Eosinophilia Following Radiation Therapy

Fm, Muggia; Na, Ghossein; Wohl, Herbert

doi:10.1159/000224727

Cited by 21 publications

(5 citation statements)

References 15 publications

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“…The low molecular weight eosinophilotactic activity was lacking in extracts of an adenocarcinoma of the lung of a patient with mild peripheral blood eosinophilia, but without eosinophil infiltration of the tumor, a renal cell carciiionoa meta'static to the lung which elicited a local eosinophilia only in the pleural space (Tables I and II PRE/NCU8AT/ON INTERVAL (mini FIGURE 5 Eosinophil chemotactic deactivation by partially purified low molecular weight ECF from tumor and normal lung and by tetrapeptide. Unpurified eosinophils, from a patient exhibiting 53% eosinophilia, were preincubated for varying time periods with factors diluted to achieve chemotactic activities of 16 net eosinophils/hpf for Dowex-1 fraction 6 of patient 3 (Fig. 3), 14 for Dowex-1 fraction 10 oflung tissue (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The appearance of peripheral blood eosinophilia inl association with ac malignant tumor is an uncommoni ocecurrence ancd tusually signifies either the development of metastatic lesions or a tissue response to irradiationi of the tumllor (1)(2)(3). In a few cases, however, peripheral eosinophilia has resolved upon removal of' the neoplasnm which implies an etiologic relationship to the tumor (1,4).…”

Section: Introductionmentioning

confidence: 99%

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Production of a Low Molecular Weight Eosinophil Polymorphonuclear Leukocyte Chemotactic Factor by Anaplastic Squamous Cell Carcinomas of Human Lung

Goetzl¹,

Tashjian²,

Rubin³

et al. 1978

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Production of a Low Molecular Weight Eosinophil Polymorphonuclear Leukocyte Chemotactic Factor by Anaplastic Squamous Cell Carcinomas of Human Lung

Goetzl¹,

Tashjian²,

Rubin³

et al. 1978

J. Clin. Invest.

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“…In human GBM primary tumor parenchyma, S100A8 and S100A9 have been identified with higher levels of S100A9 noted in the tumor regrowth parenchyma of patients that received primary resection plus irradiation compared to primary resection alone [ 152 ]. Of interest, radiation treatment of pelvic cancers has been found to induce eosinophilia and increase ECP serum levels [ 153 , 154 ]. Eosinophils cultured in GBM-cell line conditioned media in vitro have also been shown to release S100A9 [ 117 ].…”

Section: Promotionmentioning

confidence: 99%

Eosinophils in glioblastoma biology

Curran

Bertics

2012

J Neuroinflammation

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Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. The development of this malignant glial lesion involves a multi-faceted process that results in a loss of genetic or epigenetic gene control, un-regulated cell growth, and immune tolerance. Of interest, atopic diseases are characterized by a lack of immune tolerance and are inversely associated with glioma risk. One cell type that is an established effector cell in the pathobiology of atopic disease is the eosinophil. In response to various stimuli, the eosinophil is able to produce cytotoxic granules, neuromediators, and pro-inflammatory cytokines as well as pro-fibrotic and angiogenic factors involved in pathogen clearance and tissue remodeling and repair. These various biological properties reveal that the eosinophil is a key immunoregulatory cell capable of influencing the activity of both innate and adaptive immune responses. Of central importance to this report is the observation that eosinophil migration to the brain occurs in response to traumatic brain injury and following certain immunotherapeutic treatments for GBM. Although eosinophils have been identified in various central nervous system pathologies, and are known to operate in wound/repair and tumorstatic models, the potential roles of eosinophils in GBM development and the tumor immunological response are only beginning to be recognized and are therefore the subject of the present review.

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“…Eosinophil recruitment has also been indicated to occur in response to developing subdural hematomas (23) necrotic tissue (24), and radiotherapy (25), conditions known to exist in human primary GBM (16, 26). In patients with allergy and asthma, eosinophil recruitment involves cytokine (IL-3, IL-5, GM-CSF) priming in the peripheral blood that sensitizes eosinophilic adhesion molecules (CD11b/CD18, CD49d/CD29) to more effectively interact with adhesion ligands (intercellular adhesion molecule (ICAM)-1, vascular adhesion molecule (VCAM)-1) on the inflamed endothelia (27).…”

Section: Introductionmentioning

confidence: 99%

GM-CSF Production by Glioblastoma Cells Has a Functional Role in Eosinophil Survival, Activation, and Growth Factor Production for Enhanced Tumor Cell Proliferation

Curran

Evans

Bertics

2011

The Journal of Immunology

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Medicinal interventions of limited efficacy are currently available for the treatment of glioblastoma multiforme (GBM), the most common and lethal primary brain tumor in adults. The eosinophil is a pivotal immune cell in the pathobiology of atopic disease that is also found to accumulate in certain tumor tissues. Inverse associations between atopy and GBM risk suggest that the eosinophil may play a functional role in certain tumor immune responses. To assess the potential interactions between eosinophils and GBM, human primary blood eosinophils were cultured with two separate human GBM-derived cell lines (A172, U87-MG) or conditioned media generated in the presence or absence of TNF-α. Results revealed differential eosinophil adhesion and increased survival in response to co-culture with GBM cell lines. Eosinophil responses to GBM cell line-conditioned media included increased survival, activation, CD11b expression and S100A9 release. Addition of GM-CSF neutralizing antibodies to GBM cell cultures or conditioned media reduced eosinophil adhesion, survival and activation, linking tumor cell-derived GM-CSF to the functions of eosinophils in the tumor microenvironment. Dexamethasone, which has been reported to inhibit eosinophil recruitment and shrink GBM lesions on contrast enhanced scans, reduced the production of tumor cell-derived GM-CSF. Furthermore, culture of GBM cells in eosinophil-conditioned media increased tumor cell viability, and generation of eosinophil-conditioned media in the presence of GM-CSF enhanced the effect. These data support the idea of a paracrine loop between GM-CSF producing tumors and eosinophil-derived growth factors in tumor promotion/progression.

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Eosinophilia Following Radiation Therapy

Cited by 21 publications

References 15 publications

Production of a Low Molecular Weight Eosinophil Polymorphonuclear Leukocyte Chemotactic Factor by Anaplastic Squamous Cell Carcinomas of Human Lung

Production of a Low Molecular Weight Eosinophil Polymorphonuclear Leukocyte Chemotactic Factor by Anaplastic Squamous Cell Carcinomas of Human Lung

Eosinophils in glioblastoma biology

GM-CSF Production by Glioblastoma Cells Has a Functional Role in Eosinophil Survival, Activation, and Growth Factor Production for Enhanced Tumor Cell Proliferation

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