PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 62-85 colony stimulating factor 3 Homo sapiens 51-56 25805962-0 2015 Granulocyte colony-stimulating factor potentiates all-trans retinoic acid-induced granulocytic differentiation in acute promyelocytic leukemia cell line HT93A. Tretinoin 60-73 colony stimulating factor 3 Homo sapiens 0-37 25805962-7 2015 RESULTS: ATRA (100 nM) induced granulocytic differentiation (upregulation of CD11b and downregulation of CD34) and the effect was potentiated by addition of G-CSF, while G-CSF alone had no effect on HT93A cells. Tretinoin 9-13 colony stimulating factor 3 Homo sapiens 157-162 25805962-7 2015 RESULTS: ATRA (100 nM) induced granulocytic differentiation (upregulation of CD11b and downregulation of CD34) and the effect was potentiated by addition of G-CSF, while G-CSF alone had no effect on HT93A cells. Tretinoin 9-13 colony stimulating factor 3 Homo sapiens 170-175 22940758-0 2012 Granulocyte colony-stimulating factor potentiates differentiation induction by all-trans retinoic acid and arsenic trioxide and enhances arsenic uptake in the acute promyelocytic leukemia cell line HT93A. Tretinoin 101-114 colony stimulating factor 3 Homo sapiens 0-37 22940758-5 2012 G-CSF promoted differentiation-inducing activities of both ATO and ATRA. Tretinoin 67-71 colony stimulating factor 3 Homo sapiens 0-5 22940758-12 2012 G-CSF not only promotes differentiation-inducing activities of both ATRA and ATO, but also makes APL cells vulnerable to increased arsenic uptake. Tretinoin 68-72 colony stimulating factor 3 Homo sapiens 0-5 25805962-14 2015 These results suggest G-CSF activates STAT5 through the JAK pathway in combination with ATRA, resulting in myeloid differentiation in HT93A cells. Tretinoin 88-92 colony stimulating factor 3 Homo sapiens 22-27 19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 62-85 colony stimulating factor 3 Homo sapiens 244-249 19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 87-91 colony stimulating factor 3 Homo sapiens 51-56 19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 87-91 colony stimulating factor 3 Homo sapiens 244-249 19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 253-257 colony stimulating factor 3 Homo sapiens 51-56 12189565-2 2002 MATERIALS AND METHODS: ATRA was administered orally at 45 mg/m(2)/day on days 1-14 and 25 mg/m(2)/day on days 15-28 of two standard cycles (idarubicin, etoposide, cytarabine, G-CSF) and of up to three high-dose courses (cytarabine, G-CSF). Tretinoin 23-27 colony stimulating factor 3 Homo sapiens 175-180 16003389-4 2006 Granulocyte colony-stimulating factor (G-CSF) increases mitochondrial respiration and calcium accumulation capacity and subsequently blocks ATRA-induced apoptosis. Tretinoin 140-144 colony stimulating factor 3 Homo sapiens 0-37 16003389-4 2006 Granulocyte colony-stimulating factor (G-CSF) increases mitochondrial respiration and calcium accumulation capacity and subsequently blocks ATRA-induced apoptosis. Tretinoin 140-144 colony stimulating factor 3 Homo sapiens 39-44 15223604-7 2004 Moreover, in vitro and in vivo studies demonstrated that G-CSF may act as a co-stimulus augmenting the response of PML-RARalpha acute promyelocytic leukemia cells to all-trans-retinoic acid treatment. Tretinoin 176-189 colony stimulating factor 3 Homo sapiens 57-62 15068906-0 2004 Induction of differentiation of retinoic acid-resistant acute promyelocytic leukemia cells by the combination of all-trans retinoic acid and granulocyte colony-stimulating factor. Tretinoin 32-45 colony stimulating factor 3 Homo sapiens 141-178 15068906-1 2004 An acute promyelocytic leukemia (APL) cell line with natural resistance to all-trans retinoic acid (ATRA), UF-1, was induced to differentiate into mature granulocyte when treated with the combination of ATRA and granulocyte colony-stimulating factor (G-CSF), while neither of them alone was capable of inducing the differentiation effectively. Tretinoin 85-98 colony stimulating factor 3 Homo sapiens 212-249 15068906-1 2004 An acute promyelocytic leukemia (APL) cell line with natural resistance to all-trans retinoic acid (ATRA), UF-1, was induced to differentiate into mature granulocyte when treated with the combination of ATRA and granulocyte colony-stimulating factor (G-CSF), while neither of them alone was capable of inducing the differentiation effectively. