NCI CANCERLIT^® Search: Chronic Myelogenous Leukemia - September 2001

Last Modified: November 1, 2001

In vivo purging of peripheral blood stem cells obtained by apheresis, using high-dose chemotherapy and granulocyte colony-stimulating factor in chronic myelogenous leukemia patients.
Insertion (22;9)(q11;q34q21) in a patient with chronic myeloid leukemia characterized by fluorescence in situ hybridization.
[Activation of autologous hematopoietic stem cell transplants with interleukin-2]
Cutaneous reactions to STI571.
Investigation on the role of the ATM gene in chronic myeloid leukaemia.
Spontaneous cytotoxic T-cell responses against survivin-derived MHC class I-restricted T-cell epitopes in situ as well as ex vivo in cancer patients.
Chronic myeloid leukemia with a rare variant Philadelphia translocation: t(9;10;22)(q34;q22;q11).
Chronic myelogenous leukemia.
Secondary chronic myelogenous leukemia after autologous peripheral blood stem cell transplantation for lymphoma.
[Chronic myelomonocytic leukemia presenting as Guillain- Barre syndrome]
Molecular monitoring of the treatment of patients with BCR/ABL (+) chronic myelogenous leukemia.
Biologically based risk estimation for radiation-induced CML. Inferences from BCR and ABL geometric distributions.
Allogeneic marrow engraftment following whole body irradiation in a patient with leukemia. 1970.
Platelet apheresis for digital gangrene due to thrombocytosis in chronic myeloid leukaemia.
Pulmonary artery hypertension during interferon-alpha therapy for chronic myelogenous leukemia.
Classifying chronic myelomonocytic leukemia.
Occurrence of angioimmunoblastic T cell lymphoma in a patient with chronic myelomonocytic leukemia features.
Relapse of chronic myelogenous leukemia 12 years after allogeneic marrow transplantation: successful second transplantation with allogeneic peripheral blood progenitor cells.
Telomere dynamics and genetic instability in disease progression of chronic myeloid leukemia.
Influence of CD34(+) marrow cell dose on outcome of HLA-identical sibling allogeneic bone marrow transplants in patients with chronic myeloid leukaemia.
A case of chronic myelomonocytic leukaemia and factor XI deficiency with a circulating anticoagulant.
[Anti-tyrosine kinase: the beginning of molecular therapies of cancer and initial results]
Philadelphia (Ph) chromosome-positive chronic myeloid leukaemia relapsing as Ph-negative leukaemia after allogeneic bone marrow transplantation.

CancerMail from the National Cancer Institute

1
UI - 21174294
AU - Borbolla JR; Najera A; Arana RM; Lopez-Hernandez MA; Mendoza Y; Trueba E
TI - In vivo purging of peripheral blood stem cells obtained by apheresis, using high-dose chemotherapy and granulocyte colony-stimulating factor in chronic myelogenous leukemia patients.
SO - J Hematother Stem Cell Res 2001 Feb;10(1):19-21

2
UI - 21261636
AU - Martin-Subero JI; Lahortiga I; Gomez E; Ferreira C; Larrayoz MJ; Odero MD; Garcia-Delgado M; Novo FJ; Giraldo P; Calasanz MJ
TI - Insertion (22;9)(q11;q34q21) in a patient with chronic myeloid leukemia characterized by fluorescence in situ hybridization.
SO - Cancer Genet Cytogenet 2001 Mar;125(2):167-70
AD - Department of Genetics, University of Navarra, Irunlarrea s/n, 31008, Pamplona, Spain.
An unusual cytogenetic rearrangement, described as ins(22;9)(q11;q34q21), was detected in a 49-year-old male patient diagnosed with chronic myeloid leukemia (CML). Reverse transcriptase polymerase chain reaction (RT-PCR) revealed a b3a2 fusion transcript. In order to confirm the cytogenetic findings and fully characterize the inverted insertion, we performed fluorescence in situ hybridization (FISH) assays using locus-specific and whole chromosome painting probes. Our FISH analysis showed the presence of the BCR/ABL fusion gene, verified the insertion and determined that the breakpoint on chromosome 22 where the insertion took place was located proximal to the BCR gene and distal to the TUPLE1 gene on 22q11.

