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Soft Tissue Sarcomas
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Thomas F. DeLaney, David C. Harmon, Karol Sikora, Francis J. Hornicek
Dose intensity may be important. Very high-dose ifosfamide had been used with high response rates despite some toxicity. Higher-dose therapy with standard agents may require special supportive care such as bone marrow transplantation, but may offer a chance for higher CR rates and longer response duration. Considerable interest has been focused on maintaining dose intensity of chemotherapy using colony-stimulating factors to alleviate myelosuppression. Granulocyte–macrophage colony-stimulating factor (GM-CSF) or G-CSF has been used with a variety of regimens to help maintain dose intensification. In a few studies this has resulted in improved response rates. Even higher-dose chemotherapy, as used at M.D. Anderson, seems to result in higher response rates (59%–69%). Attempts to intensify treatment by increasing the dose of doxorubicin in combination with ifosfamide, although promising in phase II studies, were not confirmed in a subsequent randomized trial compared with the standard doses.48 High-dose therapy with growth factor support has been evaluated in several investigational studies but the data to date demonstrate increased toxicity without clear evidence of therapeutic gain, so this is still considered investigational treatment.
Immunomodulation in Gene Therapeutics
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Andreas Block, Susan S. Rich, Shu-Hsia Chen, Savio L. C. Woo
Granulocyte macrophage colony stimulating factor (GM-CSF) has a broad range of functions as a growth and survival factor as well as an enhancer of the function of mature blood cells [120–122]. Most of its properties affect progenitors of granulocytes, monocytes, and eosinophils as a growth factor, extending their lifespan and augmenting their functional capability. Neutrophils and macrophages show enhanced antibody-dependent cytotoxicity. In addition, GM-CSF is an important immunopotentiating factor, expanding potent antigen presenting cells [123–125] as well as augmenting antigen presenting abilities of mature macrophages [126,127], and therefore dramatically enhancing the host response to antigen.
Angiogenesis
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Insulin-like growth factor I (IGF-I) promotes chemotaxis of endothelial cells and there is evidence supporting its role in retinal neovascularization.41 A number of low molecular weight angiogenic factors (0.2 to 1 kDa) have been isolated from different sources (e.g., tumors, macrophages, serum, adipocytes).42–44 Prostaglandins are also able to stimulate angiogenesis and, furthermore, there seems to be a relation between copper ions and angiogenesis.45,46 Recently, it has been shown that macrophage colony-stimulating factor (M-CSF, 45–100 kDa) induces angiogenesis in vivo.47
Dysregulated metabolism: A friend-to-foe skewer of macrophages
Published in International Reviews of Immunology, 2023
Keywan Mortezaee, Jamal Majidpoor
Colony stimulating factor-1 (GSF-1) (also called macrophage-colony stimulating factor (M-CSF) interacts with CSF-1R for regulation of macrophage differentiation, survival and migration. CSF-1R is belonged to the receptor protein tyrosine kinase that is contributed to the induction of many types of proto-oncogenes [8]. Autocrine consumption of CSF-1 by differentiating MΦ cells is augmented under lactate exposure. In fact, under lactate exposure, expression of CD163 in macrophages is reinforced by CSF-1 and IL-6, indicating their contribution to the acquisition of M2-like phenotype in macrophages [69]. CSF-1 is highly presented in PDAC. CSF-1 inhibitors reduce the number of CD206 high TAMs in murine PDAC. Presence of CD206 high TAMs in human counterpart is associated with the poor clinical outcomes [104]. CSF-1R blockade in mouse model of breast cancer stimulates an inflamed type I IFN response and augments the efficacy of platinum-based chemotherapy [105]. CSF-1 is also released from GBM cells and turns macrophages into ‘bad macrophages’, while administration of the CSF-1R inhibitor BLZ945 mitigates tumor-promoting TAMs [106] and suppresses tumor progression [107].
The Goiânia incident, the semiotics of danger, and the next 10,000 years
Published in Clinical Toxicology, 2023
Joseph Clemons, Adam Blumenberg
Observations from serial bone marrow aspirates and biopsies corresponded with changes in granulocyte concentrations. The granulocyte recovery kinetics demonstrated a marked difference between treated and untreated individuals. Moreover, the application of granulocyte-macrophage colony-stimulating factor did not appear to influence the recovery of red blood cells or platelets. Four out of eight patients treated with granulocyte-macrophage colony-stimulating factor survived, with the fatalities being patients colonized with gram-negative bacteria prior to the initiation of granulocyte-macrophage colony-stimulating factor treatment. The side effects of granulocyte-macrophage colony-stimulating factor treatment were generally mild. Some instances of respiratory failure and/or pulmonary edema were reported during therapy, predominantly in patients with bacterial sepsis. Although these episodes were primarily attributed to infection, an effect of granulocyte-macrophage colony-stimulating factor could not be definitively excluded. Both patients who exhibited spontaneous hematological recovery survived, with one requiring forearm amputation due to severe radiation burns [15].
Colony stimulating factors for prophylaxis of chemotherapy-induced neutropenia in children
Published in Expert Review of Clinical Pharmacology, 2022
Another type of human colony stimulating factor is granulocyte-macrophage colony stimulating factor (GM-CSF). One example is sargramostim (Table 1). Similarly, GM-CSF is used to promote hematopoiesis and stimulate cellular and humoral immunity. Sargramostim stimulates hematopoietic precursor cells and increases neutrophil, eosinophil, megakaryocyte, macrophage, and dendritic cell production [24]. Compared to G-CSF, GM-CSF has similar efficacy with no difference in time to ANC recovery [27]. However, sargramostim is associated with higher frequency of clinically significant adverse effects than filgrastim such as low-grade fever, bone pain, injection site reactions, rash, headache, and diarrhea. Overall, sargramostim and filgrastim may be therapeutically equivalent and interchangeable in hospitalized patients with chemotherapy-induced neutropenia [27].