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 212-249 15068906-1 2004 An acute promyelocytic leukemia (APL) cell line with natural resistance to all-trans retinoic acid (ATRA), UF-1, was induced to differentiate into mature granulocyte when treated with the combination of ATRA and granulocyte colony-stimulating factor (G-CSF), while neither of them alone was capable of inducing the differentiation effectively. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 251-256 12627849-2 2003 Granulocyte colony-stimulating factor (G-CSF) by itself had no effect on NB4 cells but exerted additional enhancing effects on the respiratory burst activity in the presence of ATRA. Tretinoin 177-181 colony stimulating factor 3 Homo sapiens 0-37 12627849-2 2003 Granulocyte colony-stimulating factor (G-CSF) by itself had no effect on NB4 cells but exerted additional enhancing effects on the respiratory burst activity in the presence of ATRA. Tretinoin 177-181 colony stimulating factor 3 Homo sapiens 39-44 12627849-7 2003 Fundamentally identical but slightly different phenomena for the cell surface expression of CD33 and CD10 were observed in the normal human bone marrow mononuclear cells; G-CSF induced CD10 even in the absence of ATRA and down-regulated CD33 in normal cells. Tretinoin 213-217 colony stimulating factor 3 Homo sapiens 171-176 18055984-2 2007 As(2)O(3), Phenylbutyrate (PB) and G-CSF are known to potentiate ATRA effects. Tretinoin 65-69 colony stimulating factor 3 Homo sapiens 35-40 14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 99-122 colony stimulating factor 3 Homo sapiens 44-81 14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 99-122 colony stimulating factor 3 Homo sapiens 83-88 14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 124-128 colony stimulating factor 3 Homo sapiens 44-81 14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 124-128 colony stimulating factor 3 Homo sapiens 83-88 14604978-10 2004 The addition of G-CSF with ATRA during NB4 induction resulted in STAT3 phosphorylation but did not enhance differentiation. Tretinoin 27-31 colony stimulating factor 3 Homo sapiens 16-21 14745140-2 2003 Granulocyte colony-stimulating factor (G-CSF), although not having detectable effect by itself, exerted the additive effects on lipid droplet formation in NB4 cells when combined with ATRA. Tretinoin 184-188 colony stimulating factor 3 Homo sapiens 0-37 14745140-2 2003 Granulocyte colony-stimulating factor (G-CSF), although not having detectable effect by itself, exerted the additive effects on lipid droplet formation in NB4 cells when combined with ATRA. Tretinoin 184-188 colony stimulating factor 3 Homo sapiens 39-44 12873158-9 2003 Our results indicated that ATRA supplemented with vitamin D(3) and granulocyte colony-stimulating factor affords robust, rapid, and reproducible differentiation of both cell types. Tretinoin 27-31 colony stimulating factor 3 Homo sapiens 67-104 12189565-2 2002 MATERIALS AND METHODS: ATRA was administered orally at 45 mg/m(2)/day on days 1-14 and 25 mg/m(2)/day on days 15-28 of two standard cycles (idarubicin, etoposide, cytarabine, G-CSF) and of up to three high-dose courses (cytarabine, G-CSF). Tretinoin 23-27 colony stimulating factor 3 Homo sapiens 232-237 10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 63-67 colony stimulating factor 3 Homo sapiens 168-173 11172538-7 2001 In addition, when a combination of retinoic acid and the hematopoietic growth factor granulocyte colony-stimulating factor (G-CSF) is applied, the cells may be forced to undergo terminal differentiation, both in vitro and in