Bone is one of the most metastatic sites of advanced malignant tumors. With the continuous improvement of diagnosis and treatment of malignant tumors, the survival time of patients is prolonged and incidence of bone metastases also increases. Lung cancer is the leading cause of cancer-related mortality worldwide. It is estimated that the incidence of bone metastases in patients advanced lung cancer is about 30%-40%. The traditional diagnosis of bone metastases in lung cancer is based on clinical symptoms, X ray, computed tomography (CT), magnetic resonance imaging (MRI) and pathology. Recently, a large number of exploratory studies have reported blood biomarkers as indicators of bone metastasis screening and efficacy evaluation. In this review, we summarize the progress of biomarkers in diagnosis of bone metastases of lung cancer.
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Biomarkers, Tumor ; metabolism ; Bone Neoplasms ; metabolism ; physiopathology ; secondary ; Humans ; Lung Neoplasms ; pathology ; Osteogenesis

Animals ; Apoptosis ; Bone Neoplasms ; metabolism ; pathology ; Breast Neoplasms ; metabolism ; pathology ; Cell Proliferation ; Chondrosarcoma ; metabolism ; pathology ; Colorectal Neoplasms ; metabolism ; pathology ; Female ; Humans ; Male ; Ovarian Neoplasms ; metabolism ; pathology ; Prostatic Neoplasms ; metabolism ; pathology ; RNA, Messenger ; metabolism ; SOX9 Transcription Factor ; biosynthesis ; genetics ; physiology

In recent years, studies have found that mitochondrial transfer between leukemic cells and different types of cells in their bone marrow microenvironment, especially mesenchymal stem cells, plays a key role in the occurrence, development and drug resistance of hematological malignant tumors. This paper mainly introduces the role and latest research progress of mitochondrial transfer in acute and chronic myeloid leukemia, acute lymphoblastic leukemia and multiple myeloma, and briefly describes the mechanism of drug resistance caused by mitochondrial transfer in leukemic cells during chemotherapy. The aim is to provide a new idea and theoretical basis for using intercellular mitochondrial transfer as a potential therapeutic target.
Bone Marrow ; Hematologic Neoplasms/metabolism* ; Humans ; Mesenchymal Stem Cells ; Mitochondria ; Multiple Myeloma/metabolism* ; Tumor Microenvironment

OBJECTIVETo investigate the mRNA and protein expression levels of S100A8 and S100A9 in giant cell tumor (GCT) of bone, and its relation with radiological findings and biological behavior.

METHODSForty three patient with GCT of bone admitted in Ruijin Hospital Shanghai Jiaotong University School of Medicine from January 2009 to June 2012 were enrolled in the study. The expression levels of S100A8 and S100A9 mRNA and protein were detected by using semiquantitative RT-PCR and Western blotting in 43 specimens of GCT and 6 specimens of normal bone marrow. The CT and MRI findings of patients were retrospectively reviewed, its relation with tissue expression of S100A8 and S100A9 was analyzed.

RESULTSAmong 43 GCT cases 40 showed positive expression of S100A8 and S100A9 mRNA and protein, and the expression levels were significantly higher than those in normal bone marrow P<0.05). The expression level of S100A8 protein was significantly different in bone GCT with different composition ratio on MRI (P<0.05).The expression level of S100A9 protein was significantly different in GCT with different degree of bone destruction on CT scan (P<0.05).

CONCLUSIONThe expression of S100A8 and S100A9 mRNA and protein is up-regulated in GCT of bone. The expression of S100A8 and S100A9 is associated with the real composition ratio and the degree of bone destruction, respectively, indicating that S100A8 and S100A9 may be involved in the biological behavior of bone GCT.

Bone Neoplasms ; metabolism ; Calgranulin A ; metabolism ; Calgranulin B ; metabolism ; China ; Giant Cell Tumor of Bone ; metabolism ; Humans ; RNA, Messenger ; Tomography, X-Ray Computed ; Up-Regulation

Actins ; metabolism ; Bone Neoplasms ; metabolism ; pathology ; surgery ; Desmin ; metabolism ; Diagnosis, Differential ; Fibrosarcoma ; metabolism ; pathology ; Humans ; Leiomyosarcoma ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Neurilemmoma ; metabolism ; pathology ; Tibia ; Vimentin ; metabolism

OBJECTIVETo detect the expression of CXCL14 in human osteosarcoma cell lines and tissues and investigate its association with the prognosis of the patients.

METHODSRT-PCR, enzyme-linked immunosorbent assay (ELISA) and real-time PCR were used to detect the expression of CXCL14 in 4 osteosarcoma cell lines and in 40 pairs of osteosarcoma tissues and adjacent muscular tissues. CCK8 assay and colony formation assay was used to assess the effect of CXCL14 suppression mediated by two specific siRNAs on the proliferation of U2OS osteosarcoma cells. Immunohistochemistry was performed to detect the expression of CXCL14 in 58 osteosarcoma tissues, and Kaplan-Meier method and log-rank test were performed for survival analysis of the patients.

RESULTSSignificant up-regulation of CXCL14 expression was found in the osteosarcoma cell lines and in osteosarcoma tissues compared with the adjacent muscles (P<0.01). In U2OS cell, suppression of CXCL14 expression by siRNA significantly inhibited the cell proliferation (P<0.01) and colony formation rate (P<0.05). Kaplan-Meier survival analysis indicated that patients with high CXCL14 expression had worse prognosis than those with low CXCL14 expression (P=0.02).

