The usefulness of bone-marrow scintigraphy in the detection of bone metastasis from prostatic cancer

1985 ◽  
Vol 11 (8) ◽  
pp. 319-322 ◽  
Author(s):  
Nobuaki Otsuka ◽  
Masao Fukunaga ◽  
Teruki Sone ◽  
Masaya Yoneda ◽  
Noriaki Saito ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Metastasis ◽  
Prostatic Cancer ◽  
Bone Marrow Scintigraphy

99mTc-Nanocolloid Bone Marrow Scintigraphy in Prostatic Cancer

1989 ◽  
Vol 63 (5) ◽  
pp. 497-502 ◽  
Author(s):  
G. HADDOCK ◽  
H. W. GRAY ◽  
J. H. McKILLOP ◽  
R. G. BESSENT ◽  
D. KIRK
Keyword(s):  
Bone Marrow ◽  
Prostatic Cancer ◽  
Bone Marrow Scintigraphy

A Case of Synovial Sarcoma with Bone Metastasis Identified by Bone Marrow Scintigraphy

1985 ◽  
Vol 10 (4) ◽  
pp. 260-263 ◽  
Author(s):  
NOBUAKI OTSUKA ◽  
RIKUSHI MORITA ◽  
TAKASHI YAMAMOTO ◽  
AKIRA MURANAKA ◽  
TATSUSHI TOMOMITSU ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Metastasis ◽  
Synovial Sarcoma ◽  
Bone Marrow Scintigraphy

Bone Marrow Scintigraphy in Patients Treated with Chemotherapy and/or Radiotherapy

1977 ◽  
Vol 16 (02) ◽  
pp. 86-88
Author(s):  
V. Foltýnová ◽  
E. Vétrovcová ◽  
E. Tichá ◽  
J. Brousil
Keyword(s):  
Bone Marrow ◽  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Detailed Knowledge ◽  
General State ◽  
Bone Marrow Scintigraphy ◽  
Indium 111

SummaryBone marrow scintigraphy after the application of indium 111 In was compared with the results of bone marrow puncture in 18 patients with Hodgkin's disease treated with radiotherapy and/or chemotherapy. Agreement was found in 85% of the cases. When the results of bone marrow puncture were compared with the general state of haemopoiesis estimated scintigraphically agreement was found in only 65%. Bone marrow scintigraphy gives a more detailed knowledge of the general state of haemopoiesis and serves as a guide for the control of therapy with cytostatics and/or irradiation.

scholarly journals Long non‐coding RNA NORAD promotes the prostate cancer cell extracellular vesicle release via microRNA-541-3p-regulated PKM2 to induce bone metastasis of prostate cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Chuan-yi Hu ◽  
Juan Chen ◽  
Xin-hua Qin ◽  
Pan You ◽  
Jie Ma ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Bone Metastasis ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Target Molecules ◽  
Long Non Coding Rna

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.

scholarly journals Integrin alpha5 in human breast cancer is a mediator of bone metastasis and a therapeutic target for the treatment of osteolytic lesions

Oncogene ◽  
2021 ◽  
Author(s):  
Francesco Pantano ◽  
Martine Croset ◽  
Keltouma Driouch ◽  
Natalia Bednarz-Knoll ◽  
Michele Iuliani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Marrow ◽  
Bone Metastasis ◽  
Tumor Cell ◽  
Cancer Patients ◽  
Breast Cancer Patients ◽  
Osteolytic Lesions ◽  
Cell Colonization

AbstractBone metastasis remains a major cause of mortality and morbidity in breast cancer. Therefore, there is an urgent need to better select high-risk patients in order to adapt patient’s treatment and prevent bone recurrence. Here, we found that integrin alpha5 (ITGA5) was highly expressed in bone metastases, compared to lung, liver, or brain metastases. High ITGA5 expression in primary tumors correlated with the presence of disseminated tumor cells in bone marrow aspirates from early stage breast cancer patients (n = 268; p = 0.039). ITGA5 was also predictive of poor bone metastasis-free survival in two separate clinical data sets (n = 855, HR = 1.36, p = 0.018 and n = 427, HR = 1.62, p = 0.024). This prognostic value remained significant in multivariate analysis (p = 0.028). Experimentally, ITGA5 silencing impaired tumor cell adhesion to fibronectin, migration, and survival. ITGA5 silencing also reduced tumor cell colonization of the bone marrow and formation of osteolytic lesions in vivo. Conversely, ITGA5 overexpression promoted bone metastasis. Pharmacological inhibition of ITGA5 with humanized monoclonal antibody M200 (volociximab) recapitulated inhibitory effects of ITGA5 silencing on tumor cell functions in vitro and tumor cell colonization of the bone marrow in vivo. M200 also markedly reduced tumor outgrowth in experimental models of bone metastasis or tumorigenesis, and blunted cancer-associated bone destruction. ITGA5 was not only expressed by tumor cells but also osteoclasts. In this respect, M200 decreased human osteoclast-mediated bone resorption in vitro. Overall, this study identifies ITGA5 as a mediator of breast-to-bone metastasis and raises the possibility that volociximab/M200 could be repurposed for the treatment of ITGA5-positive breast cancer patients with bone metastases.

Bone Marrow Scintigraphy in Paget's Disease of Bone

1990 ◽  
Vol 31 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Ulf Rudberg ◽  
S.-O. Ahlbäck ◽  
R. Udén
Keyword(s):  
Bone Marrow ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Paget's Disease Of Bone ◽  
Bone Marrow Scintigraphy

scholarly journals Ras and Wnt Interaction Contribute in Prostate Cancer Bone Metastasis

Molecules ◽  
2020 ◽  
Vol 25 (10) ◽  
pp. 2380 ◽  
Author(s):  
Shian-Ren Lin ◽  
Ntlotlang Mokgautsi ◽  
Yen-Nien Liu
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Bone Metastasis ◽  
Signaling Pathways ◽  
Late Stage ◽  
Ras Signaling ◽  
Cancer Death ◽  
Metastatic Site ◽  
Cancer Types ◽  
Cytological Changes

Prostate cancer (PCa) is one of the most prevalent and malignant cancer types in men, which causes more than three-hundred thousand cancer death each year. At late stage of PCa progression, bone marrow is the most often metastatic site that constitutes almost 70% of metastatic cases of the PCa population. However, the characteristic for the osteo-philic property of PCa is still puzzling. Recent studies reported that the Wnt and Ras signaling pathways are pivotal in bone metastasis and that take parts in different cytological changes, but their crosstalk is not well studied. In this review, we focused on interactions between the Wnt and Ras signaling pathways during each stage of bone metastasis and present the fate of those interactions. This review contributes insights that can guide other researchers by unveiling more details with regard to bone metastasis and might also help in finding potential therapeutic regimens for preventing PCa bone metastasis.

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