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AML patients with the FLA regimen consisting of five days of treatment with a 30-minute infusion of Fluda 30 mg/sqm/day, followed four hours later by a 4-hour infusion of cytosine arabinoside (Ara-C) 2 g/sqm/day (Table 1). As reported in other studies6-9 we obrved a complete remission (CR) in a relative high proportion of cas (54%), but the median dura-tion of remission was short (4 months) (Table 2). Before therapy, the p170 expression in bone marrow blasts was evaluated by an indirect immunofluores-cence method with the anti-p170 monoclonal anti-body MRK-16 and the results were expresd as the mean fluorescence index(MFI).2Six out of 13 patients (46%) were overexpressing the p170 glycoprotein (MFI > 6.0) and only two reached a CR (cas 6 and 9) (Table 2). Out of the 6 patients who had the MFI <6, five patients reached a CR. All patients experi-enced a vere myelosuppression but the non-hema-tological toxicity was mild and the most common side effects were naua and vomiting (WHO grade I or II). The median time of granulocyte recovery (ANC >500/uL) was 22 days (range 12-35) and a platelet count >50,000/uL was reached after a median of 22 days (range 14-34). During the neutropenic pha 9 (69%) patients developed microbiologically or clini-cally proven infections.However, none of them devel-oped opportunistic infections except one, who devel-oped a lethal mucormycosis when he apparently was in CR. The results suggest that the FLA regimen is myelotoxic but not able to induce a durable complete remission in the poor-risk AML patients, such as the relapd or refractory ones. Further studies sho
uld be performed in order to define whether or not p170-positive leukemic cells can escape Fluda and Ara-C cytotoxicity, or alternatively, if the agents may lect cells with different mechanisms of resistance.10Since the non-hematological toxicity of FLA regimen was mild, the addition of a third agent like idarubicin, which is slightly involved in the MDR efflux mecha-nism, could be considered in an attempt to strenght-en the antileukemic activity of the FLA regimen. Acknowledgements
This work was supported by CNR contract n.96.00500.PF39 and by AIRC, Milan, Italy.
Key words
Acute myeloid leukemia, treatment, fludarabine, cytosine-arabinoside
在狱咏蝉骆宾王Correspondence
Dr. Domenico Russo, Clinica Ematologica, Policlinico Universi-tario, piazza S. Maria della Miricordia, Udine, Italy. Phone: inter-national +39-432-559662 •Fax: international +39-432-559661•E-mail: domenico.russo@drmm.uniud.it
References
1.Michieli M, Damiani D, Geromin A, et al. Over-
expression of multidrug resistance-associated p-170 glycoprotein in acute non-lymphocytic leukemia. Eur J Haematol 1992; 48:87-92.
2.Michieli M, Damiani D, Michelutti A, et al. Screening
of multidrug resistance in leukemia: cell reactivity to MRK-16 correlates with anthracycline retention and nsitivity of leukemic cells. Leuk Lymphoma 1996;
23:99-105.
3.Gandhi V, Estey E, Keating MJ, Plunkett W. Fluda-
rabine potentiates metabolism of cytarabine in patients with acute myelogenous leukemia during therapy. J Clin Oncol 1993; 11:116-24.梦见要搬家
4.Tosi P, Visani G, Ottaviani E, Manfroi S, Zinzani PL,
Tura S. Fludarabine+Ara-C+G-CSF: cytotoxic effect and induction of apoptosis on fresh acute myeloid leukemia cells. Leukemia 1994; 8:2076-82.
5.Michelutti A, Michieli M, Damiani D, et al. Effect of
fludarabine and arabinosylcytosine on multidrug resis-tan cells. Haematologica 1997; 82:143-7.
6.Estey E, Plunkett W, Gandhi V, Rios MB, Kantarjian H,
Keating MJ. Fludarabine and arabinosylcytosine ther-apy of refractory and relapd acute myelogenous leukemia. Leuk Lymphoma 1993; 9:343-50.
红豆八宝粥7.Visani G, Tosi P, Zinzani PL, et al. FLAG (fludarabine+
high-do cytarabine+G-CSF): an effective and toler-able protocol for the treatment of poor risk acute myeloid leukemias. Leukemia 1994; 8:1842-6.
8.Clavio M, Carrara P, Miglino M, et al. High efficacy of
fludarabine-containing therapy (FLAG-FLANG) on poor-risk acute myeloid leukemia. Haematologica 1996; 81:513-20.