3
UI - 21395234
AU - Hajek R; Koristek Z; Vinklarkova J; Janovska E; Klabusay M; Doubek M; Dvorakova D; Bourkova L; Dusek L; Adler J; Mayer J; Vorlicek J
TI - [Activation of autologous hematopoietic stem cell transplants with interleukin-2]
SO - Cas Lek Cesk 2001 Jul 19;140(14):430-5
AD - Interni hematoonkologicka klinika FN, Brno-Bohunice. r.hajek@fnbrno.cz
BACKGROUND: Recent findings of the role of the immunity in eradication of residual tumour tissue after autologous transplantation rejection leading to extensive studies on T-cell mediated specific antitumor effects or nonspecific NL-cell mediated anticancer effects. We have evaluated on the methods of adoptive cell therapy--IL-2 activation of autologous graft in the preclinical conditions. In laboratory conditions we have manipulated with autologous grafts form patients suffering with chronic myelocytic leukemia and patients suffering with multiple myeloma. METHODS AND RESULTS: Autologous graft was activated with IL-2 during 24-hours cultivation period in X-Vivo 10 medium with heparine, glutamine and Dnase. Quality of grafts after cultivation, contamination and activation of T and NK cell were evaluated. No significant differences between IL-2 activated graft and control were found. Results of autologous graft quality (CD34+, CFU-GM) were comparable with already published results. Quality of final product allowed starting of clinical experimental trials. CONCLUSIONS: We have proved the possibility to use IL-2 activated autologous graft in the clinical conditions. Based on our preclinical results experimental clinical trials have been initiated in patients suffering from chronic myelocytic leukemia and multiple myeloma.

4
UI - 21394616
AU - Brouard M; Saurat JH
TI - Cutaneous reactions to STI571.
SO - N Engl J Med 2001 Aug 23;345(8):618-9

5
UI - 21406927
AU - Melo JV; Kumberova A; van Dijk AG; Goldman JM; Yuille MR
TI - Investigation on the role of the ATM gene in chronic myeloid leukaemia.
SO - Leukemia 2001 Sep;15(9):1448-50
AD - Department of Haematology, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
Chronic myeloid leukaemia (CML) is characterised by an indolent, chronic phase (CP) preceding an acute transformation to blast crisis (BC). While the BCR-ABL fusion oncogene is strongly implicated in the CP, the molecular changes underlying BC are largely unknown. The ataxia telangiectasia gene, ATM, is a candidate gene for this transformation because the complex karyotypes associated with BC of CML suggest that DNA double-strand break repair is defective and because the ABL pathway involves the interaction between the Abl and the Atm proteins. We performed a mutational analysis for ATM in CML using genomic DNA from 14 CML cell lines and 59 CML patients in BC. No clearly deleterious nucleotide changes were observed. A new polymorphism C4138T was discovered which results in a non-conservative amino acid substitution (H1380Y). This variant lies in the Atm recognition motif for the Abl protein. While ATM is unlikely to contribute substantially to CML, further investigation of the H1380Y substitution should clarify whether it has any functional effect.

6
UI - 21397930
AU - Andersen MH; Pedersen LO; Capeller B; Brocker EB; Becker JC; thor Straten P
TI - Spontaneous cytotoxic T-cell responses against survivin-derived MHC class I-restricted T-cell epitopes in situ as well as ex vivo in cancer patients.
SO - Cancer Res 2001 Aug 15;61(16):5964-8
AD - Department of Tumor Cell Biology, Danish Cancer Society, 2100 Copenhagen, Denmark. mha@cancer.dk
Recent advances in therapeutic tumor vaccinations necessitate the identification of broadly expressed, immunogenic tumor antigens that are not prone to immune selection. To this end, the human inhibitor of apoptosis, survivin, is a prime candidate because it is expressed in most human neoplasms but not in normal, differentiated tissues. Here, we demonstrate spontaneous cytotoxic T-cell responses against survivin-derived MHC class I-restricted T-cell epitopes in breast cancer, leukemia, and melanoma patients both in situ as well as ex vivo. Moreover, survivin-reactive T cells isolated by magnetic beads coated with MHC/peptide complexes were cytotoxic against HLA-matched tumors of different tissue types. Being a universal tumor antigen, survivin may serve as a widely applicable target for anticancer immunotherapy.

