Complete Cytogenetic Response (complete + cytogenetic_response)

Distribution by Scientific Domains


Selected Abstracts


Total CD34+ cells per 10 HPF in bone marrow trephines of patients with chronic myeloid leukaemia correlates with probability of complete cytogenetic response following imatinib treatment

HISTOPATHOLOGY, Issue 6 2007
V Elliot
No abstract is available for this article. [source]


Central nervous system is a sanctuary site for chronic myelogenous leukaemia treated with imatinib mesylate

INTERNAL MEDICINE JOURNAL, Issue 6 2009
Y. Isobe
Abstract Imatinib mesylate (IM) is currently used as the first therapeutic choice against chronic myelogenous leukaemia (CML). Because IM poorly penetrates the blood-brain barrier, IM-treated CML patients may have a potential risk of central nervous system (CNS) involvement. Here we report a case with lymphoid blast crisis isolated only in CNS after bacterial meningitis, although the patient achieved and maintained complete cytogenetic response by IM therapy. It is important to consider isolated CNS blast crisis as a possible event in IM-treated CML patients. [source]


Dasatinib induces complete cytogenetic response and loss of F359C in an imatinib resistant chronic myelocytic leukemia patient,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 6 2009
Celalettin Ustun
No abstract is available for this article. [source]


Dasatinib early intervention after cytogenetic or hematologic resistance to imatinib in patients with chronic myeloid leukemia

CANCER, Issue 13 2009
Alfonso Quintás-Cardama MD
Abstract BACKGROUND: Although many patients with chronic myeloid leukemia (CML) respond well to imatinib therapy, a significant proportion loses their initial response. Loss of response on imatinib is often because of BCR-ABL mutations. Dasatinib is a 325-fold more potent inhibitor of Bcr-Abl than imatinib and has been associated with high rates of durable responses in patients with CML in chronic phase (CP) after imatinib failure. METHODS: To determine the optimal time for initiating dasatinib after loss of response on imatinib, data from dasatinib trials in CML-CP were analyzed. Patients were grouped according to whether they received early intervention with dasatinib (ie, after cytogenetic recurrence on imatinib), rather than after both cytogenetic and hematologic recurrence. RESULTS: Overall, 72% of patients who received dasatinib after loss of a major cytogenetic response (MCyR) on imatinib achieved a complete cytogenetic response (CCyR) compared with 42% of patients who were treated after loss of both MCyR and complete hematologic response (CHR). Event-free survival (EFS) also was higher after earlier dasatinib treatment (24-month EFS rates: 89% after loss of MCyR on imatinib vs 29% after loss of both MCyR and CHR). Among patients who were treated after loss of CHR on imatinib with no prior MCyR, 26% achieved a CCyR with dasatinib, and the 24-month EFS rate was 64%. In all 3 groups, CCyR rates were similar in patients with or without pre-existing BCR-ABL mutations. CONCLUSIONS: The results of the current study suggested that optimal outcomes are achieved when dasatinib is administered early after imatinib resistance. Cancer 2009. © 2009 American Cancer Society. [source]


Cytogenetic and molecular responses and outcome in chronic myelogenous leukemia

CANCER, Issue 4 2008
Need for new response definitions?
Abstract BACKGROUND. Response rates in chronic myeloid leukemia (CML) are now reported based on the cumulative incidence of a single-time best response. The study aim was to examine the significance of different response criteria for CML on imatinib therapy. METHODS. In all, 276 patients with chronic phase CML on imatinib therapy were analyzed. Cytogenetic and molecular responses were coded as to single best response and response at specific intervals of treatment. RESULTS. The cumulative incidence of complete cytogenetic response (CGCR) with imatinib was 91%; however, the incidence of CGCR at 48 months into therapy was only 78%. Similarly, the incidence of major molecular responses (best cumulative vs landmark at 48 months) were 74% versus 62%, and of undetectable BCR-ABL transcripts 38% versus 24%. There was a strong association between achievement of major cytogenetic response (Philadelphia chromosome [Ph]-positivity ,35%) at 6 months to 12 months and survival as well as progression-free survival (PFS). Achievement of major molecular response (vs lesser molecular response) in patients in complete cytogenetic response was not associated with significant differences in survival, but showed some association with PFS. Durable CGCR and major molecular responses (documented continuously for ,12 months) were associated with longer PFS duration but not with survival duration differences. Of interest, major molecular responses documented at least twice were noted in 71% of patients on imatinib therapy; undetectable BCR-ABL transcripts documented at least twice were noted in 34%. CONCLUSIONS. Achievement and durability of CGCR and of major and complete molecular responses at landmark times predict outcome in CML, and may help in comparing the efficacy of different treatments. Cancer 2008. © 2007 American Cancer Society. [source]


Treatment of chronic myeloid leukemia in the imatinib era

CANCER, Issue 6 2007
Perspective from a developing country
Abstract BACKGROUND There is paucity of data from developing countries on the efficacy and safety of imatinib mesylate in chronic myeloid leukemia (CML). The primary objective of this study was to document complete and partial cytogenetic responses to imatinib in all phases of CML. Secondary objectives included evaluations of complete hematologic response, safety, time to progression, and survival. METHODS Two hundred seventy-five patients in all phases of CML who received treatment with imatinib from January 2001 to December 2005 were included in the study. All patients had on bone marrow or BCR-ABL positive in peripheral blood by polymerase chain reaction. RESULTS After a median follow-up of 18 months, major cytogenetic responses (Ph <35%) in chronic phase (CP), accelerated phase (AP), and blastic phase (BP) were documented in 61%, 57%, and 28% of patients, respectively. A complete cytogenetic response was observed in 39.4%, 35.7%, and 14.3% of patients in CP, AP, and BP, respectively; and a complete hematologic response was observed in 90%, 86%, and 30%, respectively. The median time to progression at 18 months was 91% in CP and 68% in AP. The overall survivals in CP, AP, and BP at 18 months was 92%, 74%, and 38%, respectively. CONCLUSIONS Impressive hematologic, cytogenetic, and molecular responses to imatinib were observed, similar to the responses reported in patients from Western countries. Patients had good compliance, toxicity was limited, and overall quality of life was improved markedly. The results indicated that the biology of CML is not different in patients from developing countries. Cancer 2007 © 2007 American Cancer Society. [source]