9.Huhmann IM, Watzke HH, Geissler K, et al. FLAG (flu-
darabine, cytosine arabinoside, G-CSF) for refractory and relapd acute myeloid leukemia. Ann Hematol 1996; 73:265-71.
10.Russo D, Marie JP, Zhou DC, et al. Coexpression of
anionic glutathione-S-transfera (GST) and mul-tidrug resistance (mdr1) genes in acute myeloid and lymphoid leukemias. Leukemia 1994; 8:881-4.
Therapy-related acute leukemia associated with involvement of 11q23 after high grade non-Hodgkin lymphoma
G IOVANNI M ARTINELLI, N ICOLETTA T ESTONI, P IER L UIGI
Z INZANI, A NDREA B IONDI,* G IUSEPPE C IMINO,°S ANTE T URA nstitute of Hematology and Medical Oncology "Seràgnoli", S. Orsola Hospital, University of Bologna, Italy;*Clinica Pediatrica, University of Milan, Italy; °Department of Molecular Biology, “La Sapienza” University, Rome, Italy
Therapy-related acute myeloid leukemias with bal-anced translocations affecting the 11q23 chromo-some region are one of the most rious complica-tions of treatments with topoisomera II inhibitor drugs as epipodophillotoxins and anthracyclines.1, 2-5 The cas are usually associated with short inter-val time from previous chemotherapies, abnce of myeloid dysplastic pha, hyperleukocytosis and young age. We and others have recently identified and cloned the ALL1 gene
at 11q23 band (also named MLL, HRX, Hrxt) which is consistently altered in t-AML following therapies with topo II targeting drugs.1 However, there are few reports of cas of t-AML, clinically and biologically similar to the subtype of leukemias condary to exposure to topo II inhibitors drugs but without the involvement of the ALL1 gene. The obrvations suggest that genes other than ALL1 which are etiopathogenetically relevant for hematological neoplasias are located in this cytoge-netic region.
A 27-year-old man was admitted to our institution in June 1994 with a 4-week history of fever, anorexia and weight loss. Chest X-ray and CT scan showed a mediastinal mass with enlargement. A bone marrow (BM) aspirate and biopsy revealed normocellular BM. The diagnosis of high-grade B-cell lymphoblas-tic NHL with sclerosis was made on a needle biopsy of the mediastinal mass. No cytogenetic analysis was done on the BM at diagnosis. The clinical stage was defined as IA bulky.
From September 1994 to January 1995 the patient received 11 cours of the MACOP-B chemotherapy with cytosine arabinoside, vincristine, adriablastine, methotrexate and etoposide, achieving only partial remission due to the persistence of 20% of the initial mediastinal mass.3,4Local radiotherapy (RT) (3600 cGY/fac, with inverted fields) was administered from March to April 1995. One week after the end of RT, an hemochromocytometric analysis revealed 19ϫ109/L
WBC with 98% of blasts with monocytic features. At this time the BM biopsy showed a total substitution by leukemic blasts. On the basis of standard morpholog-ical, immunological and cytochemical criteria a diag-nosis was made of acute myeloid leukemia, FAB M4. The karyotype was 46 XX, t(7;11) (p21;q23), t(10;X) (p14;q24). The ICE protocol was administered as treatment of AML without achieving a CR.2The patient died from infective complication in June 1995.
An ALL1 germline genomic configuration was detected by Southern blot analysis of DNA from both the mediastinal mass at the time of diagnosis of NHL and from BM leukemic blasts at the ont of AML. To this purpo DNA was digested to completion with Bam HI and Hind III endonucleas and hybridized with the B859 probe, which is a cDNA inrt contain-ing the ALL1 exon 5-11 quences.
