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PubMedDate not supplied

The occurrence of variant Ph translocations in chronic myeloid leukemia (CML): a report of six cases.

Variants of Philadelphia chromosome (Ph) translocation were detected in six of 95 Ph positive chronic myeloid leukemia (CML) patients (6.3 per cent). Two of these patients showed a Ph variant of 'simple' type, involving chromosomes 10 and 12. In four patients, the variant Ph was of 'complex' type involving a third chromosome:chromosomes 1, 6, 7 and 12 in addition to 9 and 22. Two of these resulted in the occurrence of a 'masked' Ph. In addition to variant Ph translocations, variant breakpoints such as q12 (two patients) and q13 (one patient) on chromosome 22 were observed in another three patients with t(9;22).

Adult↗
PubMed1981

Prognostic value of chromosomal findings in the blast phase of Ph1-positive chronic myeloid leukaemia (CML).

Twenty-three patients in various cytological subgroups of blast phase of Ph1-positive chronic myeloid leukaemia were investigated cytogenetically The correlation between prognosis and the cytological and cytogenetic features of blast cells was studied. The best prognosis was found in the myeloid group, followed by the lymphoid, myelomonocytic, megakaryoblastic and finally the promyelocytic groups, in this order. As regards the prognostic significance of the cytogenetic finding, the survival seemed to be the longest among patients with mosaic karyotypes i.e. when further aberrations occurred in some Ph1-positive cells. The course of the disease was the most favourable in the presence of i(17q), especially in patients whose cells had i(17q) as the only aberration. The most severe course of the disease could be found in patients with +8 and/or two Ph1. The results demonstrate the usefulness of chromosome investigations in distinguishing the different cytogenetic subgroups in terminal stages of CML, which also differ prognostically from each other.

Adult↗
PubMed1988

Spatial relationship of chromosomes 9 and 22 at metaphase in patients with chronic myelogenous leukemia (CML).

One hundred patients with Ph1-chromosome-positive chronic myelogenous leukemia (CML) with t(9;22) are included in the present investigation. The position of the Ph1 chromosome in relation to the normal as well as the abnormal chromosomes 9 was localized at metaphase in 1,000 bone-marrow cells. Our study suggests that the rearranged chromosomes, i.e., Ph1 and t(9;22), are closer together than their normal homologues. This impression is based on extensive statistical analysis. The intimate relationship may be due to the fact that they carry reciprocal genetic material responsible for a power of attraction between them. Alternatively, it is tempting to hypothesize that there may be a DNA sequence homology in the bands of chromosomes 9q and 22q involved in the reciprocal translocation perpetuating this relationship in subsequently generating cells during mitotic cell divisions. Furthermore, c-abl and bcr genes might play some role in maintaining the spatial relationship.

Chromosomes, Human, Pair 22↗
PubMed1978

Ph1-positive CML in a 13;14 translocation carrier.

A 63-year-old woman with Ph1-positive CML and a constitutional 13;14 Robertsonian translocation is described. The rarity of this cytogenetic combination and the significance of the D/D translocation in the genesis of the Ph1 and other chromosome anomalies in myeloproliferative disorders is briefly discussed. It is concluded that the occurrence of the two cytogenetic anomalies and the clinical states is coincidental.

Chromosomes, Human, 13-15↗
PubMed1979

Chromosomal marker 20q- in cases of osteomyelosclerosis and CML.

Two male patients with myeloproliferative disorders (osteomyelosclerosis in one and CML in the other) were found to have a chromosomal marker 20q- in blood cells (unstimulated short time cultures). Marked erythropoietic disturbances were not revealed in these cases. The specificity of the 20q- marker for red cell disorders is discussed.

Aged↗
PubMed1984

Clonal evolution with isodicentric Ph1 chromosome in Ph1-positive CML: karyotypic conversion after bone marrow transplantation.

Clonal chromosomal evolution was observed in a 16-year-old boy suffering from Ph1-positive CML. An isodicentric Ph1 chromosome appeared 20 weeks after the initial diagnosis. At that time an allogeneic bone marrow transplantation was performed. Thereafter, during an observation period of more than 13 months, chromosome analyses showed neither the Ph1 chromosome nor the abnormal isodicentric variant. Close cytogenetic monitoring is suggested to reveal early unfavorable prognostic signs of the onset of blast crisis before it becomes evident in the bone marrow morphology.

Adolescent↗
PubMed1985

Cytogenetic heterogeneity in blast crisis (BC) of chronic myelogenous leukemia (CML).

New cytogenetic findings are reported in a patient who entered into an accelerated blastic phase of chronic myelogenous leukemia (CML). The cytogenetic findings of this case can be described as 46, xy, t (5;7) (q 31;q 11), t (9;22) (q 34;q 11), Ph'. The prognostic implications in such patients with rare and unusual cytogenetic findings are discussed.

Aged↗
PubMed1989

Translocation of c-abl oncogene and PDGFB (c-sis) gene in a case of CML with 46,XY, t(22;22).

