In this review, we discuss the genetics, diagnosis, and clinical features in Rubinstein-Taybi Syndrome with a review of the major dermatological manifestations.
Journal
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CREBBP (CREB binding protein) • EP300 (E1A binding protein p300)
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CREBBP mutation • EP300 mutation
9ms
Association of Age With Treatment-Related Adverse Events and Survival in Patients With Metastatic Colorectal Cancer. (PubMed, JAMA Netw Open)
Individual data on 1223 patients with mCRC who received first-line fluorouracil and oxaliplatin therapy in 3 clinical trials, and clinical and genomic data of 736 patients with mCRC from Moffitt Cancer Center were used to assess genomic alterations and serve as an external validation cohort. In this cohort study of 1959 patients, those with early-onset mCRC showed worse survival outcomes and unique adverse event patterns, which could be partially attributed to distinct genomic profiles. These findings may inform individualized management approaches in patients with early-onset mCRC.
Journal • Adverse events • Metastases
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HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • CREBBP (CREB binding protein)
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BRAF mutation • HER-2 amplification • CTNNB1 mutation • CREBBP mutation
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5-fluorouracil • oxaliplatin
10ms
Study of Mocetinostat in Selected Patients With Mutations of Acetyltransferase Genes in Relapsed and Refractory Diffuse Large B-Cell Lymphoma and Follicular Lymphoma (clinicaltrials.gov)
P2, N=7, Terminated, Memorial Sloan Kettering Cancer Center | Trial completion date: Oct 2023 --> May 2023 | Active, not recruiting --> Terminated | Trial primary completion date: Oct 2023 --> May 2023; Lack of accrual
Trial completion date • Trial termination • Trial primary completion date
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CREBBP (CREB binding protein)
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CREBBP mutation • EP300 mutation
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mocetinostat (MGCD0103)
11ms
Predictive value of co-existing genetic alterations and tumor mutation burden for patients with completely resected non-small cell lung cancer harboring EGFR mutation: Biomarker analysis of phase III IMPACT study. (ASCO 2023)
Sponsored by Pharmaceutical/Biotech Company, AstraZeneca K.K. Background: Although osimertinib has recently become an option for adjuvant therapy in many countries, biomarkers predicting the efficacy of adjuvant EGFR-TKI and the risk of postoperative recurrence in completely resected NSCLC harboring EGFR mutations have not been fully investigated. This IMPACT-TR study is an exploratory biomarker study for completely resected, EGFR-mutated NSCLC patients who received gefitinib or cisplatin plus vinorelbine (cis/vin) in a phase III IMPACT study (Trial registration number: UMIN000044738... This study suggested that NOTCH1 mutation may be a biomarker to predict poor response to adjuvant gefitinib and CREBBP mutation to predict poor response to cis/vin in patients with completely resected, EGFR-mutated NSCLC. Clinical trial information: UMIN000044738.
P3 data • Clinical • Tumor mutational burden
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • NOTCH1 (Notch 1) • CREBBP (CREB binding protein) • CSMD3 (CUB And Sushi Multiple Domains 3) • SYNE1 (Spectrin Repeat Containing Nuclear Envelope Protein 1)
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TP53 mutation • EGFR mutation • NOTCH1 mutation • CREBBP mutation
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Oncomine Tumor Mutation Load Assay
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cisplatin • Tagrisso (osimertinib) • gefitinib • vinorelbine tartrate
12ms
Journal
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CREBBP (CREB binding protein)
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CREBBP mutation
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Rituxan (rituximab) • Epidaza (chidamide)
1year
CREBBP/EP300 disruption promotes tumor progression and confers synthetic lethality in anaplastic thyroid cancers (AACR 2023)
The recent approval of dabrafenib plus trametinib for the treatment of BRAFV600E-mutant ATCs improved the prognosis of a subset of patients, but ineligibility and acquired resistance still limit their use. Our findings prove the oncogenicity of HAT loss in thyroid cancer progression and support exploring synthetic lethality dependencies in CREBBP/EP300-mutant ATCs. In summary, we provide pre-clinical basis to inform genomics-driven and mechanism-oriented decisions for the clinical management of patients with HAT-altered ATC.
