natgillin/translations-raw huggingface dataset:
Hvor estimeret 97% (93%) af patienterne med CCyR (PCyR) ved 12 måneder var fri for progression til accelereret fase/ blastkrise ved 60 måneder, var kun 81% af patienterne uden CCyR ved 12 måneder fri for progression til fremskreden CML ved 60 måneder (p < 0, 001 samlet, p=0, 20 mellem CCyR og PCyR).
Whereas an estimated 97% (93%) of patients with CCyR (PCyR) at 12 months were free of progression to accelerated phase/ blast crisis at 60 months, only 81% of patients without MCyR at 12 months were free of progression to advanced CML at 60 months (p < 0.001 overall, p=0.20 between CCyR and PCyR).
For patienter med CCyR og reduktion i Bcr- Abl transkripter på mindst 3 logaritmer ved 12 måneder, var sandsynligheden for at forblive fri for progression til accelereret fase/ blastkrise 100% efter 60 måneder.
For patients with CCyR and reduction in Bcr-Abl transcripts of at least 3 logarithms at 12 months, the probability of remaining free from progression to accelerated phase/ blast crisis was 100% at 60 months.
Lignende resultater fandtes baseret 15 på analysen efter 18 måneder.
Similar findings were found based on a 18-months landmark analysis.
De mere hyppige bivirkninger var gastrointestinal blødning, konjunktivitis og stigning i transaminase eller bilirubin.
The more frequent adverse reactions included gastrointestinal haemorrhages, conjunctivitis and elevation of transaminases or bilirubin.
Kronisk fase; manglende effekt med Interferon:
Chronic phase, Interferon failure:
Manglende hæmatologisk effekt (29%), manglende cytogenetisk effekt (35%) eller interferonintolerans (36%).
The patients were distributed in three main categories: haematological failure (29%), cytogenetic failure (35%), or intolerance to interferon (36%).
Patienterne havde i gennemsnit tidligere modtaget 14 måneders IFN- behandling med doser ≥25 x 106 IU/ uge og var alle i sen kronisk fase med en gennemsnitlig tid siden diagnose på 32 måneder.
Patients had received a median of 14 months of prior IFN therapy at doses ≥ 25 x 106 IU/ week and were all in late chronic phase, with a median time from diagnosis of 32 months.
Undersøgelsens primære effektvariable var graden af det cytogenetiske hovedrespons (fuldstændigt plus partielt respons, 0– 35% Ph+ - metafaser i knoglemarven).
The primary efficacy variable of the study was the rate of major cytogenetic response (complete plus partial response, 0 to 35% Ph+ metaphases in the bone marrow).
I denne undersøgelse opnåede 65% af patienterne et cytogenetisk hovedrespons, som var fuldstændigt hos 53% (bekræftet 43%) af patienterne (Tabel 4).
In this study 65% of the patients achieved a major cytogenetic response that was complete in 53% (confirmed 43%) of patients (Table 4).
Accelereret fase:
Accelerated phase:
Den primære effektvariable var graden af hæmatologisk hovedrespons, rapporteret enten som fuldstændigt hæmatologisk respons, intet tegn på leukæmi (f. eks. clearance af blaster fra knoglemarv og blod, men uden fuldstændig restitution i perifert blod som ved fuldstændigt respons) eller remission til CML i kronisk fase.
The primary efficacy variable was the rate of haematological response, reported as either complete haematological response, no evidence of leukaemia (i. e. clearance of blasts from the marrow and the blood, but without a full peripheral blood recovery as for complete responses), or return to chronic phase CML.
Der opnåedes konfirmeret hæmatologisk respons hos 71, 5% af patienterne (Tabel 4).
A confirmed haematological response was achieved in 71.5% of patients (Table 4).
Væsentligt er det, at 27, 7% af patienterne også opnåede et cytogenetisk hovedrespons, hvilket var fuldstændigt hos 20, 4% (bekræftet 16%) af patienterne.
Importantly, 27.7% of patients also achieved a major cytogenetic response, which was complete in 20.4% (confirmed 16%) of patients.
For patienter behandlet med 600 mg, var de nuværende estimater for median progressionsfri overlevelse og overlevelse i det hele taget henholdsvis 22, 9 og 42, 5 måneder.