Our ca report allows us to draw some possible etiopathogenetic suggestions on t-AML leukemogen-esis. Firstly, the obrvation from the literature that none of the rare cas of NHL with 11q23 developed a t-AML rule out the hypothesis that t-AML reprents an evolution of the natural history of the dia.7,8It is well known in fact that t-AML after NHL is a ri-ous complication of treatments including topo II inhibitors drugs usually with consistent involvement of the ALL1 gene at 11q23.3Moreover, the identifi-cation within the ALL1 breakpoint cluster region of DNA structures involved in the topo II machinery, such as high-affinity scaffold attachment regions and topoisomeras
e II binding sites, has provided a strong pathogenetic linkage in this leukemic subt between chemotherapeutic agents and targeting gene.6 However, the obrvation that the ALL1 gene is not always altered in cas with clinical, biological and cytogenetic features similar to tho of ALL1+ t-AML suggests that in the 11q23 cytogenetic band gene(s) other than ALL1 could exist that are involved in the pathogenesis of t-AML. In this respect, it is interest-ing to note at least two other genes implicated in hematological malignancies which have been identi-fied within this cytogenetic region: namely, the p54/RCK gene found altered in two B cell malignant lymphomas with t(11;14) (q23;q32) cytogenetic translocation, and the PLZF gene coding a ZF protein which is fud to the RARA in acute promyelocytic leukemia with t(11;17)(q23;q21) abnormality.6-10In conclusion, the prent ca provides further evi-dence of the need to arch for other gene(s) locat-ed in this region which could be involved in the pathogenetic mechanism leading to t-AML after exposure to chemotherapeutic treatments. Funding
This work was supported by Associazione Italiana per la Ricerca sul Cancro (A.I.R.C), by Italian C.N.R “A.C.R.O.”no. 94.01222 and by 95.2206 C.N.R. target projects. Key words
Non-Hodgkin’s lymphoma, 11q23, acute leukemia Correspondence
Dr. Giovanni Martinelli, Institute of Hematology and Med-ical Oncology “Seràgnoli”, University of Bologna, S.Orsola Hospital, via Massarenti 9, 40138 Bologna, Italy. Phone: international +39-51-6364075 •Fax: international +39-51-398973.
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Scientific letters
References羊肉炒饭
1.Roulston D, Anastasi J, Rudinsky R, et al. Therapy-
related acute leukemia associated with t(11q23) after primary acute myeloid leukemia with t(8;21): a report of two cas. Blood 1995; 86:3613-4.
2.Clavio M, Carrara P, Miglino M, et al. High efficacy of
fludarabine-containing therapy (FLAG-FLANG) in poor risk acute myeloid leukemia. Haematologica 1996;
81:513-20.
睾丸潮湿吃什么药3.Cimino G, Moir DT, Canaani O, et al. Cloning of ALL-
1, the locus involved in leukemias with the t(4;11) (q21;q23), t(9;11)(p22;q23), and t(11;19) (q23;p13) chromosome translocations. Cancer Res 1991; 51: 6712-4.
4.Cimino G, Lo Coco F, Biondi A, et al. ALL-1 gene at
chromosome 11q23 is consistently altered in acute leukemia of early infancy. Blood 1993; 82:544-6.
5.Gallagher A, Darley RL, Padua R. The molecular basis
of myelodysplastic syndromes. Haematologica 1997;
82:191-204.
6.Broeker PL, Super HG, Thirman MJ, et al. Distribution
of 11q23 breakpoints within the MLL breakpoint clus-ter region in de novo acute leukemia and in treatment-related acute myeloid leukemia: correlation with scaf-fold attachment regions and topoisomera II con-nsus binding sites. Blood 1996; 87:1912-22.
胰岛素是什么东西
7.Bloomfield CD, Arthur DC, Frizzera G, Levine EG,
Peterson BA, Gajl-Peczalaska KJ. Nonrandom chro-mosome abnormalities in lymphoma. Cancer Res 1983; 43:2975-84.
8.Cabanillas F, Pathak S, Trujillo J, et al. Cytogenetic fea-
tures of Hodgkins’ dia suggest possible origin from
a lymphocyte. Blood 1988; 71:1615-7.
9.Zinzani PL, Bendandi M, Gherlinzoni F, et al. VNCOP-
言听计从什么意思
B regimen in the treatment of high-grade non-Hodgk-
in’s lymphoma in the elderly. Haematologica 1993;
78:378-2.
10.Kubonishi I, Niiya K, Yamashita M, et al. Characteri-
zation of a new human lymphoma cell line (RC-K8) with t(11;14) chromosome abnormality. Cancer 1986;
58:1453-60.