Synthetic lethality
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CREBBP (CREB binding protein) • EP300 (E1A binding protein p300)
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BRAF V600E • BRAF V600 • CREBBP mutation • EP300 mutation
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Mekinist (trametinib) • Tafinlar (dabrafenib)
1year
Different treatment response in several head and neck squamous cell carcinoma (HNSCC) cell lines reflecting underlying genomic and molecular signatures (AACR 2023)
PI3K/mTOR dual inhibition, PI3Kalpha inhibitor, AKT inhibitor, FGFR inhibitor, ALK/IGF1R inhibitor, CDK4/6 inhibitor, BCl2 inhibitor, WEE1 inhibitor, ATR inhibitor, DNA-PK inhibitor, AT2AR inhibitor, Mcl-1 inhibitor, MEK1/2 inhibitor, EZH2 inhibitor, HDAC inhibitor, CDK9 inhibitor, DNMT3 inhibitor, BRD4/BET inhibitor, JAK2 inhibitor, CXCR4 inhibitor, FAK inhibitor, BTK inhibitor, eribulin, & VEGFR2/ PDGFR/FGFR or VEGFR2/c-MET/Axl triple blockage might be effective on TW2.6 and reverse treatment refractoriness, maybe through the inhibition of mesenchymal transformation, pRB, & PI3K/AKT /mTOR signaling and the modulation of stemness & PD1/PDL1 pathway...All cell lines will be tried to be categorized as TCGA subtypes for the reference of future drug combinations.Cell linesSCC25KBSASCAL27FaDuSCC15SCC9SCC4TW2.6Differ- entiationWellPoorPoorPoorPoorWellWellWellWell, but rapidly replicated, with high hyper-diploidy & complex rearrangementsHPV statusHPV 16/18HPV18--HPV 16/18--HPV 6/11-EGFR statusMediumLowHighHighMediumHighLowMedium to highUnknownDocetaxel sensitivity+++++++++++++ to +++++-+Cisplatin sensitivity+++++++++++++- to +-- to +5-FU sensitivity+++++++++++-+ to ++-- to +Afatinib sensitivity+++- to +-+++++ to +++++++++-Polo-like kinase Inhibitor sensitivity+++++++++++++ to +++- to +-- to +VEGFR2 Inhibitor sensitivity----+++++--++PI3K/ mTOR inhibitorAll cell lines sensitiveCDK4/6 Inhibitor response+++- to ++++++ to +++++++++++++ to +++Western blotsWeak p-AKT & VEGF-A, mild PDL1 and BMI-1, Gli-1(+)Weak p-AKT, mild PDL1 and strong VEGF-A & BMI-1, p16(+)Moderate p-AKT & BMI-1, high PDL1, mild VEGF-AHigh p-AKT & VEGF-A, mild PDL1 & BMI-1High VEGF-A, moderate p-AKT & PDL1, weak BMI-1, Gli-1(+)Weak p-AKT & VEGF-A, mild PDL1 & BMI-1Weak p-AKT, VEGF-A, & BMI-1, moderate PDL1Moderate p-AKT & VEGF-A, strong BMI-1, mild PDL1, Gli-1(+)High p-AKT, PDL1, & VEGF-A and moderate BMI-1NGSCCND1 gain, CDKN2A deletion, FRG1 mutation, HGF mutation, p53 mutation, ATR mutation, SMO mutation, RUNX1T1 mutationSTK11 mutation, PDGFRA mutation, IGF1 mutation, BCOR mutation, EGFR mutation, NOTCH1 mutation, MET mutation, IKZF1 mutation, NFKB1 mutation, DPYD mutation, FGFR4 mutation, BRCA1 mutation, MSH2 mutation, DNMT3A mutationKRAS mutation, MDM2 mutation, TMB-H, AXIN1 loss, RAD51D mutation, NOTCH1/2 mutation, ERBB4 mutation, PALB2 mutation, p53 mutation, POLE mutation, CASP8 mutation, BRCA2 mutation, RNF43 mutation, LRP1B mutation, MET mutationCDKN2A deletion, EGFR amplification, SMAD4 mutation, TMB-H, LRP1B