For the patients treated at 600 mg, the current estimates for median progression-free-survival and overall survival were 22.9 and 42.5 months, respectively.
Myeloid blastkrise:
Myeloid blast crisis:
95 (37%) havde tidligere modtaget kemoterapi til behandling af enten accelereret fase eller blastkrise (” tidligere behandlede patienter ”), hvorimod 165 (63%) ikke havde (” ubehandlede patienter ”).
95 (37%) had received prior chemotherapy for treatment of either accelerated phase or blast crisis (“ pretreated patients”) whereas 165 (63%) had not (“ untreated patients”).
I denne undersøgelse opnåede 31% af patienterne et hæmatologisk respons (36% af de tidligere ” ubehandlede patienter ” og 22% af de ” tidligere behandlede patienter ”).
The rate of
Hovedresponsniveauet var også større hos patienter behandlet med 600 mg (33%) sammenlignet med patienter behandlet med 400 mg (16%, p=0, 0220).
16 response was also higher in the patients treated at 600 mg (33%) as compared to the patients treated at 400 mg (16%, p=0.0220).
Den aktuelle estimerede gennemsnitlige overlevelse hos tidligere ” ubehandlede ” og ” behandlede patienter ” var henholdsvis 7, 7 og 4, 7 måneder.
The current estimate of the median survival of the previously untreated and treated patients was 7.7 and 4.7 months, respectively.
Incidensen af hæmatologisk respons var 70% med en varighed på 2– 3 måneder.
The rate of haematological response was 70% with a duration of 2– 3 months.
16 Tabel 4
Table 4
Respons hos voksne CML- patienter
Response in adult CML studies
Undersøgelse 0110 37 måneders data Kronisk fase, IFN - svigt (n=532) 1
Study 0110
Undersøgelse 0109 40, 5 måneders data Accelereret fase (n=235)% patienter (CI95%)
Study 0109
Undersøgelse 0102 38 måneders data Myeloid blastkrise (n=260)
Study 0102
Hæmatologisk
40.5-month data
respons 95% (92, 3- 96, 3)
Chronic phase, IFN failure (n=532)
71% (65, 3- 77, 2)
Accelerated phase (n=235)
31% (25, 2– 36, 8)
Myeloid blast crisis (n=260)
Fuldstændigt hæmatologisk respons (CHR)
% of patients (CI95%) 1 Haematological response Complete haematological response (CHR)
95%
95% (92.3– 96.3) 95%
42%
71% (65.3– 77.2) 42%
8%
31% (25.2– 36.8) 8%
12% 17%
12%
Cytogenetisk hovedrespons2 Fuldstændigt
Major cytogenetic response Complete
65% (61, 2- 69, 5) 53%
65% (61.2– 69.5) 53%
28% (22, 0- 33, 9) 20%
28% (22.0– 33.9) 20%
(Bekræftet3) [95% CI] Delvist
(Confirmed3) [95% CI] Partial
(43%) [38, 6- 47, 2] 12%
(43%) [38.6– 47.2] (16%) [11.3– 21.0] 12% 7%
[0, 6- 4, 4] 8%
[0.6– 4.4] 8%
Hæmatologiske responskriterier (hvert respons skal bekræftes ≥4 uger):
Haematological response criteria (all responses to be confirmed after ≥ 4 weeks):
CHR:
CHR:
RTC: < 15% blaster I BM og PB, < 30% blaster + promyelocytter in BM og PB, < 20% basofilocytter i PB, ingen ekstramedullær sygdom andet end milt og lever (kun 0102 og 0109).
Study 0110 [WBC < 10 x 109/ l, platelets < 450 x 109/ l, myelocyte+metamyelocyte < 5% in blood, no blasts and promyelocytes in blood, basophils < 20%, no extramedullary involvement] and in studies 0102 and 0109 [ANC ≥ 1.5 x 109/ l, platelets ≥ 100 x 109/ l, no blood blasts, BM blasts < 5% and no extramedullary disease] NEL Same criteria as for CHR but ANC ≥ 1 x 109/ l and platelets ≥ 20 x 109/ l (0102 and 0109 only) RTC < 15% blasts BM and PB, < 30% blasts+promyelocytes in BM and PB, < 20% basophils in PB, no extramedullary disease other than spleen and liver (only for 0102 and 0109).
