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  • 1
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    Cell competition is a tumour suppressor mechanism in the thymus
    Springer Science and Business Media LLC ; 2014
    In:  Nature Vol. 509, No. 7501 ( 2014-05-22), p. 465-470
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 509, No. 7501 ( 2014-05-22), p. 465-470
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/nature13317
    RVK:
    TA 1000
    RVK:
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    RVK:
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2014
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  • 2
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    Abstract 1023: Activation of proto-oncogenes by enhancer-hijacking in high-risk neuroblastoma
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 1023-1023
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 1023-1023
    Abstract: Background: Neuroblastoma (NB), a neural crest-derived tumor of the sympathetic nervous system, is the most common extracranial solid tumor in children. We have previously shown that genomic rearrangements activate proto-oncogenic telomerase by juxtaposing active enhancer elements to the TERT gene in a large fraction of high-risk NBs. In the present study, we applied a global approach integrating whole genome sequencing (WGS), Chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq) data of NB cells and tumors to identify further key oncogenes activated by enhancer-hijacking in NB. Methods: WGS was applied to search for structural rearrangements in 120 NB tumors and five NB cell lines. Corresponding RNA-seq data were used to discover mono-allelic and/or outlier expression of candidate genes potentially involved in enhancer hijacking events. ChIP-seq of 34 NB tumors and 17 NB cell lines was applied to identify active enhancer elements in NB. Circular chromatin conformation capture sequencing (4C-seq) was used to confirm physical promoter-enhancer interactions in NB cell lines. Results: WGS analyses revealed that chromosomal rearrangements are common events in NB tumors and cell lines and frequently affect regions harboring proto-oncogenes and lineage specific enhancers. ChIP-seq analyses of the chromatin mark histone 3 lysine 27 acetylation (H3K27ac), surrogate for enhancer activity, confirmed that these rearrangements recurrently juxtapose active enhancer elements to oncogenes including MYCN and MYC in NB. Intriguingly, quantification of H3K27ac ChIP-seq profiles uncovered that the enhancer elements translocated to MYC were among the most active ones within the respective epigenomes. 4C-seq analyses proofed physical interactions between translocated enhancer elements and promoters of the respective oncogenes, which is in line with their elevated expression in rearranged cases. Conclusions: Our study reveals that structural rearrangements in high-risk neuroblastoma frequently juxtapose strong enhancers to key oncogenes, including MYCN and MYC, leading to physical promoter-enhancer interactions which likely drive overexpression of the oncogenes observed in rearranged cases. The common mechanism of oncogene activation by enhancer-hijacking may open a therapeutic window for epigenetic drugs including BET or CDK7 inhibitors in high-risk NBs. Citation Format: Daniel Dreidax, Moritz Gartlgruber, Sebastian Steinhauser, Larisa Savelyeva, Ron Schwessinger, Umut Toprak, Nati Ha, Dilafruz Juraeva, Martin Peifer, Matthias Fischer, Stefan Gröschel, Kai-Oliver Henrich, Young-Gyu Park, Benedikt Brors, Matthias Schlesner, Carl Herrmann, Frank Westermann. Activation of proto-oncogenes by enhancer-hijacking in high-risk neuroblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1023. doi:10.1158/1538-7445.AM2017-1023
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-1023
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 3
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    A Systematic Approach to Defining the microRNA Landscape in Metastasis
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15 ( 2015-08-01), p. 3010-3019
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15 ( 2015-08-01), p. 3010-3019
    Abstract: The microRNA (miRNA) landscape changes during the progression of cancer. We defined a metastasis-associated miRNA landscape using a systematic approach. We profiled and validated miRNA and mRNA expression in a unique series of human colorectal metastasis tissues together with their matched primary tumors and corresponding normal tissues. We identified an exclusive miRNA signature that is differentially expressed in metastases. Three of these miRNAs were identified as key drivers of an EMT-regulating network acting though a number of novel targets. These targets include SIAH1, SETD2, ZEB2, and especially FOXN3, which we demonstrated for the first time as a direct transcriptional suppressor of N-cadherin. The modulation of N-cadherin expression had significant impact on migration, invasion, and metastasis in two different in vivo models. The significant deregulation of the miRNAs defining the network was confirmed in an independent patient set as well as in a database of diverse malignancies derived from more than 6,000 patients. Our data define a novel metastasis-orchestrating network based on systematic hypothesis generation from metastasis tissues. Cancer Res; 75(15); 3010–9. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-15-0997
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 4
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    MET ex14 ctDNA dynamics & resistance mechanisms detected in liquid biopsy (LBx) from patients (pts) with MET ex14 skipping NSCLC treated with tepotinib.
