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In: Blood, American Society of Hematology, Vol. 140, No. Supplement 1 ( 2022-11-15), p. 6774-6775

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2022-168228

Language: English

Publisher: American Society of Hematology

Publication Date: 2022

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 140, No. Supplement 1 ( 2022-11-15), p. 6782-6783

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2022-167927

Language: English

Publisher: American Society of Hematology

Publication Date: 2022

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 118, No. 21 ( 2011-11-18), p. 4455-4455

Abstract: Abstract 4455 Introduction: The CML Registry was developed by the Argentine Society of Hematology as a part of the centralized RAEH. Results from epidemiologic and clinical data related to CML, will enable to determine the geographic distribution of the target population, to establish associated environmental causes, and mainly to rationalize resources supply. Objective: a) To analyze characteristics of CML patients registered in the RAEH; b) To evaluate the CML Registry performance through its first year. Materials and Methods: Patients with CML registered in the RAEH from January 1st, 2011 up to July 31st, 2011. The protocol allowed to enroll de novo patients as well as patients diagnosed from 2000 on. Result: Data reported by 15 hospitals were included: 224 patients were registered. Mean age was 50 (18–86 y) and gender distribution was female: 102, male: 122. Occupational data showed no a characteristic pattern. 96.5% of patients were diagnosed in chronic phase, while 3.5% were diagnosed in accelerated phase/blast crisis. In 6% of patients cytogenetic tests detected 8 abnormalities besides t(9,22): double Philadelphia chromosome and monosomy 12 were the most frequent findings. FISH tests were recorded for 18% of patients at the time of diagnosis. Bone marrow biopsy was reported as a diagnostic procedure in 51%. Qualitative BCR/ABL was recorded for 31% of patients at the time of diagnosis. Molecular RQ-PCR tests for follow-up of treatment response were reported for 51% of patients. Of the registered population, 21% received interferon as previous therapy to Imatinib (IM); 89% received IM 400mg daily; 6% required dose increase. Second line treatment with dasatinib or nilotinib was recorded in 34% and 14% of patients, respectively. At 60 months mean follow-up 8% of the registered population had developed blast crisis and 6% had died. Conclusions. The RAEH’s first year of performance in CML was assessed. This only reflects the experience with 15 sites. Data registered will allow us in the following years to learn about disease epidemiology and available resources to improve patient accessibility. Disclosures: No relevant conflicts of interest to declare.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V118.21.4455.4455

Language: English

Publisher: American Society of Hematology

Publication Date: 2011

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 132, No. Supplement 1 ( 2018-11-29), p. 1753-1753

