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PubMed1999

[Leukemias induced by anticancer chemotherapies].

The frequency of leukemia and myelodysplasia following treatment with cytotoxic agents is increasing. Theses treatment-related leukemias raise both theoretical and practical concerns. On a theoretical basis, cytogenetic and molecular abnormalities described constitute useful models to study leukemogenesis. On a practical basis, prognosis of treatment related-leukemia is somehow unfavorable and implies to take in account this risk in the development of combination therapy for solid tumors or hematological malignancies. There are two distinctive types of treatment-induced leukemia: those secondary after alkylating agents and those secondary after topoisomerase-II- inhibitors. These two types of leukemia after regarding their clinical and their hematological characteristics, but also regarding their prognosis and their associated molecular abnormalities. Leukemias induced by alkylating agents occur generally 5 or 6 years after the beginning of the chemotherapy and are preceded by a more or less long phase of pancytopenia or myelodysplasia and according to their cytologic aspects are difficult to be classified within FAB classification. Their prognosis is pejorative. The most commonly found cytogenetic abnormalities associated with these types of induced leukemia are losses or deletions of chromosomes 5 and 7. Leukemias induced by topoisomerase-II-inhibitors occur shortly after the treatment (12 to 30 months), they begin generally suddenly without preleukemia prodom and their more frequent cytological aspects are M4 and M5 type. The prognosis is less severe than alkylating agent related forms with higher response rates and is dependant of discovered cytogenetic abnormalities. The more frequent molecular abnormalities are not chromosome deletions but balanced translocations. They affect particularly the MLL gene located at band 11q23. Other translocations have been described in this type of leukemia and are comparable to the one found in the de novo leukemia (t8;21, t15;17) for example. The evaluation of the risk of treatment-related leukemia for a given chemotherapeutic agent is difficult as for as current treatment use the combination of several agents potentially leukemogenic (chemotherapy and radiotherapy, combination chemotherapy). It is necessary to set up an up-dated data register in order to centralize all therapy-related myelodysplasia and leukemia within the treatment of a given type of cancer.

Acute Disease↗
PubMed2001

[Telepathology in diagnostic consultations for controversial neoplastic growths in the lung--personal experience].

The authors assessed the diagnostic accuracy of the static telepathology (sTP) for practical consultations in the controversial pulmonary oncology cases. The short characteristics of the diagnostic cases is included. We reported the results of 6 difficult clinico-pathological cases submitted to Dept Quantitative Pathology [DQP] for consultations (5F and 1M, age: 26-68 yrs). Digital images of histological or cytological samples were captured at DQP and transmitted to telepathologist (TPat) in Thoraxklinik, Heidelberg or AFIP, Washington DC. Simultaneously, the same slides (or with a paraffin block) were mailed to TPats for re-evaluation with the conventional microscope (dgn-zwPat). The controversial cases presented 2 types of diagnostic problems: 1/rare entities, 2/common difficulties in the routine work of pathologist, but with indefinitely proved diagnosis. The first group encounters TPat diagnoses as follows: * case A: pulmonary plasma cell granuloma with lymphoidal interstitial infiltrates [LIP]--preleukemia; * case B: microfoci of early metastases of benign uterine leiomyoma; * case D: small cell carcinoma spreading along pleura. The second group included: * case C: invasive epidermoidal carcinoma in bronchus; *case E: probably metastatic adenocarcinoma of colon; *case F: synchronous or metastasising 2 lung tumours sharing NE morphology or NE immunohistochemical features. There was very high concordance between referring pathologist (ref-Pat) diagnoses and TPat diagnoses as well as a consensus in zw-TPat diagnoses. In 2 cases the conceptual problem was solved by TPat. Telepathology offered a support or improved the quality of the final diagnosis. The implementation of sTP remarkably reduced the time of consultations and allowed to present the diagnostic problems to the international group of experts.

Adenocarcinoma↗
PubMed1992

Combined differentiation therapy in myelodysplastic syndrome with retinoid acid, 1 alpha,25 dihydroxyvitamin D3, and prednisone.