vivo. Tretinoin 35-48 colony stimulating factor 3 Homo sapiens 124-129 10428509-8 1999 Simultaneous treatment with G-CSF and zVAD-fmk additively blocked ATRA-induced apoptosis. Tretinoin 66-70 colony stimulating factor 3 Homo sapiens 28-33 11721444-0 1999 The relationship between the levels of granulocyte colony-stimulating factor and leukocytosis induced by all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 105-128 colony stimulating factor 3 Homo sapiens 39-76 11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 229-242 colony stimulating factor 3 Homo sapiens 97-134 11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 229-242 colony stimulating factor 3 Homo sapiens 136-141 11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 244-248 colony stimulating factor 3 Homo sapiens 97-134 11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 244-248 colony stimulating factor 3 Homo sapiens 136-141 11721444-4 1999 After ATRA treatment, both serum G-CSF level and WBC number increased in 68.1% of the cases. Tretinoin 6-10 colony stimulating factor 3 Homo sapiens 33-38 10199205-11 1999 Although ATRA was administered at a dose of 80 mg/day for more than 2 months, the number of myelocytes and promyelocytes increased Finally CAG (cytarabine, aclarubicin, G-CSF) therapy was initiated, but the patient died due to intracranial invasion and hemorrhage accompanied by disseminated intravascular coagulation. Tretinoin 9-13 colony stimulating factor 3 Homo sapiens 169-174 10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 colony stimulating factor 3 Homo sapiens 161-166 10414449-7 1999 Furthermore, G-CSF, through its potent differentiating activity, may increase the risk of such complications during ATRA treatment. Tretinoin 116-120 colony stimulating factor 3 Homo sapiens 13-18 10194425-2 1999 Granulocyte colony-stimulating factor (G-CSF) has been considered to be potentially synergistic with ATRA in this regard. Tretinoin 101-105 colony stimulating factor 3 Homo sapiens 0-37 10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 3 Homo sapiens 60-65 10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 3 Homo sapiens 93-98 10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 3 Homo sapiens 93-98 10221506-6 1999 Among them, granulocyte colony-stimulating factor (G-CSF) is unique in that it preferentially stimulates clonal growth, but not self-renewal, in many APL cases, and synergistically enhances the differentiation-inducing effect of ATRA when used in combination. Tretinoin 229-233 colony stimulating factor 3 Homo sapiens 12-49 10221506-6 1999 Among them, granulocyte colony-stimulating factor (G-CSF) is unique in that it preferentially stimulates clonal growth, but not self-renewal, in many APL cases, and synergistically enhances the differentiation-inducing effect of ATRA when used in combination. Tretinoin 229-233 colony stimulating factor 3 Homo sapiens 51-56 9578604-2 1998 G-CSF enhanced O-2 generating ability of HL-60 cells whose differentiation had been initiated by dimethylsulfoxide (DMSO) or retinoic acid (RA). Tretinoin 125-138 colony stimulating factor 3 Homo sapiens 0-5 9590146-4 1998 Based on these observations, we administered recombinant human G-CSF to a patient with APL in the third relapse that was resistant to both cytotoxic agents and all trans retinoic acid, in an attempt to sensitize the leukemic cells to cell-cycle-dependent agents. Tretinoin 170-183 colony stimulating factor 3 Homo sapiens 63-68 9578604-2 1998 G-CSF enhanced O-2 generating ability of HL-60 cells whose differentiation had been initiated by dimethylsulfoxide (DMSO) or retinoic acid (RA). Tretinoin 140-142 colony stimulating factor 3 Homo sapiens 0-5 9194390-9 1997 ATRA was restarted along with granulocyte-colony stimulating factor (G-CSF). Tretinoin 0-4 colony stimulating factor 3 Homo sapiens 69-74 9277051-0 1997 Prediction of growth sensitivity of acute promyelocytic leukemia cells to granulocyte colony-stimulating factor using 7AAD/PY during