PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10812245-1 2000 OBJECTIVE: To determine whether the compound STI571 (formerly known as CGP571418B), a selective inhibitor of the protein tyrosine kinase (PTK) activity of ABL and BCR-ABL proteins, preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors (CFU-GM) from patients with chronic myeloid leukemia while sparing normal CFU-GM and to compare responses of CML and normal cells with STI571 and IFN-alpha. Imatinib Mesylate 45-51 interferon alpha 1 Homo sapiens 419-428 22684027-0 2012 Pretreatment with IFN-alpha increases resistance to imatinib mesylate in patients with chronic myelocytic leukemia. Imatinib Mesylate 52-69 interferon alpha 1 Homo sapiens 18-27 25814086-7 2015 Some of the clinical trials testing IFNalpha plus imatinib combination therapy suggest that addition of IFNalpha increases the speed and rate of responses with imatinib therapy. Imatinib Mesylate 50-58 interferon alpha 1 Homo sapiens 104-112 25814086-7 2015 Some of the clinical trials testing IFNalpha plus imatinib combination therapy suggest that addition of IFNalpha increases the speed and rate of responses with imatinib therapy. Imatinib Mesylate 160-168 interferon alpha 1 Homo sapiens 36-44 25814086-7 2015 Some of the clinical trials testing IFNalpha plus imatinib combination therapy suggest that addition of IFNalpha increases the speed and rate of responses with imatinib therapy. Imatinib Mesylate 160-168 interferon alpha 1 Homo sapiens 104-112 25765803-0 2015 [Treatment-free molecular remission achieved by combination therapy with imatinib and IFNalpha in CML with BIM deletion polymorphism relapsed after stop imatinib]. Imatinib Mesylate 153-161 interferon alpha 1 Homo sapiens 86-94 25712735-8 2015 In conclusion, an IFN/imatinib induction treatment followed by a temporary IFN maintenance therapy may enable a high rate of treatment discontinuation in CML patients in at least MMR when stopping imatinib. Imatinib Mesylate 197-205 interferon alpha 1 Homo sapiens 18-21 25712735-8 2015 In conclusion, an IFN/imatinib induction treatment followed by a temporary IFN maintenance therapy may enable a high rate of treatment discontinuation in CML patients in at least MMR when stopping imatinib. Imatinib Mesylate 197-205 interferon alpha 1 Homo sapiens 75-78 24553365-4 2014 Under treatment, significant lowest levels were observed in imatinib+IFN arm. Imatinib Mesylate 60-68 interferon alpha 1 Homo sapiens 69-72 23934954-3 2014 Interferon alpha (IFN) induces hematologic and cytogenetic remissions and interestingly, improved outcome was reported with the combination of interferon and imatinib. Imatinib Mesylate 158-166 interferon alpha 1 Homo sapiens 18-21 21143150-9 2011 Imatinib, a tyrosine kinase inhibitor, is now first line treatment for CML, but two large randomized studies show improved outcome when pegylated IFN-alpha is added to the treatment with imatinib. Imatinib Mesylate 0-8 interferon alpha 1 Homo sapiens 146-155 21821707-3 2011 We found that pretreatment of CML cells with imatinib mesylate augments the antigrowth effects of IFNalpha. Imatinib Mesylate 45-62 interferon alpha 1 Homo sapiens 98-106 20922524-5 2011 Imatinib mesylate was administered upon cytogenetic relapse or disease progression while on IFN-alpha. Imatinib Mesylate 0-17 interferon alpha 1 Homo sapiens 92-101 21143150-9 2011 Imatinib, a tyrosine kinase inhibitor, is now first line treatment for CML, but two large randomized studies show improved outcome when pegylated IFN-alpha is added to the treatment with imatinib. Imatinib Mesylate 187-195 interferon alpha 1 Homo sapiens 146-155 21143150-10 2011 One explanation for this might be that IFN-alpha, contrary to imatinib, stimulates the quiescent stem cells to proliferate and thereby potentially increases sensitivity to imatinib. Imatinib Mesylate 172-180 interferon alpha 1 Homo sapiens 39-48 20845478-6 2011 RESULTS: For patients who received imatinib after failing on IFN-alpha, the 7-year EFS rate was 61%, whereas the CEFS rate was 69%. Imatinib Mesylate 35-43 interferon alpha 1 Homo sapiens 61-70 17692911-6 2008 These results indicate that patients induced into CCR by IFN treatment represent a subset with very favourable prognosis, which can significantly improve molecular response with imatinib and further support investigative treatment schedules combining these two drugs. Imatinib