Direct inhibition of human acute myeloid leukemia cell growth by IL-12

Ferretti, Elisa; Carlo, Emma Di; Cocco, Claudia; Ribatti, Doménico; Sorrentino, Carlo; Ognio, Emanuela; Montagna, Daniela; Pistoia, Vito; Airoldi, Irma

doi:10.1016/j.imlet.2010.08.002

Cited by 33 publications

(32 citation statements)

References 27 publications

(33 reference statements)

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“…In this study, we investigated that p35 and p40 mRNA expression was both up-regulated in ND AML patients compared to controls, suggesting that IL-12 was increased in adult ND AML patients. This increase of IL-12 is consistent with the previous report in which IL-12 acts directly on AML cell growth, and blockage of IL-12 may limit AML cell proliferation as potential therapy for AML [25]. It has been reported that IL-27 reduces AML cell proliferation and modulates the expression of different genes involved in the angiogenic or spreading process [26].…”

Section: Suppression Of T-cell Proliferation (2) Conversion Of Naivesupporting

confidence: 92%

Elevated IL-35 in bone marrow of the patients with acute myeloid leukemia

et al. 2015

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Section: Suppression Of T-cell Proliferation (2) Conversion Of Naivesupporting

confidence: 92%

Elevated IL-35 in bone marrow of the patients with acute myeloid leukemia

et al. 2015

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“…These cytokines are predominantly produced by antigen-presenting cells in response to microbial or host immune stimuli and are involved in the regulation of immune responses against infections and tumor development (2). Recent preclinical studies showed the direct antitumor activities of IL-12 family cytokines in different human hematologic malignancies, including pediatric acute leukemias and multiple myeloma, as well as in solid tumors (3)(4)(5)(6)(7). Here, we report and discuss recent advances in the role of IL-27 and IL-23 in multiple myeloma cells and their microenvironment and in human normal plasma cells.…”

Section: Introductionmentioning

confidence: 99%

Novel Insights into the Role of Interleukin-27 and Interleukin-23 in Human Malignant and Normal Plasma Cells

Giuliani

Airoldi

2011

Clinical Cancer Research

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Multiple myeloma is a monoclonal postgerminal center tumor that has phenotypic features of plasmablasts and/or plasma cells and usually localizes at multiple sites in the bone marrow. The pathogenesis of multiple myeloma is complex and dependent on the interactions between tumor cells and their microenvironment. Different cytokines, chemokines, and proangiogenic factors released in the tumor microenvironment are known to promote multiple myeloma cell growth. Here, we report recent advances on the role of 2 strictly related immunomodulatory cytokines, interleukin-27 (IL-27) and IL-23, in human normal and neoplastic plasma cells, highlighting their ability to (i) act directly against multiple myeloma cells, (ii) influence the multiple myeloma microenvironment by targeting osteoclast and osteoblast cells, and (iii) modulate normal plasma cell function. Finally, the therapeutic implication of these studies is discussed.

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“…This anti-angiogenesis has been mediated through down-regulation of pro-angiogenic gene vascular endothelial growth factor (VEGF)-C, as well as the pro-angiogenic proteins, VEGF and basic fibroblast growth factor (BFGF) on tumor cells and supporting fibroblast cells. CD8 + T lymphocytes and NK cells have shown to contribute to this anti-angiogenesis effect on some models, especially by direct endothelial cell directed toxicity and cytolysis [137,138].…”

Section: Other Interleukinsmentioning

confidence: 99%