7
UI - 21411573
AU - Emberger W; Behmel A; Tschernigg M; Seewann HL; Petek E; Kroisel PM; Wagner K
TI - Chronic myeloid leukemia with a rare variant Philadelphia translocation: t(9;10;22)(q34;q22;q11).
SO - Cancer Genet Cytogenet 2001 Aug;129(1):76-9
AD - Institute of Medical Biology and Human Genetics, University of Graz, Harrochgasse 21/8, A-8010 Graz, Austria. werner.emberger@kfunigraz.ac.at
We report a 59-year-old, male, chronic myeloid leukemia patient with a rare variant Philadelphia (Ph) translocation t(9;10;22)(q34;q22;q11). Fluorescence in situ hybridization with whole chromosome paints was used to confirm the cytogenetic findings. With a BCR/ABL-specific probe, the known rearrangement on the derivative chromosome 22 was found. The prognostic implications as well as the relevance of the additional breakpoint region 10q22 are discussed.

8
UI - 21400885
AU - Kalidas M; Kantarjian H; Talpaz M
TI - Chronic myelogenous leukemia.
SO - JAMA 2001 Aug 22-29;286(8):895-8
AD - Department of Bioimmunotherapy, M.D. Anderson Cancer Center, 1515 Holcombe Blvd, Box 422, Houston, TX 77030, USA. mtalpaz@mail.mdanderson.org

9
UI - 21265652
AU - Hsiao HH; Liu TC; Chang CS; Sue YC; Chen TP; Lin SF
TI - Secondary chronic myelogenous leukemia after autologous peripheral blood stem cell transplantation for lymphoma.
SO - Int J Hematol 2001 Jan;73(1):126-8
AD - Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan.
A 31-year-old woman was diagnosed with intestinal lymphoma (high-grade mucosa-associated lymphoid tissue lymphoma, stage IIE) in September 1996. Eleven courses of chemotherapy were administered, but the results were poor. She received autologous peripheral blood stem cell transplantation (PBSCT) in September 1997. Leukocytosis was noted, and chronic myelogenous leukemia was diagnosed 8 months after the PBSCT, progressing to blast phase 10 months later. We report this case because secondary chronic myelogenous leukemia after stem cell transplantation is rare.

10
UI - 21334502
AU - Fernandez del Campo R; Polo Zarzuela M; Prieto del Portillo I; Poyo-Guerrero Lahoz R
TI - [Chronic myelomonocytic leukemia presenting as Guillain- Barre syndrome]
SO - Med Clin (Barc) 2001 Jun 2;116(20):797

11
UI - 21388771
AU - Ruiz-Arguelles GJ; Lopez-Martinez B; Ramirez-Cabrera JM; Reyes-Nunez V; Rodriguez-Cedeno HM; Garces-Eisele J
TI - Molecular monitoring of the treatment of patients with BCR/ABL (+) chronic myelogenous leukemia.
SO - Rev Invest Clin 2001 May-Jun;53(3):235-9
AD - Centro de Hematologia y Medicina Interna de Puebla, Universidad de las Americas-Puebla. gruizl@clinicaruiz.com
BACKGROUND: The molecular follow-up of patients with chronic myelogenous leukemia (CML) has been described as useful in other countries, but there are not data reported in Mexico. METHODS: All patients studied at Laboratories Clinicos de Puebla/Centro de Hematologia y Medicina Interna de Puebla in which the BCR-ABL hybrid gene was identified by means of polymerase chain reaction were analyzed. In 22 individuals the molecular marker of the disease was studied at diagnosis and in different instances afterwards; these patients were treated with chemotherapy, interferon, autologous or allogeneic bone marrow transplantation. RESULTS: Only the six patients that were allografted from HLA-identical siblings cleared the molecular marker of the disease; the rest of them did not achieve molecular remissions. The median survival (SV) of the whole group has not been reached, whereas the 53-month SV is 68%. One of the allografted patients died as a result of complications of graft versus-host disease. CONCLUSIONS: We have found useful the molecular monitoring of the treatment of patients with CML. Using this approach, we found that molecular remissions can be accomplished only with allografting; however, other therapeutic approaches may also result in long-lasting hematologic remissions.