Abstract: Background RESPONSE is a randomized (1:1), open-label, phase 3 study of rux vs BAT in pts with PV who are resistant/intolerant of HU. In RESPONSE, significantly more pts achieved the primary composite end point (hematocrit control [Hct] and a ≥ 35% reduction in spleen volume [SVR] ) with rux compared to BAT (23% vs 1%; P ˂ .0001). The 4-year (y) follow-up confirmed that primary and clinicohematologic (CLHM) responses were sustained with the rux treatment, and the safety profile was consistent with previous reports. Here, we report the long-term efficacy and safety after 5 ys (256 weeks [wks]) of treatment (after last pt first treatment visit) in RESPONSE. Methods PV pts resistant/intolerant of HU (per modified ELN criteria) with splenomegaly requiring phlebotomy (PBT) for Hct control were randomized to rux 10 mg BID or BAT (selected based on investigator's choice). The primary response was a composite end point of achieving both Hct control without PBT (defined as no PBT eligibility between wks 8 to 32 with no more than 1 PBT eligibility from randomization to wk 8) through wk 32 and a ≥ 35% SVR by imaging at wk 32. Key secondary endpoints were durability of the primary response, overall CLHM (Hct control without PBT, platelet count ≤ 400 × 109/L, WBC count ≤ 10 × 109/L, SVR ≥35% by imaging), and long-term safety. Overall survival (OS) was an exploratory end point. Pts randomized to BAT could cross over (CO) to rux after wk 32. Results Pts were randomized to rux (n = 110) and BAT (n = 112). Baseline characteristics were mostly balanced between arms. At baseline, pts randomized to rux were reported to have longer prior exposure to HU compared to BAT (162.9 vs 145.6 wks) and higher frequency of prior nonmelanoma skin cancer (NMSC) or pre-cancerous skin conditions (10.9 vs 6.3%). No pt remained on randomized BAT treatment after wk 80 and median CO time was 34.7 wks. At study completion, 72 pts (66%) in the rux arm and 64 of the 98 pts (65%) who crossed over from BAT completed 5 ys of on-study treatment. Main reason for discontinuation in the BAT arm was lack of efficacy (89%). Adverse events (AEs; 15% and 16%), disease progression (11% and 9% ) and pt decision (6% and 6%) primarily led to treatment discontinuations in the rux arm and CO population, respectively. At final analysis, the KM estimated probability of maintaining primary response for 224 wks (starting from wk 32) in the rux arm was 0.74 (95% CI: 0.51, 0.88) (Figure 1); 6/25 primary responders had progressed by the time of study completion. The probability of maintaining CLHM response for 224 wks (starting from wk 32) was 0.67 (95% CI: 0.54, 0.77) with 21/70 pts who achieved CLHM at wk 32 had progressed. Median duration of primary and CLHM responses had not been reached. In the intent-to-treat analysis not accounting for CO, KM estimates for OS at 5 ys in the rux and BAT arms were 91.9% (95% CI: 84.4, 95.9) and 91.0% (95% CI: 82.8, 95.4), respectively (HR = 0.95 [95% CI: 0.38, 2.41]). There were 2 on-treatment deaths in the rux arm (adenocarcinoma gastric [n = 1, investigator suspected event to be related to study drug] and neoplasm malignant [n = 1, not related to study drug]). In the CO population, 4 pts had fatal AEs leading to 4 on-treatment deaths (not related to rux). No pt died while on BAT. With longer exposure of rux, there was no notable increase in rate of AEs. The most common AEs (exposure-adjusted rate ≥ 5) in the rux arm and CO population were anemia (8.9 and 8.8), pruritus (7.0 and 6.1), diarrhea (7.0 and 3.6), weight increased (6.1 and 4.2), headache (5.8 and 5.2), arthralgia (5.6 and 3.3), fatigue (5.1 and 3.9) and muscle spasms (5.1 and 3.3). Rates (per 100 pt-y) of thromboembolic events were lower in rux-treated pts (1.2) and the CO population (2.7) compared to BAT pts (8.2). The exposure adjusted rates of second malignancies were 7.0 (rux) vs 4.5 (CO) vs 4.1 (BAT). The exposure-adjusted rate of NMSC was 5.1 (rux) vs 2.7 (CO) vs 2.7 (BAT). Rates of transformation to myelofibrosis and acute myeloid leukeimia in the rux arm were 2.1 and 0.2 per 100 pt-y, 1.8 and 0.6 per 100 pt-y in CO population, and 1.4 and 0.0 per 100 pt-y in BAT arm, respectively. Conclusion In HU resistant/intolerant PV pts, clinical benefits of rux treatment (Hct control and CLHM) were durable with long-term therapy. Considering that the OS findings from this analysis are confounded by extensive CO, the observed HR from this analysis represents a conservative estimate of rux benefit. The long-term safety was consistent with previous findings. Disclosures Kiladjian: AOP Orphan: Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding; Celgene: Membership on an entity's Board of Directors or advisory committees. Hino:Otsuka Pharmaceutical Co., Ltd.: Research Funding; Novartis: Research Funding. Pane:Novartis: Research Funding, Speakers Bureau; BMS: Speakers Bureau; AMGEN: Speakers Bureau. Masszi:Pfizer: Consultancy; BMS: Consultancy; AbbVie: Consultancy; Janssen-Cilag: Consultancy; Novartis: Consultancy; Takeda: Consultancy. Harrison:Celgene: Consultancy, Honoraria, Speakers Bureau; Roche: Consultancy, Honoraria; CTI BioPharma: Consultancy, Honoraria; Gilead: Honoraria, Speakers Bureau; Novartis: Consultancy, Honoraria, Research Funding, Speakers Bureau. Mesa:CTI: Research Funding; Promedior: Research Funding; Celgene: Research Funding; Incyte: Research Funding; Gilead: Research Funding; Galena: Consultancy; Ariad: Consultancy; Novartis: Consultancy. Miller:Gilead: Honoraria, Research Funding; Incyte: Consultancy, Honoraria, Research Funding, Speakers Bureau; CTI: Research Funding; Novartis: Honoraria, Speakers Bureau. Passamonti:Janssen: Consultancy, Speakers Bureau; Celgene: Consultancy, Speakers Bureau; Novartis: Consultancy, Honoraria, Speakers Bureau; Roche: Consultancy. Durrant:Novartis: Honoraria, Speakers Bureau. Griesshammer:Novartis: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau. Kirito:Novartis Pharma KK: Honoraria. Besses:Novartis: Honoraria, Research Funding; Shire: Honoraria. Francillard:Novartis: Employment. Dong:Novartis: Employment, Equity Ownership. Wroclawska:Novartis: Employment, Equity Ownership. Verstovsek:Incyte: Consultancy; Italfarmaco: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Celgene: Membership on an entity's Board of Directors or advisory committees.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2018-99-115129