Thalidomide therapy in adult patients with myelodysplastic syndrome

CANCER, Issue 4 2006
A North Central Cancer Treatment Group phase II trial
Abstract BACKGROUND. Thalidomide has shown promise for the treatment of patients with myelodysplastic syndrome. The current prospective multicenter study examined the efficacy and toxicity of thalidomide in adult patients with myelodysplastic syndrome. METHODS. Using the International Prognostic Scoring System (IPSS), patients were stratified into 2 groups: favorable (IPSS score, 0,1.0) or unfavorable (IPSS score, 1.5,3.5). Seventy-two patients (42 of whom were favorable and 30 of whom were unfavorable) received a starting dose of oral thalidomide of 200 mg daily. The dose was increased by 50 mg per week to a targeted maximum daily dose of 1000 mg. RESULTS. According to the International Working Group response criteria for myelodysplastic syndrome, 1 patient in the unfavorable group achieved a partial remission with a complete cytogenetic response. Overall, 2 patients (5%) in the favorable group and 4 patients (14%) in the unfavorable group experienced either a hematologic improvement or a partial response. The most frequent Grade 3 or 4 (grading was based on the National Cancer Institute's Common Toxicity Criteria [version 2.0]) nonhematologic adverse events were fatigue (24%), infection (19%), neuropathy (13%), dyspnea (8%), and constipation (7%). CONCLUSIONS. Thalidomide alone, at the schedule and dose levels used in the current study, is not a safe and viable therapeutic option for patients with myelodysplastic syndrome. Limited efficacy and increased toxicity were observed in the current Phase II trial. Cancer 2006. © 2006 American Cancer Society. [source]


Phase I/II trial of adding semisynthetic homoharringtonine in chronic myeloid leukemia patients who have achieved partial or complete cytogenetic response on imatinib

CANCER, Issue 9 2005
David Marin M.D.
Abstract BACKGROUND A Phase I/II study was designed to show whether the addition of semisynthetic homoharringtonine (sHHT) would reduce the level of residual disease in patients with Ph-positive chronic myeloid leukemia who appeared to have achieved a suboptimal response to imatinib alone. METHODS Patients with CML who had achieved , 35% Ph-negativity on imatinib were included. All patients had been treated with imatinib at , 400 mg/day for at least 2 years and had achieved a plateau in BCR-ABL transcripts defined by measuring BCR-ABL transcripts on at least 4 occasions over a minimum period of 1 year with the latest value not lower than the previous minimum value. Initially sHHT was given subcutaneously at a dose of 1.25 mg/m2 twice daily for 1 day. Courses were repeated every 28 days. The dosage of sHHT was escalated by adding one day of treatment every two days. Efficacy was assessed by serial monitoring of blood levels of BCR-ABL transcripts. RESULTS Of 10 evaluable patients, 7 had an appreciable decline in BCR-ABL transcript levels; in 5 cases the reduction was greater than 1 log. Asthenia (n = 10) and cytopenias (n = 3) were prominent side-effects, but the drug was generally well tolerated. Mutations in the P-loop of the BCR-ABL kinase domain were found in 2 of the patients who responded to the addition of sHHT. CONCLUSIONS The addition of sHHT should be considered for patients on imatinib who fail to obtain low levels of minimal residual disease. Cancer 2005. © 2005 American Cancer Society. [source]


Long-term survival estimates for imatinib versus interferon-, plus low-dose cytarabine for patients with newly diagnosed chronic-phase chronic myeloid leukemia,,

CANCER, Issue 11 2004
Kevin J. Anstrom Ph.D.
Abstract BACKGROUND The authors estimated survival among patients with chronic myeloid leukemia for a cost-effectiveness analysis of imatinib versus interferon-, plus low-dose cytarabine (IFN+LDAC). METHODS Two-year survival and cytogenetic response were determined using data from 553 patients who received first-line imatinib in the International Randomized Interferon versus ST571 Study (IRIS). Long-term survival was modeled on complete cytogenetic response (CCyR) after 2 years. Long-term survival for patients with a CCyR was modeled using data from a cohort study of 317 patients with CCyRs. Long-term survival for patients without a CCyR was modeled using data from a trial of 275 patients who were treated with IFN+LDAC. Computation of lifetime survival estimates for imatinib assumed a proportional hazards relation between survival for an age-matched and gender-matched cohort and survival for patients with and without a CCyR. RESULTS For IRIS patients receiving imatinib, the estimated survival was 95.8% and the CCyR rate was 73.8%. The average residual life expectancy was estimated to be 16.71 years for CCyR patients and 5.78 years for non-CCyR patients. The estimated life expectancy after treatment with imatinib was 15.30 years, compared with 9.07 years for patients who were treated with IFN+LDAC in previous studies. CONCLUSIONS Assuming the relation between CCyR and survival with interferon-, holds for imatinib, higher CCyR rates with imatinib therapy will result in an estimated 6.23 life-years gained compared with treatment with IFN+LDAC. Cancer 2004. © 2004 American Cancer Society. [source]