12
UI - 21257359
AU - Radivoyevitch T; Kozubek S; Sachs RK
TI - Biologically based risk estimation for radiation-induced CML. Inferences from BCR and ABL geometric distributions.
SO - Radiat Environ Biophys 2001 Mar;40(1):1-9
AD - Department of Mathematics, University of California, Berkeley 94720, USA. radivot@musc.edu
Chronic myeloid leukemia (CML) invites biologically based radiation risk modeling because CML is simultaneously well-understood, homogeneous and prevalent. CML is known to be caused by a translocation involving the ABL and BCR genes, almost all CML patients have the BCR-ABL translocation, and CML is prevalent enough that its induction is unequivocally detected among Hiroshima A-bomb survivors. In a previous paper, a linear-quadratic-exponential (LQE) dose-response model was used to estimate the lifetime excess risk of CML in the limit of low doses of gamma-rays, R gamma. This estimate assumed that BCR-ABL translocation dose-response curves in stem cells for both neutrons and gamma-rays, differ only by a common proportionality constant from dicentric aberration dose-response curves in lymphocytes. In the present paper we challenge this assumption by predicting the BCR-ABL dose response. The predictions are based on the biophysical theory of dual radiation action (TDRA) as it applies to recent BCR-to-ABL distance data in G0 human lymphocytes; this data shows BCR and ABL geometric distributions that are not uniform and not independent, with close association of the two genes in some cells. The analysis speaks against the previous proportionality assumption. We compute 11 plausible LQE estimates of R gamma, 2 based on the proportionality assumption and 9 based on TDRA predictions. For each estimate of R gamma we also compute an associated estimate of the number of CML target cells, N; the biological basis of the LQE model allows us to form such estimates. Consistency between N and hematological considerations provides a plausibility check of the risk estimates. Within the group of estimates investigated, the most plausible lifetime excess risk estimates tend to lie near R gamma = 0.01 Gy-1, substantially higher than risk estimates based on the proportionality assumption.

13
UI - 21259853
AU - Buckner CD; Epstein RB; Rudolph RH; Clift RA; Storb R; Thomas ED
TI - Allogeneic marrow engraftment following whole body irradiation in a patient with leukemia. 1970.
SO - J Hematother Stem Cell Res 2001 Apr;10(2):201-8

14
UI - 21315521
AU - Win N; Mitchell DC
TI - Platelet apheresis for digital gangrene due to thrombocytosis in chronic myeloid leukaemia.
SO - Clin Lab Haematol 2001 Feb;23(1):65-6
AD - National Blood Service - South London Centre, UK. Nay.Win@nbs.nhs.uk
Thrombocytosis is a frequent presenting feature of myeloproliferate disorders and is associated with increased incidence of thrombotic and haemorrhage complications. However, these complications are rare in chronic myeloid leukaemia (CML). We describe a case of CML which presented with digital gangrene due to thrombocytosis. Reduction of the platelet count by plateletpheresis lead to rapid symptomatic relief and recovery from the gangrene.

15
UI - 21339571
AU - Fruehauf S; Steiger S; Topaly J; Ho AD
TI - Pulmonary artery hypertension during interferon-alpha therapy for chronic myelogenous leukemia.
SO - Ann Hematol 2001 May;80(5):308-10
AD - Department of Internal Medicine V, University of Heidelberg, Germany. stefan_fruehauf@med.uni-heidelberg.de
In the conventionally treated group of patients with chronic myelogenous leukemia (CML) the prognosis has been significantly improved by interferon-alpha (IFN-alpha). Several side effects in association with IFN-alpha treatment have been reported. Here we present the first case of a CML patient with reversible pulmonary artery hypertension (PAH) during IFN-alpha therapy. The patient received IFN-alpha-2b (up to 10 million U/day) for 6 months until he started to complain of dyspnea on exertion and an afebrile non-productive cough. An echocardiography and right heart catheterization showed signs of right heart failure with PAH (80 mmHg). A reduced carbon monoxide diffusion capacity and partial respiratory insufficiency were noted. Inflammatory markers were not elevated and pulmonary infiltrates could not be detected. Respiratory infections, thromboembolic causes or autoimmune diseases were carefully ruled out. IFN-alpha was suspected as causative agent, because experimental investigations in sheep showed that IFN-alpha can stimulate the thromboxane cascade which resulted in transient PAH. A reduced pulmonary diffusion capacity had been observed secondary to PAH. After discontinuation of IFN-alpha, our patient's clinical status improved rapidly. After 6 months the pulmonary artery pressure had returned to near normal values (35 mmHg) and the pulmonary diffusion capacity was normal. It took one year until the electrocardiogram reverted to the pre-IFN-alpha pattern. PAH should be included in the differential diagnosis of patients treated with IFN-alpha who complain of exertional dyspnea in the absence of inflammatory signs.