Language: English

Publisher: American Society of Hematology

Publication Date: 2018

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 4766-4766

Abstract: Introduction: The evaluation of response to imatinib in CML patients (pts) as guide to clinical management is undergoing substantial changes of criteria. The degree of reduction of total leukemia cell mass by imatinib as measured by FISH and RQ-PCR studies, correlates with progression-free survival. Therapeutic decisions, as dose scalation, is mandatory in pts with rising level of bcr/abl transcripts. Purpose: To determine the potential of RQ-PCR to predict the duration of response in pts in complete cytogenetic remission (CCyR). Patients and Methods: A total of 160 CML pts in first chronic phase, in CCyR treated with imatinib 400mg daily were studied prospectively since November 2005 (147 pts from 30 hematology centers in Argentina and 13 pts from 2 centers in Uruguay). According to previous treatment they were divided in two groups: 83 pts (51%) received as first line treatment IFN/Cytarabine and 77 pts (49%) received imatinib as first line. According to Sokal Index, 72% were low risk, 19% intermediate risk and 9% high risk. At baseline all pts were first evaluated by FISH and RQ-PCR under EAC program protocol and recommendations of T.P. Hughes, et al (Blood 108:28–37, 2006). Only RQ-PCR is being performed at 6 and 18 months from the beginning of the study. The median duration since beginning with imatinib treatment was 28 months (range 6–58). Results: At the time of first RQ-PCR evaluation, 93% had undetectable bcr/abl fusion gene by FISH and 7% had low level FISH positivity ( 0,1 – 5%). The distribution of the type of molecular responses (MR) in the 160 pts was: Complete (CMR)≥4 log red, U/ & lt;0.01% bcr-abl/c-abl : 23%; Major (MaMR) ≥ 3log red, & lt;0,1%bcr-abl/c-abl : 17%; Minor (MiMR) & gt;2 log red, 1–0,1 % bcr-abl/c-abl : 34%; MiMR & lt; 2log red, 10–1% bcr-abl/c-abl : 15%; Nule (NuMR) & lt;1 log red, & gt; 10%bcr-abl/c-abl : 11%. Pts with Fish (+) showed association with MiMR. Thirty eight percent of pts with a follow-up between 6–24 months since the beginning of imatinib treatment achieved MaMR and CMR, similar rate as the observed in the group with & gt; 24 months on imatinib (42%). Up to July 2006, 53 pts underwent a 2nd RQ-PCR evaluation at 6 months: 15% of pts improved molecular response, 68% maintained it while 17% showed worse response. The 87.5% of pts with decreasing bcr-abl transcripts level at 2nd evaluation corresponded to imatinib treatment as first line. The 78% of pts with rising levels at 2nd evaluation showed MiMR at beginning of this study. Up to now, no pts showed hematological relapse. Conclusion: This is an on-going study in CML pts in CCyR, where 93% showed a negative FISH study, and 7% had low FISH positivity. By RQ-PCR, 40% of pts presented CMR or MaMR (≥3 log red). In 2nd RQ-PCR evaluation, 83% of pts improved or maintained the molecular response. Up to now all pts remain in hematological remission.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V108.11.4766.4766