2 Cytogenetiske responskriterier:
BM = bone marrow, PB = peripheral blood 2 Cytogenetic response criteria:
3 Fuldstændigt cytogenetisk respons bekræftet ved endnu en cytogenetisk knoglemarvsundersøgelse udført mindst 1 måned efter den initial knoglemarvsundersøgelse.
A major response combines both complete and partial responses: complete (0% Ph+ metaphases), partial (1– 35%) 3 Complete cytogenetic response confirmed by a second bone marrow cytogenetic evaluation performed at least one month after the initial bone marrow study.
Ialt 26 pædiatriske patienter i alderen < 18 år med enten CML i kronisk fase (n=11) eller CML i blastkrise eller Ph+ akut leukæmi (n=15) blev inkluderet i en fase I undersøgelse med dosis- eskalering.
A total of 26 paediatric patients of age < 18 years with either chronic phase CML (n=11) or CML in blast crisis or Ph+ acute leukaemias (n=15) were enrolled in a dose-escalation phase I trial.
Det var en population af patienter, der i udtalt grad tidligere havde modtaget anden behandling, eftersom 46% tidligere havde modtaget BMT og 73% tidligere havde modtaget multi- stof kemoterapi.
This was a population of heavily pretreated patients, as 46% had received prior BMT and 73% a prior multi-agent chemotherapy.
Patienterne blev behandlet med Glivec- doser på 260 mg/ m2/ dag (n=5), 340 mg/ m2/ dag (n=9), 440 mg/ m2/ dag (n=7) og 570 mg/ m2/ dag (n=5).
Patients were treated at doses of Glivec of 260 mg/ m2/ day (n=5), 340 mg/ m2/ day (n=9), 440 mg/ m2/ day (n=7) and 570 mg/ m2/ day (n=5).
Af 9 patienter med kronisk fase CML og tilgængelige cytogenetiske data opnåede henholdsvis 4 (44%) og 3 (33%) fuldstændigt og delvist cytogenetisk respons, med en McyR- rate på 77%.
Out of 9 patients with chronic phase CML and cytogenetic data available, 4 (44%) and 3 (33%) achieved a complete and partial cytogenetic response, respectively, for a rate of MCyR of 77%.
Hvis der ikke var dosisbegrænsende toksicitet, blev patienterne behandlet med 340 mg/ m2/ dag uden afbrydelse.
Patients were treated with Glivec 340 mg/ m2/ day, with no interruptions in the absence of dose limiting toxicity.
Glivec- behandling inducerer et hurtigt respons hos nydiagnosticerede pædiatriske CML- patienter med en CHR hos 78% efter 8 ugers behandling.
Glivec treatment induces a rapid response in newly diagnosed paediatric CML patients with a CHR of 78% after 8 weeks of therapy.
Derudover sås partielt cytogetisk respons (PCyR) hos 16%, dermed MCyR hos 81%.
The
Hovedparten af patienterne, som opnåede CCyR, udviklede dette mellem 3. og 10. måned med en mediantid til respons på 5, 6 måneder baseret på et Kaplan- Meier estimat.
17 majority of patients who achieved a CCyR developed the CCyR between months 3 and 10 with a median time to response based on the Kaplan-Meier estimate of 5.6 months.
Kliniske studier ved Ph+ ALL Nydiagnostiseret Ph+ ALL:
Clinical studies in Ph+ ALL Newly diagnosed Ph+ ALL:
I et kontrolleret studie (ADE10) hvor imatinib blev sammenlignet med kemoterapi- induktion hos 55 nydiagnostiserede patienter i alderen 55 år og derover, gav imatinib brugt som monoterapi anledning til en signifikant højere ratio af hæmalogisk respons end kemopterapi
In a controlled study (ADE10) of imatinib versus chemotherapy induction in 55 newly diagnosed patients aged 55 years and over, imatinib used as single agent induced a significantly higher rate of complete haematological response than chemotherapy (96.3% vs.
17 (96, 3% versus 50%, p=0, 0001).
50%; p=0.0001).