16
UI - 21424072
AU - Yavorkovsky LL; Cook P
TI - Classifying chronic myelomonocytic leukemia.
SO - J Clin Oncol 2001 Sep 1;19(17):3790-2

17
UI - 21319922
AU - Gaulier A; Jary-Bourguignat L; Serna R; Pulik M; Davi F; Raphael M
TI - Occurrence of angioimmunoblastic T cell lymphoma in a patient with chronic myelomonocytic leukemia features.
SO - Leuk Lymphoma 2000 Dec;40(1-2):197-204
AD - Service de Pathologie, Hjpital V. Dupouy, Argenteuil, France. gaulier@club-internet.fr
In a patient with recently diagnosed chronic myelomonocytic leukemia features, the biopsy of a peripheral lymphadenopathy seven months later revealed disorganised lymphoid tissue with a few large EBER (+) LMP1 (+) B-lymphocytes before any treatment was given. At this time, a clonal TCR gamma rearrangement and very faint clonal IgH rearrangement were demonstrated, and the diagnosis of angioimmunoblastic T-cell lymphoma was made. Treatment with MOPP was started, followed by Hydroxycarbamide and CHOP but the outcome was fatal. During the evolution, there was no blastic transformation of the chronic myelomonocytic leukemia. The T-cell lymphoma extended to abdominal lymph nodes, Waldeyer ring and bone marrow and the percentage of large LMPI EBER (+) B-cells increased in the lymph nodes. These findings do not support a common stem cell abnormality leading to myelodysplasia in the bone marrow and lymphoma in peripheral lymph nodes. The lack of a clearcut light chain restriction in the EBV infected B-cell is suggestive of a persistant EBV infection in polyclonal or oligoclonal activated B-cells as described in immunodepressed patients. The association of CMML features and an angioimmunoblastic T-cell lymphoma is discussed.

18
UI - 21319925
AU - Reiter E; Rabitsch W; Greinix HT; Keil F; Mitterbauer G; Hinterberger W; Haas OA; Lechner K; Kalhs P
TI - Relapse of chronic myelogenous leukemia 12 years after allogeneic marrow transplantation: successful second transplantation with allogeneic peripheral blood progenitor cells.
SO - Leuk Lymphoma 2000 Dec;40(1-2):215-8
AD - Department of Medicine I, University of Vienna, Austria.
We report on a 31-year old female patient who relapsed with CML in blast crisis 12 years after a successful BMT for CML in chronic phase from her HLA-identical sister. Because of her good performance status and the long time elapsed since her first BMT, PBPC transplantation of the originial donor was planned. Therefore, the patient was conditioned with busulfan and cyclophosphamide and then received unmanipulated PBPCs from her sister. GVHD prophylaxis consisted of MTX and CsA. She had early engraftment but considerable hepatotoxicity which resolved after more than six months. Furthermore, she developed acute GVHD of the skin grade 2, which responded to corticosteroids. Fifteen months after second transplantation the patient is alive and well in molecular remission and without signs of chronic GVHD.

19
UI - 21319905
AU - Ohyashiki K; Iwama H; Tauchi T; Shimamoto T; Hayashi S; Ando K; Kawakubo K; Ohyashiki JH
TI - Telomere dynamics and genetic instability in disease progression of chronic myeloid leukemia.
SO - Leuk Lymphoma 2000 Dec;40(1-2):49-56
AD - First Department of Internal Medicine, Tokyo Medical University, Japan. ohyashik@rr.iij4u.or.jp
Chronic myeloid leukemia (CML) is characterized by a Philadelphia (Ph) translocation creating a novel BCR-ABL oncoprotein, and CML patients have a chronic phase for several years followed by an intractable blast cell proliferation, called blast transformation. In the blast phase, more than 60% of patients show additional cytogenetic changes, e. g., double Ph, +8, i(17q). In this review, we would like to address genetic changes, including genome instability, cytogenetic changes, and telomere dynamics that relate to karyotypic instability. In the chronic phase, approximately 60% of CML patients show reduced telomere length without highly elevated telomerase activity or microsatellite alterations, indicating that telomere reduction may be linked to cell replication. Therefore, the Ph translocation might be a first event to immortalize cell proliferation. In the blast phase, 50% of CML patients have high levels of elevated telomerase activity and the same number of patients had microsatellite changes. Of note is that most patients with telomerase up-regulation in the blast phase had additional cytogenetic changes and >60% of them showed microsatellite changes at least at one locus. In contrast, most patients without telomerase activity did not show microsatellite changes. These findings may indicate that telomerase up-regulation in the blast phase of CML patients is closely associated with microsatellite changes (representative of genome instability), while blast cells in the remaining patients (30%) maintain their proliferative capability without microsatellite changes and telomerase up-regulation. This further suggests that there is also an unknown mechanism for genome stability without the process of telomerase up-regulation in some patients with CML in blast crisis.