Mesylate 178-186 interferon alpha 1 Homo sapiens 57-60 20142590-4 2010 PATIENTS AND METHODS: Imatinib therapy was stopped in 20 patients who had concomitantly been pretreated with imatinib and IFN for a median of 2.4 years (range, 0.2 to 4.8 years) and 2.5 years (range, 0.2 to 4.9 years), respectively. Imatinib Mesylate 22-30 interferon alpha 1 Homo sapiens 122-125 20142590-11 2010 CONCLUSION: Treatment with IFN enables discontinuation of imatinib in most patients after prior imatinib/IFN combination therapy and may result in improved molecular response. Imatinib Mesylate 58-66 interferon alpha 1 Homo sapiens 27-30 20142590-11 2010 CONCLUSION: Treatment with IFN enables discontinuation of imatinib in most patients after prior imatinib/IFN combination therapy and may result in improved molecular response. Imatinib Mesylate 96-104 interferon alpha 1 Homo sapiens 27-30 19062090-3 2009 Here, we describe five cases of CML in late CP, which were switched to imatinib while in CCR after interferon alpha (IFN alpha) and reached complete and stable molecular remission with intermittent drug administration at 400mg/every 20 days/month. Imatinib Mesylate 71-79 interferon alpha 1 Homo sapiens 117-126 18679373-2 2008 To study the results of treatment with IM after IFN failure/intolerance versus allogeneic BMT (allo-BMT), we retrospectively analyzed 264 patients treated for CML in first chronic phase in three different institutions. Imatinib Mesylate 39-41 interferon alpha 1 Homo sapiens 48-51 17932248-11 2008 Imatinib continues to be an effective and safe therapy for patients with CP CML after failure of IFN. Imatinib Mesylate 0-8 interferon alpha 1 Homo sapiens 97-100 17970609-22 2007 The International randomized Interferon versus STI571 clinical trial was the first to document the efficacy of imatinib as a first-line therapy for patients in CP. Imatinib Mesylate 111-119 interferon alpha 1 Homo sapiens 29-39 17607681-2 2007 The question of whether IFN-alpha-responsive patients can experience further improvements with imatinib has not been answered. Imatinib Mesylate 95-103 interferon alpha 1 Homo sapiens 24-33 17607681-10 2007 Every patient who had already achieved an MMR while receiving IFN-alpha (n = 7 patients) maintained an MMR while receiving imatinib. Imatinib Mesylate 123-131 interferon alpha 1 Homo sapiens 62-71 17607681-12 2007 CONCLUSIONS: These data suggest that switching IFN-alpha-responsive patients to imatinib leads to a rapid improvement in achieving an MMR, a response with established prognostic value, and is well tolerated. Imatinib Mesylate 80-88 interferon alpha 1 Homo sapiens 47-56 17106015-11 2006 Although combinations of imatinib with IFN alpha show small improvements compared to imatinib therapy alone, the biggest improvements were seen when imatinib doses were doubled. Imatinib Mesylate 85-93 interferon alpha 1 Homo sapiens 39-48 17106015-11 2006 Although combinations of imatinib with IFN alpha show small improvements compared to imatinib therapy alone, the biggest improvements were seen when imatinib doses were doubled. Imatinib Mesylate 85-93 interferon alpha 1 Homo sapiens 39-48 15245690-7 2004 RESULTS: Intention-to-treat analysis showed that imatinib was associated with complete CR at 12 months follow-up of 68% compared with 20% for the IFN-alpha plus Ara-C group. Imatinib Mesylate 49-57 interferon alpha 1 Homo sapiens 146-155 16630657-6 2006 We here report on a Ph(+) CML case in long lasting CCR following interferon-alpha treatment (IFN) which reached CMR with imatinib but soon relapsed at molecular level after this latter drug discontinuation; we considered the present observation also in the light of previously reported data. Imatinib Mesylate 121-129 interferon alpha 1 Homo sapiens 93-96 16533530-4 2006 Although protein expression did not consistently match mRNA levels, a role for the two cell cycle regulators in the IFN-alpha signaling pathway is suggested as well as a relation with the resistance to IFN-alpha or imatinib therapy. Imatinib Mesylate 215-223 interferon alpha 1 Homo sapiens 116-125 17263225-3 2006 We present results of a multicenter phase II study on the use of imatinib in chronic phase after failure to interferon-alpha (IFN-alpha). Imatinib Mesylate 65-73 interferon alpha 1 Homo sapiens 126-135 16042686-8 2005 Imatinib and IFN appear to have divergent effects on CML progenitors at different stages