mutation, APC mutation, CASP8 mutation, CREBBP mutation, PIK3CG mutation, NRAS mutation, ABL1 mutation, FGF23 mutation, HGF mutation, ATRX mutation, p53 mutation, ERBB2 mutation, ROS1 mutation, EP300 mutation, NRAS mutation, CDKN1A mutation, KDM6A mutation, FLT4 mutationCCND1 gain, CDKN2A deletion, FLCN mutation, TMB-H, LRP1B mutation, SMAD4 loss, SF3B1 mutation, FAT1 mutation, VHL mutation, NOTCH3 mutation, EPHA5 mutation, p53 mutation, ERCC2 mutationCCND1 gain, EGFR amplification, SMO mutation, ATR mutation, FAT1 loss, NTRK1 mutation, KMT2D mutation, p53 mutation, NOTCH3 mutationCDKN2A deletion, AXIN2 amplification, SMAD3 loss, HRAS mutation, ATR mutation, NF1 mutation. IGF1R mutation, FLCN mutation, KEAP1 mutation, ASXL1 mutation, PMS2 mutationCCND1 gain, NF1 loss, LRP1B mutation, NSD1 mutation, KMT2D mutation, p53 mutation, EPHA2 mutationFAT1 loss, CCND3/FGF10 amplification, PIK3CA H1047R mutation, STK11 mutation, RICTOR/FLCN amplification, VEGF-A amplification , TSC2 mutation, EPHB1 mutation, MAP2K4 mutation, KDM5A mutation, PDGFRB mutation, SETD2 mutation, RPTOR mutation, APC mutation, DDR2 mutation, ATM mutation, MDM2 mutation, p53 mutation, CDK12 mutation, HRAS mutation, MYC mutation, CDK8 mutation, ARID1B lossOutcomesBest; like TCGA CL (HPV+) subtypeLike TCGA basal subtype, but responded to particular treatments eachBasalBasalLike TCGA mesen-chymal subtype (HPV+)Like TCGA CL(HPV-) subtype, different characters between these 3 cell linesCL(HPV-) subtypeCL(HPV-) subtypeWorse; like TCGA EMT subtype (HPV-)Potential treatmentsAll sensitive maybe; Hedgehog inhibitor , HGF/c-MET inhibitor, and I/O could be tried(1) Taxane, cisplatin, PLKi (2) mTORi (3) IGF1Ri, METi, PDGFRi, FGFRi (4) Epigenetics (5) I/O(1) Taxane, cisplatin, 5-FU, PLKi (2) CDK4/6i (3) I/O (4) DDRi (5) KRASi, METi, HERi (6) p53 reactivator and MDM2/Mcl-1 inhibitor(1) Taxane, cisplatin, 5-FU, PLKi (2) CDK4/6i (3) Mild EGFRi response (4) I/O (5) NRASi, FGFRi, HGF/c-METi/ROS1i/HERi (6) p53 reactivator/DDRi/Epigenetics(1) Cisplatin, 5-FU (2) EGFRi and VEGFR2i (3) Weak to PLKi & CDK4/6i (4) I/O (5) mTORi (6) Ephi (7) DDR/Epigenetics (8) p53 reactivator (9) HIFi(1) Taxane and PLKi (2) EGFRi, VEGFR2i, CDK4/6i (3) NTRKi (4) Hedgehog inhibitor (5) DDRi, epigenetics,& p53 reactivator(1) Taxane &5-FU (2) EGFRi (3) HRASi (4) DDRi/Epigenetics (5) I/O (6) IGF1Ri (7) mTORi(1) EGFRi (2) CDK4/6i (3) I/O (4) Epigenetics (5) Ephi (6) p53 reactivator(1) CDK4/6 inhibitor (2) Multi-targeted VEGFR TKI (3) PI3K/AKT/mTOR inhibitor (4) ICIs combination (5) p53 reactivator/ DDR interventions/Epigenetics (6) Dasatinib, HRASi, EphB1/B4 interventions Further NGS analysis may translate these HNSCC cell lines to represent TCGA subtypes for the reference of future drug combinations, esp... Further NGS analysis may translate these HNSCC cell lines to represent TCGA subtypes for the reference of future drug combinations, esp. immunotherapy, basic/translational research, and animal models. LRP1B will be a potential ICIs efficacy biomarker in HNSCC.