20
UI - 21218709
AU - Morariu-Zamfir R; Rocha V; Devergie A; Socie G; Ribaud P; Esperou H; Parquet N; Guardiola P; Dal Cortivo L; Bittencourt H; Garnier F; Traineau R; Marolleau JP; Chevret S; Gluckman E
TI - Influence of CD34(+) marrow cell dose on outcome of HLA-identical sibling allogeneic bone marrow transplants in patients with chronic myeloid leukaemia.
SO - Bone Marrow Transplant 2001 Mar;27(6):575-80
AD - Laboratory of Cellular Therapy, Saint Louis Hospital, Paris, France.
In order to study the influence of bone marrow CD34(+) cell dose on the outcome of allogeneic bone marrow transplantation (BMT), we analysed the results of BMT from HLA-identical siblings donors in 50 patients with chronic myeloid leukaemia (CML). The median numbers of nucleated cells (NC) and CD34(+) cells infused were 2.18 x 10(8)/kg (0.05-4.14 x 10(8)/kg) and 3.12 x 10(6)/kg (0.35-8.52 x 10(6)/kg), respectively. All patients engrafted. In univariate analysis, there was no correlation between the number of CD34(+) cells infused and the time to neutrophil recovery (P = 0.17). The Kaplan-Meier estimate of grade II-IV acute graft-versus-host disease (GVHD) at day 100 was 53 +/- 14% and 2-year survival was 46 +/- 15%. A number of CD34(+) cells infused greater than the median was the main factor increasing survival (P = 0.0006) and decreasing 100 day transplant-related mortality (P = 0.009). Patient-, disease- and transplant-related characteristics were not statistically different among patients receiving more or less than the median number of CD34(+) cells. The rate of infectious deaths was significantly higher in patients receiving less than 3.12 x 10(6) CD34/kg (48% vs 16%, P = 0.01). In a multivariable analysis, two factors associated with increased risk of death were advanced disease status at transplant (HR: 2.5 (95% CI: 1.09-5.75), P = 0.03) and a lower number of marrow CD34(+) cells infused/kg (HR: 4.55 (95% CI: 1.87-10.90), P = 0.0008).

21
UI - 21336328
AU - Billon S; Blouch MT; Escoffre-Barbe M; Le Niger C; Le Roux AM; Abgrall JF
TI - A case of chronic myelomonocytic leukaemia and factor XI deficiency with a circulating anticoagulant.
SO - Haemophilia 2001 Jul;7(4):433-6
AD - Clinical Department of Hematology, Hopital Morvan, Brest, France Laboratory of Hematology, Hopital Morvan, Brest, France. sandrine.billon@univ-brest.fr
Inhibitors against factor XI (FXI) have been frequently described in patients who acquired inhibitors (due to auto-immune disorders, malignancies or infections), but less often in those with a congenital deficiency of this factor, who had received plasma infusions. The present report concerns one such inhibitor found in the plasma of a patient with chronic myelomonocytic leukaemia and infected by B19 parvovirus, who was neither a heterozygote nor a homozygote for FXI deficiency, and who had no bleeding tendency despite a very low FXI level. Taking this case into account, we discuss and present the clinical and biological features of acquired FXI deficiency caused by an inhibitor.

22
UI - 21387135
AU - Guilhot F
TI - [Anti-tyrosine kinase: the beginning of molecular therapies of cancer and initial results]
SO - Bull Cancer 2001 Jul;88(7):659-60
AD - Service d'oncologie hematologique et de therapie cellulaire, CHU La Miletrie, 86021 Poitiers. f.guilhot@chu-poitiers.fr

23
UI - 21421112
AU - Au WY; Lie AK; Ma SK; Wan TS; Liang R; Leung YH; Kwong YL
TI - Philadelphia (Ph) chromosome-positive chronic myeloid leukaemia relapsing as Ph-negative leukaemia after allogeneic bone marrow transplantation.
SO - Br J Haematol 2001 Aug;114(2):365-8
AD - Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong.
Two patients with Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukaemia (CML) relapsed 1.5 and 5 years after allogeneic bone marrow transplantation (BMT). Although the leukaemias were of recipient origin, t(9;22) could no longer be detected using conventional cytogenetics/fluorescence in situ hybridization or molecularly. Both patients responded to immunotherapy with donor lymphocytes/peripheral blood stem cells, although one patient ultimately relapsed again. These patients were similar to the occurrence of Ph(-) leukaemias previously described in Ph(+) CML after treatment with interferon or autologous BMT, and might be relevant in the pathogenesis and monitoring of treatment after BMT in CML.