    American Society of Clinical Oncology (ASCO) ; 2021
    In:  Journal of Clinical Oncology Vol. 39, No. 15_suppl ( 2021-05-20), p. 9012-9012
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 39, No. 15_suppl ( 2021-05-20), p. 9012-9012
    Abstract: 9012 Background: In the VISION study, tepotinib in METex14 skipping NSCLC pts (Cohort A) had robust and durable clinical activity. Serial LBx samples were collected for biomarker analyses, presented herein. Methods: LBx samples taken at baseline (BL), Week 6, 12, & end of treatment (EOT) were analyzed using Guardant360 ® CDx (73 genes). Investigator (INV)-assessed clinical outcome was evaluated per BL biomarker profiles and by molecular response (MR; defined as 〉 75% depletion from BL in METex14 variant allele frequency [VAF] ctDNA confirmed in 2 consecutive samples) or molecular progression (MP; defined as VAF increase 〉 0 from BL). Acquired resistance was investigated in EOT samples, following progression per INV. Results: LBx pts (n = 99) had a median age of 72 yrs (range 49–88), 53% were male, 44% never smokers, 85% had adenocarcinoma. INV ORR was 53% (95% CI 42, 63); ORR in 1L (n = 44) was 59% (43, 74) & ≥2L (n = 55) was 47% (33, 61). 94 pts had BL biomarker profiles; these were similar in 1L and ≥2L pts, except EGFR amp: 1/43 1L [2%] vs 8/51 ≥2L [16%] . Outcomes were not impacted by location/type of METex14 alteration. 1 pt with concomitant MET M1250T mutation had a PFS of 17.3 months. A trend towards better efficacy was seen in pts with concomitant MET amp (6 responses in 8 pts). Response to tepotinib occurred both in pts with wt or mutant TP53; however, there was a trend for longer mDOR in pts with wt TP53 (18.3 [95% CI 9.7, ne] vs 7.1 [4.7, 10.9] months) and mPFS (9.5 [6.7, 19.7] vs 5.1 [2.8, 6.9] months). Concomitant oncogenic mutations were rare, with no responses in 3 pts with KRAS, NRAS alterations and 3 responses in 5 pts with PI3K/AKT alterations. 65 pts had 2 consecutive on-treatment samples: 46 (71%) had confirmed MR, 5 (8%) had confirmed MP, 14 (22%) had no change in VAF or lacked confirmation. MR was associated with clinical response and MP was associated with no response/short PFS (Table). 52 pts with progression had EOT LBx samples. Emerging MET resistance mutations (Y1230H/C & D1228H/N) occurred in 7 (13%) pts, all responders and 5/7 had PFS 〉 10 months. Analyses on non-MET-driven resistance mechanisms will be presented. Conclusions: LBx biomarker analysis from the largest on-treatment data set for a MET inhibitor in METex14 skipping NSCLC, showed that ctDNA depletion in METex14 VAF is associated with improved clinical response in pts treated with tepotinib. This suggests serial LBx could help us to monitor response/non-response, understand resistance, and guide trials that test escalation/de-escalation strategies to improve outcomes and maximize QOL. Clinical trial information: NCT02864992. [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2021.39.15_suppl.9012
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2021
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  • 5
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    Changes in ctDNA levels as an early indicator of outcomes in advanced NSCLC treated with TKI: Initial findings from a retrospective aggregate analysis of 8 clinical trials.