The myelodysplastic syndrome (MDPS) provides an opportunity for identifying host factors (genetic, endocrine, immune) involved in initiation and progression of preleukemia into frank acute myeloid leukemia. The aim of this study was to identify bone marrow (BM) cellular and humoral dysfunctions central to the development of MDPS and useful in therapeutic follow-up studies. Our preclinical studies have shown that (1) the characteristic stromal cell composition of the normal BM microenvironment was impaired in MDPS and in AML in 67 and 86% of the cases, respectively; (2) the 1 alpha,25(OH)2D3 concentration in BM plasma was abnormal in 50% of MDPS and 30% of AML; and (3) an inverse correlation existed in MDPS between the 1 alpha,25(OH)2D3 concentration and the frequency of F-CFU, (r = 0.41, p < 0.02), suggestive of a regulatory interaction between this secosteroid hormone and BM stromal cells. The analysis of clonal extinction of BM blast cells in response to all trans retinoic acid (RA), 1 alpha,25(OH)2D3, and colony stimulating factors (PHA-LCM), either alone or in various combinations, revealed individual patterns of responses in the cases of MDPS or AML. The results indicate the necessity for preclinical studies to select patients for combined differentiation therapy. Our ongoing clinical trials suggest that RA (Roaccutan, 20 mg/day continuously) as induction therapy, followed at weeks 6 to 8 by prednisone (40 mg/day for 15 days) and 1 alpha,25(OH)2D3 (Rocaltrol, 3 x 0.25 micrograms/day for 3 months) may induce a long-lasting hematological remission in MDPS.

Bone Marrow↗
PubMed1992

Long-term outcome of high-dose cytarabine-based consolidation chemotherapy for adults with acute myelogenous leukemia.

Modern induction chemotherapy produces 60% to 80% complete remissions in adults with newly diagnosed acute myelogenous leukemia. A major challenge is to eradicate subclinical disease in remission and prevent leukemic relapse. We analyzed the long-term results of high-dose cytarabine-anthracycline consolidation chemotherapy without maintenance treatment and examined the effect of major prognostic factors, including age, sex, history of preleukemia, and cytogenetics. Two hundred twenty-seven patients with newly diagnosed acute leukemia were enrolled on two sequential studies conducted from 1982 to 1991. One hundred fifty-one patients (67%) achieved a complete remission. One hundred twenty-three patients were eligible for high-dose cytarabine-based consolidation administered in two to three courses. After a median follow-up of 4.8 years, 40 patients remain alive, with 28 in continued remission. Median remission duration for all eligible patients is 12.8 months, and actuarial leukemia-free survival (LFS) at 5 years is 26% +/- 8%. Advanced age and male sex were negative prognostic indicators for LFS. For patients < or = 45 years of age, 5-year LFS was 35% +/- 13%, as compared with 18% +/- 11% for patients greater than age 45 (P = .03). Toxicity of consolidation chemotherapy included treatment-related death in nine patients and serious neurotoxicity in five. Our results show an improved LFS for younger patients treated with high-dose cytarabine-based consolidation. There was no apparent benefit for older patients compared with reported data with less intensive regimens.

Adult↗
PubMed2004

Transformation of myelodysplastic syndromes into acute myeloid leukemias.

BACKGROUND: Myelodysplastic syndromes (MDSs), also called preleukemias, are a group of myeloid hematopoietic malignant disorders. We studied the transformation of MDS into acute myeloid leukemia (AML). METHODS: Leukemic transformation in 151 patients with MDS was dynamically followed up. The clinical manifestation, peripheral blood and bone marrow condition, karyotypes, immunophenotypes, response to treatment, and prognosis of AML evolution from MDS (MDS-AML) were also observed. RESULTS: During the course of this study, over the past eight years and seven months, 21 (13.91%) of 151 MDS patients progressed to overt leukemia, with a median interval of 5 (1 - 23) months. There were no significant differences between rates of leukemic transformation in comparison with the refractory anemia (RA), RA with excess of blasts (RAEB), and RAEB in transformation (RAEB-t) patient groups. Transformation occurred either gradually or rapidly. There were five parameters positively correlated to leukemic transformation: under 40 years of age, pancytopenia of 3 lineages, more than 15% blasts in the bone marrow, at least two abnormal karyotypes, and treatment with combined chemotherapy. All of the 21 patients with leukemia suffered from MDS-AML, and most of them were M2, M4, or M5. Two (9.52%) MDS-AML patients developed extramedullary infiltration. Leukopenia was found in 47.62% of these patients. Two thirds of these patients, whose bone marrows were generally hypercellular, suffered from neutropenia. After developing AML, 8 (47.06%) patients developed abnormal karyotypes. High expression of immature myeloid antigens, including CD33 [(49.83 +/- 24.50)%], CD13 [(36.38 +/- 33.84)%], monocytic antigen CD14 [(38.50 +/- 24.60)%], and stem cell marker CD34 [(34.67 +/- 30.59)%], were found on bone marrow mononuclear cells from MDS-AML patients after leukemic transformation. In some cases, lymphoid antigens, such as CD5, CD7, CD9, and CD19, coexisted with myeloid antigens. A low complete remission rate (31.25%) and a short survival time, with median survival of 6 (1 - 28) months, were found in patients with MDS-AML treated by induction chemotherapy. CONCLUSIONS: MDS has a high risk of developing into AML, either gradually or rapidly. Patients with MDS-AML have specific biological characteristics and a worse prognosis.