Preclinical • Tumor mutational burden • BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • ATM (ATM serine/threonine kinase) • STK11 (Serine/threonine kinase 11) • HRAS (Harvey rat sarcoma viral oncogene homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • DNMT3A (DNA methyltransferase 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NOTCH1 (Notch 1) • NF1 (Neurofibromin 1) • KEAP1 (Kelch Like ECH Associated Protein 1) • POLE (DNA Polymerase Epsilon) • AXL (AXL Receptor Tyrosine Kinase) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • CCND1 (Cyclin D1) • MDM2 (E3 ubiquitin protein ligase) • PALB2 (Partner and localizer of BRCA2) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • PDGFRB (Platelet Derived Growth Factor Receptor Beta) • KMT2D (Lysine Methyltransferase 2D) • LRP1B (LDL Receptor Related Protein 1B) • FGFR4 (Fibroblast growth factor receptor 4) • MSH2 (MutS Homolog 2) • RNF43 (Ring Finger Protein 43) • CDK12 (Cyclin dependent kinase 12) • SMAD4 (SMAD family member 4) • IKZF1 (IKAROS Family Zinc Finger 1) • ERCC2 (Excision repair cross-complementation group 2) • PMS2 (PMS1 protein homolog 2) • VHL (von Hippel-Lindau tumor suppressor) • APC (APC Regulator Of WNT Signaling Pathway) • ATRX (ATRX Chromatin Remodeler) • TSC2 (TSC complex subunit 2) • IGF1R (Insulin-like growth factor 1 receptor) • NOTCH2 (Notch 2) • CREBBP (CREB binding protein) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • SMO (Smoothened Frizzled Class Receptor) • BCOR (BCL6 Corepressor) • ERBB4 (erb-b2 receptor tyrosine kinase 4) • FAT1 (FAT atypical cadherin 1) • KDM6A (Lysine Demethylase 6A) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • PIK3CG (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma) • NOTCH3 (Notch Receptor 3) • ARID1B (AT-Rich Interaction Domain 1B) • EP300 (E1A binding protein p300) • FLT4 (Fms-related tyrosine kinase 4) • IGF1 (Insulin-like growth factor 1) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • RAD51D (RAD51 paralog D) • RICTOR (RPTOR Independent Companion Of MTOR Complex 2) • EPHA2 (EPH receptor A2) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • CASP8 (Caspase 8) • CCND3 (Cyclin D3) • BRD4 (Bromodomain Containing 4) • DDR2 (Discoidin domain receptor 2) • FLCN (Folliculin) • KDM5A (Lysine Demethylase 5A) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • DPYD (Dihydropyrimidine Dehydrogenase) • EPHA5 (EPH Receptor A5) • EPHB1 (EPH Receptor B1) • FGF10 (Fibroblast Growth Factor 10) • FGF23 (Fibroblast Growth Factor 23) • MAP2K4 (Mitogen-Activated Protein Kinase Kinase 4) • SMAD3 (SMAD Family Member 3)
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TP53 mutation • KRAS mutation • BRCA2 mutation • BRCA1 mutation • EGFR mutation • TMB-H • NRAS mutation • PIK3CA mutation • EGFR amplification • ATM mutation • PIK3CA H1047R • STK11 mutation • DNMT3A mutation • PALB2 mutation • POLE mutation • NF1 mutation • NOTCH1 mutation • ASXL1 mutation • CDKN2A deletion • BCL2 overexpression • KEAP1 mutation • SF3B1 mutation • CDKN2A mutation • KMT2D mutation • CDK12 mutation • LRP1B mutation • VHL mutation • PIK3CA amplification • HRAS mutation • APC mutation • ATR mutation • ATRX mutation • CCND1 amplification • PDGFRA mutation • CREBBP mutation • MSH2 mutation • RNF43 mutation • ROS1 mutation • SMAD4 mutation • BCOR mutation • FGFR4 mutation • KDM6A mutation • RAD51D mutation • TSC2 mutation • FAT1 mutation • MYC mutation • ARID1B mutation • NOTCH3 mutation • PMS2 mutation • SMO mutation • IKZF1 mutation • MDM2 mutation • NTRK1 mutation • EP300 mutation • ERBB4 mutation • NSD1 mutation • PIK3CA H1047R + PIK3C2B amplification • PIK3CG mutation • SETD2 mutation • EPHA5 mutation • EPHB1 mutation • ERCC2 mutation • FGF10 amplification • FGF23 mutation • FLCN mutation • HGF mutation • PDGFRB mutation • RAD51 mutation
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cisplatin • Gilotrif (afatinib) • dasatinib • 5-fluorouracil • Halaven (eribulin mesylate)
1year
Journal • Next-generation sequencing • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • BCL6 (B-cell CLL/lymphoma 6) • NOTCH2 (Notch 2) • CREBBP (CREB binding protein) • CD5 (CD5 Molecule) • TNFRSF14 (TNF Receptor Superfamily Member 14) • STAT6 (Signal transducer and activator of transcription 6) • TNFRSF18 (TNF Receptor Superfamily Member 18)
|
EZH2 mutation • CREBBP mutation • BCL6 rearrangement • NOTCH2 mutation • BCL2 rearrangement
1year
Effects of the Omega-3 Fatty Acid DHA on histone and p53 acetylation in Diffuse Large B-Cell Lymphoma. (PubMed, Biochem Cell Biol)
qRT-PCR results revealed significant changes in expression of multiple genes, including increased expression of CREBBP and of PRDM1 (required for differentiation into plasma cells or memory B-cells). Taken together, our results provide (to our knowledge) the first characterization of the epigenetic effects of omega-3 fatty acids in DLBCL.
