Inhibition of graft-versus-host reaction by treatment of immature thymocytes with eicosanoids

Juzan, M.; Gualde, N.

doi:10.1016/s0952-3278(98)90132-6

Cited by 1 publication

(1 citation statement)

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“…One such report has shown that CD4 − CD8 − double negative thymocytes cultured with LTB 4 and IL-2 led to the generation of CD8 + suppressor thymocytes and that these suppressive T cells are involved in tolerance to self antigens, which could be extended to include tumor antigens [134]. Another study examined the effect of LBT 4 treated thymocytes in a graft-versus-host disease (GVHD) model and reported that LTB 4 could influence the behavior of immature thymocytes and in the setting of allostimulation, as is in the case of GVHD, it induces a state of tolerance [135]. These studies support the theory that certain lipoxygenase products may play a role in preventing effecter anti-tumor immune responses while actively enhancing immune tolerance to tumors.…”

Section: Regulation Of Adhesion Migration and Invasion By Loxmentioning

confidence: 99%

Lipoxygenase metabolism: roles in tumor progression and survival

Pidgeon

Lysaght

Krishnamoorthy

et al. 2007

Cancer Metastasis Rev

263

206

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The metabolism of arachidonic acid through lipoxygenase pathways leads to the generation of various biologically active eicosanoids. The expression of these enzymes vary throughout the progression of various cancers, and thereby they have been shown to regulate aspects of tumor development. Substantial evidence supports a functional role for lipoxygenase-catalyzed arachidonic and linoleic acid metabolism in cancer development. Pharmacologic and natural inhibitors of lipoxygenases have been shown to suppress carcinogenesis and tumor growth in a number of experimental models. Signaling of hydro[peroxy]fatty acids following arachidonic or linoleic acid metabolism potentially effect diverse biological phenomenon regulating processes such as cell growth, cell survival, angiogenesis, cell invasion, metastatic potential and immunomodulation. However, the effects of distinct LOX isoforms differ considerably with respect to their effects on both the individual mechanisms described and the tumor being examined. 5-LOX and platelet type 12-LOX are generally considered pro-carcinogenic, with the role of 15-LOX-1 remaining controversial, while 15-LOX-2 suppresses carcinogenesis. In this review, we focus on the molecular mechanisms regulated by LOX metabolism in some of the major cancers. We discuss the effects of LOXs on tumor cell proliferation, their roles in cell cycle control and cell death induction, effects on angiogenesis, migration and the immune response, as well as the signal transduction pathways involved in these processes. Understanding the molecular mechanisms underlying the anti-tumor effect of specific, or general, LOX inhibitors may lead to the design of biologically and pharmacologically targeted therapeutic strategies inhibiting LOX isoforms and/or their biologically active metabolites, that may ultimately prove useful in the treatment of cancer, either alone or in combination with conventional therapies.

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Section: Regulation Of Adhesion Migration and Invasion By Loxmentioning

confidence: 99%