Adolescent↗
PubMed1992

Prevalence of N-ras mutations in children with myelodysplastic syndromes and acute myeloid leukemia.

The ras proto-oncogene family encodes a group of 21 kDa nucleotide-binding proteins. Activating mutations of ras genes are associated with certain types of malignancies, indicating that they are related in some way to the malignant process. We have examined bone marrow cells from nine children with myelodysplastic syndromes (MDS) and 35 with acute myeloid leukemia (AML) for activating point mutations of ras genes by in vitro amplification using polymerase chain reaction (PCR), oligonucleotide hybridization and sequencing of PCR products. We found N-ras mutations in cells from 3 of 9 children (33%) with MDS and only 2 of 35 children with AML (6%; 95% confidence interval is 0.7-19%). All mutations the second nucleotide of codon 12 or the first nucleotide of codon 61 of N-ras. There was no apparent correlation with clinical or laboratory characteristics, including karyotype; however, an association of N-ras activation with the most aggressive type of MDS was noted. Among the patients with MDS, 2 of 6 with monosomy 7 had N-ras mutations; however, three children with monosomy 7 which presented with AML lacked ras mutations. One patient was studied at time of diagnosis of MDS and again after progression to AML. At the preleukemic stage of disease, an N-ras mutation was identified; however, after development of AML this mutation was not present in the leukemic clone. In conclusion, these data show that ras mutations, while not necessary for leukemic transformation, may be important for the initiation of preleukemias evolving into overt AML.

Adolescent↗
PubMed2004

Growth factor priming in therapy of acute myelogenous leukemia.

Treatment of acute myelogenous leukemia (AML) incorporates the use of growth factors towards several objectives, including abbreviating the time of neutropenia, reducing susceptibility to infections, reducing length of hospitalization, and increasing susceptibility of the blasts to chemotherapy drugs, or priming. Priming is defined as the driving of leukemia cells into cell cycle in order to increase response to S-phase-specific drugs such as cytarabine (Ara-C). Growth factors that have been used in priming include both filgrastim (G-CSF) and sagramostim (GM-CSF). Priming has often been applied in the treatment of older patients, who do not respond as well to standard treatment regimens, and whose disease was transformed from a myelodysplastic syndrome (MDS), or preleukemia. Recent, large randomized trials have demonstrated that although subgroups of patients may benefit, there does not appear to be any improvement in the complete remission rate sustained by inclusion of growth factor priming as part of the initial therapy of acute myelogenous leukemia.

Clinical Trials as Topic↗
PubMed1992

Molecular genetic aspects of myelodysplastic syndromes.