Achromobacter xylosoxidans bacteremia in patients with hematologic malignancies
J OSÉ-A NGEL H ERNÁNDEZ,* R ODRIGO M ARTINO,
R OSER P ERICAS,°A NNA S UREDA, S ALUT B RUNET,
A NDREU D OMINGO-A LBÓS†
†in memoriam
Unitat d’Hematologia Clinica, Departament d’Hematologia and °Servei de Microbiologia, Hospital de la Santa Creu i Sant Pau, Barcelona; *Servei d’Hematologia-Hemoterapia, Hospital Ger-mans Trias i Pujol, Badalona, Barcelona, Spain
We report nine cas of Achromobacter xylosoxidans bacteremia diagnod in patients with hematol
ogic malignancies. There was not an obvious epidemio-logic link between cas and the organism was not isolated from any source. Outcome was cure in all nine cas. In our experience, catheter removal is generally required for eradication of A. xylosoxidans.
Achromobacter xylosoxidans is a non-fermenting gram-negative rod widely distributed in the environment, like hospital fluids, from which outbreaks of nosoco-mial infections may occur.1-3About 90 cas lo-soxidans bacteremia have been reported, twenty-one out of the in patients with hematologic malignan-cies, though eleven occurred as an infectious outbreak in a hematology ward.4-6
Between January 1993 and April 1997, the data of 8 patients from the department of hematology who losoxidans bacteremia were recorded. One patient had two infections parated by 8 months and has been included twice.
Tables 1 and 2 show the patients characteristics of the ries. All cas of bacteremia were not related with each other by time or space losoxidans was not isolated in hospital environment nor any other source than blood cultures. Patients received empiric broad spectrum antibiotics and they were changed if resistance was demonstrated.
None of the patients developed ptic complica-tions or deep-ated infections, suggesting lo-soxidans is a non-virulent organism even in highly com-promid hosts. Six isolates were nsitive to ampi-cillin and eight to amoxicillin-clavulanate. Six cas were resistant to all first and cond generation cephalosporins and two to ceftazidime. All species were resistant to gentamicin and tobramicin and two cas were nsitive to amikacin. On the other hand, susceptibility to the fluorquinolones, ticarcillin, pipe-racillin and carbapenems was universal. One ca was resistant to co-trimoxazole.
losoxidans bacteremia is uncommon, we have obrved nine episodes in the last four years. During this period, 541 adult patients received inten-
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285 Scientific letters
ing the 9 cas losoxidans reported herein (1.6% of all patients). This bacteria can be found in aque-ous environments, such as disinfectants and fluids. Thus, we might suspect in a common source, but there was no epidemiological relationship between cas. Moreover, three episodes were diagnod as outpatients.
In our ries, the majority of patients had vere neutropenia, and it is possible that mucositis and breakdown of the intestinal barrier allowed invasion of bloodstream losoxidans. Clinical prenta-tions were highly persistant fever and chills, but nei-ther death nor psis syndrome occurr
ed despite poor respon to antibiotic therapy in most cas. This is in contrast with other non-fermenting gram-negative infections, which are often associated with high morbidity and mortality.9
The antibiotic susceptibility profile of isolates was similar to previous reports,4,5with special emphasis on the almost universal in vitro resistance to amino-glycosides and aztreonam. As with other non-fer-menting gram-negative bacilli, most isolates were sus-ceptible to broad-spectrum -lactams, co-trimoxa-zole and fluoroquinolones. The most important con-clusion, from our experience, is that the infections are usually catheter-related, and despite their appar-ently low morbidity, removal of the catheter is gen-erally required for definitive eradication of the micro-organism. Appropriate in vitro antibiotic therapy may be ineffective or lead only temporary control of the infection.
Key words
Bacteremia, hematologic malignancies Correspondence
落花生作者José Angel Hernández, Servei d’Hematologia-Hemote-rapia, Hospital Universitari Germans Trias i Pujol, Ctra. Canyet s/n, 08916 Badalona (Barcelona), Spain. Fax: inter-national +34-3-3954206.References
1.Pickett MJ, Hollis DG, Bottone EJ. Miscellaneous
gram-negative bacteria. In: Balows A, Hausler WJ Jr, Herrmann KL, Inberg HD, Shadomy HJ, eds. Man-ual of clinical microbiology. 5th ed. Washington, DC: American Society for Microbiology; 1991:410-28. 2.Spear JB, Fuhrer J, Kirby BD. Achromobacter xylosoxidans
(Alcaligenes xylosoxidans subsp. xylosoxidans) bacteremia associated with a well-water source: ca report and review of the literature. J Clin Microbiol 1988; 26:598-9.
3.Reina J, Antich M, Siquier B, Alomar P. Nosocomial
outbreak of Achromobacter xylosoxidans associated with
a diagnostic contrast solution. J Clin Pathol 1988;
41:920-1.