administration of all-trans retinoic acid. Tretinoin 161-174 colony stimulating factor 3 Homo sapiens 74-111 9277051-5 1997 In one patient, APL cells harvested from marrow during the first 3 weeks of ATRA administration showed distinct growth sensitivity to G-CSF ex vivo, and the cells harvested after a 4-week exposure to ATRA appeared to have lost this sensitivity. Tretinoin 76-80 colony stimulating factor 3 Homo sapiens 134-139 9277051-6 1997 In this patient, G-CSF could be safely administered after 4 weeks of ATRA therapy. Tretinoin 69-73 colony stimulating factor 3 Homo sapiens 17-22 9277051-7 1997 7AAD/PY analysis is useful for predicting growth sensitivity of APL cells to G-CSF during ATRA administration. Tretinoin 90-94 colony stimulating factor 3 Homo sapiens 77-82 9331973-9 1997 In conclusion, DMSO- or RA-treated HL-60 cells are useful for the measurement of bioactivity of hG-CSF. Tretinoin 24-26 colony stimulating factor 3 Homo sapiens 96-102 9150345-1 1997 All-trans-retinoic acid (ATRA) has been used as a potent therapeutic agent to induce differentiation of acute promyelocytic leukemia (APL) cells, and granulocyte colony-stimulating factor (G-CSF) has been reported to enhance this effect of ATRA in vitro. Tretinoin 0-23 colony stimulating factor 3 Homo sapiens 189-194 9150345-1 1997 All-trans-retinoic acid (ATRA) has been used as a potent therapeutic agent to induce differentiation of acute promyelocytic leukemia (APL) cells, and granulocyte colony-stimulating factor (G-CSF) has been reported to enhance this effect of ATRA in vitro. Tretinoin 240-244 colony stimulating factor 3 Homo sapiens 150-187 9150345-1 1997 All-trans-retinoic acid (ATRA) has been used as a potent therapeutic agent to induce differentiation of acute promyelocytic leukemia (APL) cells, and granulocyte colony-stimulating factor (G-CSF) has been reported to enhance this effect of ATRA in vitro. Tretinoin 240-244 colony stimulating factor 3 Homo sapiens 189-194 8753812-2 1996 G-CSF protein was neither produced during PMA-induced differentiation nor in response to retinoic acid (RA) alone. Tretinoin 89-102 colony stimulating factor 3 Homo sapiens 0-5 8923783-0 1996 Administration of granulocyte colony-stimulating factor during remission induction therapy with all-trans retinoic acid for acute promyelocytic leukemia. Tretinoin 106-119 colony stimulating factor 3 Homo sapiens 18-55 8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 140-153 colony stimulating factor 3 Homo sapiens 0-37 8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 140-153 colony stimulating factor 3 Homo sapiens 39-44 8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 155-159 colony stimulating factor 3 Homo sapiens 0-37 8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 155-159 colony stimulating factor 3 Homo sapiens 39-44 8923783-2 1996 Accordingly, we initiated a pilot study on G-CSF in APL patients who developed neutropenia and severe infection during remission induction therapy with ATRA. Tretinoin 152-156 colony stimulating factor 3 Homo sapiens 43-48 8923783-5 1996 Our findings suggest that administration of G-CSF combined with ATRA can improve the hematological state in APL patients not previously receiving ATRA therapy. Tretinoin 146-150 colony stimulating factor 3 Homo sapiens 44-49 8753812-0 1996 Production of granulocyte colony-stimulating factor by THP-1 cells in response to retinoic acid and phorbol ester is mediated through the autocrine production of interleukin-1. Tretinoin 82-95 colony stimulating factor 3 Homo sapiens 14-51 9387319-2 1996 ELISA method was used in detecting levels of serum granulocyle colony-stimulating factor (G-CSF) in 47 cases of APL during treatment with ATRA. Tretinoin 138-142 colony stimulating factor 3 Homo sapiens 51-88 9387319-2 1996 ELISA method was used in detecting levels of serum granulocyle colony-stimulating factor (G-CSF) in 47 cases of APL during treatment with ATRA. Tretinoin 138-142 colony stimulating factor 3 Homo sapiens 90-95 9387319-4 1996 After ATRA treatment, both serum G-CSF level and WBC number increased in 68.1% of the cases. Tretinoin 6-10 colony stimulating factor 3 Homo sapiens 33-38 8997128-9 1996 These findings suggest that combined therapy of ATRA and G-CSF is effective to the low responder to ATRA and that combined use of ATRA and prednisolone reduces the side effect of ATRA without diminishing the favorable effect on differentiation. