We evaluated the immunohistochemical profile and specificity of CD138 reactivity in 238 specimens from hematopoietic and nonhematopoietic neoplasms. In 91 bone marrow biopsies, CD138 reactivity was observed for nonneoplastic plasma cells, neoplastic plasma cells in multiple myeloma cases (43/43), and the plasmacytic component in lymphoplasmacytic lymphoma cases (4/4). Stromal reactivity was noted in 7 multiple myeloma cases. Of 9 bone marrow specimens involved by metastatic carcinoma, tumor cells were CD138+ in 5 cases; stromal reactivity was noted in 7 cases. Studies of 76 nodal and extranodal lymphomas (B-cell, 49; T-cell, 8; Hodgkin lymphoma, 19), 1 Langerhans cell histiocytosis, and 14 nonneoplastic lymph nodes revealed CD138 reactivity only for nonneoplastic plasma cells, the neoplastic cells of 2 large B-cell lymphomas (immunoblastic type, plasmacytoid features), and the clonal plasmacytic component of 3 of 3 extranodal and 1 nodal marginal zone lymphoma. Evaluation of 56 epithelial and nonepithelial tumors revealed CD138 positivity for neoplastic cells of carcinomas of various types (30/33), frequently with associated stromal reactivity, and for neoplasms of mesenchymal, melanocytic, and other tumor types (12/23). Within the hematopoietic system, CD138 is an excellent marker of plasmacytic differentiation. Based on its broad staining profile, CD138 reactivity for neoplastic cells is not a definitive marker for plasmacytic derivation, unless a hematolymphoid origin has been established.
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http://dx.doi.org/10.1309/617D-WB5G-NFWX-HW4L | DOI Listing |
Platelets
December 2024
Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Karolinska Institutet, Stockholm, Sweden.
Drugs blocking the renin-angiotensin-aldosterone system may offer benefit on endothelial function, inflammation, and hemostasis in addition to the effects of reducing blood pressure. We have shown antithrombin effects by treatment with the angiotensin converting enzyme (ACE) inhibitor ramipril. As thrombin is a key inducer of platelet aggregation, we hypothesized that treatment with ramipril could modulate platelet reactivity and endothelial glycocalyx (eGCX) function.
View Article and Find Full Text PDFCancer Lett
December 2024
Shandong Provincial Key Laboratory of Precision Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, 250117, China. Electronic address:
Bone marrow stromal cells (BMSCs) are vital for preventing chemotherapy induced apoptosis of multiple myeloma (MM), but roles and machinery in other forms of cell death have not been well elucidated. Here, using an in vitro BMSC-MM interacting model, we observed BMSCs protected MM cells from labile iron pool (LIP) and reactive oxygen species (ROS) triggered ferroptosis by elevating glutathione peroxidase 4 (GPX4). Mechanistically, direct interaction with BMSCs upregulated the expression of SUMO-specific protease 3 (SENP3) in MM cells through CD40/CD40L signaling pathway, and SENP3 de-conjugated SUMO2 at lysine 75 residue to stabilize GPX4 protein, thereby consuming ROS to obviate ferroptosis in MM cells from the Vk∗MYC mouse model, as well as in CD138B220 cells separated from the Cd40l;Prx1 mice (CD40-CKO) and Sumo2 knock out (SUMO2-KO) mice.
View Article and Find Full Text PDFJ Inflamm Res
November 2024
Emergency Medical Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, People's Republic of China.
Objective: To evaluate and predict adverse outcomes associated with serum Syndecan-1 (SYN-1) levels in patients with early sepsis, and to explore the prognostic risk factors in sepsis and septic shock.
Methods: This retrospective single-center observational study included 168 sepsis patients admitted to the Emergency Department of Beijing Chao-Yang Hospital Shijingshan Branch, Capital Medical University, from October 2020 to October 2021. Patients were categorized into sepsis (n=114) and septic shock (n=54) groups based on Sepsis 3.
Kidney Int Rep
November 2024
Universite Paris Est Creteil, INSERM IMRB U955, Créteil, France.
Microvasc Res
January 2025
Institute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China; International Center of Microvascular Medicine, Chinese Academy of Medical Sciences, Beijing 100005, China. Electronic address:
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