Da imatinib blev givet som ” salvage therapy ” til patienter, som ikke responderede eller som responderede dårligt på kemoterapi, opnåedes komplet hæmatologisk respons hos 9 (81, 8%) ud af 11 patienter.
When salvage therapy with imatinib was administered in patients who did not respond or who responded poorly to chemotherapy, it resulted in 9 patients (81.8%) out of 11 achieving a complete haematological response.
Denne kliniske effekt var efter 2 ugers behandling forbundet med en højere reduktion i bcr- abl transkriptionen hos de imatinibbehandlede patienter end i kemoterapiarmen (p=0, 02).
This clinical effect was associated with a higher reduction in bcr- abl transcripts in the imatinib-treated patients than in the chemotherapy arm after 2 weeks of therapy (p=0.02).
Alle patienter blev efter induktion behandlet med imatinib og standard kemoterapi (se Tabel 5), og bcr- abl transkriptionerne var identiske i de to arme efter 8 ugers behandling.
All patients received imatinib and consolidation chemotherapy (see Table 5) after induction and the levels of bcr-abl transcripts were identical in the two arms at 8 weeks.
Som det var forventet på basis af studiedesignet, sås ingen forskel i varighed af remission, sygdomsfri overlevelse eller generel overlevelse, skønt patienter med komplet molekylær respons og forblivende i minimal residual sygdom havde større udbytte af behandlingen i form af både varighed af remission (p=0, 01) og sygdomsfri overlevelse (p=0, 02).
As expected on the basis of the study design, no difference was observed in remission duration, disease-free survival or overall survival, although patients with complete molecular response and remaining in minimal residual disease had a better outcome in terms of both remission duration (p=0.01) and disease-free survival (p=0.02).
Imatinib givet i kombination med kemoterapi- induktion (se Tabel 5) resulterede i en komplet hæmatologisk responsrate på 93% (147 ud af 158 evaluerbare patienter), og i en væsentlig cytogenetisk responsrate på 90% (19 ud af 21 evaluerbare patienter).
Imatinib in combination with chemotherapy induction (see Table 5) resulted in a complete haematological response rate of 93% (147 out of 158 evaluable patients) and in a major cytogenetic response rate of 90% (19 out of 21 evaluable patients).
Sygdomsfri overlevelse (disease- free survival DFS) og overordnede overlevelse (overall survival OS) var konstant mere end 1 år og var superior til historiske kontroller (DFS p < 0, 001; OS p < 0, 0001) i to studier (AJp01 og AUS01).
Disease-free survival (DFS) and overall survival (OS) constantly exceeded 1 year and were superior to historical control (DFS p < 0.001; OS p < 0.0001) in two studies (AJP01 and AUS01).
Kemoterapiregime anvendt i kombination med imatinib
Chemotherapy regimen used in combination with imatinib
DEX 10 mg/ m2 oral, dag 1- 5; CP 200 mg/ m2 i. v., dag 3, 4, 5; MTX 12 mg intrathecal, dag 1
DEX 10 mg/ m2 oral, days 1-5; CP 200 mg/ m2 i. v., days 3, 4, 5; MTX 12 mg intrathecal, day 1
DEX 10 mg/ m2 oral, dag 6- 7, 13- 16; VCR 1 mg i. v., dag 7, 14; IDA 8 mg/ m2 i. v.
DEX 10 mg/ m2 oral, days 6-7, 13-16; VCR 1 mg i. v., days 7, 14; IDA 8 mg/ m2 i. v.
(0, 5 time), dag 7, 8, 14, 15; CP 500 mg/ m2 i. v. (1 time) dag 1; Ara- C 60 mg/ m2 i. v., dag 22- 25, 29- 32
(0.5 h), days 7, 8, 14, 15; CP 500 mg/ m2 i. v. (1 h) day 1; Ara- C 60 mg/ m2 i. v., days 22-25, 29-32
Konsoliderende behandling I, III, V Konsoliderende behandling II, IV Studie AAU02
Consolidation therapy I, III, V
(24 timer), dag 1, 15; 6- MP 25 mg/ m2 oral, dag 1 - 20 Ara- C 75 mg/ m2 i. v.
