The expression of vascular endothelial platelet endothelial cell adhesion molecule-1 is not regulated by IFN-gamma treatment of C6 tumors in vivo.

Jonas, N K; Saleh, Mary

doi:10.3892/ijo.17.5.939

Cited by 4 publications

(5 citation statements)

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“…[28][29][30] Staining serial sections of IFN-␥-treated tumors with antibodies that detect PECAM or Factor VIII-related antigen produced identical results. 25 Thus, IFN-␥ did not appear to alter the staining pattern of PECAM expression in our C6 tumor model. The quanti-fication of vessels in tumors visualized by PECAM staining was therefore confirmed by staining for Factor VIIIrelated antigen.…”

Section: /Tcr Monoclonal Antibody (453(mca)); (D) Mouse Anti-rat Macrmentioning

confidence: 95%

“…The quanti-fication of vessels in tumors visualized by PECAM staining was therefore confirmed by staining for Factor VIIIrelated antigen. 25 The mechanism of IFN-␥ regulation of tumor vascularization remains unclear. Studies are now underway to examine the role of this cytokine in tumor angiogenesis in vitro and in vivo.…”

Section: /Tcr Monoclonal Antibody (453(mca)); (D) Mouse Anti-rat Macrmentioning

confidence: 99%

“…In the brain, the dividing cells are primarily the tumor cells and the tumorassociated vascular endothelium. The retroviruses we have produced in this and other studies 6,24,25 predominantly transduce the proliferating vascular endothelium rather than C6 cells. It is the transduced cells within the tumor mass that produce sustained high levels of IFN-␥ in vivo for a prolonged antitumorigenic response.…”

Section: Introductionmentioning

confidence: 99%

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The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

et al. 2000

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Current treatments for malignant gliomas are still largely ineffective in significantly improving prognosis. We have investigated the efficacy of treating established rat C6 glioma by in situ retroviral delivery of IFN-␥ cDNA. Ecotropic retrovirus packaging cells were transfected with a retroviral vector containing the mouse IFN-␥ gene. The IFN-␥ packaging cells were stereotactically implanted into established intracranial C6 glioma in immunocompetent Wistar rats, resulting in the eradication of these tumors. All IFN-␥-treated rats survived to 92 days after C6 implantation (an arbitrary

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Section: /Tcr Monoclonal Antibody (453(mca)); (D) Mouse Anti-rat Macrmentioning

confidence: 95%

Section: /Tcr Monoclonal Antibody (453(mca)); (D) Mouse Anti-rat Macrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

et al. 2000

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“…28 Findings of both animal and human studies have indicated that IFN␣ and IFN␥ may upregulate MHC Class I molecules on various types of normal cells [20][21][22]28,33,46,49 and neoplasms, [1][2][3]7,36 including GBMs. 12,23,34,37 Augmentation of MHC Class I expression has been shown to effectively regulate and activate CTLs, 18,47 which are the primary effectors of anti-tumor cellular immune responses.…”

mentioning

confidence: 98%

Modulation of major histocompatibility complex Class I molecules and major histocompatibility complex—bound immunogenic peptides induced by interferon-α and interferon-γ treatment of human glioblastoma multiforme

Yang¹,

Kremen²,

Giovannone³

et al. 2004

Journal of Neurosurgery

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Interferon-alpha and IFN-gamma can significantly upregulate the MHC Class I molecules that are expressed on the cell surface of human GBM cells as well as the potentially immunogenic peptides bound to the MHC. These results may help explain the molecular basis for increased immunogenicity with IFN treatment of human GBMs and might provide added insight into the design of future antitumor vaccines for human brain tumors.

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“…It can mediate cell adhesion through the upregulation of integrin and plays important roles in the transendothelial migration of leukocytes, the inhibition of T-cell-mediated signal transduction, and the regulation of platelet function. 7 – 10 On the other hand, it can exert anti-inflammatory effects by increasing the threshold for leukocyte activation, suppressing the generation of proinflammatory cytokines, and maintaining the integrity of the vascular barrier. 10 …”

Section: Introductionmentioning

confidence: 99%

Asn563Ser polymorphism of CD31/PECAM-1 is associated with atherosclerotic cerebral infarction in a southern Han population

Song¹,

Li²,

Long³

et al. 2014

NDT

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BackgroundCD31, also called platelet endothelial cell adhesion molecule-1 (PECAM-1), is thought to play a role in the pathological mechanisms of atherosclerosis. Leu125Val polymorphism and elevated plasma levels of soluble PECAM-1 (sPECAM-1) were found to be associated with cerebral infarction. Our aim was to investigate the association between the Asn563Ser polymorphism of CD31/PECAM-1, plasma level of sPECAM-1, and the risk of atherosclerotic cerebral infarction (ACI) in the southern Han population of the People’s Republic of China.Subjects and methodsA total of 147 subjects with ACI and 114 controls were enrolled in the study. The Asn563Ser CD31/PECAM-1 polymorphism was detected using the polymerase chain reaction–restriction fragment length polymorphism method. The plasma spECAM-1 level was measured using the enzyme-linked immunosorbent assay method.ResultsIn this study, statistically significant differences in Asn563Ser genotype and allele distribution were found between the cases and controls (P<0.05). Furthermore, logistic regression analysis showed that the GG genotype is associated with increase in ACI risk (odds ratio =4.862, P<0.001). The plasma level of sPECAM-1 was associated with ACI (odds ratio =1.431, P=0.038). In both the ACI and the control groups, the plasma sPECAM-1 level in subjects with the GG genotype was higher than that in subjects carrying the AA or GA genotype (P<0.05).ConclusionOur study showed that the Asn563Ser polymorphism of CD31/PECAM-1 gene and elevated plasma sPECAM-1 level are related to ACI risk in the southern Han population of People’s Republic of China.

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The expression of vascular endothelial platelet endothelial cell adhesion molecule-1 is not regulated by IFN-gamma treatment of C6 tumors in vivo.

Cited by 4 publications

References 0 publications

The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

Modulation of major histocompatibility complex Class I molecules and major histocompatibility complex—bound immunogenic peptides induced by interferon-α and interferon-γ treatment of human glioblastoma multiforme

Asn563Ser polymorphism of CD31/PECAM-1 is associated with atherosclerotic cerebral infarction in a southern Han population

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The expression of vascular endothelial platelet endothelial cell adhesion molecule-1 is not regulated by IFN-gamma treatment of C6 tumors in vivo.

Cited by 4 publications

References 0 publications

The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

Modulation of major histocompatibility complex Class I molecules and major histocompatibility complex—bound immunogenic peptides induced by interferon-α and interferon-γ treatment of human glioblastoma multiforme

Asn563Ser polymorphism of CD31/PECAM-1 is&nbsp;associated with atherosclerotic cerebral infarction in a southern Han population

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Asn563Ser polymorphism of CD31/PECAM-1 is associated with atherosclerotic cerebral infarction in a southern Han population