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 57-62 8997128-9 1996 These findings suggest that combined therapy of ATRA and G-CSF is effective to the low responder to ATRA and that combined use of ATRA and prednisolone reduces the side effect of ATRA without diminishing the favorable effect on differentiation. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 57-62 8997128-9 1996 These findings suggest that combined therapy of ATRA and G-CSF is effective to the low responder to ATRA and that combined use of ATRA and prednisolone reduces the side effect of ATRA without diminishing the favorable effect on differentiation. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 57-62 8753812-2 1996 G-CSF protein was neither produced during PMA-induced differentiation nor in response to retinoic acid (RA) alone. Tretinoin 104-106 colony stimulating factor 3 Homo sapiens 0-5 8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 colony stimulating factor 3 Homo sapiens 50-55 8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 colony stimulating factor 3 Homo sapiens 220-225 8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 67-69 colony stimulating factor 3 Homo sapiens 83-88 8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 162-164 colony stimulating factor 3 Homo sapiens 83-88 8753812-6 1996 Finally, we demonstrated that RA can also enhance IL-1-induced G-CSF production in primary monocytes of human peripheral blood. Tretinoin 30-32 colony stimulating factor 3 Homo sapiens 63-68 8767533-7 1996 A patient with Vaquez"s disease, in remission for 15 years and presenting a progressive increase in bone marrow and peripheral myeloblasts, did not have a positive response to the administration of ATRA; however, the association of G-CSF to ATRA was followed by a complete remission. Tretinoin 241-245 colony stimulating factor 3 Homo sapiens 232-237 8624378-12 1996 This pilot study demonstrates that treatment with ATRA/G-CSF/EPO/tocopherol is well tolerated, leading to normalization of neutrophil counts in most, and to improvement of platelets and red blood cells in a significant subgroup of patients. Tretinoin 50-54 colony stimulating factor 3 Homo sapiens 55-60 8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 33-46 colony stimulating factor 3 Homo sapiens 341-346 8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 48-50 colony stimulating factor 3 Homo sapiens 341-346 8929647-3 1995 Culture of his marrow cells at diagnosis showed that granulocyte colony-stimulating factor (G-CSF) promoted cell proliferation, while all-trans retinoic acid (ATRA) inhibited the proliferative effect of G-CSF and induced differentiation. Tretinoin 144-157 colony stimulating factor 3 Homo sapiens 203-208 8547662-6 1996 Retinoic acid (RA) was the strongest inducer of defensin mRNA accumulation, even at doses too low to effect morphologic changes; the initial (first 48 hours), gradual increase resulted from transcriptional activation and was enhanced by granulocyte colony-stimulating factor. Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 237-274 8929647-3 1995 Culture of his marrow cells at diagnosis showed that granulocyte colony-stimulating factor (G-CSF) promoted cell proliferation, while all-trans retinoic acid (ATRA) inhibited the proliferative effect of G-CSF and induced differentiation. Tretinoin 159-163 colony stimulating factor 3 Homo sapiens 203-208 7535055-4 1995 Challenge of NB4 cells with G-CSF, dbcAMP and ATRA causes a much higher induction of LAP relative to that observed in the presence of ATRA+G-CSF or ATRA+dbcAMP. Tretinoin 46-50 colony stimulating factor 3 Homo sapiens 139-144 21552804-0 1995 Retinoic Acid potently stimulates the production of granulocyte-colony-stimulating factor in the human monocytic thp-1 cell-line. Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 52-89 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 colony stimulating factor 3 Homo sapiens 94-131 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 colony stimulating factor 3 Homo sapiens 133-138 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 colony stimulating factor 3 Homo sapiens 94-131 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 colony stimulating factor 3 Homo sapiens 133-138 7540644-0 1995 Modulation of human G-CSF receptor mRNA and protein in normal and leukemic myeloid cells by G-CSF and retinoic acid. Tretinoin 102-115 colony stimulating factor 3 Homo sapiens 20-25 7540644-10 1995 Furthermore, the ability of retinoic acid to up-regulate G-CSF receptor may account for the synergistic effect of G-CSF and retinoic acid in differentiation induction of acute promyelocytic leukemia. Tretinoin 28-41 colony stimulating factor 3 Homo sapiens 57-62 7540644-10 1995 Furthermore, the ability of retinoic acid to up-regulate G-CSF receptor may account for the synergistic effect of G-CSF and retinoic acid in differentiation induction of acute promyelocytic leukemia. Tretinoin 124-137 colony stimulating factor 3 Homo sapiens 57-62 7543855-5 1995 G-CSFR-expressing clones (a) acquired the capacity to respond to the differentiation-inducing properties of G-CSF and retinoic acid, (b) formed colonies which exhibited a dispersed phenotype, and (c) exhibited near diploid DNA ploidy. Tretinoin 118-131 colony stimulating factor 3 Homo sapiens 0-5 21566987-5 1994 Further experiments indicated that interleukin 1 (IL-1), one of the mediators of LPS activity, also synergized with t-RA to stimulate G-CSF secretion. Tretinoin 116-120 colony stimulating factor 3 Homo sapiens 134-139 7511442-13 1994 In NB4 cells, ATRA induces G-CSF, alpha, and beta retinoic acid receptor transcripts, whereas G-CSF has minor effects on the expression of these mRNAs. Tretinoin 14-18 colony stimulating factor 3 Homo sapiens 27-32 7524761-0 1994 All-trans retinoic acid directly inhibits granulocyte colony-stimulating factor-induced proliferation of CD34+ human hematopoietic progenitor cells. Tretinoin 10-23 colony stimulating factor 3 Homo sapiens 42-79 7524761-6 1994 Retinoids also significantly inhibited G-CSF-induced colony formation in semisolid medium, with 88% inhibition observed at a concentration of retinoic acid of 1 mumol/L. Tretinoin 142-155 colony stimulating factor 3 Homo sapiens 39-44 7523800-0 1994 Modulation of IL-8, IL-1 beta, and G-CSF secretion by all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 64-77 colony stimulating factor 3 Homo sapiens 35-40 7523800-9 1994 Interestingly, the increase of IL-1 beta and G-CSF production in the presence of ATRA was highly correlated to an increase in APL cell count in vitro and in vivo hyperleukocytosis, resulting in fatal outcome. Tretinoin 81-85 colony stimulating factor 3 Homo sapiens 45-50 7520101-4 1994 In contrast, cells induced by G-CSF or GM-CSF alone showed increased DNA syntheses, the levels of which were not significantly affected by the combination of ATRA with CSFs. Tretinoin 158-162 colony stimulating factor 3 Homo sapiens 30-35 7520101-5 1994 Interestingly, G-CSF or GM-CSF potentiated the capability of ATRA-induced cells to reduce nitroblue tetrazolium (NBT), while G-CSF or GM-CSF alone induced no NBT reduction. Tretinoin 61-65 colony stimulating factor 3 Homo sapiens 15-20 7520101-6 1994 Furthermore, in several patients examined, APL cells induced by ATRA with G-CSF showed an increased activity of chemotaxis and CD11a expression. Tretinoin 64-68 colony stimulating factor 3 Homo sapiens 74-79 7520101-7 1994 These findings suggest that G-CSF or GM-CSF can potentiate differentiation of ATRA-induced APL cells while