(24 h), days 1, 15; 6-MP 25 mg/ m2 oral, days 1-20
(1 time), dag 1- 5; VM26 60 mg/ m2 i. v.
(1 h), days 1-5; VM26 60 mg/ m2 i. v.
(1 time), dag 1- 5
(1 h), days 1-5
Daunorubicin 30 mg/ m2 i. v., dag 1- 3, 15- 16; VCR 2 mg total dose i. v., dag 1, 8, 15, 22; CP 750 mg/ m2 i. v., dag 1, 8; prednison 60 mg/ m2 oral, dag 1- 7, 15- 21; IDA 9 mg/ m2 oral, dag 1- 28; MTX 15 mg intrathecal, dag 1, 8, 15, 22; Ara- C 40 mg intrathecal, dag 1, 8, 15, 22; methylprednisolon 40 mg intrathecal, dag 1, 8, 15, 22
Daunorubicin 30 mg/ m2 i. v., days 1-3, 15-16; VCR 2 mg total dose i. v., days 1, 8, 15, 22; CP 750 mg/ m2 i. v., days 1, 8; prednisone 60 mg/ m2 oral, days 1-7, 15-21; IDA 9 mg/ m2 oral, days 1-28; MTX 15 mg intrathecal, days 1, 8, 15, 22; Ara-C 40 mg intrathecal, days 1, 8, 15, 22; methylprednisolone 40 mg intrathecal, days 1, 8, 15, 22
Konsoliderende behandling (de novo Ph+ ALL) Studie ADE04
Consolidation (de novo Ph+ ALL) Study ADE04
Ara- C 1. 000 mg/ m2/ 12 timer i. v. (3 timer), dag 1- 4; mitoxantron 10 mg/ m2 i. v. dag 3- 5; MTX 15 mg intrathecal, dag 1; methylprednisolon 40 mg intrathecal, dag 1
Ara-C 1,000 mg/ m2/ 12 h i. v. (3 h), days 1-4; mitoxantrone 10 mg/ m2 i. v. days 3-5; MTX 15 mg intrathecal, day 1; methylprednisolone 40 mg intrathecal, day 1
DEX 10 mg/ m2 oral, dag 1- 5; CP 200 mg/ m2 i. v., dag 3- 5; MTX 15 mg intrathecal, dag 1
DEX 10 mg/ m2 oral, days 1-5; CP 200 mg/ m2 i. v., days 3-5; MTX 15 mg intrathecal, day 1
Induktionsbehandling I Induktionsbehandling II Konsoliderende behandling Studie AJP01
Induction therapy I
DEX 10 mg/ m2 oral, dag 1- 5; VCR 2 mg i. v., dag 6, 13, 20; daunorubicin 45 mg/ m2 i. v., dag 6- 7, 13- 14 CP 1 g/ m2 i. v.
DEX 10 mg/ m2 oral, days 1-5; VCR 2 mg i. v., days 6, 13, 20; daunorubicin 45 mg/ m2 i. v., days 6-7, 13-14
(1 time), dag 26, 46; Ara- C 75 mg/ m2 i. v.
(1 h), days 26, 46; Ara-C 75 mg/ m2 i. v.
(1 time), dag 28 - 31, 35- 38, 42- 45; 6- MP 60 mg/ m2 oral, dag 26- 46 DEX 10 mg/ m2 oral, dag 1- 5; vindesin 3 mg/ m2 i. v., dag 1; MTX 1, 5 g/ m2 i. v.
DEX 10 mg/ m2 oral, days 1-5; vindesine 3 mg/ m2 i. v., day 1; MTX 1.5 g/ m2 i. v.
(24 timer), dag 1; etoposid 250 mg/ m2 i. v.
(24 h), day 1; etoposide 250 mg/ m2 i. v.
(1 time) dag 4- 5; Ara- C 2x 2 g/ m2 i. v.
(1 h) days 4-5; Ara- C 2x 2 g/ m2 i. v.
(3 timer), dag 1; daunorubicin 60 mg/ m2 i. v.
(3 h), day 1; daunorubicin 60 mg/ m2 i. v.