4.Duggan JM, Goldstein SJ, Chenoweth CE, Kauffman
CA, Bradley SF. Achromobacter xylosoxidans bacteremia: report of four cas and review of the literature. Clin Infect Dis 1996; 23:569-76.
5.Legrand C, Anaissie E. Bacteremia due to Achromobac-
ter xylosoxidans in patients with cancer. Clin Infect Dis 1992; 14:479-84.
6.Knippschild M, Schmid EN, Uppenkamp M, et al.
Infection by Alcaligenes xylososidans subsp. xylososidans in neutropenic patients. Oncology 1996; 53: 258-62.
7.Mandell WF, Garvey GJ, Neu HC. A chromobacter xylosox-
idans bacteremia. Rev Infect Dis 1987; 9:1001-5. 8.McGann KA, Provencher M, Hoegg C, Talbot GH.
Achromobacter xylosoxidans bacteremia. Infect Control Hosp Epidemiol 1990; 11:539-41.
9.Martino R, Martínez C, Pericas R, et al. Bacteremia
due to gluco non-fermenting gram-negative bacilli in patients with hematologic neoplasias and solid tumors. Eur J Clin Microbiol 1996; 15:610-5.
Unexpected late graft failure 9 months after HLA-identical bone marrow transplant (BMT) for chronic myeloid leukemia (CML): treatment with a cond BMT
J UAN J OSÉG IL-F ERNÁNDEZ, R EYES A RRANZ, R AFAEL CÁMARA, A DRIAN A LEGRE, A NGELA F IGUERA, J OSÉM ARIA F ERNÁNDEZ-R AÑADA
Hematology Department, Hospital Universitario de la Princesa, Madrid, Spain
We describe a patient with CML in 1st chronic pha (CP) who experienced a graft failure 9 months after an HLA genotypically identical sibling BMT. Drug tox-icity, viral infections, chronic graft-versus-host-dis-ea (GVHD) or leukemic relap were excluded. Chimerism study showed 85% of donor marrow cells. She underwent a cond BMT, reengrafted but died of grade IV acute GVHD.
Late graft failure (LGF) after allogeneic BMT is defined as pancytopenia with marrow hypoplasia after complete engraftment.1It is obrved after haplo-identical or T-cell-depleted BMT and in heavily trans-fud aplastic anaemia patients receiving identical grafts.2,3The reported incidence of this event is about 0.4%.3Cyclosporine withdrawal, interferon-␣treat-
286Scientific letters
ment, human herpes virus-6 (HHV-6) infection, chron-ic GVHD, increasing recipient’s age or lower do of BM cells infud,1, 4-7have been implicated.
A 44-year-old female was diagnod of CML in CP on July 1993. She was treated with hydroxyurea and subquently interferon-␣2b for 24 months without cytogenetic respon. On January, 1996, she under-went a BMT from her genotypically identical brother conditioned with busulphan (16 mg/kg) and cyclo-phosphamide (120 mg/kg) and 4.81ϫ108unmanip-ulated bone marrow (BM) mononuclear cells (MNC) per kg of recipient were infud. GVHD prophylaxis consisted of cyclosporine and short methotrexate. She reached complete engraftment with complete cytogenetic chimerism on day +90. Chronic GVHD screening was negative and cyclosporine was with-drawn on day +180. On day +258, isolated throm-bocytopenia of 61ϫ109/L was detected, that evolved to pancytopenia (leukocytes 0.6ϫ109/L, hemoglobin 9.6 g/dL and platelets 2ϫ109/L) in 12 days. Physical exam revealed fever and herpetic lesions on no and lips. Biochemical parameters, including rum B12 and folic acid levels, liver function tests and LDH, were normal. Autoimmunity screening, Coombs’ and Ham’s tests were negative. Chest-x-ray was normal. Red blood cell group and antigens were of donor type (O+). A marrow aspirate was very hypocellullar with lymphocytes, hystiocytes, plasma cells and masto-cytes. Genomic amplification studies by PCR in mar-row specimen were negative fo
r herpes virus (HSV-I and II, CMV, EBV, HZV, HHV-6) and Parvovirus B19. BM cariotype was 46 XY and RT-PCR of bcr/abl transcripts was negative. Chimerism study by PCR of VNTR loci on MNC from BM revealed 85% of MNC of donor and 15% of receptor. Hemotherapy, broad spectrum antibiotics, amphotericin-
B and acyclovir were administered.