Journal
|
TP53 (Tumor protein P53) • CREBBP (CREB binding protein) • EP300 (E1A binding protein p300) • PRDM1 (PR/SET Domain 1)
|
CREBBP mutation • EP300 mutation
1year
Inflammatory brain lesions preceding primary central nervous system lymphoma: a case report and genetic analysis. (PubMed, Neurol Sci)
Our present case is the first to demonstrate inflammatory brain lesions heralding PCNSL from genetic and pathological perspectives. This may help clinicians to select new auxiliary diagnostic methods for timely diagnosis of patients with suspected PCNSL.
Review • Journal
|
CREBBP (CREB binding protein) • RELN (Reelin) • PCLO (Piccolo Presynaptic Cytomatrix Protein)
|
CREBBP mutation
over1year
Mutation analysis performed on tumor biopsies from patients with newly-diagnosed germinal center aggressive B cell lymphomas. (PubMed, Oncotarget)
CREBBP mutations may be frequent and predict for inferior DFS in patients with newly-diagnosed GCB DLBCL/HGBL. Furthermore, CLMA may be practically-applied to translate experimental findings into those with more direct application to risk stratification and clinical trial design in subsets of patients with DLBCL/HGBL.
Journal
|
CREBBP (CREB binding protein)
|
CREBBP mutation
over1year
Diffuse large B-cell lymphoma and red cell autoimmunity: clinical role and pathogenesis. (PubMed, Pathology)
Mutation analysis of these five samples demonstrated high frequency of mutations in several genes, including CREBBP and NCOR2. Further research could explore if mutations in CREBBP and NCOR2 work in conjunction with the preserved QW and AVY motifs to promote lymphomagenesis in IGHV4-34-expressing B cells, and if so, could guide future targeted therapy.
Journal
|
KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein) • BIRC3 (Baculoviral IAP repeat containing 3) • CARD11 (Caspase Recruitment Domain Family Member 11) • EP300 (E1A binding protein p300) • NCOR2 (Nuclear Receptor Corepressor 2)
|
CREBBP mutation
over1year
Clinical Laboratory Mutation Analysis Performed on Tumor Biopsies from Patients with First Relapsed/Refractory Aggressive B Cell Lymphoma Treated with Curative-Intent Immunochemotherapy (ASH 2022)
Given the low rate of 2y DFS as well as a shift in practice to the use of chimeric antigen receptor-modified T cells (CART) as 2Ltx for pts with early R/R DLBCL/HGBL, these data do not support further investigation of CLMA performed on a larger sample of tumor bx from all pts at the time of first R/R disease who are candidates for CART. However, performance of CLMA could further explored in the subset of DLBCL/HGBL pts with late first R/R disease for whom the standard of care 2Ltx remains curative-intent IC, as the presence of absence of mut predicting for disease response/DFS in this pt population may inform tx decisions given the availability of non-cytotoxic agents as 2L tx as well as CART at the time of subsequent R/R disease.