In a case of CML with a variant Philadelphia translocation (Ph1 or Ph) t(22;22) (q11;q13) in bone marrow cells and unstimulated peripheral blood cells, no cytogenetically detectable involvement of chromosome 9 was observed. Southern blot experiments using probes specific for bcr and c-sis however revealed rearrangement of the bcr, but not of PDGFB (c-sis) gene. Northern blot analysis of bone marrow RNA showed a very weak signal with the c-sis probe, while in a lymph-node biopsy PDGFB m-RNA could not be detected. Chromosomal in situ hybridization gave evidence for translocation of c-abl from chromosome 9 to Ph and of PDGFB from chromosome 22 to chromosome 9, as the result of a threefold translocation t(9;22;22).

Bone Marrow↗
PubMed1988

Treatment with natural human interferon alpha of a CML-patient with antibodies to recombinant interferon alpha-2b.

A patient with Philadelphia-chromosome positive chronic myelogenous leukemia developed interferon antibodies on treatment with recombinant interferon alpha-2b. Clinically this event corresponded with progressive disease. No cross-reactivity of antibodies with human leukocyte interferon was found by Western blot. Treatment was switched to human leukocyte interferon with an obvious clinical effect: WBC was reduced and platelet count stabilized, but the effect was transient and no hematologic remission was achieved. Human leukocyte interferon may be an alternative in CML-patients with neutralizing antibodies to recombinant interferon alpha.

Antibody Formation↗
PubMed1983

Definition of four HLA-A2 subtypes by CML typing and biochemical analysis.

The population of HLA-A2-positive individuals, currently considered serologically homogeneous, can be divided into three subtypes on the basis of antigen recognition by various HLA-A2-specific cytotoxic T lymphocytes (CTLs). When these three types of HLA-A2 antigens were analyzed biochemically, they were found to be distinct. Isoelectric focusing (IEF) of HLA antigens digested with neuraminidase (NANAse) suggested that the difference(s) reside in the polypeptide backbone of the HLA-A2 heavy chain. Biochemical analysis distinguishes three distinct categories of HLA-A2 antigens: (1) a major subtype, designated HLA-A2.I, (2) a minor subtype, designated HLA-A2.II, possessing a more basic isoelectric point (IEP) and (3) a minor HLA-A2 subtype more acidic in its IEP than HLA-A2.I, designated HLA-A2.III. A fourth HLA-A2 subtype could be defined by discordance between cell-mediated lympholysis (CML) typing and biochemical analysis. The latter HLA-A2 antigen was defined as a variant by CTL, but was biochemically indistinguishable from the major subtype HLA-A2.I.

Electrophoresis, Polyacrylamide Gel↗
PubMed1992

Relation between leukocyte counts and cortisol secretion in CML patients undergoing combined TNF alpha/IFN alpha therapy.

During long-term interferon alpha-2b (IFN) therapy of Philadelphia chromosome-positive chronic myelogenous leukemia (CML) patients, short-term effects of tumor necrosis factor alpha (TNF) on peripheral leukocyte counts, as well as cortisol and corticotropin (ACTH) release were studied. TNF (40-160 micrograms/m2) was given as a 2-h infusion on 5 consecutive days every 3 weeks, in addition to s.c. daily IFN injections (4 mio U/m2), to four (two male/two female) patients, who had been treated for more than 8 months with IFN and additionally for 0-7 months with TNF. Leukocyte counts, cortisol, and ACTH were determined at 30-min intervals between 4 p.m. and midnight. Profiles were determined the day before and on day 1 of TNF therapy. Leukocyte numbers decreased 30 min after start of TNF administration and increased 30-60 min later with a rebound until the next TNF application. The increase of leukocyte counts was due mostly to neutrophil granulocytes. ACTH levels increased 30 min, cortisol 60 min, and leukocyte counts 90 min after start of TNF infusion. Metopirone, an inhibitor of cortisol synthesis given to one patient, suppressed the TNF-induced stimulation of cortisol secretion and subsequent increase of leukocyte counts, while ACTH blood levels were enhanced. It was concluded that leukocyte count increases after TNF/IFN administration might be related to TNF-evoked cortisol secretion.

Adrenocorticotropic Hormone↗
PubMed1999

IFN-alpha regulates IL 10 production by CML cells in vitro.

High levels of spontaneous in vitro IL 10 secretion by a subset of untreated chronic phase CML patients' cells are shown to be decreased in the presence of IFN-alpha. However, the lower level of spontaneous IL 10 secretion by healthy control cells are was not depressed by IFN-alpha. In contrast to its effects on IL 10 production, IFN-alpha increased the low spontaneous secretion of IL 1alpha by patients' cells, bud did not further increase the higher levels of spontaneous IL 1beta secretion by normal cells. It had no effect on secretion of TNF-alpha by patients or normals. Spontaneous secretion of IL-1alpha (or IFN-gamma) by patients' cells was not observed whether or not IFN-alpha was present. Therefore, one mechanism of action of IFN-alpha in vivo may involve decreasing endogenous IL 10 secretion (thereby reducing suppressive effects on T cell reactivity) and increasing IL 1beta secretion (thereby enhancing antigen presentation).