Language: English

Publisher: American Society of Hematology

Publication Date: 2006

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 4811-4811

Abstract: Imatinib induces complete cytogenetic response (CCyR) in 82% of patients with CML in chronic phase. There is a subset of patients who either failed to achieve or lose hematological/CCyR. Kinase domain mutations have emerged as a potential cause for treatment failure. Aims: In the current study we have investigated ABL kinase domain mutations, amplifications and quantification of BCR-ABL transcripts by Q-PCR in Imatinib resistant patients. Patients and Methods: A total of 84 patients (pts) with CML treated with Imatinib were studied and 82 were evaluable. Sixty-one (74%) were in chronic phase (CP), eleven (14%) were in accelerated phase (AP), and ten (12%) were in blast crisis (BC).We analyzed the DNA from blood samples. Mutations were screened by conformation sensitive gel electrophoresis (CSGE). The amplification products displaying an abnormal pattern were sequenced using automatic system. The amplification of BCR-ABL rearrangement was studied in interphase nuclei using Vysis extra-signaling probe. Real time quantitative PCR (RQ-PCR) of BCR-ABL transcripts was performed in a subset of 44 patients to assess molecular response, using Light Cycler (Roche®), Syber Green Method. Results: Eleven mutations from 82 evaluable patients were detected (13%). Seven were in p- loop: M244R (1), L247A (1), G250E (2), Q252H (1), E255K (2), and four in the Imatinib binding: T315I (3), H318L (1). Two patients had BCR-ABL amplifications with 4–6 signals in interphase nucleous and one of them showed extramedullary involvement in skin nodules. Five patients had clonal evolution with double Ph chromosome. Most of mutations were found in patients in late chronic phase (6/11: 54%). The detection occurred at a median of 49 months (range 12–154) after diagnosis. Eighty four percent of cases studied with RQ-PCR, had null molecular response ( & lt;1Log Reduction). Imatinib dose in patients with mutations had been escalated to 600–800 mg/day previously. Conclusion: This is the first multicentric study in spanish-speaking South America. T315I was the most frequent mutation detected in our study and was associated with poor outcome. We found 13% of resistant cases with point mutations, all of them located in the p-loop or imatinib binding.This is an ongoing study and further recruitment is needed to confirm these findings. Early detection of mutations can have prognostic implication and allow therapeutic intervention such as dose escalation, combination therapy or second generation tyrosine kinase inhibitors.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V108.11.4811.4811

Language: English

Publisher: American Society of Hematology

Publication Date: 2006

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 136, No. Supplement 1 ( 2020-11-5), p. 3-5

