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Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity [array]

ABSTRACT: We tested the relationship between IgH subclone diversity in B-ALL and the number of resolved chromosomal breaks as assessed by chromosome microarray analysis (CMA).

ORGANISM(S): Homo sapiens

PROVIDER: GSE201170 | GEO | 2025/04/08

REPOSITORIES: GEO

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Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity [sequencing]

Project description:It remains unclear whether the variable biologic features of B-lymphoblastic leukemia (B-ALL) reflect distinct cells of origin in the hierarchy of early B cell development. Recombination activating genes (RAG) 1 and 2 rearrange the immunoglobulin heavy chain (IgH) locus in B lymphoid progenitors, resulting in unique variable (Vh), diversity (D), and joining (Jh) gene rearrangements. To test whether discrete properties of each B-ALL reflect derivation from distinct developmental B cell stages, we assessed the relationship between IgH variable gene (IGHV) characteristics and gene expression. Using targeted, pre-treatment IgH sequencing of 22 patients’ B-ALL, we discovered 2 distinct groups: leukemias with RAG-mediated intra-clonal IGHV sequence diversification (‘diverse’; N=9, 40.9%) and those lacking diversity (‘homogeneous’; N=10, 45.5%). Three patients (13.6%) lacked a dominant IgH sequence. In the ‘diverse’ cohort, we observed extensive subclone evolution arising from Vh gene recombination after neoplastic transformation (median: 482 subclones; range 2-2600). In the ‘homogeneous’ cohort, all IgH clones lacked subclone evolution. The ‘diverse’ cohort demonstrated enriched expression of genes associated with regulation of a hematopoietic stem cell state, while ‘homogeneous’ cases showed enriched expression of genes involving cell fate commitment. Furthermore, distinct IgH clonotypes within a single patient could be individually diverse or homogenous. Single cell analysis indicated that within a single patient, only occasional IgH clonotypes were expressed; IGHV-expressing leukemia cells were characterized by distinctive phenotypes including RAG1 pathway up-expression. In summary, pre-treatment IgH composition reflects the B cell stage at leukemic initiation and provides insights about the biologic mechanisms of genetic diversity in B-ALL.

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Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity

Project description:This SuperSeries is composed of the SubSeries listed below.

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Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity

Project description:Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity

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Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity [array]

Project description:Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity [array]

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Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity [sequencing]

Project description:Biologic characteristics of B-lymphoblastic leukemia correspond to immunoglobulin gene diversity [sequencing]

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Ultrasonographic characteristics, genetic features, and maternal and fetal outcomes in fetuses with omphalocele: a single tertiary center experience

Project description:Routine karyotyping combined with CMA testing should be provided for fetuses with omphalocele. WES is an option if karyotype and CMA tests are normal. In addition, if conventional karyotype, CMA detection and WES detection are normal, then further molecular biology methods can be used to rule out disease phenotypes like BWS syndrome. We analyzed the ultrasonographic features, genetic characteristics, and maternal and fetal outcomes of fetuses with omphalocele and provide a reference for perinatal management of such cases.

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PTIP promotes chromatin changes critical for immunoglobulin class switch recombination

Project description:Programmed genetic rearrangements in lymphocytes require transcription at antigen receptor genes to promote accessibility for initiating double-strand break (DSB) formation critical for DNA recombination and repair. Here we show that activated B cells deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3) /MLL4 complex display impaired histone methylation (H3K4me3) and transcription initiation of downstream switch regions at the immunoglobulin heavy-chain (Igh) locus leading to defective immunoglobulin class-switching. We also show that PTIP accumulation at DSBs contributes to class-switch recombination (CSR) and genome stability independently from Igh switch transcription. These results demonstrate that PTIP promotes specific chromatin changes that control the accessibility of the Igh locus to CSR, and suggest a non-redundant role for the MLL3/MLL4 complex in altering antibody effector function. Genome-wide analysis of histone modifications, PTIP, and Pol II in PTIP-WT and PTIP-KO mouse activated B cells.

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The Chromatin Reader ZMYND8 Regulates Igh Enhancers to Promote Immunoglobulin Class Switch Recombination

Project description:Class Switch Recombination (CSR) is a DNA recombination reaction that diversifies the effector component of antibody responses. CSR is initiated by activation-induced cytidine deaminase (AID), which targets transcriptionally active immunoglobulin heavy chain (Igh) switch donor and acceptor DNA. The 3’ Igh super-enhancer, 3’ Regulatory Region (3’RR), is essential for acceptor region transcription, but how this function is regulated is unknown. Here we identify the chromatin reader ZMYND8 as an essential regulator of the 3’RR and CSR. In B cells, ZMYND8 binds promoters and super-enhancers, including the 3’RR, and controls its activity by modulating the enhancer transcriptional status. In its absence, there is increased 3’RR polymerase loading, and decreased acceptor region transcription and CSR. In addition to CSR, ZMYND8 deficiency impairs somatic hypermutation (SHM) of Igh, which is also dependent on the 3’RR. Thus ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 3’ Igh super-enhancer.

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Deciphering the importance of the palindromic architecture of the immunoglobulin heavy chain 3â?? regulatory region.

Project description:The IgH 3â?? regulatory region (3â??RR) controls class switch recombination (CSR) and somatic hypermutation (SHM) in B cells. The mouse 3â??RR contains four enhancer elements with hs1,2 flanked by inverted repeated sequences and the center of a 25-kb palindrome bounded by two hs3 enhancer inverted copies (hs3a and hs3b). hs4 lies downstream of the palindrome. Evolution maintained in mammals this unique palindromic arrangement suggesting that it is functionally significant. We report that deconstructing the palindromic IgH 3â??RR strongly impacts its function even when enhancers are preserved. CSR and IgH transcription appear poorly dependent from the 3â??RR architecture and are more or less preserved provided 3â??RR enhancers are present. By contrast, an â??architectural effectâ?? significantly lowers VH germline transcription, AID recruitment and SHM. In conclusion, this work indicates that the IgH 3â??RR does not simply pile up enhancer units but also optimally expose them into a functional architecture of crucial importance. RNAseq analysis of B-cell splenocytes with (S=stimulated) or without (R=resting) LPS activation from wt, delta2leftPAL, and deltaIRIS mice.

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