Idiopathic LGF was diagnod. She underwent a c-ond BMT from the same brother conditioned with cyclophosphamide (50 mg/kg/day for 4 days) and ATG (30 mg/kg/day for 3 days), with infusion of 4.6ϫ108unmanipulated marrow MNC per kg of recipient 17 days after LGF obrvation. Cyclosporine with short methotrexate were again given. She recov-ered >1.0ϫ109/L neutrophiles on +15 and >50ϫ109/L platelets on +40. Acute GVHD of skin and liver devel-oped and she was treated with corticosteroids (2 mg/kg/day). On +33, she was discharged in good condition with 6.8ϫ109/L leukocytes and 43ϫ109/L platelets. BM karyotype was 46 XY and 100% of BM cells were of donor origin. She was readmitted on day +51, with naua, vomiting and slight diarrea. Intra-venous nutrition and incread immunosuppression were given under suspicion of GVHD progression. CMV antigenemia was detected and Gancyclovir started. Her condition worned, with liver function deterioration (bilirubin 40 mg/dL), gastrointestinal bleeding and hepatic encephalopathy. She died on
day +75. Autopsy was denied.
LGF has been rarely described after unmanipulat-ed grafts for CML.5,6In previously reported cas of LGF occurring more than 6 months after BMT, a cau could be found (T-cell depletion, HHV-6 infec-tion, chronic GVHD or leukemic relap).5,6,8The mechanism of LGF is unknown.11Residual host lym-phocytes with in vitro inhibitory effect against donor hemopoietic cells have been sometimes detected.6 Second transplants have a high transplant-related mortality in this condition2,10and immunosuppres-sion treatment alone or combinated with stem cells reinfusion or hematopoietic growth factors.1,4,5,8,9fre-quently induce autologous hematopoietic recovery.1,8 In our patient, a cond BMT was decided becau of the long interval between first BMT and graft fail-ure and good patient’s performance status. Engraft-ment was successful but lethal GVHD developed. The optimal approach to manage this complication is unclear and reports are scarce and heterogeneous. Key words
HLA-identical BMT, chronic myeloid leukemia, graft failure Correspondence
Juan José Gil-Fernández, MD, Hematology Department, Hospital Universitario de la Princesa, Diego de León 62, 28006 Madrid, Spain. Fax: international +34-1-520-23-26. References
1.Hows J, Palmer S, Gordon-Smith EC. Cyclosporine
and graft failure following bone marrow transplanta-
tion for vere aplastic anaemia. Br J. Haematol 1985;
60:611-7.
2.Kernan NA, Bordignon C, Heller G, et al. Graft failure
after T-depleted human leukocyte antigen identical
marrow transplants for leukemia. I. Analysis of risk
factors and results of condary transplants. Blood
1989; 74:2227-36.
3.Anatti C, Amos D, Beatty PG, et al. Effect of HLA
compatibility on engraftment of bone marrow trans-
plants in patients with leukemia or lymphoma. N.
Engl J Med 1989; 320:197-204.
4.De Souza MH, Abdelhay E, Silva ML, et al. Late mar-
row allograft rejection following alpha-interferon ther-
apy for hepatitis in a patient with paroxymal noctur-
nal hemoglobinuria. Bone Marrow Transplant 1992;
9:495-7.
5.Ronfeld CS, Rybka WB, Weinbaum D, et al. Late
graft failure due to dual bone marrow infection with variants A and B human herpervirus-6. Exp Hematol 1995; 23:626-9.
6.Nakao S, Nakatsumi T, Chuhjo T, et al. Analysis of
late graft failure after allogeneic bone marrow trans-
plantation: detection of residual host cells using amplification of variable number of tandem repeats loci. Bone Marrow Transplant 1992; 9:107-11.
7.Berthou C, Devergie A, Espérou-Bourdeau H, Traineau
R, Thierry D, Gluckman E. Late marrow failure occur-
ring after HLA identical bone marrow transplant. Bone
Marrow Transplant 1991; 7(suppl 2):50.
8.Jackson N, Franklin IM. Successful treatment of late
graft failure following T cell depleted bone marrow
transplantation. Br J. Haematol 1986; 63:207-9.
9.Vannucchi AM, Bosi A, Laszlo D, Guidi S, Saccardi R,
