Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
 6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eosinophilia of the blood and bone marrow may be encountered in patients with disseminated malignancies. It is unrelated to the histologic type of the tumor but usually reflects its aggressiveness and prognostic outlook. Its pathogenesis is controversial. The presence of eosinophil colony-stimulating factor(s) in serum and malignant tissue extracts was evaluated in two cases of malignancies accompanied by marked blood and bone marrow eosinophilia. When compared with controls, serum and tumor tissue extracts stimulated the growth of G, M, and Eo colonies in semisolid cultures of human bone marrow. Such stimulating effect was inhibited by the addition of antibodies to granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3. Thus, the colony-stimulating factor(s) play a role in the pathogenesis of the eosinophilia associated with some malignant tumors, and these factors appear to include GM-CSF, interleukin-3, and probably others.
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PMID:Blood and bone marrow eosinophilia in malignant tumors. Role and nature of blood and tissue eosinophil colony-stimulating factor(s) in two patients. 206 75

Prostate cancer represents a heterogeneous disease entity with varying degrees of behavior, aggressiveness, patterns of metastasis, and response to therapy. Progressive metastatic prostate cancer is associated with a formidable array of morbidity that ultimately contributes to death of the patient. Thus far, there has been no convincing evidence to support routine use of non-hormonal chemotherapeutic agents or combinations over symptomatic treatment only. Furthermore, no single compound or combination has shown a dramatic improvement in conventional quality of life parameters over symptomatic treatment only. Androgen ablation remains the primary systemic therapeutic modality for this disease, yet the intense delineation of mechanisms involved in tumor cell metastasis has lead to new therapeutic strategies, ranging from cytotoxic to cytostatic, including immunomodulators. Among those strategies currently being studied are granulocyte-macrophage colony-stimulating factor-transduced prostate cancer vaccines, differentiation therapy, gene therapy, inducers of apoptosis, antimetastatic agents, angiogenesis inhibitors, radiation therapy (local and systemic), and systemic approaches targeted at prostate cancer morbidity. The difficult issue is which agents should be developed and how should we best assess the response using standard and newly identified endpoints. Certainly, the future of advanced prostate cancer therapy will undergo dramatic changes as a result of the continued interaction between the laboratory and the clinic.
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PMID:Prostate cancer treatment strategies based on tumor-specific biological principles: future directions. 899 87

Tumor growth and progression are critically controlled by alterations in the microenvironment often caused by an aberrant expression of growth factors and receptors. We demonstrated previously that tumor progression in patients and in the experimental HaCaT tumor model for skin squamous cell carcinomas is associated with a constitutive neoexpression of the hematopoietic growth factors granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), causing an autocrine stimulation of tumor cell proliferation and migration in vitro. To analyze the critical contribution of both factors to tumor progression, G-CSF or GM-CSF was stably transfected in factor-negative benign tumor cells. Forced expression of GM-CSF resulted in invasive growth and enhanced tumor cell proliferation in a three-dimensional culture model in vitro, yet tumor growth in vivo remained only transient. Constitutive expression of G-CSF, however, caused a shift from benign to malignant and strongly angiogenic tumors. Moreover, cells recultured from G-CSF-transfected tumors exhibited enhanced tumor aggressiveness upon reinjection, i.e., earlier onset and faster tumor expansion. Remarkably, this further step in tumor progression was again associated with the constitutive expression of GM-CSF strongly indicating a synergistic action of both factors. Additionally, expression of GM-CSF in the transfected tumors mediated an earlier recruitment of granulocytes and macrophages to the tumor site, and expression of G-CSF induced an enhanced and persistent angiogenesis and increased the number of granulocytes and macrophages in the tumor vicinity. Thus both factors directly stimulate tumor cell growth and, by modulating the tumor stroma, induce a microenvironment that promotes tumor progression.
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PMID:Cooperative autocrine and paracrine functions of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor in the progression of skin carcinoma cells. 1552 Jan 86