stimulating their proliferating activity as well, and that G-CSF, rather than GM-CSF, may be a useful adjunct to promote ATRA-induced differentiation of APL. Tretinoin 78-82 colony stimulating factor 3 Homo sapiens 28-33 7520101-7 1994 These findings suggest that G-CSF or GM-CSF can potentiate differentiation of ATRA-induced APL cells while stimulating their proliferating activity as well, and that G-CSF, rather than GM-CSF, may be a useful adjunct to promote ATRA-induced differentiation of APL. Tretinoin 228-232 colony stimulating factor 3 Homo sapiens 166-171 21566987-4 1994 The stimulation of t-RA on LPS-mediated G-CSF secretion was dose-dependent and was observed at t-RA concentration of as low as 10(-10) M. Some other retinoids were also as effective as t-RA, whereas other steroids were either less or not effective or inhibitory on LPS-mediated G-CSF secretion. Tretinoin 19-23 colony stimulating factor 3 Homo sapiens 40-45 21566987-4 1994 The stimulation of t-RA on LPS-mediated G-CSF secretion was dose-dependent and was observed at t-RA concentration of as low as 10(-10) M. Some other retinoids were also as effective as t-RA, whereas other steroids were either less or not effective or inhibitory on LPS-mediated G-CSF secretion. Tretinoin 19-23 colony stimulating factor 3 Homo sapiens 278-283 21566987-4 1994 The stimulation of t-RA on LPS-mediated G-CSF secretion was dose-dependent and was observed at t-RA concentration of as low as 10(-10) M. Some other retinoids were also as effective as t-RA, whereas other steroids were either less or not effective or inhibitory on LPS-mediated G-CSF secretion. Tretinoin 95-99 colony stimulating factor 3 Homo sapiens 40-45 8200851-4 1994 For the samples in group C, RA inhibited the colonies formed by granulocyte colony-stimulating factor (G-CSF) but stimulated those by granulocyte macrophage CSF (GM-CSF). Tretinoin 28-30 colony stimulating factor 3 Homo sapiens 64-101 7512172-6 1994 Indomethacin shifted the G-CSF dose-response curve of cells treated with 10 nM RA to lower G-CSF concentrations. Tretinoin 79-81 colony stimulating factor 3 Homo sapiens 25-30 8200851-4 1994 For the samples in group C, RA inhibited the colonies formed by granulocyte colony-stimulating factor (G-CSF) but stimulated those by granulocyte macrophage CSF (GM-CSF). Tretinoin 28-30 colony stimulating factor 3 Homo sapiens 103-108 7512172-6 1994 Indomethacin shifted the G-CSF dose-response curve of cells treated with 10 nM RA to lower G-CSF concentrations. Tretinoin 79-81 colony stimulating factor 3 Homo sapiens 91-96 7504151-4 1993 G-CSF markedly enhanced RA-induced granulocytic differentiation in APL cells obtained from all four cases. Tretinoin 24-26 colony stimulating factor 3 Homo sapiens 0-5 7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 16-29 colony stimulating factor 3 Homo sapiens 323-328 7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 31-35 colony stimulating factor 3 Homo sapiens 323-328 7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 314-318 colony stimulating factor 3 Homo sapiens 41-78 7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 314-318 colony stimulating factor 3 Homo sapiens 80-85 7509208-6 1994 mRNA of NAP is known to be induced by in vitro treatment of the cells with granulocyte colony-stimulating factor (G-CSF), which is enhanced by a simultaneous addition of retinoic acid. Tretinoin 170-183 colony stimulating factor 3 Homo sapiens 75-112 7509208-6 1994 mRNA of NAP is known to be induced by in vitro treatment of the cells with granulocyte colony-stimulating factor (G-CSF), which is enhanced by a simultaneous addition of retinoic acid. Tretinoin 170-183 colony stimulating factor 3 Homo sapiens 114-119 7508772-5 1993 This case supports the concept that G-CSF accelerates ATRA-induced neutrophilic differentiation of blast cells in APL. Tretinoin 54-58 colony stimulating factor 3 Homo sapiens 36-41 1372669-6 1992 The combination of retinoic acid with interferon gamma was most effective in