Myelodysplastic syndromes originate from a pluripotent stem cell. This view, previously suggested by G-6-PD and cytogenetic investigations, has been established unequivocally by X-chromosome inactivation analysis based on DNA polymorphisms and by studies of mutated oncogenes. Two genomic alterations associated with MDS have been analyzed in more detail. Activation of the RAS oncogenes, preferentially N-RAS, is demonstrated in approximately 35% of MDS patients. Mutations in the FMS gene, encoding the CSF-1 receptor, are found in 16% of cases. Interestingly, RAS and FMS mutations are predominantly observed in disorders of myelomonoctic differentiation, i.e., the CMML subtype in MDS and the AML FAB type M4. Moreover, homozygous deletion of the FMS gene may be an important event in the genesis of the MDS variant 5q- syndrome. Preliminary data indicate that defects in tumor-suppressor genes, namely p53, may also contribute to the development of MDS. Different lines of evidence suggest that clinical preleukemia is preceded by a phase in which genetic alterations accumulate without any hematologic change. Cases in point are the detection of RAS and FMS mutations in healthy individuals who had been treated in the past with cytotoxic therapy for lymphoma, the frequent observation of clonal remission in AML patients, or the identification of oncogene mutations in healthy individuals without even a history of malignancy or chemotherapy. Possibly, either germline mutations of oncogenes or tumor-suppressor genes and the process of genomic imprinting may constitute additional factors that predispose hematopoietic stem cells to malignant transformation. Limited as they are, the currently available data suggest that accumulation of genomic lesions, rather than their precise order of development with respect to one another, characterize the multistep process of leukemogenesis in which MDS already represent more advanced stages. The prognostic significance of oncogene mutations in MDS patients is controversially discussed. This issue awaits prospective analyses taking into account the influence of treatment modalities. However, the clinical relevance of molecularly defined parameters has already been established for their use as clonal markers in determining the mode of action and efficiency of different therapeutic approaches.

Chromosome Deletion↗
PubMed1987

[The value of cell cultures in leukemias, aplastic anemias and bone marrow transplantations].

In a survey different methods of culture are represented for the purpose of identifying and quantifying haemopoietic stem cells (CFU-GEMM, CFU-GM, CFU-E/BFU-E) in human bone-marrow or peripheral blood respectively. On the basis of findings from international medical literature their validity is explained in the diagnostics and prognosis of some haematological diseases, such as acute and chronic myeloic leukemia, aplastic anemia, preleukemia. Special attention is given to their significance within bone-marrow transplantation. Their importance in evaluating transplantations after their preceding in-vitro manipulation as to the separation of rest tumour and T-cells is particularly referred to.

Anemia, Aplastic↗
PubMed1989

Reticulocytosis: defective reticulin degradation, a case report.

In summary, this case illustrates a previously unrecognized syndrome of reticulocytosis secondary to a defect in reticulin degradation. We are aware of two other case reports in the literature which also describe patients with an elevated reticulocyte count who's red cells appeared to lack the ability to degrade reticulin (Lofters et. al.1978, Tulliez et. al. 1982). Both of these cases however, demonstrated only mild reticulocytosis and appeared to be related to preleukemic syndromes. Our patient had no evidence of preleukemia and indeed, has been followed for over four years without evidence of other hematologic abnormalities. The mild anemia that has persisted in this patient may suggest that although no evidence of hemolysis is obvious in this patient, some minor amount of hemolysis may be occurring. Due to the relative insensitivity of other measures of early red cell death (51Cr survival, bone marrow biopsy, etc...), and the loss of the the reticulocyte count as a sensitive index of hemolysis, a minor amount of hemolysis cannot be excluded. This does not decrease the validity of the observations noted above, since this massive reticulocytosis cannot be explained by minimal hemolysis. Whether this patient's reticulocytosis represents an acquired or congenital syndrome is unsettled at present. Although his brother is unaffected, and we have on record only a mildly elevated reticulocyte count from 1981, there remains a possibility that this syndrome is congenital. We are, at present, in the process of further characterizing the specific defect in these red cells. Further assays of Lipoxygenase and protease activity, the ability to ubiquitinate proteins, specific identification of the mitochondria-like structures, and protein synthesis assays are in progress or are planned. The inability to degrade reticulin in this patient's red cells and the impact of this upon other cellular physiologic processes afford an excellent opportunity to enhance our understanding of normal red cell physiology, particularly, we suspect in this patient, of Ubiquitin-ATP-dependent proteolysis.

Aged↗
PubMed1989

Novel vitamin D analogs that modulate leukemic cell growth and differentiation with little effect on either intestinal calcium absorption or bone mobilization.