of maturation, with imatinib more active against differentiated CML progenitors and IFN more active against primitive CML progenitors. Imatinib Mesylate 0-8 interferon alpha 1 Homo sapiens 173-176 16042686-8 2005 Imatinib and IFN appear to have divergent effects on CML progenitors at different stages of maturation, with imatinib more active against differentiated CML progenitors and IFN more active against primitive CML progenitors. Imatinib Mesylate 109-117 interferon alpha 1 Homo sapiens 13-16 15794712-7 2005 The pivotal registration study for newly diagnosed CML was a large randomised trial comparing 400 mg/day of imatinib to a combination of IFN-alpha and cytarabine, which demonstrated a significantly higher complete haematological and cytogenetic response rate in the imatinib arm. Imatinib Mesylate 266-274 interferon alpha 1 Homo sapiens 137-146 15739029-12 2005 The results of current study indicate that imatinib has a significant therapy benefit in CML patients in whom treatment with IFN alpha had failed. Imatinib Mesylate 43-51 interferon alpha 1 Homo sapiens 125-134 15671523-1 2005 UNLABELLED: Imatinib mesylate (Gleevec, Novartis Pharmaceuticals East Manruer, NJ) received accelerated approval on May 10, 2001 for the treatment of patients with chronic myeloid leukemia (CML) in (a) chronic phase after failure of IFN-alpha therapy, (b) accelerated phase, and (c) blast crisis. Imatinib Mesylate 12-29 interferon alpha 1 Homo sapiens 233-242 15671523-30 2005 CONCLUSIONS: The results confirm those of the interim analysis and suggest that imatinib mesylate represents an effective therapeutic agent for the treatment of patients with CML in chronic phase after failure of IFN-alpha therapy, in blast crisis, and in accelerated phase. Imatinib Mesylate 80-97 interferon alpha 1 Homo sapiens 213-222 15161340-4 2004 Imatinib mesylate was also effective in patients with chronic-phase CML refractory to or intolerant of treatment with IFNalpha (as 400 mg/day) and in those with blast-crisis or accelerated-phase CML (600 mg/day). Imatinib Mesylate 0-17 interferon alpha 1 Homo sapiens 118-126 15128424-3 2004 Imatinib mesylate was started in April 2002 after failure of IFN-alpha to induce a cytogenetic response. Imatinib Mesylate 0-17 interferon alpha 1 Homo sapiens 61-70 14635203-8 2003 One patient continued IFN when treatment with imatinib was started. Imatinib Mesylate 46-54 interferon alpha 1 Homo sapiens 22-25 14669283-2 2003 This was most likely because approximately 90% of patients receiving IFN-alpha plus ara-C changed to imatinib therapy after a median of 8 months into therapy. Imatinib Mesylate 101-109 interferon alpha 1 Homo sapiens 69-78 14734453-0 2004 Survival advantage with imatinib mesylate therapy in chronic-phase chronic myelogenous ;eukemia (CML-CP) after IFN-alpha failure and in late CML-CP, comparison with historical controls. Imatinib Mesylate 24-41 interferon alpha 1 Homo sapiens 111-120 14734453-1 2004 PURPOSE: The purpose of this research was to compare the survival of patients with Philadelphia chromosome (Ph) -positive chronic myelogenous leukemia (CML) post-IFN-alpha failure treated with imatinib to historical experiences with standards of care or other therapies. Imatinib Mesylate 193-201 interferon alpha 1 Homo sapiens 162-171 14734453-13 2004 CONCLUSIONS: This analysis provides evidence for a survival advantage with imatinib versus other therapies in chronic-phase CML post-IFN failure, and for a survival advantage with imatinib versus IFN in late chronic-phase CML. Imatinib Mesylate 75-83 interferon alpha 1 Homo sapiens 133-136 14635203-13 2003 In nine patients imatinib treatment was followed by a rise in leukocyte and platelet counts that required combination with HU or IFN. Imatinib Mesylate 17-25 interferon alpha 1 Homo sapiens 129-132 12970765-2 2003 A significant proportion of chronic myeloid leukemia (CML) patients achieve a major cytogenetic remission (MCR) to imatinib therapy after failing interferon (IFN) alpha-based protocols. Imatinib Mesylate 115-123 interferon alpha 1 Homo sapiens 146-168 14523462-7 2003 We conclude that (i) treatment with imatinib in newly diagnosed CML patients is associated with a rapid decrease of BCR-ABL transcript levels; (ii) nested PCR may reveal residual BCR-ABL transcripts in samples that are negative by real-time PCR; (iii) BCR-ABL transcript levels parallel cytogenetic