18 dag 1- 3; vinkistin 1, 3 mg/ m2 i. v., dag 1, 8, 15, 21; prednisolon 60 mg/ m2/ dag oral
(1 h), days 1-3; vincristine 1.3 mg/ m2 i. v., days 1, 8, 15, 21; prednisolone 60 mg/ m2/ day oral
Supplerende kemoterapi omgange: høj- dosis kemoterapi med MTX 1 g/ m2 i. v.
Alternating chemotherapy course: high dose chemotherapy with MTX 1 g/ m2 i. v.
(24 timer), dag 1, og Ara- C 2 g/ m2 i. v.
(24 h), day 1, and Ara-C 2 g/ m2 i. v.
(q 12 timer), dag 2- 3, i 4 cyklus
(q 12 h), days 2-3, for 4 cycles
Vedligeholdelse Studie AUS01
Maintenance Study AUS01
VCR 1, 3 g/ m2 i. v., dag 1; prednisolon 60 mg/ m2 oral, dag 1- 5
VCR 1.3 g/ m2 i. v., day 1; prednisolone 60 mg/ m2 oral, days 1-5
Induktions - konsoliderende behandling
Induction- consolidation therapy
Hyper- CVAD regimen:
Hyper-CVAD regimen:
(3 timer, q 12 timer), dag 1- 3; vinkristin 2 mg i. v., dag 4, 11; doxorubicin 50 mg/ m2 i. v.
(3 h, q 12 h), days 1-3; vincristine 2 mg i. v., days 4, 11; doxorubicine 50 mg/ m2 i. v.
(24 timer), dag 4; DEX 40 mg/ dag på dag 1- 4 og 11- 14, supplerende med MTX 1 g/ m2 i. v.
(24 h), day 4; DEX 40 mg/ day on days 1-4 and 11-14, alternated with MTX 1 g/ m2 i. v.
(24 timer), dag 1, Ara- C 1 g/ m2 i. v.
(24 h), day 1, Ara-C 1 g/ m2 i. v.
(2 timer, q 12 timer), dag 2- 3 (total af 8 omgange)
(2 h, q 12 h), days 2-3 (total of 8 courses)
VCR 2 mg i. v. månedligt i 13 måneder; prednisolon 200 mg oral, 5 dag per måned i 13 måneder
VCR 2 mg i. v. monthly for 13 months; prednisolone 200 mg oral, 5 days per month for 13 months
inkluderer administration af steroider mod CNS profylakse
All treatment regimens include administration of steroids for CNS prophylaxis.
Ara- C: cytosin arabinosid; CP: cyclophosphamid; DEX: dexamethason; MTX: methotrexat; 6 - MP:
Ara-C: cytosine arabinoside; CP: cyclophosphamide; DEX: dexamethasone; MTX: methotrexate; 6-MP:
6- mercaptopurin; VM26: teniposid; VCR: vinkristin; IDA: idarubicin; i. v.: intravenøs
Teniposide; VCR: vincristine; IDA: idarubicine; i. v.: intravenous
Recidiverendet/ refraktær Ph+ ALL:
Relapsed/ refractory Ph+ ALL:
Da imatinib blev brugt som enkeltstofbehandling ved recidiverende/ refraktær Ph+ ALL var resultatet hos 53 ud af 411 evaluerbare patienter en hæmatologisk responsrate på 30% (9% komplet) og en væsentlig cytogenetisk responsrate på 23%.
When imatinib was used as single agent in patients with relapsed/ refractory Ph+ ALL, it resulted, in the 53 out of 411 patients evaluable for response, in a haematological response rate of 30% (9% complete) and a major cytogenetic response rate of 23%.
Mediantid før progression varierede i den samlede population af 411 patienter med recidiverende/ refraktær Ph+ ALL fra 2, 6 til 3, 1 måned, og median for samlet overlevelse hos de 401 evaluerbare patienter varierede fra 4, 9 til 9 måneder.
(Of note, out of the 411 patients, 353 were treated in an expanded access program without primary response data collected.) The median time to progression in the overall population of 411 patients with relapsed/ refractory Ph+ ALL ranged from 2.6 to 3.1 months, and median overall survival in the 401 evaluable patients ranged from 4.9 to 9 months.