Abstract: Introduction: Treatment-free remission (TFR) is an emerging treatment goal for chronic myeloid leukemia (CML) patients in deep molecular response (DMR). Current evidence shows that 40%-60% of patients relapse while in TFR; and nearly all regain response once tyrosine kinase inhibitors (TKIs) treatment are reinitiated. However a robust predictor of prolonged TFR has not been reported yet. Considering real-life setting, 2 key factors may affect TFR outcome if not properly done: Access to serial molecular monitoring at optimal timepoints and quality laboratory terms as accuracy, sensitivity and rapid results. This motivated the creation of the AST study in our region to guarantee adequate molecular monitoring for TFR in Argentina and characterize new prognostic biomarkers helpful to identify more accurately patients who will be able to sustain TFR. We aimed to assess the proportion of patients with sustained major molecular response (MMR) after TKIs discontinuation and define precise conditions for stopping treatment. Methods: This prospective, multicentre Argentina Stop Trial (AST) trial is recruiting chronic phase CML patients under TKI treatment for at least ≥ 4 years, in DMR (≥MR4.0) sustained for ≥ 2 years in standardized laboratory, confirmed typical BCR-ABL1 transcripts b3a2 and/or b2a2 and aged & gt; 18 years. Molecular tests are centralized in 2 harmonized laboratories and performed monthly for the first 6 months, every 2 months until the first year, and every 3 months during the second year. If patients lost MMR, TKI was restarted immediately. Molecular relapse Free Survival was estimated by Kaplan-Meier method. Difference between survival variables was evaluated through log-rank test. Multivariate analysis was performed through Cox proportional hazards model. The cutoffs of the numerical variables were considered according to the log-rank test. Results: Between February 2019 and July 2020, we evaluated 50 CML patients of whom 46 were enrolled from 7 centers in Argentina and 4 were screening failures. Recruitment was interrupted due to COVID-19 pandemic. Patient median age was 57.5 years (range 24-85). Before discontinuation, TKI treatment was as follows: Imatinib 37/46 (80%), Nilotinib 5/46 (11%) and Dasatinib 4/46 (9%), 2G-TKI as 1st line, 11% of the patients received non-branded treatment. Sokal risk score showed to be low in 22 patients (48%), intermediate in 14 (30%) and high in 10 (22%). Median follow-up was 10 months (range 4-17) and the estimated molecular relapse-free survival was 80.2% (95%CI 69-93) at 6 months Fig 1. Longer DMR durations before discontinuation were associated with increased probability of maintaining response at 6 and 12 months: 83.2% for patients who had & gt;54 months in DMR vs 70% with & lt;54 months and 72% vs 23.3% respectively (p=0.0453) Fig 2. Cox multivariate analysis was performed including different variables as age at diagnosis, time in DMR, time in TKI previous to discontinuation and Sokal risk. The only significant variable associated to improved prognosis was time in DMR (HR 2.8 95%CI 1.002-8.07 p=0.0495). Our cohort had a long time on TKI treatment previous to discontinuation, median 10.5 years (4.16-17.5) probably considering it a favorable factor for the high TFR rates described at 6 months. Among the 46 patients included, 15 (33%) lost MMR, all restarted treatment with the same TKI used before discontinuation, 12/15 (80%) regained MMR with a median time of 3 months (range1-8) and 9/15(60%) obtained MR 4.0 with a median time of 3 months (range1-5). Conclusion: This is the first multicenter study of TKI discontinuation in CML patients in Argentina showing that TKI can be safely discontinued in those who achieve and maintain a DMR before discontinuation. We observed high rates of molecular relapse free survival, although longer follow-up is needed. We must continue with this approach for patients participating in TFR trials or TFR programs in order to decrease the risk of relapse and make this goal a fact in our region. This discontinuation study will allow in a near future significant saving of economic resources and might improve patients quality of life specially in those who are currently experiencing treatment adverse events. Disclosures Pavlovsky: Novartis: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; BMS: Speakers Bureau; Pfizer: Speakers Bureau; Pint Pharma: Speakers Bureau. Varela:Novartis: Consultancy, Speakers Bureau. Pavlovsky:Janssen: Membership on an entity's Board of Directors or advisory committees, Other: travel grants, Speakers Bureau; Abbvie: Membership on an entity's Board of Directors or advisory committees, Other: Travel grants, Speakers Bureau; Astra Zeneca: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Varifarma: Speakers Bureau. Moiraghi:BMS: Speakers Bureau; Novartis: Speakers Bureau.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2020-142416