Clinical • IO biomarker
|
TP53 (Tumor protein P53) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • BCL2 (B-cell CLL/lymphoma 2) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • BCL6 (B-cell CLL/lymphoma 6) • CREBBP (CREB binding protein) • SOCS1 (Suppressor Of Cytokine Signaling 1)
|
TP53 mutation • BCL2 expression • MYC expression • CREBBP mutation • MYC rearrangement • BCL6 rearrangement • BCL2 rearrangement
over1year
Identification of Histone Acetylation Regulator KAT2A As a Potential Prognostic Biomarker in Diffuse Large B-Cell Lymphoma (ASH 2022)
Additionally, our study shows that KAT2A is associated with prognosis in patients with DLBCL. Further study of the mechanisms of KAT2A in DLBCL may help clinicians to individualize the treatment of this patient population.
Epigenetic controller
|
CD19 (CD19 Molecule) • CREBBP (CREB binding protein)
|
CREBBP mutation
over1year
Genetic Alterations of Crebbp Are Associated with Radiosensitivity in Follicular Lymphoma (ASH 2022)
Clinicodemographic factors associated with durable FL response to RT are crude and though there are many predictive models of response to rituximab or chemotherapy, there are no known genetic markers of FL radiosensitivity...Additionally, as histone acetylation by CREBBP is implicated in the radiosensitivity of FL, it is possible that agents targeting epigenetic processes may have a role in increasing radiosensitivity during FL treatment. The genetic landscape of FL patients being treated with radiotherapy, especially VLDRT, may be incorporated into clinical decision making to improve patient and dose selection for RT.
IO biomarker
|
TP53 (Tumor protein P53) • BCL2 (B-cell CLL/lymphoma 2) • KMT2D (Lysine Methyltransferase 2D) • B2M (Beta-2-microglobulin) • CREBBP (CREB binding protein) • IRF8 (Interferon Regulatory Factor 8) • TNFRSF14 (TNF Receptor Superfamily Member 14) • STAT6 (Signal transducer and activator of transcription 6) • TNFRSF18 (TNF Receptor Superfamily Member 18)
|
CREBBP mutation
|
MSK-IMPACT
|
Rituxan (rituximab)
over1year
Long-Term Outcome of Patients with Follicular Lymphoma Is Not Fundamentally Affected By KMT2D, EZH2, and Crebbp Mutational Status (ASH 2022)
Initial treatment in this series of 295 patients with FL included monoclonal antibody + chemotherapy (57%), single-agent rituximab (15%), chemotherapy (2%), radiotherapy alone (8%), and other treatments (6%). Exploratory analysis with WES was performed on 16 FLEP cases and 10 FLLP cases. There were no significant differences in the occurrence of gene mutations between FLEP and FLLP cases in the WES cohort. Only 1 gene, SETD1B, appeared in the WES panel that is not covered in the HemePACT and clinical IMPACT targeted signaling platforms.
Clinical • IO biomarker
|
KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein)
|
KMT2D mutation • EZH2 mutation • CREBBP mutation
|
Rituxan (rituximab) • Mepact (mifamurtide)
over1year
Mutations Associated with Progression in Follicular Lymphoma Predict Inferior Outcomes in Newly Diagnosed Patients (Alliance 151303) (ASH 2022)
In summary, our analyses highlight a set of MAPs that may offer unique insight into progression risk in FL, which may be more generalizable than the m7-FLIPI. Future studies are warranted to validate the poor prognosis associated with the presence of MAPs in pts with untreated FL, which could facilitate prospective studies of novel therapies in this subset of high risk pts.
Clinical • Tumor Mutational Burden
|
TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • ARID1A (AT-rich interaction domain 1A) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • B2M (Beta-2-microglobulin) • CREBBP (CREB binding protein) • CARD11 (Caspase Recruitment Domain Family Member 11) • EP300 (E1A binding protein p300) • SOCS1 (Suppressor Of Cytokine Signaling 1) • STAT6 (Signal transducer and activator of transcription 6) • IGLL5 (Immunoglobulin Lambda Like Polypeptide 5)
|
TP53 mutation • ARID1A mutation • EZH2 mutation • CREBBP mutation
over1year
Expanding the High-Risk Definition for Children with Newly Diagnosed Acute Myeloid Leukemia (ASH 2022)
Retrospective incorporation of candidate HR alterations into COG's contemporary risk classification system would have increased the number of patients allocated to allogenic donor SCT. While all 6 candidate alterations had a consistently inferior EFS over successive trials, patients w/ co-occurring LR alterations had a more favorable OS, suggesting they can be salvaged via SCT. Before these alterations can be considered HR, further investigation is required, including corroboration from other large pediatric and adult consortium trials and the benefit of this re-allocation will need to be validated prospectively.
