Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Light chains from seven of eight monoclonal Ig detected in the serum of patients with chronic myelocytic leukaemia (CML) were of the lambda isotype. Although the presence of monoclonal Ig in CML is distinctly unusual, this prevalence of lambda chains is unlikely to be a mere coincidence. All patients had otherwise typical clinical, chromosomal and molecular (bcr rearrangements) features of classical CML. The lambda locus appeared unaltered. Only two patients had an excess of dystrophic plasma cells suggestive of multiple myeloma.
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PMID:Prevalence of monoclonal Ig with lambda light chains in chronic myelocytic leukaemia. 251 66

The BCR gene on chromosome 22 has received increasing attention because of its involvement in the Philadelphia (Ph') translocation. For most restriction enzymes, this locus has been found to be nonpolymorphic. Two alleles have only been found when Taql-digested DNA is hybridized to a 5' bcr-specific probe. We describe another two-allele polymorphism detected by the same probe in PvuII-digested DNA. The polymorphism is characterized by an additional PvuII site in the bcr region: this causes the appearance of an additional band of about 2.3 kb or 2.5 kb besides a 4.8-kb fragment in hybridizations with the 5' bcr or a 3' bcr probe. The incidence of the second allele is very low. It has only been found in some patients with hematopoietic malignancies and in a group of volunteers having a leukemia patient in their families.
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PMID:A PvuII polymorphism of the bcr region in patients with hematopoietic disorders and their families. 256 65

To elucidate the mechanism of leukemia induced by radiation, we studied both chromosome abnormalities and bcr rearrangements of seven CML patients with a history of atomic bomb exposure and 14 CML patients without the exposure. All patients, irrespective of radiation exposure, had 9;22 translocation and rearrangement of the bcr gene in the leukemic cells. Further analysis of breakpoints within the bcr gene demonstrated no distinct difference between the exposed and the non-exposed groups. The present study suggests that formation of the chimeric bcr-abl gene and its genetic products may play an important role in the development of leukemia in either radiation-induced or de novo CML.
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PMID:9;22 translocation and bcr rearrangements in chronic myelocytic leukemia patients among atomic bomb survivors. 261 51

Results of our study on the activation of N-ras oncogene by point mutation in human leukemia and myelodysplastic syndrome have been described in this article. Point mutation was observed mainly on the 12th, 13th and 61st amino acid codon of ras genes. Therefore, oligomers containing mutations at these codons were used as probes for dot blot analysis of DNA derived from patient's bone marrow cells or leukemia cells. Polymerase chain reaction technique was used to amplify the DNA of ras genes containing 12th, 13th and 61st codons. By this technique, sensitivity of the method to detect the point mutations in ras oncogene was remarkably increased. Detection of the mutation in ras gene is considered to be very useful for the diagnosis, determination of remission and finding of relapse at an early stage. Study on the fused gene of bcr-abl, its mRNA and protein in chronic myelogenous leukemia is a good and reliable method to prove the existence of Ph1 positive chromosome by gene technology. Identification of the Ph1 acute lymphoblastic leukemia (ALL) has become possible by studying abl oncogene in Ph1 positive ALL. This method can be used also for the diagnosis of Ph1 ALL.
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PMID:[Oncogenes in human leukemia]. 265 Jun 33

In the Philadelphia positive bcr negative acute leukemias (Ph1+bcr- AL), the chromosomal breakpoints on chromosome 22 have been shown clustered within 10.8kb (bcr2) and 5kb (bcr3) fragments of the first intron of the BCR gene. We previously reported that the breakpoints were localized in Alu repeats on chromosomes 9 and 22 in a Ph1+bcr- acute lymphoblastic leukemia with a rearrangement involving bcr2. Molecular data of two other Ph1 translocations, one a Ph1+bcr- acute myeloblastic leukemia in the bcr2 region, and the other an acute lymphoblastic leukemia in the bcr3 region are presented. In the former, the breakpoints on chromosomes 9 and 22 are localized in Alu repeats, in regions with two inverted Alu sequences, as in our previously reported case. In the second leukemia, the breakpoints are not located in Alu sequences, but such repeats are found in their vicinity. The implications of these findings are discussed.
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PMID:Structural alterations of the BCR and ABL genes in Ph1 positive acute leukemias with rearrangements in the BCR gene first intron: further evidence implicating Alu sequences in the chromosome translocation. 267 2