reducing CFU-L recovering (8 responsive/15 AML cases), G-CSF and M-CSF displayed either inhibitory or stimulatory activity in different AML cases. Tretinoin 19-32 colony stimulating factor 3 Homo sapiens 132-137 7689128-1 1993 Recombinant human granulocyte colony-stimulating factor (rhG-CSF) not only enhanced the growth of HL-60 cells, but also significantly increased NBT-reducing ability and alkaline phosphatase (ALP) activity of the cells, which were enhanced by the treatment with retinoic acid (RA). Tretinoin 261-274 colony stimulating factor 3 Homo sapiens 18-55 7686602-2 1993 Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF). Tretinoin 56-69 colony stimulating factor 3 Homo sapiens 274-311 7686602-2 1993 Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF). Tretinoin 56-69 colony stimulating factor 3 Homo sapiens 313-318 1373689-0 1992 Retinoic acid acts to neutralize the inhibitory effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on alkaline phosphatase activity of neutrophils that is induced by granulocyte colony-stimulating factor (G-CSF). Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 183-220 1373689-0 1992 Retinoic acid acts to neutralize the inhibitory effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on alkaline phosphatase activity of neutrophils that is induced by granulocyte colony-stimulating factor (G-CSF). Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 222-227 1721002-5 1991 The results suggest that RA not only inhibits the proliferative action of G-CSF, but also retains and enhances the action of G-CSF to induce differentiation. Tretinoin 25-27 colony stimulating factor 3 Homo sapiens 74-79 1721002-5 1991 The results suggest that RA not only inhibits the proliferative action of G-CSF, but also retains and enhances the action of G-CSF to induce differentiation. Tretinoin 25-27 colony stimulating factor 3 Homo sapiens 125-130 1704851-3 1991 Treatment of neutrophils with both G-CSF and retinoic acid augmented the amount of mRNA for NAP over the amount obtained by G-CSF alone, which was most marked at 24 h. These results show that both G-CSF-mediated NAP induction and its potentiation by retinoic acid are due to the increased levels of mRNA for NAP. Tretinoin 45-58 colony stimulating factor 3 Homo sapiens 124-129 1704851-3 1991 Treatment of neutrophils with both G-CSF and retinoic acid augmented the amount of mRNA for NAP over the amount obtained by G-CSF alone, which was most marked at 24 h. These results show that both G-CSF-mediated NAP induction and its potentiation by retinoic acid are due to the increased levels of mRNA for NAP. Tretinoin 45-58 colony stimulating factor 3 Homo sapiens 124-129 1704851-3 1991 Treatment of neutrophils with both G-CSF and retinoic acid augmented the amount of mRNA for NAP over the amount obtained by G-CSF alone, which was most marked at 24 h. These results show that both G-CSF-mediated NAP induction and its potentiation by retinoic acid are due to the increased levels of mRNA for NAP. Tretinoin 250-263 colony stimulating factor 3 Homo sapiens 35-40 1705636-8 1991 The results suggest that G-CSF stimulates RA-induced morphological and functional differentiation of HL-60 cells, but the differentiation-enhancing effects of GM-CSF are limited, whereas the growth-stimulating effect of GM-CSF on HL-60 cells is greater than that of G-CSF. Tretinoin 42-44 colony stimulating factor 3 Homo sapiens 25-30 2481663-5 1989 G-CSF significantly enhanced the RA-induced granulocytic differentiation of APL cells in vitro. Tretinoin 33-35 colony stimulating factor 3 Homo sapiens 0-5 2451772-2 1988 The phosphorylation of 22 kD, pI 6.0 and 5.8 proteins (pp22) in HL-60 cells or myeloid leukemic cells from patients, was enhanced by treatment with granuloid inducers such as retinoic acid, dimethyl sulfoxide or G-CSF, in common with prostaglandin E2 and theophylline, or dibutyryl c-AMP, which increased intracellular c-AMP. Tretinoin 175-188 colony stimulating factor 3 Homo sapiens 212-217