    American Society of Clinical Oncology (ASCO) ; 2023
    In:  Journal of Clinical Oncology Vol. 41, No. 16_suppl ( 2023-06-01), p. 3030-3030
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 41, No. 16_suppl ( 2023-06-01), p. 3030-3030
    Abstract: 3030 Background: To determine whether changes in circulating tumor DNA (ctDNA) levels reflect treatment outcome, Friends of Cancer Research created the ctDNA to Monitor Treatment Response (ctMoniTR) Project with collaborators from industry, government, academia, and advocacy. A prior ctMoniTR effort analyzing 5 clinical trials (CT) showed an association between decreases in ctDNA levels and improved outcomes in patients with advanced non-small cell lung cancer (aNSCLC) treated with an anti-PD-(L)1. The current study expands that work and focuses on CT investigating tyrosine kinase inhibitors (TKI) treatment in oncogene-driven aNSCLC. Methods: We performed a retrospective analysis of patient-level clinical and ctDNA data across 8 CT representing 1,015 patients with aNSCLC treated with TKI (i.e., anti-EGFR, ALK, RET, or MET). Patients included in the analysis had a baseline ctDNA measurement (T0), an on treatment ctDNA measurement within 10 weeks of treatment initiation (for those with multiple ctDNA measurements within 10 weeks, we used the lowest measurement within 10 weeks) (T1), and overall survival (OS) data (n=749). CT used different ctDNA collection timepoints and assays. We randomly divided the dataset into training (2/3 of the data) and validation (1/3 of the data) datasets stratified by CT cohort (i.e., arm), age, tumor stage, and prior lines of therapy, then ran initial analyses on the training dataset (n=501; reported herein). ctDNA change was calculated as the percent change in maximum variant allele frequency (VAF) between T0 and T1 using tumor-derived variants provided by sponsors for each unique patient sample. CT used either ddPCR or an NGS assay. ctDNA limits of detection were assay specific and varied across CT. Multivariate analyses are ongoing and validation dataset analyses will be conducted. Results: At T0, 141 patients had non-detected (ND) ctDNA and 360 patients had detected (D) ctDNA. Of these, 27% (n=136) had ND ctDNA at both T0 and T1 (“ND/ND”), 52% (n=260) had changes from D at T0 to ND at T1 (“D/ND”), 12% (n=60) had at least a 50% decrease from T0 to T1 (“decrease”) and 9% (n=45) had an increase or a less pronounced decrease in ctDNA. In a univariate analysis, patients with ND/ND and D/ND were associated with improved OS compared to the decrease group. In addition to other characteristics, patients with max VAF ≤0.5% or ND at T0 (n=214, 43%) had improved OS (HR=0.44, P 〈 0.001) compared to those with max VAF 〉 0.5% at T0 (n=287, 57%). Conclusions: In a retrospective aggregate analysis of 8 CT, ND ctDNA at T1 was associated with improved OS in patients with aNSCLC treated with TKI. Changes in ctDNA levels, particularly from D to ND, may provide an early indication of treatment benefit and predict long-term outcomes in this population. Additional ctMoniTR analyses are ongoing to validate the potential use of ctDNA as an early endpoint.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2023.41.16_suppl.3030
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2023
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  • 6
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    Landscape and Clonal Dominance of Co-occurring Genomic Alterations in Non–Small-Cell Lung Cancer Harboring MET Exon 14 Skipping
    American Society of Clinical Oncology (ASCO) ; 2021
    In:  JCO Precision Oncology , No. 5 ( 2021-11), p. 1802-1812
    Details
    In: JCO Precision Oncology, American Society of Clinical Oncology (ASCO), , No. 5 ( 2021-11), p. 1802-1812
