Potentiation of retinoid-induced differentiation of HL-60 and U937 cell lines by cytokines

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

“…TNF has been shown to synergize with ATRA for proliferation and dierentiation of dierent hematopoietic cells (Trincheiri et al, 1987;Tobler et al, 1987;Peck et al, 1991). In addition, we have shown that ATRA inhibits TNF production by macrophages stimulated by lipopolysaccharide and interferon (IFN)-g (Mehta et al, 1994).…”

“…It has been reported that TNF is a potent inducer of manganese superoxide dismutase in A549 cells (Pogrebniak et al, 1991), which can block TNF-induced NF-kB activation (Manna et al, 1998). Whether conversion of A549 cells to a TNF-sensitive phenotype by ATRA is entirely due to induction of TNF receptors is also less likely.…”

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

“…TNF has been shown to synergize with ATRA for proliferation and dierentiation of dierent hematopoietic cells (Trincheiri et al, 1987;Tobler et al, 1987;Peck et al, 1991). In addition, we have shown that ATRA inhibits TNF production by macrophages stimulated by lipopolysaccharide and interferon (IFN)-g (Mehta et al, 1994).…”

“…It has been reported that TNF is a potent inducer of manganese superoxide dismutase in A549 cells (Pogrebniak et al, 1991), which can block TNF-induced NF-kB activation (Manna et al, 1998). Whether conversion of A549 cells to a TNF-sensitive phenotype by ATRA is entirely due to induction of TNF receptors is also less likely.…”

All Trans Retinoic Acid in Primary and Relapsed Acute Promyelocytic Leukemia

“…All trans retinoic acid is a safe and highly effective treatment for acute promyclocytic leukemia as reported in other studies [7,8], Interferons and other cytokines may potentiate the anti proliferative and differentiation inducing capacity of ATRA [6], Futhcr approaches for maintenance therapy are required.…”

Effects of retinoic acid combined with interferon-gamma on the expression of a tumor rejection antigen (heat shock protein gp96) in human cervical cancer

“…A growing body of evidence from both laboratory and clinical research support the concept that simultaneous exposure to both retinoids and IFNs can result in enhanced antiproliferative, differentiative, and antiangiogeneic effects when compared to treatment with either agent alone( 6, 15, 27). The mechanism of action of these two biologic response modifiers is still unknown, but there is evidence to suggest that IFNs may modulate the RA system by inducing or increasing retinoic acid receptor expression or by changing the expression of cellular retinoic acid‐binding proteins, thus rendering cells more sensitive to retinoid action( 27).…”

“…Taken together, these results suggest that combined IFN‐γ/retinoid therapy may provide a beneficial effect in the treatment of cervical cancer that is more effective than either modality alone. Both agents are active in up‐regulating immunologically important cell surface antigens and could inhibit cervical cell proliferation via distinct, but reinforcing pathways( 6, 15, 27). Moreover, the previously unrecognized effects described in this study on the expression of Hsp‐gp96 strongly suggest that they may further contribute to enhance immune recognition of cervical tumor cells.…”

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

“…TNF has been shown to synergize with ATRA for proliferation and dierentiation of dierent hematopoietic cells (Trincheiri et al, 1987;Tobler et al, 1987;Peck et al, 1991). In addition, we have shown that ATRA inhibits TNF production by macrophages stimulated by lipopolysaccharide and interferon (IFN)-g (Mehta et al, 1994).…”

“…It has been reported that TNF is a potent inducer of manganese superoxide dismutase in A549 cells (Pogrebniak et al, 1991), which can block TNF-induced NF-kB activation (Manna et al, 1998). Whether conversion of A549 cells to a TNF-sensitive phenotype by ATRA is entirely due to induction of TNF receptors is also less likely.…”

All Trans Retinoic Acid in Primary and Relapsed Acute Promyelocytic Leukemia

“…All trans retinoic acid is a safe and highly effective treatment for acute promyclocytic leukemia as reported in other studies [7,8], Interferons and other cytokines may potentiate the anti proliferative and differentiation inducing capacity of ATRA [6], Futhcr approaches for maintenance therapy are required.…”

Effects of retinoic acid combined with interferon-gamma on the expression of a tumor rejection antigen (heat shock protein gp96) in human cervical cancer

“…A growing body of evidence from both laboratory and clinical research support the concept that simultaneous exposure to both retinoids and IFNs can result in enhanced antiproliferative, differentiative, and antiangiogeneic effects when compared to treatment with either agent alone( 6, 15, 27). The mechanism of action of these two biologic response modifiers is still unknown, but there is evidence to suggest that IFNs may modulate the RA system by inducing or increasing retinoic acid receptor expression or by changing the expression of cellular retinoic acid‐binding proteins, thus rendering cells more sensitive to retinoid action( 27).…”

“…Taken together, these results suggest that combined IFN‐γ/retinoid therapy may provide a beneficial effect in the treatment of cervical cancer that is more effective than either modality alone. Both agents are active in up‐regulating immunologically important cell surface antigens and could inhibit cervical cell proliferation via distinct, but reinforcing pathways( 6, 15, 27). Moreover, the previously unrecognized effects described in this study on the expression of Hsp‐gp96 strongly suggest that they may further contribute to enhance immune recognition of cervical tumor cells.…”

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

“…TNF has been shown to synergize with ATRA for proliferation and dierentiation of dierent hematopoietic cells (Trincheiri et al, 1987;Tobler et al, 1987;Peck et al, 1991). In addition, we have shown that ATRA inhibits TNF production by macrophages stimulated by lipopolysaccharide and interferon (IFN)-g (Mehta et al, 1994).…”

“…It has been reported that TNF is a potent inducer of manganese superoxide dismutase in A549 cells (Pogrebniak et al, 1991), which can block TNF-induced NF-kB activation (Manna et al, 1998). Whether conversion of A549 cells to a TNF-sensitive phenotype by ATRA is entirely due to induction of TNF receptors is also less likely.…”

All Trans Retinoic Acid in Primary and Relapsed Acute Promyelocytic Leukemia

“…All trans retinoic acid is a safe and highly effective treatment for acute promyclocytic leukemia as reported in other studies [7,8], Interferons and other cytokines may potentiate the anti proliferative and differentiation inducing capacity of ATRA [6], Futhcr approaches for maintenance therapy are required.…”

Effects of retinoic acid combined with interferon-gamma on the expression of a tumor rejection antigen (heat shock protein gp96) in human cervical cancer

“…A growing body of evidence from both laboratory and clinical research support the concept that simultaneous exposure to both retinoids and IFNs can result in enhanced antiproliferative, differentiative, and antiangiogeneic effects when compared to treatment with either agent alone( 6, 15, 27). The mechanism of action of these two biologic response modifiers is still unknown, but there is evidence to suggest that IFNs may modulate the RA system by inducing or increasing retinoic acid receptor expression or by changing the expression of cellular retinoic acid‐binding proteins, thus rendering cells more sensitive to retinoid action( 27).…”

“…Taken together, these results suggest that combined IFN‐γ/retinoid therapy may provide a beneficial effect in the treatment of cervical cancer that is more effective than either modality alone. Both agents are active in up‐regulating immunologically important cell surface antigens and could inhibit cervical cell proliferation via distinct, but reinforcing pathways( 6, 15, 27). Moreover, the previously unrecognized effects described in this study on the expression of Hsp‐gp96 strongly suggest that they may further contribute to enhance immune recognition of cervical tumor cells.…”