Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 170 patients with chronic myeloid leukemia (CML), 107 in chronic phase (CP) and 63 in blastic phase (BP) of the disease, 187 patients with "de novo" acute myelogenous leukemia (AML) and 175 patients with myelodysplastic syndrome (MDS), 164 patients with primary and 11 with secondary MDS, were cytogenetically examined. All patients with CML were Ph positive, additional chromosomal changes were ascertained in 29% of patients in CP and in 71% of patients in BP. The most frequent chromosomal abnormalities were trisomy 8, additional Ph, (i(17q] and loss of Y chromosome. More favorable course of the disease was observed for group of patients with Ph chromosome as solitary chromosomal abnormality in CP. Acquired chromosomal aberrations were proved in 137 patients with AML (73.3%). Except specific chromosomal changes delineated according to the specific subtype of AML we were concerned with evaluation of nonrandom chromosomal abnormalities, specially those involving chromosome 5 and 7. Numerical and morphological changes of those chromosomes were found in 33 patients (17.6%). In MDS patients abnormal chromosomal clones were found in 68.8% of patients, those involving chromosome 5 and/or 7 in 68 patients (38.8% of all examined). The frequency of these abnormalities in AML does not differ significantly from the results quoted by the other studies. However, in our MDS patients these so called "mutagen-associated" chromosome abnormalities were significantly more frequent than in all studies published so far. Prognostic value of cytogenetic examination was evaluated on the basis of cumulative survival of patients with normal and abnormal chromosomal clones present in bone marrow cells.
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PMID:Cytogenetic abnormalities in 532 patients with myeloid leukemias and myelodyplastic syndrome. The Czechoslovak MDS Cooperative Group. 208 40

Serial cytogenetic studies were performed on 64 patients with chronic myelogenous leukemia (CML) after T cell-depleted allogeneic bone marrow transplantation (BMT). Forty patients with CML in chronic phase (CP) received cytoreduction followed by BMT with HLA-matched T cell-depleted allogeneic marrow. The remaining 24 patients were transplanted in second chronic, accelerated, or blastic phase, or received T cell-depleted grafts with a dose of T cells added back. The Y chromosome and autosomal heteromorphisms were used to distinguish between donor and host cells. Mixed hematopoietic chimerism (presence of donor and host cells) was identified in 90% of patients in first CP. The Philadelphia (Ph) chromosome reappeared in 16 of the 40 first CP CML patients. As expected, patients who had detectable Ph chromosome positive cells at any time during the posttransplant period had a high likelihood of subsequent clinical relapse. Transient disappearance of the Ph positive clone was rarely observed, and was followed by reappearance of the Ph chromosome or clinical relapse. A subset of engrafted patients with greater than 25% host cells within 3 months post-BMT had a significantly shorter survival time free of cytogenetic or clinical relapse compared with other patients. In patients who had received donor T cells added to the T cell-depleted graft, there was a higher proportion of complete chimerism. Clonal progression of Ph positive as well as negative cells was observed and may be the result of radiation induced breakage. Serial cytogenetic studies of patients post-BMT can provide useful information regarding the biologic and clinical behavior of CML.
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PMID:Cytogenetic analysis of chimerism and leukemia relapse in chronic myelogenous leukemia patients after T cell-depleted bone marrow transplantation. 231 Aug 31

The fate of the donor graft in allogeneic bone marrow transplantation, the presence of chimaerism and early relapse can be monitored by identification of the donor or recipient origin of haemopoietic cells in peripheral blood and bone marrow. We have done this by the use of highly informative locus-specific hypervariable DNA probes in two sex and blood group matched transplants. In four sex mismatched transplants the Y chromosome was identified by in situ hybridization using a biotinylated Y probe. Early engraftment by day 13 was detected in five of the six patients. Transient chimaerism occurred in half of the cases and was accompanied by the temporary appearance of the Philadelphia chromosome in one patient with chronic myeloid leukaemia without subsequent relapse. Persistence of the graft in the face of falling peripheral counts was documented in four of the six patients studied. The morphology as well as origin of the haemopoietic cells could be characterized by the Y probe analysis. In one patient, recipient lymphocytes were shown to co-exist with myeloid series of donor origin. We conclude that both techniques are highly specific, sensitive and can provide information within 24-48 h. Thus they are of value in guiding early therapeutic intervention in allogeneic transplantation.
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PMID:Rapid identification of donor and recipient cells after allogeneic bone marrow transplantation using specific genetic markers. 266 22