Induction of terminal differentiation of leukemic and preleukemic cells is a therapeutic approach to leukemia and preleukemia. The 1 alpha, 25-dihydroxyvitamin D3 [1,25(OH)2D3], the hormonally active form of vitamin D3, can induce differentiation and inhibit proliferation of leukemia cells, but concentrations required to achieve these effects cause life-threatening hypercalcemia. Seven new analogs of 1,25(OH)2D3 were discovered to be either equivalent or more potent than 1,25(OH)2D3 as assessed by: (a) inhibition of clonal proliferation of HL-60, EM-2, U937, and patients' myeloid leukemic cells: and (b) induction of differentiation of HL-60 promyelocytes. Furthermore, these analogs stimulated clonal growth of normal human myeloid stem cells. The most potent analog, 1,25-dihydroxy-16ene-23yne-vitamin D3, was about fourfold more potent than 1,25(OH)2D3. This analog decreased clonal growth and expression of c-myc oncogene in HL-60 cells by 50% within ten hours of exposure. Effects on calcium metabolism of these novel analogs in vivo was assessed by intestinal calcium absorption (ICA) and bone calcium mobilization (BCM). Each of the analogs mediated markedly less (10 to 200-fold) ICA and BCM as compared with 1,25(OH)2D3. To gain insight into the possible mechanism of action of these new analogs, receptor binding studies were done with 1,25(OH)2-16ene-23yne-D3 and showed that it competed only about 60% as effectively as 1,25(OH)2D3 for 1,25(OH)2D3 receptors present in HL-60 cells and 98% as effective as 1,25(OH)2D3 for receptors present in chick intestinal cells. In summary, we have discovered seven novel vitamin D analogs that are more potent than the physiologic 1,25(OH)2D3 as measured by a variety of hematopoietic assays. In contrast, these compounds appear to have the potential to be markedly less toxic (induction of hypercalcemia). These novel vitamin D compounds may be superior to 1,25(OH)2D3 in a number of clinical situations including leukemia/preleukemia; they will provide a tool to dissect the mechanism of action of vitamin D seco-steroids in promoting cellular differentiation.

Animals↗
PubMed1979

Acute myeloblastic leukemia considered as a clonal hemopathy.

Acute myeloblastic leukemia, like certain other hematologic disorders, originates in pluripotent stem cells. Two general biologic processes underlie development of the disease. Over long times, clonal progression leads from normal polyclonal hemopoiesis through clonal preleukemia to leukemia. Overt leukemia is characterized by the emergence of blast cell populations. Over shorter times, clonal expansion yields cellular diversity based upon randomizing events. The analysis indicates that that blast population is of crucial importance. Characteristics of a colony assay for blast cell progenitors are presented.

Clone Cells↗
PubMed1979

[Cytochemical aspects in bone marrow cells in macrocytic anemias].

Cytochemical investigations are useful for the characterization of different kinds of macrocytic anemias. Vitamin B12 and folate defects or chronic alcoholic myelopathy, induce in the erythroblasts cytochemical patterns which can be distinguished from those seen in preleukemia, erythroleukemia, or in drug induced toxic anemia. Tests for alpha-naphthol-acetate-esterase, for acid phosphatase, for iron, and for polysaccharides (PAS-stain), are especially valuable for these diagnostic procedures.

Anemia, Macrocytic↗
PubMed1986

[Erythromyelosis in the outcome of partial red cell aplasia].

The authors describe two women with a history of partial red-cell aplasia of the bone marrow without any remissions for 2 and 3 years, followed by the development of erythromyelosis. The latter lasted from 1 to 2 years, the total illness duration being 4 to 5 years. All the attempts to achieve remissions with the use of splenectomy, mono- and polychemotherapy with a purpose of immunosuppression ended in failure. Partial red-cell aplasia is viewed as preleukemia.

Adult↗
PubMed1987

Bone marrow transplantation for leukemia following a new busulfan and cyclophosphamide regimen.

Busulfan 16 mg/kg and cyclophosphamide 120 mg/kg were used as conditioning prior to allogeneic marrow transplantation in 50 adult patients with acute nonlymphocytic leukemia (ANLL), acute lymphocytic leukemia (ALL), and chronic myelogenous leukemia (CML). A standard risk group of 20 patients included those with acute leukemia in remission and CML in chronic phase. A high-risk group of 30 patients included individuals with refractory acute leukemia, acute leukemia in relapse, acute leukemia following preleukemia, and CML in accelerated and blastic phase. Complete remission and sustained complete engraftment were achieved in all evaluable patients. The duration of aplasia was remarkably short (median of 8 days), resulting in a low infection rate during the period of neutropenia, a reduced need for blood product support, and a short length of hospital stay. Three-year actuarial relapse-free survival in both standard-risk (88.9% +/- 10.5%) and high-risk (50.5% +/- 9.6%) groups compares favorably with that reported with total body irradiation (TBI) containing regimens.