Humans↗
PubMed2002

Candida arthritis in a patient with chronic myelogenous leukemia (CML) in blastic transformation, unresponsive to fluconazole, but treated effectively with liposomal amphotericin B.

Candida arthritis is quite rare and might be caused either by direct intra-articular inoculation of Candida or secondary to hematogeneous seeding of Candida in immunocompromised hosts. Until now less than 50 cases of Candida arthritis have been reported in the literature. We report a case of Candida arthritis, which occurred in a patient with chronic myelogenous leukemia (CML) in blastic transformation. Aggressive chemotherapy and broad-spectrum antibiotics for a prolonged period for febrile neutropenia had been given to the patient. Arthritis of the left knee appeared during the recovery phase of leukopenia. Despite treatment with fluconazole, no clinical or microbiological improvement was obtained. Thus, administration of liposomal amphotericin B was started and after 3 days there was improvement. We can conclude that fluconazole might not be sufficient in some Candida arthritis cases and liposomal amphotericin B might be a good alternative in these resistant cases.

Amphotericin B↗
PubMed2003

Pulmonary nocardiosis in a patient with CML relapse undergoing imatinib therapy after bone marrow transplantation.

We describe a case of pulmonary nocardiosis in a female patient with graft-versus-host disease (GVHD) underwent therapy with imatinib mesylate for a relapse of chronic myeloid leukemia (CML) after allogeneic bone marrow transplantation (BMT). The patient developed chronic GVHD 8 months after the use of imatinib and was on corticosteroid therapy. Three months after the development of chronic GVHD, she acquired pulmonary nocardiosis and a computed tomography (CT) scan of the chest showed multiple nodular lesions with cavitations over both lungs. She was successfully treated with single-agent trimethoprim-sulfamethoxazole (TMP/SMX) and the infection did not recur. Our case indicated that pulmonary nocardiosis could occur in patients with GVHD undergoing imatinib and corticosteroid therapy and might be treated by single-agent TMP/SMX.

Adrenal Cortex Hormones↗
PubMed2004

Modern diagnostics in chronic myeloproliferative diseases (CMPDs).

According to the new WHO classification a group of chronic myeloproliferative diseases (CMPDs) were defined: chronic myeloid leukemia (CML), chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia and hypereosinophilic syndrome (CEL/HES), polycythemia vera (PV), chronic idiopathic myelofibrosis (with extramedullary hematopoiesis, CIMF), essential thrombocythemia (ET), and so called CMPD/unclassifiable. As clinical features and laboratory findings differ widely between these diseases several diagnostic approaches are mandatory at diagnosis for classification and are needed also for follow up studies, especially for the measurement of minimal residual disease (MRD). We here outline the laboratory set up at diagnosis and during follow up in CMPDs with specific focus on the respective therapeutical consequences. Only by using a comprehensive diagnostic panel including cytomorphology, cytogenetics, and molecular genetic methods establishing the correct diagnosis, optimizing treatment as well as evaluating treatment response is possible in CMPDs today.

Blood Cell Count↗
PubMed2005

Conventional cytogenetics of myeloproliferative diseases other than CML contribute valid information.

In chronic myeloproliferative disorders other than CML (CMPD) recurrent cytogenetic abnormalities occur, but specific patterns of chromosomal aberrations in the specific entities have so far not been detected. Thus, the value of conventional cytogenetics in the routine diagnostic setting of CMPD remains to be clarified. We performed a cytogenetic study on 409 patients with different CMPD [polycythemia vera, essential thrombocytosis (ET), idiopathic osteomyelofibrosis, chronic myelomonocytic leukemia (proliferative subtype), idiopathic hypereosinophilic syndrome (HES), myeloproliferative syndrome (unclassifiable)] and on 102 patients with suspected CMPD. Cytogenetic abnormalities occurred in different frequencies ranging from 3 to 40% depending on the subtype, and showed some specific differences with respect to their type. The highest frequency and the most complex pattern of clonal aberrations were observed in idiopathic osteomyelofibrosis. However, clonal aberrations were also found in 10% of patients with suspected CMPD establishing the diagnosis of a malignant disease. In conclusion, cytogenetics are essential in the routine diagnostic setting of CMPD or cases suspicious for CMPD. In ET and in HES the aberration rate was only 3 and 7%, respectively. Thus, cytogenetics can be omitted. However, in some of these cases molecular procedures should be integrated into the routine diagnostic process.

Adult↗
PubMed1990

Class II MHC antigen-positive macrophages from human placentae suppress strong MLR and CML reactions.

Placental adherent cells (PAC), derived by mild enzymic digestion of human placentae and adherence to plastic, were tested for their ability to suppress MLR and CML reactions. Stimulation of allogeneic T cells by cord blood mononuclear cells or by a strongly stimulatory B lymphoblastoid cell line were consistently inhibited by all PAC preparations tested. PAC were fractionated by Fc rosetting and Percoll gradients to produce a number of bands. Suppression correlated with the content of macrophages in each band and was strongest in band 5 which generally contained 94-100% macrophages. The suppressive effect was not inhibited by indomethacin. The possible role of macrophages in suppressing immune reactivity in the placenta is discussed.

Cell Separation↗