Fifty-six patients with blood disorders (23 with chronic myeloid leukemia, 14 with acute myeloblastic leukemia, seven with acute lymphoblastic leukemia, one with chronic lymphocytic leukemia, and 11 with preleukemia states) were studied. A quantitative and objective method of C band length analysis with well-matched controls was used. The C bands of chromosome pairs 1, 9, and 16 presented a normal distribution that was similar in patients and controls, whereas the Y chromosome presented an abnormal distribution. Smaller C bands in 1qh and higher indexes of intrapair heteromorphism in pairs 1 and 9 were detected in the CML group; the group of acute leukemias (myeloblastic and lymphoblastic) presented a smaller index only in pair 1qh. No other differences in length, heteromorphism, inversion frequency, or sex were detected.
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PMID:Densitometric measurements of C bands of chromosomes 1, 9, 16, and Y in leukemic and preleukemic disorders. 276 53

To examine whether determination of (1) the copynumber or restriction pattern of certain oncogenes or (2) the mutational activation of the N-ras gene might contribute to the risk classification of acute lymphoblastic leukemia of childhood (ALL), we investigated DNA isolated from lymphoblasts of untreated patients. Restriction enzyme analysis of cellular oncogenes was performed on DNA of 25 patients. No rearrangements could be demonstrated within or near the genes c-myc, c-myb, c-abl, bcr, c-Ki-ras, and N-ras. No amplifications of these genes nor of N-myc or c-Ha-ras were present. Eight of 21 patients were heterozygote for "rare" Ha-ras allelic restriction fragments that have been associated with an increased risk of developing a malignancy. These patients were clinically indistinguishable from patients lacking these fragments. The breakpoint cluster region (bcr) that is rearranged in all patients with Philadelphia chromosome positive chronic myeloid leukemia, was normal in all cases, including at least one patient with Philadelphia chromosome positive ALL. A 2.8 kb HindIII fragment of a hitherto unknown gene or pseudogene related to v-myb probably derives from the Y chromosome. Nineteen patients were examined for point mutations in the N-ras gene, using a novel synthetic oligonucleotide hybridization assay. In two patients activating point mutations were present, both in positions 1 of the 12th codon. Both patients were somewhat older than the others (16 and 11 years), had L2 morphology, and were shown to have high growth fractions of tumor in their bone marrow.
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PMID:Absence of oncogene amplifications and occasional activation of N-ras in lymphoblastic leukemia of childhood. 301 Nov 51

2 cases of chronic myelocytic leukemia (CML) without Y chromosome are reported. One is a 45-year-old man with Philadelphia-positive CML, and the other a 74-year-old patient with Philadelphia-negative CML. Cytogenetic analysis of bone marrow and peripheral blood cultures with and without PHA stimulation was carried out. The Philadelphia-positive patient died after 15 months, whereas in the case of the Philadelphia-negative patient, the survival time of 27 months exceeded the median survival time usually reported for Philadelphia-negative CML patients, thus indicating a prognostic relevance of the missing Y chromosome.
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PMID:Missing Y chromosome in 2 patients with chronic myelocytic leukemia. 309 29

A 16-year-old boy with leukemia had a marked leucocytosis (165 x 10(9)/L) at presentation. The large number of neutrophils, myelocytes, and metamyelocytes and negative leucocyte alkaline phosphatase reaction raised the possibility of chronic myeloid leukemia. Cytogenetic analysis showed a deletion of chromosome 7, a t (8;21), a missing Y chromosome, and, in some cells, duplication of the der(21). The Philadelphia chromosome was not detected, nor was the breakpoint cluster region of chromosome 22 found to be rearranged. Myeloid leukemia with t (8;21) can therefore be associated with a greater degree of granulocytic hyperplasia than has so far been apparent, and cytogenetic analysis in this case has been crucial in distinguishing leukemia types.
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PMID:Translocation t (8;21) associated with marked granulocytic hyperplasia. 316 93