Adolescent↗
PubMed1986

Acute myelomonocytic leukemia in a horse.

A 7-year-old Quarter Horse stallion with a myeloproliferative disorder was examined because of colic, and an enterolith was removed surgically. The horse experienced secondary complications after abdominal surgery, and leukopenia and thrombocytopenia were detected. Five months later, the horse was examined for recurrent peripheral edema and for repair of an abdominal incisional hernia. Acute myelomonocytic leukemia was diagnosed, and treatment with low-dose (noncytocidal) cytosine arabinoside was unsuccessful. Necropsy revealed neoplastic infiltrate in the spleen, liver, lung, adrenal gland, testes, and eye. The persistent hematologic abnormalities before the onset of overt leukemia may represent hematopoietic dysplasia or preleukemia.

Animals↗
PubMed1987

Cellular control of in vitro progression of murine myeloid leukemia: progression accompanies acquisition of independence from growth factor and stromal cells.

The ability of bone marrow stroma cells of normal WCB6F1 (+/+) mice versus their congenic Sl/Sld stromal-defective littermates to support sustained proliferation and leukemic transformation of the growth factor-dependent myeloid cell line FDC-P1 was studied. Extensive proliferation of factor-dependent cells occurred on (+/+) normal long-term marrow culture stroma without the addition of growth factor, whereas factor-dependent cells dissipated from Sl/Sld stromal cultures after addition. The sustained proliferation that occurred on +/+ stromal layers later resulted in the appearance of factor-independent cell lines that were no longer dependent upon stroma. Factor-independent cell lines were cloned by limiting dilution and analyzed for expression of cell surface antigens to prove their origin from FDC-P1. Factor-independent cells, but not factor-dependent cells, formed tumors in syngeneic mice. These studies demonstrate a critical role for marrow stroma in the stepwise development of murine leukemia and are concordant with the previous data obtained in in vivo studies by McCool et al. that the splenic stroma of irradiated Sl/Sld mice do not support growth of Friend virus-induced preleukemic cell colonies. The present data demonstrate in a preleukemia model not induced by Friend virus complex that normal (+/+) stromal cells promote the in vitro proliferation of factor-dependent preleukemic cells and their subsequent transition to factor-independent leukemia cells, but Sl/Sld defective stroma do not efficiently promote this transition.

Animals↗
PubMed1986

Bone marrow transplantation in patients aged 45 years and older.

Increasing age has been reported to be a poor prognostic factor for survival after bone marrow transplantation. We evaluated causes of death and frequency and type of complications after marrow grafting in 24 syngeneic and 39 allogeneic recipients who were 45 to 68 years old at the time of transplant. Most patients were in an advanced stage of hematologic malignancy. Among patients given syngeneic transplants, actuarial disease-free survival at 7 years is 20%. The major causes of death were relapse of leukemia and idiopathic interstitial pneumonia. Among allogeneic recipients, 9 (23%) are currently alive, and actuarial disease-free survival at 7 years is 11%. Cytomegalovirus pneumonia and septicemia were the most frequent causes of death. Patients over 50 years of age had the poorest survival rate (1/13), but many of these were transplanted in an advanced stage of their disease. However, among 12 patients transplanted while in remission or at an early stage of their disease, 5 are surviving 65 to 1,160 days after transplantation, with an actuarial survival rate of 22% at 3 years. This is in contrast to those who received their transplant in relapse: 2 out of 20 patients (10%) became long-term survivors, with a probability of survival of 15% at 3 years. The actuarial incidence of grade II through IV acute graft-v-host disease (GVHD) was 30% for allogeneic recipients 45 to 50 years of age. This was not significantly different from the incidence in younger patients. In patients 51 to 62 years of age, the actuarial incidence of acute GVHD was 79%; however, this group included three partially HLA-mismatched transplants. Ten of 15 patients surviving at least 3 months developed chronic GVHD. These results suggest that marrow transplantation is feasible and should be considered in patients over 45 years, especially if recipients are in good clinical condition and are at an early stage of their disease, such as the chronic phase of chronic myelogenous leukemia and preleukemia. For patients more than 50 years of age, allogeneic marrow grafting cannot presently be considered first-line therapy.

Adult↗