response, and (iv) imatinib is superior to IFN/Ara-C in terms of the speed and degree of molecular responses, but residual disease is rarely eliminated. Imatinib Mesylate 36-44 interferon alpha 1 Homo sapiens 342-345 14508830-2 2003 The objective of the current study was to evaluate the benefit of adding imatinib to the treatment sequence of patients with early chronic phase Ph-positive CML who received interferon alpha (IFN)-based regimens as frontline therapy. Imatinib Mesylate 73-81 interferon alpha 1 Homo sapiens 192-195 14555307-0 2003 Imatinib mesylate therapy of chronic phase chronic myeloid leukemia resistant or intolerant to interferon: results and prognostic factors for response and progression-free survival in 150 patients. Imatinib Mesylate 0-17 interferon alpha 1 Homo sapiens 95-105 14555307-2 2003 The results of imatinib treatment in chronic-phase CML patients resistant or intolerant to interferon (IFN) and the factors predicting therapeutic response and progression-free survival were analyzed. Imatinib Mesylate 15-23 interferon alpha 1 Homo sapiens 91-107 14555307-3 2003 DESIGN AND METHODS: One hundred and fifty patients with chronic-phase CML resistant (n=111) or intolerant (n=39) to IFN were treated with imatinib. Imatinib Mesylate 138-146 interferon alpha 1 Homo sapiens 116-119 14555307-13 2003 INTERPRETATION AND CONCLUSIONS: Imatinib is highly effective in chronic-phase CML patients resistant or intolerant to IFN, especially in those with normal platelet counts and in those not requiring prolonged treatment discontinuation due to neutropenia. Imatinib Mesylate 32-40 interferon alpha 1 Homo sapiens 118-121 14513038-2 2003 Experimental data suggest that interferon-alpha (IFN-alpha) enhances the antileukemic activity of imatinib. Imatinib Mesylate 98-106 interferon alpha 1 Homo sapiens 49-58 12857554-3 2003 We describe the immunologic findings in patients with chronic myeloid leukemia resistant to or intolerant of interferon (IFN) a who were treated with imatinib. Imatinib Mesylate 150-158 interferon alpha 1 Homo sapiens 109-127 12783377-2 2003 Imatinib (Gleevec) (formerly STI571), a potent inhibitor of BCR-ABL, is very effective in inducing CgRs in chronic-phase CML patients, even in late chronic-phase patients in whom interferon (IFN) was unsuccessful. Imatinib Mesylate 0-8 interferon alpha 1 Homo sapiens 179-195 12389876-5 2002 Imatinib is indicated for the treatment of patients with CML who failed interferon (IFN)-alpha therapy and for the treatment of patients with gastrointestinal stromal tumors (GISTs) expressing the tyrosine kinase receptor c-kit. Imatinib Mesylate 0-8 interferon alpha 1 Homo sapiens 72-94 12389876-12 2002 In cases of CML, imatinib should be further limited to patients who have tried and failed IFN-alpha therapy or who are not candidates for an allogeneic stem cell transplant. Imatinib Mesylate 17-25 interferon alpha 1 Homo sapiens 90-99 11526598-9 2001 Low-dose IFN-alpha may be given after imatinib mesylate-induced remission as a specific immune stimulant to consolidate the remission. Imatinib Mesylate 38-55 interferon alpha 1 Homo sapiens 9-18 11526598-10 2001 Recent data showing a possible additive effect of imatinib mesylate and IFN-alpha suggest that concurrent use of these agents may also be more effective than single use, particularly in advanced stages of CML where imatinib mesylate has activity but resistance develops. Imatinib Mesylate 215-232 interferon alpha 1 Homo sapiens 72-81 12374669-1 2002 PURPOSE: Imatinib mesylate (Gleevec; Novartis, East Hanover, NJ)is a receptor tyrosine kinase inhibitor approved previously in 2001 by the United States Food and Drug Administration for the treatment of chronic myelogenous leukemia in blast crisis, accelerated phase, or in chronic phase after failure of IFN-alpha therapy. Imatinib Mesylate 9-26 interferon alpha 1 Homo sapiens 305-314 12114418-10 2002 In a subset analysis, survival rates among 161 patients with Ph-positive CML after hematological or cytogenetic failure after IFN-alpha who had been treated with imatinib mesylate were better than those for similar patients treated previously with other regimens. Imatinib Mesylate 162-179 interferon alpha 1 Homo sapiens 126-135 12114418-11 2002 In summary, imatinib mesylate is highly effective in chronic-phase CML after IFN-alpha failure. Imatinib Mesylate 12-29 interferon alpha 1 Homo sapiens 77-86