Granulocyte–macrophage colony-stimulating factor: not just another haematopoietic growth factor

Francisco‐Cruz, Alejandro; Aguilar‐Santelises, Miguel; Ramos-Espinosa, Octavio; Mata-Espinosa, Dulce; Marquina‐Castillo, Brenda; Barrios-Payán, Jorge; Hernández-Pando, Rogelio

doi:10.1007/s12032-013-0774-6

Cited by 110 publications

(88 citation statements)

References 107 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…GM-CSF is a potent immune stimulator promoting the differentiation of progenitor cells into dendritic cells. It also increases the number and function of white blood cells in patients (39). Tumor cell death caused by virus replication is expected to result in the release of tumor antigens and may elicit an in situ, patient-specific antitumor response which could be enhanced by hGM-CSF expressed by NDV.…”

Section: Discussionmentioning

confidence: 99%

Genetic Modification of Oncolytic Newcastle Disease Virus for Cancer Therapy

Cheng

Wang

et al. 2016

J Virol

View full text Add to dashboard Cite

Clinical development of a mesogenic strain of Newcastle disease virus (NDV) as an oncolytic agent for cancer therapy has been hampered by its select agent status due to its pathogenicity in avian species. Using reverse genetics, we have generated a lead candidate oncolytic NDV based on the mesogenic NDV-73T strain that is no longer classified as a select agent for clinical development. This recombinant NDV has a modification at the fusion protein IMPORTANCEAvian paramyxovirus type 1, NDV, has been an attractive oncolytic agent for cancer virotherapy. However, this virus can cause epidemic disease in poultry, and concerns about the potential environmental and economic impact of an NDV outbreak have precluded its clinical development. Here we describe generation and characterization of a highly potent oncolytic NDV variant that is unlikely to cause Newcastle disease in its avian host, representing an essential step toward moving NDV forward as an oncolytic agent. Several attenuation mechanisms have been genetically engineered into the recombinant NDV that reduce chicken pathogenicity to a level that is acceptable worldwide without impacting viral production in cell culture. The selective tumor replication of this recombinant NDV, both in vitro and in vivo, along with efficient tumor cell killing makes it an attractive oncolytic virus candidate that may provide clinical benefit to patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Genetic Modification of Oncolytic Newcastle Disease Virus for Cancer Therapy

Cheng

Wang

et al. 2016

J Virol

View full text Add to dashboard Cite

show abstract

“…Administration of GM-CSF has been shown to enhance killing of M. tuberculosis in mice (31,32). In addition, the absence of GM-CSF has been reported to increase the severity of M. tuberculosis infection in GM-CSF null animals (29).…”

Section: Discussionmentioning

confidence: 99%

Keratinocyte Growth Factor Administration Attenuates Murine Pulmonary Mycobacterium tuberculosis Infection through Granulocyte-Macrophage Colony-stimulating Factor (GM-CSF)-dependent Macrophage Activation and Phagolysosome Fusion

Pasula

Azad

Gardner

et al. 2015

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Mycobacterium tuberculosis is a major cause of morbidity and mortality worldwide, and chemotherapeutic treatments are not always effective. Results: Keratinocyte growth factor (KGF) administration results in an epithelium-dependent, GM-CSF-mediated induction of microbicidal programs in alveolar macrophages. Conclusion: KGF induces GM-CSF and enhances clearance of M. tuberculosis from the lungs of mice. Significance: KGF may be a useful adjunctive strategy for treatment of infection with M. tuberculosis.

show abstract

“…GM-CSF is a cytokine that stimulates stem cells to produce neutrophils, monocytes, and macrophages (106). In the immunosuppressive phase of sepsis, patients who were ventilator dependent were treated with recombinant GM-CSF and had fewer ventilator and ICU days (107,108).…”

Section: Introductionmentioning

confidence: 99%

Sepsis-induced immune dysfunction: can immune therapies reduce mortality?

Delano¹,

Ward²

2016

Journal of Clinical Investigation

502

472

View full text Add to dashboard Cite

Sepsis affects the immune system by directly altering the lifespan, production, and function of the effector cells responsible for Sepsis is a systemic inflammatory response induced by an infection, leading to organ dysfunction and mortality. Historically, sepsis-induced organ dysfunction and lethality were attributed to the interplay between inflammatory and antiinflammatory responses. With advances in intensive care management and goal-directed interventions, early sepsis mortality has diminished, only to surge later after "recovery" from acute events, prompting a search for sepsis-induced alterations in immune function. Sepsis is well known to alter innate and adaptive immune responses for sustained periods after clinical "recovery," with immunosuppression being a prominent example of such alterations. Recent studies have centered on immune-modulatory therapy. These efforts are focused on defining and reversing the persistent immune cell dysfunction that is associated with mortality long after the acute events of sepsis have resolved.

show abstract

Granulocyte–macrophage colony-stimulating factor: not just another haematopoietic growth factor

Cited by 110 publications

References 107 publications

Genetic Modification of Oncolytic Newcastle Disease Virus for Cancer Therapy

Genetic Modification of Oncolytic Newcastle Disease Virus for Cancer Therapy

Keratinocyte Growth Factor Administration Attenuates Murine Pulmonary Mycobacterium tuberculosis Infection through Granulocyte-Macrophage Colony-stimulating Factor (GM-CSF)-dependent Macrophage Activation and Phagolysosome Fusion

Sepsis-induced immune dysfunction: can immune therapies reduce mortality?

Contact Info

Product

Resources

About