Clinical
|
TP53 (Tumor protein P53) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • KMT2A (Lysine Methyltransferase 2A) • CREBBP (CREB binding protein) • CSF3R (Colony Stimulating Factor 3 Receptor) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
|
TP53 mutation • NPM1 mutation • CREBBP mutation • MLL mutation
over1year
Crebbp Mutations Are Associated with Shorter Time to Progression in Limited-Stage Follicular Lymphoma Treated with Radiation (ASH 2022)
In conclusion, we found an association between CREBBP mutations and shorter time to progression in limited-stage FL treated with RT. To our knowledge, this represents a novel genetic prognostic finding in limited-stage FL. Further studies with larger sample sizes are required to confirm the association.
IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein) • TNFRSF14 (TNF Receptor Superfamily Member 14) • STAT6 (Signal transducer and activator of transcription 6) • TNFRSF18 (TNF Receptor Superfamily Member 18)
|
KMT2D mutation • CREBBP mutation • BCL2 mutation
over1year
Prognostic biomarkers correlated with immune infiltration in non-small cell lung cancer. (PubMed, FEBS Open Bio)
Gene set enrichment analysis (GSEA) revealed that cell cycle, the Notch signaling pathway, the insulin signaling pathway, and the mTOR signaling pathway are related to LRP1B mutations in the immune system. LRP1B mutations may be of clinical importance in enhancing the anti-tumor immune response and may be a promising biomarker for predicting immunotherapy responsiveness.
Journal • Tumor Mutational Burden • IO biomarker
|
EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • RB1 (RB Transcriptional Corepressor 1) • KMT2D (Lysine Methyltransferase 2D) • LRP1B (LDL Receptor Related Protein 1B) • CREBBP (CREB binding protein) • FAT1 (FAT atypical cadherin 1)
|
TP53 mutation • EGFR mutation • TMB-H • KMT2D mutation • LRP1B mutation • CREBBP mutation
over1year
Study of Mocetinostat in Selected Patients With Mutations of Acetyltransferase Genes in Relapsed and Refractory Diffuse Large B-Cell Lymphoma and Follicular Lymphoma (clinicaltrials.gov)
P2, N=7, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Oct 2022 --> Oct 2023 | Trial primary completion date: Oct 2022 --> Oct 2023
Trial completion date • Trial primary completion date
|
CREBBP (CREB binding protein)
|
CREBBP mutation • EP300 mutation
|
mocetinostat (MGCD0103)
over1year
Association of CREBBP mutation with favorable outcome with immune checkpoint inhibitors in bladder cancer (ESMO 2022)
Conclusions CREBBP mutation shows a favorable link between CREBBP mutation with efficacy of ICIs. Furthermore, validation of the predictive value of CREBBP in prospective trials and more fundamental exploration are needed in future.
Checkpoint inhibition • Tumor Mutational Burden • IO biomarker
|
TMB (Tumor Mutational Burden) • CREBBP (CREB binding protein)
|
TMB-H • CREBBP mutation
over1year
Patients deriving long-term benefit from immune checkpoint inhibitors demonstrate conserved patterns of site-specific mutations. (PubMed, Sci Rep)
Thus, this study identified several genes that may have utility as predictive biomarkers for therapeutic responses in patients receiving ICIs. As many have no known relationship to immunotherapy or ICIs, these genes warrant continued exploration, particularly for cancers in which established biomarkers such as PD-L1 expression or TMB have little predictive value.