Four patients with Philadelphia (Ph') positive chronic myeloid leukemia (CML) were studied before, after, and on relapse following allogeneic bone marrow transplantation (BMT). Southern analysis of DNA from cells collected before and at relapse after BMT was performed in order to investigate the origin of the leukemia at relapse. Using minisatellite probes we showed that the relapse occurred in cells of host origin in all four patients and this was confirmed with a Y chromosome specific probe in two male patients who had a female donor. Furthermore, using two probes for the breakpoint cluster region (bcr) on chromosome 22, we showed that leukemic cells at relapse bore identical rearrangements to those in the disease at time of presentation of each patient. We conclude that relapse in all four patients is due to re-emergence of the original leukemic clone.
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PMID:Molecular analysis of relapse in chronic myeloid leukemia after allogeneic bone marrow transplantation. 330 66

Chromosome studies on bone marrow cells and unstimulated peripheral lymphocytes from a patient with chronic myelogenous leukemia revealed the presence in all cells of two apparent Philadelphia chromosomes: one resulting from the classical translocation with a chromosome #9, and the other arising from a translocation between chromosomes #22 and #7. There was no normal chromosome #22. Some of the cells also had an i(17q), indicative of blast crisis. Repeated chromosome studies at different times during the course of the disease revealed the evolution of additional karyotypic changes. All cells from later samples had an extra #8; some of these cells had a third Philadelphia chromosome, whereas, others had a second Y chromosome. Although a few normal cells were seen in PHA-stimulated lymphocyte cultures, indicating that the patient has a normal constitutional karyotype, most of the cells had a karyotype identical to that found in unstimulated cultures. This unusual karyotype, 46,XY,t(7;22)(p22;q11),t(9;22)(q34;q11), represents the first case in which two apparent Philadelphia chromosomes are present in the leukemic cells from a patient in the absence of a normal #22 chromosome.
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PMID:Two apparent Philadelphia chromosomes arising from translocations with different chromosomes in a patient with CML: 46,XY,t(7;22)(p22;q11),t(9;22)(q34;q11). 345 23

Between 1965 and 1982, 105 patients with a diagnosis of Philadelphia chromosome-negative chronic myelogenous leukemia were referred to our institution with minimal or no prior therapy. The median age was 63 years and 64% were males. The overall median survival from time of referral was 14 months; 53% of patients survived 1 year and only 10% survived beyond 5 years. At the time of analysis, 92 patients (88%) were dead, 56% of deaths being preceded by a blastic crisis. Compared with Philadelphia chromosome-positive disease, patients with Philadelphia chromosome-negative chronic myelogenous leukemia were older and had a significantly higher incidence of anemia, thrombocytopenia, monocytosis, marrow blasts, decreased marrow megakaryocytes and a lower incidence of basophilia and thrombocytosis. Chromosomal abnormalities occurred in 33% of patients and consisted most frequently of trisomy 8, or an additional chromosome C, loss of the Y chromosome, or abnormalities in chromosomes #5 and #7. Of nine pretreatment characteristics significantly associated with poor survival, a multivariate analysis identified four to have independent additive prognostic significance: severe thrombocytopenia, hemoglobin levels less than 10 g/dl, increasing peripheral blasts and promyelocytes, and age 60 years or older. Monocytosis was not of prognostic significance. The derived prognostic model divided patients into three risk groups, low, intermediate, and high, with median survivals of 36, 16, and 3 months, respectively. The authors conclude that Philadelphia chromosome-negative chronic myelogenous leukemia is a distinct entity among the myeloproliferative syndromes with characteristic clinical and laboratory features and a poor prognosis. Prognostic factors and related risk categories were demonstrated within this disease entity.
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PMID:Clinical and prognostic features of Philadelphia chromosome-negative chronic myelogenous leukemia. 346 97


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