    Abstract: MET exon 14 skipping alterations ( METex14) comprise a diverse set of actionable oncogene drivers in non–small-cell lung cancer (NSCLC). Recent studies have established the efficacy of tyrosine kinase inhibitors for this patient population. The landscape of co-occurring genetic alterations in METex14 NSCLC and their potential impact to therapeutic sensitivities has not yet been fully described. MATERIALS AND METHODS METex14 NSCLC cases were collected from three cohorts: the VISION trial, and data sets from Guardant360 and GenePlus. Clinicopathologic characteristics and METex14 mutation sites were analyzed and compared across data sets. Co-occurring genetic alterations and the clonality relationships to METex14 were evaluated. RESULTS Of 40,824 NSCLCs, 692 METex14 cases (1.7%) were identified, including 332 in Guardant360, 188 in VISION, and 172 in GenePlus. The demographics and mutation type and/or sites were similar in the Asian versus Western cohorts. MET amplification, which were found to be associated with sensitivity to MET kinase inhibitors, co-occurs in 7.6%-13.8% of cases, whereas kinase domain secondary mutation of MET co-occurs in 5%-6%. When co-occurring with METex14, EGFR mutations were often identified as the dominant clone (78%, 7 of 9), whereas when co-occurring, METex14 (39%, 7 of 18) and KRAS (44%, 8 of 18) had similar rates of clonal dominance. PIK3CA and PTEN mutations were almost always subclones (89%, 16 of 18) to METex14. Moreover, RET-CCDC6 fusion and EGFR mutation were detected following crizotinib treatment in two patients, suggesting novel mechanisms of resistance. CONCLUSION METex14 mutations frequently co-occur with other potential driver oncogenes with differing patterns of clonal dominance observed among the drivers. This cellular context can provide insights into whether METex14 is acting as a primary oncogenic driver or resistance mechanism and help guide treatment choices.
    Type of Medium: Online Resource
    ISSN: 2473-4284
    URL: Article
    DOI: 10.1200/PO.21.00135
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2021
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  • 7
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    Clinical response to tepotinib according to circulating tumor (ct) DNA biomarkers in patients with advanced NSCLC with high-level MET amplification ( MET amp) detected by liquid biopsy (LBx).
    American Society of Clinical Oncology (ASCO) ; 2022
    In:  Journal of Clinical Oncology Vol. 40, No. 16_suppl ( 2022-06-01), p. 9121-9121
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 40, No. 16_suppl ( 2022-06-01), p. 9121-9121
    Abstract: 9121 Background: Tepotinib, a potent, highly selective, oral, MET inhibitor, showed meaningful activity in patients (pts) with NSCLC with high-level METamp by LBx in VISION. Exploratory biomarker analyses are presented herein. Methods: Pts had 0–2 prior therapy lines, high-level METamp by LBx (Guardant360; MET copy number ≥2.5), and no MET exon 14 skipping or EGFR/ ALK alterations. Pts received tepotinib 500 mg once daily (450 mg active moiety). Primary endpoint was objective response by independent review; data cut-off: Aug 20, 2021. Exploratory biomarker analysis included LBx at baseline (BL), on treatment, and end of treatment (EOT). Early molecular response (eMR) was defined as undetectable METamp 6–8 weeks on treatment. Results: 24 pts were enrolled (median age: 63.4 years [yrs]; smokers: 88%; ECOG PS 1: 88%; adenocarcinoma: 67%). Treatment duration was ≥1 yr in five pts and ≥2 yrs in two pts (both ongoing). Overall, objective response rate (ORR) was 41.7% (95% CI: 22.1, 63.4). Treatment-naïve pts (n=7) had an ORR of 71.4% (29.0, 96.3), median (m) DOR was 14.3 months (2.8, not estimable [ne] ), and mPFS was 15.6 months (1.4, ne). BL biomarker analyses according to clinical benefit (CR/PR/SD [n=11] vs PD/NE [n=13] ) showed association with better outcomes in pts with focal METamp, or without MYCamp or RB1 mutation (Table). MYCamp/ RB1 mutation was detected in 4/7 pts with neuroendocrine/not otherwise specified histology; MYCamp in 2/3 pts with neuroendocrine histology. Low BL ctDNA mutant allele frequency (MAF) was associated with better outcomes. 14 pts had eMRs (ORR 71.4%); persistent METamp (n=4) was associated with lack of clinical response. 2/9 pts with EOT biomarker profiles had emerging resistance mechanisms (MET kinase domain mutations Y1230 and D1228); both had METamp re-emergence. Treatment-related adverse events included edema (composite term; any grade: 46%; Grade 3: 13%) and constipation (any grade: 17%; Grade ≥3: 0%). Conclusions: Tepotinib showed meaningful activity, especially in first line, in the first trial of a MET inhibitor in EGFR WT NSCLC with high-level METamp to enroll based on a convenient LBx assay. BL biomarker analyses indicated focal METamp, MYC/RB1 WT, and low ctDNA MAF were associated with improved outcomes. Serial LBx could monitor molecular response and evaluate resistance. Clinical trial information: NCT02864992. [Table: see text]