A break in chromosome 22 within the major breakpoint cluster region (M-bcr) is a characteristic of Philadelphia chromosome-positive CML. We have determined the zone of the breakpoint in 80 chronic myelogenous leukemia (CML) patients and have confirmed our previous observation that a relationship does exist between the subregion of the breakpoint within the M-bcr and the average length of the chronic phase of the disease. Patients with a 3' breakpoint have a statistically shorter chronic phase (25 months) than patients with a 5' break (55 months). Thus, a molecular analysis of the M-bcr may provide a prognostically useful indicator of the probable length of the chronic phase, although the underlying mechanism of blast transformation, and the role (if any) of the hybrid phl-abl mRNA, is still unclear.
Leukemia 1989 Dec
PMID:Further evidence that the site of the breakpoint in the major breakpoint cluster region (M-bcr) may be a prognostic indicator. 268 75

A case of acute myelocytic leukemia (AML-M2) with a late appearance of Philadelphia chromosome (Ph1) is presented. Chromosome analysis revealed a normal karyotype at the time of diagnosis and for 23 months, when hematological relapse occurred, accompanied by abnormal clones, 46, XX, t(9;22) (q34;q11) (78%) and 45,XX, -16, t(9;22) (q34;q11), del (5) (q13q31) (22%). The patient died of GVHD after bone marrow transplantation. Molecular analysis confirmed bcr gene rearrangement in the cells with Ph1 chromosome. Acquisition of Ph1 chromosome during the course of hematological malignancies other than CML is extremely rare. This case is undoubtedly important for the understanding of leukemogenesis and the evolution of leukemia clones. The authors discussed possible mechanisms of Ph1 acquisition in the late stages of AML.
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PMID:[Late appearance of Philadelphia chromosome with bcr gene rearrangement in an acute myelocytic leukemia patient]. 269 64

A new Philadelphia chromosome (Ph1-positive) acute lymphoblastic leukemia (ALL) cell line was established in nude mice by direct and serial transplantation of peripheral blood leukemia cells from an adult patient. Although the patient's leukemia cells did not grow in vitro, they were successfully transplanted for 8 serial passages, giving rise to progressive growth of tumors with frequent involvement of lymph nodes, liver, spleen, bone marrow, and meninges. The tumor cells could also be passaged in an ascites form. This in vivo cell line, designated PALL-I, retained the Ph1 chromosome, t(9;22) (q34;q11), and pre-B-cell phenotype (SmIg-, CpIg-, CD10+, CD19+, OKIaI+, and CD38+), like the original leukemia cells. Molecular genetic analysis of PALL-I cells revealed neither bcr rearrangement nor 8.5-kb abI-related mRNA that is characteristically seen in Ph1-positive chronic myelogenous leukemia (CML). Thus, the PALL-I cell line is genetically distinct from CML. It may provide a useful model for an understanding of the cellular and molecular biology of Ph1-positive ALL without classical bcr rearrangement.
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PMID:Direct and serial transplantation of Ph1-positive acute lymphoblastic leukemia into nude mice. 273 4

Despite the major breakthrough in the knowledge of the molecular events underlying the t(9;22) translocation, still no consistent data have been found on the evolution of Ph1 positive CML from the chronic to the accelerated or blastic phase of the disease. In most patients in fact the bcr/abl rearrangements are identical both in chronic phase and in blast crisis, and overall differences in chronic phase duration, related to different location of breakpoints inside the bcr region, were found to be marginal. We approached this problem by studying the molecular features of the bcr/abl abnormality in rare CML patients with very long, atypical chronic phase. The three patients studied, whose chronic phase duration is 17, 19, and 21 years, respectively, have typical genomic bcr rearrangements, and two of them show, hybridizing Northern blots to c-abl, the 8.5 kb mRNA, as that typically present in CML. It seems that genomic alterations within bcr and abl cannot account, alone, for the duration of the chronic phase of Ph1 positive CML and those quantitative and/or qualitative alterations of the p210 bcr/abl protein, unluckily awkward to prove, might be responsible for the atypical clinical features of these CML long survivors.
Leukemia 1989 Jul
PMID:Philadelphia-positive chronic myelogenous leukemia with typical bcr/abl molecular features and atypical, prolonged survival. 273 55

Seven patients with Philadelphia (Ph) chromosome positive essential thrombocythemia (ET) were investigated for the presence of a rearrangement within the major breakpoint cluster region (M-bcr) using the Southern blot technique and, in six cases, for the presence of the hybrid bcr-abl mRNA using the polymerase chain reaction (PCR). The molecular studies showed rearrangement of M-bcr in all cases; there was evidence of the b2a2 mRNA junction in one case and of b3a2 junction in five cases. These findings are identical to what might have been expected in Ph-positive chronic myeloid leukemia. These features may explain the poor prognosis of Ph-positive ET in comparison with cytogenetically normal cases. Conversely, the differences in clinical presentation may be due to other genetic changes.
Leukemia 1989 Aug
PMID:Molecular analysis of Philadelphia positive essential thrombocythemia. 274 91


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