Reiner Siebert
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View article: Towards a WHO classification of genetic tumour syndromes
Towards a WHO classification of genetic tumour syndromes Open
Almost 70 years ago, the World Health Organization (WHO) decided to propose a “Classification of Tumours”. Since then, a systematic and extensive classification system for tumours has been continuously developed in successive editions and …
View article: Mosaicism in genetic tumour syndromes
Mosaicism in genetic tumour syndromes Open
Inherited pathogenic variants in a series of cancer-associated genes cause monogenic genetic tumour syndromes (GTS). Nevertheless, in a subset of tumour-predisposed individuals, such variants have not been inherited through the germline bu…
View article: Divergent molecular pathways drive monomorphic epitheliotropic and enteropathy-associated intestinal T-cell lymphoma
Divergent molecular pathways drive monomorphic epitheliotropic and enteropathy-associated intestinal T-cell lymphoma Open
Enteropathy-associated intestinal T-cell lymphoma (EATL) and monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL) have distinctive clinical context, morphology, and immunophenotype. To characterize their genetic and molecular spe…
View article: Malignant Rhabdoid Tumors of the Liver Are Associated With Inferior Outcomes Compared to Other Extracranial Rhabdoid Tumors
Malignant Rhabdoid Tumors of the Liver Are Associated With Inferior Outcomes Compared to Other Extracranial Rhabdoid Tumors Open
Background Extracranial malignant rhabdoid tumors (eMRT) are rare, highly aggressive pediatric neoplasms. While the liver is a relatively common anatomic site of presentation, the clinical course of patients with hepatic eMRT (eMRT‐L) is n…
View article: <scp><i>APC</i></scp>‐related multiple salivary gland lesions: spatial transcriptomic analysis reveals progressive <scp>WNT</scp> activation
<span><i>APC</i></span>‐related multiple salivary gland lesions: spatial transcriptomic analysis reveals progressive <span>WNT</span> activation Open
Attenuated familial adenomatous polyposis (AFAP) is a disorder caused by germline pathogenic variants in APC and is characterized by the presence of <100 colonic polyps and a high lifetime risk of developing colorectal cancer. Salivary gla…
View article: Supplementary Table S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
RAG1/2 levels, IGK/LV gene rearrangements, IGH dependency and sensitivity to inhibitors of BCR signaling, in HGBCL-DH-BCL2(-BCL6) primary specimens and cell lines.
View article: Supplementary Table S2 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S2 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Bulk and spatial gene expression data of MYC and BCL2 dual expressor DLBCL and HGBCL-DH-BCL2 (-BCL6).
View article: Supplementary figure S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
AID expression in IGH+ and IGHUND HGBCL-DH-BCL2
View article: Supplementary Table S1 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S1 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
DLBCL cases included in the study.
View article: Supplementary figure S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
IGG transcript a protein analyses in HGBCL-DH-BCL2(-BCL6) cell lines and HEK293T cells before and after complementation with IG expression vectors
View article: Supplementary Table S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
IGH and CD79B expression and interaction in HGBCL-DH-BCL2(-BCL6), and relation to follicular lymphoma.
View article: Supplementary figure S2 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S2 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Transcriptional programs of IGH+ and IGHUND HGBCL-DH-BCL2
View article: Supplementary figure S1 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S1 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
IGH shutdown in DLBCL
View article: Supplementary Table S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Non synonymus SNVs, IGHV gene rearrangements, AID expression status and N-glycosylation motifs in IGHV domains of HGBCL-DH-BCL2(-BCL6).
View article: Supplementary figure S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
IGH cytogenetics, RAG1/2 expression and IG light chain V gene editing in HGBCL-DH-BCL2(-BCL6)
View article: Supplementary figure S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S4 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
IGH and CD79B expression, complex formation and IGH isotype choice in DLBCL and HGBCL-DH-BCL2
View article: Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
List of tools and reagents.
View article: Supplementary figure S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Cytogenetic of COH-DHL1 and COH-THL1 HGBCL-DH-BCL2(-BCL6) cell line models (A-D); In vivo secondary Ighv gene rearrangements in BCR-less murine lambda-MYC lymphomas (E-J)
View article: Supplementary Table S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Configuration of IGH, MYC and BCL2 loci in HGBCL-DH-BCL2(-BCL6) and RAG1/2 involvement in t(8;22).
View article: Supplementary figure S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
AID expression in IGH+ and IGHUND HGBCL-DH-BCL2
View article: Supplementary Table S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Configuration of IGH, MYC and BCL2 loci in HGBCL-DH-BCL2(-BCL6) and RAG1/2 involvement in t(8;22).
View article: Supplementary Table S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S3 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Non synonymus SNVs, IGHV gene rearrangements, AID expression status and N-glycosylation motifs in IGHV domains of HGBCL-DH-BCL2(-BCL6).
View article: Supplementary figure S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S5 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
IGH cytogenetics, RAG1/2 expression and IG light chain V gene editing in HGBCL-DH-BCL2(-BCL6)
View article: Supplementary figure S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary figure S6 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
Cytogenetic of COH-DHL1 and COH-THL1 HGBCL-DH-BCL2(-BCL6) cell line models (A-D); In vivo secondary Ighv gene rearrangements in BCR-less murine lambda-MYC lymphomas (E-J)
View article: Data from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Data from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
The B-cell receptor (BCR) is critical for mature B-cell lymphomas (BCL), serving as a therapeutic target. We show that high-grade BCLs with MYC and BCL2 rearrangements [HGBCL–double-hit (DH)–BCL2] predominantly exhibit immunoglobulin heavy…
View article: Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements
Supplementary Table S7 from B-cell Receptor Silencing Reveals the Origin and Dependencies of High-Grade B-cell Lymphomas with <i>MYC</i> and <i>BCL2</i> Rearrangements Open
List of tools and reagents.