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2022.40.16_suppl.9121
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2022
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  • 8
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    Molecular Classification Substitutes for the Prognostic Variables Stage, Age, and MYCN Status in Neuroblastoma Risk Assessment
    Elsevier BV ; 2017
    In:  Neoplasia Vol. 19, No. 12 ( 2017-12), p. 982-990
    Details
    In: Neoplasia, Elsevier BV, Vol. 19, No. 12 ( 2017-12), p. 982-990
    Type of Medium: Online Resource
    ISSN: 1476-5586
    URL: Article
    DOI: 10.1016/j.neo.2017.09.006
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
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  • 9
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    A distinct human NKp30+FcɛRIγ+CD8+ T cell population exhibiting high NK-like anti-tumor potential
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 200, No. 1_Supplement ( 2018-05-01), p. 124.6-124.6
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 200, No. 1_Supplement ( 2018-05-01), p. 124.6-124.6
    Abstract: CD8+ T cells are considered prototypical cells of adaptive immunity. Here, we uncovered a distinct CD8+ T cell population, expressing the activating NK receptor, NKp30, in peripheral blood of healthy individuals. We revealed that IL-15 could de novo induce NKp30 expression in a population of CD8+ T cells, and further drive their differentiation towards a broad innate transcriptional landscape. The adapter FcɛRIγ was concomitantly induced, and shown to be crucial to enable NKp30 cell surface expression and function in CD8+ T cells. FcɛRIγ de novo expression required promoter demethylation and was accompanied by the acquisition of the signaling molecule Syk and the “innate” transcription factor PLZF. IL-15-induced NKp30+CD8+ T cells exhibited high NK-like anti-tumor activity in vitro, able to synergize with TCR-signaling. Importantly, this population potently controlled tumor growth in a preclinical xenograft mouse model. Our study, while blurring borders between innate and adaptive, reveals a unique NKp30+FcɛRIγ+CD8+ T cell population with high anti-tumor therapeutic potential.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.200.Supp.124.6
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
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  • 10
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    The genomic and transcriptional landscape of primary central nervous system lymphoma
    Springer Science and Business Media LLC ; 2022
    In:  Nature Communications Vol. 13, No. 1 ( 2022-05-10)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2022-05-10)
    Abstract: Primary lymphomas of the central nervous system (PCNSL) are mainly diffuse large B-cell lymphomas (DLBCLs) confined to the central nervous system (CNS). Molecular drivers of PCNSL have not been fully elucidated. Here, we profile and compare the whole-genome and transcriptome landscape of 51 CNS lymphomas (CNSL) to 39 follicular lymphoma and 36 DLBCL cases outside the CNS. We find recurrent mutations in JAK-STAT, NFkB, and B-cell receptor signaling pathways, including hallmark mutations in MYD88 L265P (67%) and CD79B (63%), and CDKN2A deletions (83%). PCNSLs exhibit significantly more focal deletions of HLA-D (6p21) locus as a potential mechanism of immune evasion. Mutational signatures correlating with DNA replication and mitosis are significantly enriched in PCNSL. TERT gene expression is significantly higher in PCNSL compared to activated B-cell (ABC)-DLBCL. Transcriptome analysis clearly distinguishes PCNSL and systemic DLBCL into distinct molecular subtypes. Epstein-Barr virus (EBV)+ CNSL cases lack recurrent mutational hotspots apart from IG and HLA-DRB loci. We show that PCNSL can be clearly distinguished from DLBCL, having distinct expression profiles, IG expression and translocation patterns, as well as specific combinations of genetic alterations.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-022-30050-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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