CONCLUSIONCXCL14 is up-regulated in both osteosarcoma cell lines and primary osteosarcoma tissues to promote the proliferation of osteosarcoma cells. A high CXCL14 expression in osteosarcoma tissues is associated with a poor prognosis, suggesting the that CXCL14 serve as a potential therapeutic target for osteosarcoma.

Bone Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; Chemokines, CXC ; metabolism ; Humans ; Osteosarcoma ; metabolism ; pathology ; Prognosis

Multiple myeloma (MM) is a common hematologic tumor characterized by malignant proliferation of clonal plasma cells, the exact pathogenesis of which is not yet fully understood. The extracellular vesicles (EV) are structures released by cells into their surroundings that do not have a functional nucleus and can communicate between cells or deliver biologically active proteins and nucleic acids to target cells. EV play an important role in the interaction between myeloma cells and the bone marrow microenvironment, and they can promote MM progression. In this paper, we summarize the recent research progress in the mechanism of action of EV on MM in order to provide inspiration for exploring new strategies for MM treatment and prognostic stratification.
Bone Marrow/metabolism* ; Extracellular Vesicles/pathology* ; Hematologic Neoplasms/metabolism* ; Humans ; Multiple Myeloma/pathology* ; Nucleic Acids/metabolism* ; Tumor Microenvironment

OBJECTIVETo explore the expression of the epithelial cell adhesion molecule (EpCAM) in prostate cancer (PCa) and its clinical significance.

METHODSWe collected tissue samples from 63 cases of PCa, 46 cases of prostatic intraepithelial neoplasia (PIN), and 58 cases of benign prostatic hyperplasia (BPH) adjacent to PCa and determined the expression of EpCAM in the epithelial and stromal cells by immunohistochemistry.

RESULTSThe positive expression rates of EpCAM in the epithelial cells were significantly higher in PCa and PIN than in PCa-adjacent BPH (98. 4 and 97. 8 vs 51.7%, P <0. 01), and so was that in the stromal cells of PCa than in those of PCa-adjacent PIN (89.5 vs 50.0%, P <0.01). The expression of EpCAM.was remarkably higher in the stromal cells of bone metastasis than in those of non-bone metastasis tissue (100. 0 vs 40. 0%, P <0. 01) but showed no statistically significant differences between the highly and poorly differentiated PCa tissues (88.5 vs 91.9%, P >0.05).

CONCLUSIONThe expression level of EpCAM in the stromal cells of PCa is related to the occurrence, progression, and bone metastasis of the tumor, and therefore may be used as a marker in the early diagnosis of PCa as well as a predictor of bone metastasis of the tumor.

Antigens, Neoplasm ; metabolism ; Biomarkers ; metabolism ; Bone Neoplasms ; metabolism ; secondary ; Cell Adhesion Molecules ; metabolism ; Disease Progression ; Epithelial Cell Adhesion Molecule ; Epithelial Cells ; metabolism ; Humans ; Immunohistochemistry ; Male ; Prostatic Hyperplasia ; metabolism ; Prostatic Intraepithelial Neoplasia ; metabolism ; Prostatic Neoplasms ; metabolism ; Stromal Cells ; metabolism

Skeletal metastases result in significant morbidity and mortality. This is particularly true of cancers with a strong predilection for the bone, such as breast, prostate, and lung cancers. There is currently no reliable cure for skeletal metastasis, and palliative therapy options are limited. The Wnt signaling pathway has been found to play an integral role in the process of skeletal metastasis and may be an important clinical target. Several experimental models of skeletal metastasis have been used to find new biomarkers and test new treatments. In this review, we discuss pathologic process of bone metastasis, the roles of the Wnt signaling, and the available experimental models and treatments.
Animals ; Bone Neoplasms ; drug therapy ; metabolism ; radiotherapy ; secondary ; surgery ; Breast Neoplasms ; metabolism ; pathology ; Disease Models, Animal ; Drug Delivery Systems ; Female ; Humans ; Lung Neoplasms ; metabolism ; pathology ; Male ; Mice ; Prostatic Neoplasms ; metabolism ; pathology ; Wnt Proteins ; metabolism ; Wnt Signaling Pathway ; beta Catenin ; metabolism

Granulocyte-colony stimulating factor (G-CSF) is a naturally occurring glycoprotein that stimulates the proliferation and maturation of precursor cells in the bone marrow into fully differentiated neutrophils. Several reports of G-CSF-producing malignant tumors have been published, but scarcely any in the hepatobiliary system, such as in hepatocellular carcinoma (HCC). Here, we encountered a 69-yr-old man with a hepatic tumor who had received right hepatic resection. He showed leukocytosis of 25,450/microL along with elevated serum G-CSF. Histological examination of surgical samples demonstrated immunohistochemical staining for G-CSF, but not for G-CSF receptor. The patient survived without recurrence for four years, but ultimately passed away with multiple bone metastases. In light of the above, clinicians may consider G-CSF-producing HCC when encountering patients with leukocytosis and a hepatic tumor. More cases are needed to clarify the clinical picture of G-CSF-producing HCC.
Aged ; Bone Neoplasms/secondary ; Carcinoma, Hepatocellular/*metabolism/pathology ; Fatal Outcome ; Granulocyte Colony-Stimulating Factor/*metabolism ; Humans ; Liver Neoplasms/*metabolism/pathology ; Male ; Receptors, Granulocyte Colony-Stimulating Factor/metabolism