Cytokine and cytokine receptor serum levels in adult bone sarcoma patients: Correlations with local tumor extent and prognosis

Rutkowski, Piotr; Kamińska, Janina; Kowalska, M; Ruka, W.; Steffen, Jan

doi:10.1002/jso.10305

Cited by 111 publications

(88 citation statements)

References 51 publications

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“…A larger study evaluated serum VEGF and bFGF levels in 72 patients with nonmetastatic bone sarcoma compared with healthy controls and patients with benign bone tumors. 39 Patients with bone sarcomas had higher levels of serum VEGF and bFGF than healthy controls but not greater than patients with benign bone tumors. Higher serum VEGF levels were observed in bone sarcoma patients with larger tumors, higher grade tumors, and more locally invasive tumors.…”

Section: Skeletal Sarcomasmentioning

confidence: 85%

“…Serum VEGF and bFGF levels did not correlate with prognosis and did not differ between patients with osteosarcoma, Ewing sarcoma, or chondrosarcoma. 39 The prognostic impact of serum VEGF, bFGF, and placental growth factor levels was evaluated in a series of 16 patients with osteosarcoma. 40 Patients with metastatic disease at diagnosis or who developed metastatic disease within 1 year of diagnosis had significantly higher serum levels of VEGF than patients without early metastatic disease.…”

Section: Skeletal Sarcomasmentioning

confidence: 99%

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Markers of angiogenesis and clinical features in patients with sarcoma

DuBois

Demetri

2007

Cancer

129

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Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function. Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered. Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage. Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed. ANN NEUROL 2011;

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Section: Skeletal Sarcomasmentioning

confidence: 85%

Section: Skeletal Sarcomasmentioning

confidence: 99%

Markers of angiogenesis and clinical features in patients with sarcoma

DuBois

Demetri

2007

Cancer

129

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“…Four months later, AX cells were transplanted into mice intraperitoneally and survival curves were drawn (n ¼ 5). osteosarcoma patients, 9 and IL-6 is implicated in the development of various tumors. [15][16][17] Thus, we transplanted AX cells into IL-6-deficient or wild-type mice in order to compare mouse survival rates (Figure 1b).…”

Section: Introductionmentioning

confidence: 99%

TNFα promotes osteosarcoma progression by maintaining tumor cells in an undifferentiated state

et al. 2013

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Chronic inflammation is frequently associated with tumorigenesis in elderly people. By contrast, young people without chronic inflammation often develop tumors considered independent of chronic inflammation but driven instead by mutations. Thus, whether inflammation has a significant role in tumor progression in tumors driven by mutations remains largely unknown. Here we show that TNFa is required for the tumorigenesis of osteosarcoma, the most common tumor in children and adolescents. We show that transplantation of AX osteosarcoma cells, which harbor mutations driving c-Myc overexpression and Ink4a-deficiency, in wildtype mice promotes lethal tumorigenesis accompanied by ectopic bone formation and multiple metastases, phenotypes seen in osteosarcoma patients. Such tumorigenesis was completely abrogated in TNFa-deficient mice. AX cells have the capacity to undergo osteoblastic differentiation; however, that activity was significantly inhibited by TNFa treatment, suggesting that TNFa maintains AX cells in an undifferentiated state. TNFa inhibition of AX cell osteoblastic differentiation occurred through ERK activation, and a pharmacological TNFa inhibitor effectively inhibited both AX cell tumorigenesis and increased osteoblastic gene expression and increased survival of tumor-bearing mice. Lethal tumorigenesis of AX cells was also abrogated in IL-1a/IL-1b doubly deficient mice. We found that both TNFa and IL-1 maintained AX cells in an undifferentiated state via ERK activation. Thus, inflammatory cytokines are required to promote tumorigenesis even in mutation-induced tumors, and TNFa/IL-1 and ERK may represent therapeutic targets for osteosarcoma.

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“…Due to the central role of VEGF in tumour angiogenesis, the VEGF-VEGF receptor (VEGFR) pathway has become a major focus of research and antiangiogenic drug development in oncology [3]. Although a close relationship between a high serum VEGF levels and poor prognosis has been suggested [19,20], the lack of prospective evaluation has made its value uncertain for predicting prognosis in patients with osteosarcoma. Measuring serum VEGF levels using enzyme-linked immunosorobent assay (ELISA) appears to be a more promising quantification procedure than immunohistochemical staining for tissue VEGF [4].…”

Section: Introductionmentioning

confidence: 99%

Role of vascular endothelial growth factor as a tumour marker in osteosarcoma: a prospective study

Rastogi

Kumar

Sankineani

et al. 2012

International Orthopaedics (SICOT)

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Cytokine and cytokine receptor serum levels in adult bone sarcoma patients: Correlations with local tumor extent and prognosis

Abstract: These findings indicate that cytokines and soluble cytokine receptors, both physiologically involved in bone destruction and bone formation, have an essential role in the progression of malignant bone tumors.

Cited by 111 publications

References 51 publications

Markers of angiogenesis and clinical features in patients with sarcoma

Markers of angiogenesis and clinical features in patients with sarcoma

TNFα promotes osteosarcoma progression by maintaining tumor cells in an undifferentiated state

Role of vascular endothelial growth factor as a tumour marker in osteosarcoma: a prospective study

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