Language: English

Publisher: American Society of Hematology

Publication Date: 2020

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 4267-4267

Abstract: Background: Since the introduction of Imatinib (IM), the treatment of chronic myeloid leukemia (CML) experienced its most important change. As this drug became the first line for the treatment of CML, we learned that under-dosing was associated with a delay in achieving cytogenetic response and the development of acquired resistance. Last year we presented a case-control study that analyzed how compliance affects the cytogenetic response to Imatinib. This is an update of that data. Materials and Methods: Twenty-four patients with newly diagnosed Ph (+) chronic phase CML (CP-CML) were included and followed for 24 months. Patients received 400mg of IM and were asked to note down all taken doses, and reasons for non-compliance. Follow up visits were scheduled every 28–30 days and prescriptions were filled in order to last for only 30 days. During each visit, the medication was counted and non-adherence reasons were determined. Adverse events were graded according to the CTC and modifications in the Imatinib dose were only allowed with related adverse events with a CTC score ≥3. As a control group, we matched each case with a Phi + CP-CML patient from our data base of the same sex and similar age as the case patient. All control patients had to have complete information about dosing and response. They all received initial treatment with IM 400mg; thereafter, dose was adjusted according to each physician’s criteria. Compliance was measured as: mg prescribed/mg taken during the study period. Results: Twenty-four patients, 14 males median age 56 yo (range: 24–83), were included in the study. Three were lost to follow up, leaving only twenty-one for analysis of compliance. At the end of the first year, all patients had complete hematological response. Compliance during these 12 months was 96.1, which is clearly superior to the 80% reported in the setting of clinical trials. All patients had a complete hematological response, 89.9 achieved a major cytogenetic response (MCyR) and 87.4 a complete cytogenetic response (CCyR), compared to 60 of the control group with a MCyR (p=0.027) and 57.8 a CCyR (p=0.025). During the second year, four patients lost CCyR, three responded to an increase in IM dose and one progressed to an accelerated phase and died. Compliance fell slightly during this period to 90.86% which was reflected in 81.66% CCyR, which was still statistically higher than the 54% of major responses in the control group (p=0.033). In both groups, none of the patients not achieving MCyR at 12 months achieved MCyR at 24 months. Hematological toxicity was more frequently observed within the first 6 months of treatment and after the increase in dosage. Severity and incidence of adverse events were similar in both groups, and were the main reasons for interruption or reduction of IM dose in the control group. The only additional difference besides compliance between the two groups was the average IM dose prescribed during the duration of the study (cases group: 430mg – control group: 330mg). Conclusions: Adherence to Imatinib is associated with an improvement in cytogenetic response that can be seen even at two years after the start of therapy. Since outcome and development of resistance seem to be associated with compliance to therapy, emphasis should be put on maintaining treatment at an adequate dose for as long as possible.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V112.11.4267.4267

Language: English

Publisher: American Society of Hematology

Publication Date: 2008

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 34, No. 15_suppl ( 2016-05-20), p. 7054-7054

Type of Medium: Online Resource

ISSN: 0732-183X , 1527-7755

URL: Article

DOI: 10.1200/JCO.2016.34.15_suppl.7054

Language: English

Publisher: American Society of Clinical Oncology (ASCO)

Publication Date: 2016

detail.hit.zdb_id: 2005181-5

In: Clinical Lymphoma Myeloma and Leukemia, Elsevier BV, Vol. 11, No. 3 ( 2011-06), p. 280-285

Type of Medium: Online Resource

ISSN: 2152-2650

URL: Article

DOI: 10.1016/j.clml.2011.03.016

Language: English

Publisher: Elsevier BV

Publication Date: 2011

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detail.hit.zdb_id: 2193618-3