Osteoblastic bone metastasis with unusual synthesis of trabeculae in the bone marrow space: A case report with a node-strut analysis

2000 ◽  
Vol 18 (4) ◽  
pp. 223-225 ◽  
Author(s):  
Katsumitsu Arai ◽  
Tatsuhiko Tanizawa
Author(s):  
Christian Ulm ◽  
Georg D. Strbac ◽  
Andreas Stavropoulos ◽  
Azadeh Esfandeyari ◽  
Toni Dobsak ◽  
...  

Author(s):  
Chuan-yi Hu ◽  
Juan Chen ◽  
Xin-hua Qin ◽  
Pan You ◽  
Jie Ma ◽  
...  

Abstract Background Bone metastasis is the leading cause of mortality and reduced quality of life in patients with metastatic prostate cancer (PCa). Long non-coding RNA activated by DNA damage (NORAD) has been observed to have an abnormal expression in various cancers. This article aimed to explore the molecular mechanism underlying the regulatory role of NORAD in bone metastasis of PCa. Methods NORAD expression in clinical PCa tissues and cell lines was detected with the application of qRT-PCR. Cancer cells were then transfected with plasmids expressing NORAD, after which Transwell assay and CCK-8 assay were carried out to detect proliferation, migration, and bone metastasis of PCa. NORAD downstream target molecules were screened through bioinformatics analysis, followed by further verification using dual luciferase assay. Extracellular vesicles (EVs) were labeled with PKH67 and interacted with bone marrow stromal cells. The gain- and loss-function method was applied to determine the internalization and secretion of PCa cells-derived EVs under the intervention of downstream target molecules or NORAD. Results PCa tissues and cell lines were observed to have a high expression of NORAD, particularly in tissues with bone metastasis. NORAD knockdown resulted in reduced secretion and internalization of EVs, and suppressed proliferation, migration, and bone metastasis of PCa cells. It was indicated that NORAD interacted with miR-541-3p, leading to the upregulation of PKM2. Forced expression of PKM2 promoted the transfer of PKH67-labeled EVs to bone marrow stromal cells. Conclusions NORAD might serve as a ceRNA of miR-541-3p to promote PKM2 expression, thereby enhancing the development of bone metastasis in PCa by promoting internalization and transfer of EVs of cancer cells, providing an insight into a novel treatment for the disorder.


2021 ◽  
Author(s):  
Kenta Yoshida ◽  
Takao Oyama ◽  
Takenori Takahata ◽  
Sae Kudo ◽  
Yuki Sato ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Samin Alavi ◽  
Maryam Ebadi ◽  
Alireza Jenabzadeh ◽  
M. T. Arzanian ◽  
Sh. Shamsian

Herein, the first case of childhood erythrophagocytosis following chemotherapy for erythroleukemia in a child with monosomy 7 is reported. A 5-year-old boy presented with anemia, thrombocytopenia, and hepatosplenomegaly in whom erythroleukemia was diagnosed. Prolonged pancytopenia accompanied by persistent fever and huge splenomegaly and hepatomegaly became evident after 2 courses of chemotherapy. On bone marrow aspiration, macrophages phagocytosing erythroid precursors were observed and the diagnosis of HLH was established; additionally, monosomy 7 was detected on bone marrow cytogenetic examination. In conclusion, monosomy 7 can lead to erythrophagocytosis associated with erythroid leukemia and should be considered among the chromosomal abnormalities contributing to the association.


2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Pankit Vachhani ◽  
Prithviraj Bose

Myeloid sarcoma represents the proliferation of myeloblasts of acute myeloid leukemia (AML) at extramedullary sites. While extramedullary involvement in AML is uncommon in itself, isolated myeloid sarcomas, that is, myeloid sarcomas without any bone marrow involvement, are extremely rare and pose a diagnostic and therapeutic challenge. Here, we present the case of a middle-aged woman with isolated myeloid sarcoma in the stomach—an organ seldom involved by this disease. Additionally, the literature on the epidemiology, diagnosis, pathology, prognosis, and therapeutic options in myeloid sarcomas has been reviewed.


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