Kliniske undersøgelser vedrørende MDS/ MPD Der er meget begrænset erfaring med Glivec ved denne indikation, og den er baseret på hæmatologiske og cytogenetiske responsrater.
Clinical studies in MDS/ MPD Experience with Glivec in this indication is very limited and is based on haematological and cytogenetic response rates.
Der er udført et åbent multicenter, klinisk fase II- studie (studie B2225) med henblik på vurdering af Glivec i en blandet patientpopulation med livstruende sygdomme forbundet med Abl, Kit eller PDGFR protein- tyrosinkinaser.
One open label, multicentre, phase II clinical trial (study B2225) was conducted testing Glivec in diverse populations of patients suffering from life-threatening diseases associated with Abl, Kit or PDGFR protein tyrosine kinases.
I dette studie indgik 7 patienter med MDS/ MPD, som blev behandlet med 400 mg Glivec daglig.
This study included 7 patients with MDS/ MPD who were treated with Glivec 400 mg daily.
På tidspunktet for den oprindelige analyse, havde 3 af 4 patienter med konstateret PDGFR- omlejring opnået hæmatologisk respons (2 CHR og 1 PHR).
At the time of the original analysis, three of the four patients with detected PDGFR gene rearrangements developed haematological response (2 CHR and 1 PHR).
Derudover er yderligere 24 patienter med MDS/ MPD beskrevet i 13 publikationer.
In addition a further 24 patients with MDS/ MPD were reported in 13 publications.
Opdaterede oplysninger om 6 af disse 11 patienter, som er publiceret for nylig, viste, at alle disse patienter forblev i cytogenetisk remission (32- 38 måneder).
In a recent publication updated information from 6 of these 11 patients revealed that all these patients remained in cytogenetic remission (range 32-38 months).
Der var i samme publikation oplysning om længere varende opfølgningsdata fra 12 MDS/ MPD- patienter med PDGFR- omlejring (5 patienter fra studie B2225).
The same publication reported long term follow-up data from 12 MDS/ MPD patients with PDGFR gene rearrangements (5 patients from study B2225).
Elleve patienter opnåede hurtig CHR; hos 10 patienter var cytogenetiske abnormaliteter svundet fuldstændig og der sås mindskning eller forsvinden af fusion- transcripts målt med RT- PCR.
Eleven patients achieved rapid CHR; ten had complete resolution of cytogenetic abnormalities and a decrease
19 PDGFR- proteintyrosinkinaser.
19 or disappearance of fusion transcripts as measured by RT-PCR.
I dette studie blev 14 patienter med HES/ CEL behandlet med 100 mg - 1. 000 mg Glivec daglig.
Glivec administration to patients without the genetic translocation generally results in no improvement.
Yderligere er 162 patienter med HES/ CEL i alderen 11 til 78 år omtalt i 35 publicerede kasuistikker og behandlingsserier.
In this study, 14 patients with HES/ CEL were treated with 100 mg to 1,000 mg of Glivec daily.
De blev behandlet med GLivec i doser fra 75 mg til 800 mg daglig.
A further 162 patients with HES/ CEL, reported in 35 published case reports and case series received Glivec at doses from 75 mg to 800 mg daily.
Af disse 117 patienter var 61 positive for FIP1L1- PDGFRα fusionkinase.
In 61 of these 117 patients FIP1L1-PDGFRα fusion kinase was identified.
Yderligere 4 HES patienter blev fundet FIP1L1- PDGFRα positive i 3 andre publicerede kasuistikker.
An additional four HES patients were found to be FIP1L1-PDGFRα - positive in other 3 published reports.
Alle 65 FIP1L1- PDGFRα fusionkinase- positive patienter opnåede CHR, som vedvarede i måneder (varighed fra 1+ til 44+ måneder censureret på opgørelsestidpunktet).
All 65 FIP1L1-PDGFRα fusion kinase positive patients achieved a CHR sustained for months (range from 1+ to 44+ months censored at the time of the reporting).
Som beskrevet i en nylig publikation opnåede 21 af disse 65 patienter også komplet molekylær remission med en median opfølgningstid på 28 måneder (varierende fra 13- 67 måneder).
As reported in a recent publication 21 of these 65 patients also achieved complete molecular remission with a median follow-up of 28 months (range 13-67 months).