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Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis [bulkRNA-seq]

ABSTRACT: Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis [bulkRNA-seq]

PROVIDER: PRJNA1021159 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26176164_1.fastq.gz	Fastqsanger.gz
	SRR26176164_2.fastq.gz	Fastqsanger.gz
	SRR26176165_1.fastq.gz	Fastqsanger.gz
	SRR26176165_2.fastq.gz	Fastqsanger.gz
	SRR26176166_1.fastq.gz	Fastqsanger.gz

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Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis [bulkRNA-seq]

Project description:The RVd therapy, combining lenalidomide, bortezomib, and dexamethasone, is a mainstay treatment for multiple myeloma, typically eliciting immune activation and myeloma cell clearance, alleviating anemia and associated symptoms. In a unique multiple myeloma case, the patient developed pure red cell aplasia (PRCA) following RVd treatment, despite the absence of common PRCA triggers. In vitro analyses revealed severe erythropoiesis impairment in this patient, with lenalidomide emerging as a pivotal disruptor of erythroid development, potentially driving PRCA. Single-cell transcriptome analysis unveiled a notable increase in hyperactive cluster of differentiation (CD)8+ T cells in the patient's bone marrow. The few remaining erythroid progenitors in the patient's bone marrow exhibited developmental dysfunction and immune-related pathway activation. Unexpectedly, these erythroid cells displayed abnormally high expression of major histocompatibility class I (MHCI). Functional assays demonstrated that the addition of lenalidomide further augmented MHCI expression in the patient's erythroid progenitors. Drug-induced increases in antigen presentation by immune erythrocytes emerged as the potential driving force behind hyperactive T cell attacks and subsequent development of PRCA. This study not only elucidates the mechanism underlying lenalidomide-induced PRCA in this rare case, but also underscore the importance of considering the MHCI gene in erythroid cells during clinical trials and drug administration.

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Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis

Project description:Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis

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Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis [scRNA-seq]

Project description:Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis [scRNA-seq]

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Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis [scRNA-seq]

2025-02-28 | GSE244044 | GEO

Lenalidomide-induced pure red cell aplasia analysis

Project description:The RVd therapy, combining lenalidomide, bortezomib, and dexamethasone, is a mainstay treatment for multiple myeloma. A multiple myeloma patient developed pure red cell aplasia (PRCA) following RVd treatment, despite the absence of common PRCA triggers. In vitro analyses revealed lenalidomide as a pivotal disruptor of erythropoiesis. Single-cell transcriptome analysis unveiled hyperactive CD8+ T cells and impaired erythropoiesis in the patient's bone marrow. Unexpectedly, the patient's erythroid cells displayed abnormally high expression of genes in the antigen presentation pathway, particularly those for major histocompatibility class I (MHC-I) molecules. Functional assays demonstrated that lenalidomide treatment further augmented MHC-I expression in the patient's erythroid cells. Blocking MHC-I or depleting T cells alleviate the defective erythropoiesis of PRCA, suggesting that the interaction between erythroid cells with elevated MHC-I and T cells in the bone marrow might contribute to PRCA. Taken together, our study revealed a novel mechanism underlying lenalidomide-induced PRCA in treating cancer patients.

2024-09-03 | PXD055495 |

Lenalidomide-induced pure red cell aplasia: clinical characteristics and mechanistic analysis

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

2025-02-28 | GSE244045 | GEO

Secondary pure red cell aplasia in multiple myeloma treated with lenalidomide.

Project description:Pure red cell aplasia (PRCA) is a rare disorder characterized by marked erythroid hypoplasia with maturation arrest in the bone marrow. Secondary acquired PRCA may be associated with hematologic disorders. A few case reports have described PRCA associated with multiple myeloma (MM). However, the clinical course and mechanism of PRCA associated with MM remain unknown. We herein report two cases of PRCA associated with MM in patients undergoing treatment with lenalidomide.

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Protein composition of the extracellular matrix in idiopathic germ cell aplasia

Project description:The somatic microenvironment supports spermatogonial stem cell differentiation into sperm. Extracellular matrix (ECM) plays multiple roles in the stem cell niche, including self-renewal, proliferation, differentiation and survival of spermatogonial cells. The pathophysiology of male infertility might be representative of a progressive degenerative process of the testicular tissue, including ECM, rather than a defective genetic background, thus outlining the existence of chronic etiological agents/pathways. In this context, we sought to identify potential causative factors responsible for a number of modifications of the testicular somatic microenvironment associated with idiopathic germ cell aplasia in human beings. Proteomic analysis of the decellularized ECM was performed to study testis parenchyma from 10 idiopathic non-obstructive azoospermic (iNOA) men, dichotomized according to positive sperm retrieval versus germ cell aplasia. Germ cell aplasia was characterized by an increased nuclear distribution of the retinoic acid receptor in Sertoli cells which was associated with decreased expression of the ECM markers, Nidogen-2 and Heparan sulfate proteoglycan-2. Decreased levels of the interstitial matrisome associated Factor IX and its regulator VKORC1 were instead coupled with decreased signaling of vitamin K in Leydig cells. This study identified pathogenetic signature of the somatic testicular microenvironment and provide mechanistic insights into the molecular determinants of human idiopathic germ cell aplasia.

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Lenalidomide-induced pure red cell aplasia is associated with elevated expression of MHC-I molecules on erythrocytes.

Project description:The RVd therapy, combining lenalidomide, bortezomib, and dexamethasone, is a mainstay treatment for multiple myeloma. A multiple myeloma patient developed pure red cell aplasia (PRCA) following RVd treatment, despite the absence of common PRCA triggers. In vitro analyses reveal lenalidomide as a pivotal disruptor of erythropoiesis. Single-cell transcriptome analysis unveils hyperactive CD8+ T cells and impaired erythropoiesis in the patient's bone marrow. Unexpectedly, the patient's erythroid cells display abnormally high expression of genes in the antigen presentation pathway, particularly those for major histocompatibility class I (MHC-I) molecules. Functional assays demonstrate that lenalidomide treatment further augmented MHC-I expression in the patient's erythroid cells. Blocking MHC-I or depleting T cells alleviates the defective erythropoiesis of PRCA, suggesting that the interaction between erythroid cells with elevated MHC-I and T cells in the bone marrow might contribute to PRCA. Taken together, our study implicates a mechanism underlying lenalidomide-induced PRCA in treating cancer patients.

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