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Articles by Gregor Hoermann
MDS without clonal marker: when depth outperforms breadth
Myelodysplastic neoplasms (MDS) are a heterogeneous group of clonal myeloid neoplasms. The interplay of mutations shapes disease phenotype, progression, and response to therapy, highlighting clonal hematopoiesis (CH) as a central feature of MDS biology. However, in around 10–20% of MDS patients no clonal aberrations are found by standard diagnostic workup [1,2,3].
Multiple myeloma with concomitant chronic lymphocytic leukemia: evidence for independent clonal origin
Multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) are hematologic malignancies originating from different stages during B-cell development. While MM affects the final stage of B-cell differentiation and is characterized by proliferation of monoclonal plasma cells (PC) in the bone marrow (BM) [1], CLL involves mature naïve B-cells or memory B-cells that have not become differentiated PC and that accumulate in blood, BM, and secondary lymphoid tissues [2].
Two ways to complex karyotype in MDS—the role of del(5q) and TP53 - Blood Cancer Journal
Dear Editor, Myelodysplastic neoplasms (MDS) are defined as clonal hematopoietic stem cell neoplasms characterized by cytopenias and morphological dysplasia, and ineffective hematopoiesis with an increased risk of leukemic transformation [1]. In addition, MDS are very heterogeneous with respect to their underlying genetic landscape encompassing also cytogenetic abnormalities [2].
Relevance of blast counts for genetic subclassification in MDS - Leukemia
To the Editor: We read the paper by Al Amri et al. on the independent prognostic significance of blast count in a large cohort of patients with myelodysplastic neoplasms (MDS) with great interest [1].
Parallel genomic analysis from paired bone marrow and peripheral blood samples of 200 cytopenic patients - Leukemia
To the Editor: Bone marrow (BM) analysis is required for morphological and genetic assessment in patients evaluated for myelodysplastic neoplasms (MDS) and thus currently represents the gold standard in patients with unexplainable cytopenia [1, 2].
Genomic landscape of CCUS compared to MDS and its implications on risk prediction - Leukemia
To the Editor: The 5th edition of the WHO classification (WHO HAEM5) newly included myeloid precursor lesions introducing clonal cytopenia of undetermined significance (CCUS) as an entity [1]. CCUS is defined as clonal hematopoiesis (CH) in the presence of unexplained, persistent cytopenia requiring detection of either somatic mutations in certain genes or clonal chromosomal abnormalities. Discriminating CCUS from MDS primarily relies on morphologic bone marrow (BM) dysplasia.
CAR virus receptor mediates erythroid differentiation and migration and is downregulated in MDS - Leukemia
Abstract Myelodysplastic syndromes (MDS) are myeloid neoplasms presenting with dysplasia in the bone marrow (BM) and peripheral cytopenia. In most patients anemia develops. We screened for genes that are expressed abnormally in erythroid progenitor cells (EP) and contribute to the pathogenesis of MDS. We found that the Coxsackie-Adenovirus receptor (CAR = CXADR) is markedly downregulated in CD45low/CD105+ EP in MDS patients compared to control EP.
This paper is only available as a PDF. To read, Please Download here. Abstract Mast cell (MC) neoplasms are an emerging challenge in the fields of internal medicine, allergy, immunology, dermatology, laboratory medicine and pathology. In this review, we discuss the current standards for the diagnosis and prognostication of MC neoplasms with special reference to clinically relevant germline and somatic gene variants.
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