Retrospective data • Journal • Checkpoint inhibition • Tumor Mutational Burden • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • TMB (Tumor Mutational Burden) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • RNF43 (Ring Finger Protein 43) • VHL (von Hippel-Lindau tumor suppressor) • CREBBP (CREB binding protein) • NOTCH3 (Notch Receptor 3) • ZFHX3 (Zinc Finger Homeobox 3) • EPHA7 (EPH Receptor A7) • LATS1 (Large Tumor Suppressor Kinase 1) • NCOA3 (Nuclear Receptor Coactivator 3)
|
PD-L1 expression • VHL mutation • CREBBP mutation • RNF43 mutation • NOTCH3 mutation • LATS1 mutation
over1year
Study to Evaluate CCS1477 in Advanced Tumours (clinicaltrials.gov)
P1/2, N=350, Recruiting, CellCentric Ltd. | N=200 --> 350 | Trial completion date: Jun 2022 --> Mar 2024 | Trial primary completion date: Jun 2022 --> Mar 2024
Enrollment change • Trial completion date • Trial primary completion date
|
MYC (V-myc avian myelocytomatosis viral oncogene homolog) • AR (Androgen receptor) • ARID1A (AT-rich interaction domain 1A) • CREBBP (CREB binding protein)
|
ARID1A mutation • CREBBP mutation • EP300 mutation
|
Lynparza (olaparib) • Tecentriq (atezolizumab) • enzalutamide capsule • abiraterone acetate • Nubeqa (darolutamide) • inobrodib (CCS1477)
almost2years
Analysis of CREBBP as a Potential Biomarker for Immune Checkpoint Therapy in Solid Tumors and Its Correlation With Immune Microenvironment (IASLC-WCLC 2022)
The results showed that the CREBBP had a high correlation in solid tumors with TMB, MSI and PD-L1. The CREBBP might a potential biomarker for ICIs therapy, and the immune microenvironment may be a factor affecting it.
Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • TMB (Tumor Mutational Burden) • CREBBP (CREB binding protein) • CD4 (CD4 Molecule)
|
PD-L1 expression • TMB-H • CREBBP mutation
|
PD-L1 IHC 22C3 pharmDx
almost2years
Periocular Pigmented Basal Cell Carcinomas: Clinicopathologic Features and Mutational Profile. (PubMed, Ophthalmic Plast Reconstr Surg)
In this large cohort of a relatively uncommon variant of BCC, the clinicopathological features and tumor behavior of PBCC was similar to periocular non-PBCC. The somatic mutation spectrum of PBCC resembles that reported in nonperiocular cutaneous BCC with novel drivers identified. We identified several potential actionable mutations that could be targeted with molecular therapy.
Journal
|
TERT (Telomerase Reverse Transcriptase) • PTCH1 (Patched 1) • CREBBP (CREB binding protein) • SMO (Smoothened Frizzled Class Receptor) • FANCD2 (FA Complementation Group D2)
|
PTCH1 mutation • CREBBP mutation • TERT mutation • SMO mutation
almost2years
Genetic characterization and drug sensitivity study of newly derived HGBL double/triple-hit lymphoma cell lines. (PubMed, Blood Adv)
Silvestrol and Dinaciclib generally showed outstanding activities and the newly derived cell lines tended to be most responsive. The BL cell line Jijoye showed a completely different pattern of response. A panel of well characterized D/TH lymphoma lines would be very helpful in preclinical studies of targeted agents.
Preclinical • Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • BCL6 (B-cell CLL/lymphoma 6) • KMT2D (Lysine Methyltransferase 2D) • CREBBP (CREB binding protein) • EP300 (E1A binding protein p300)
|
EZH2 mutation • CREBBP mutation • BCL6 rearrangement • BCL2 rearrangement
|
dinaciclib (MK-7965)
almost2years
Molecular and immune landscape of FH-mutated cancers. (ASCO 2022)
FH alterations are found in multiple cancers. A41V was the most common VUS mutation and is associated with a distinct molecular profile compared to K477dup-mt and R233-mt tumors; it was associated with worse survival in all-comers and after chemotherapy compared to P+LP mutations. This highlights the significance of this mutation and the need for further investigation into how this specific and other FH mutations contribute to cancer progression and treatment outcomes.
PD(L)-1 Biomarker • MSi-H Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • CREBBP (CREB binding protein) • FH (Fumarate Hydratase) • DICER1 (Dicer 1 Ribonuclease III) • PRKDC (Protein Kinase, DNA-Activated, Catalytic Subunit)
|
TMB-H • MSI-H/dMMR • FBXW7 mutation • CREBBP mutation • PRKDC mutation
|
PD-L1 IHC 22C3 pharmDx • VENTANA PD-L1 (SP142) Assay • PD-L1 IHC 28-8 pharmDx