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

A drug-resistant cartridge was employed in the construction of families of insertion mutants of a cosmid clone. The cartridge contains a cml gene and has identical restriction enzyme sites, EcoRI, BamHI, SalI, and PstI, on both ends. The families of mutants were made by ligation of the cartridge to the cosmid, which was linearized or partially digested, followed by in vitro packaging and transduction. From these families we selected cosmid derivatives which either have a unique BamHI site at a predetermined site in the cosmid or have deletions covering different portions of the original clone. The extent of a large gene cluster cloned into the original cosmid was identified by confirming the gene function in some of the deletion mutants. The possibility for further and various uses of this cartridge is discussed.
Plasmid 1990 Sep
PMID:The use of a drug resistance cartridge for in vitro insertion and deletion mutagenesis of a cosmid clone. 196 47

About 950 genes (or a part of them) have been cloned. Using them as probes, DNA diagnosis is now available in hundreds of hereditary diseases and some malignant diseases. In many of them, detailed analysis into the mechanisms underlying the diseases has become possible. Examples of this capability include 21 hydroxylase deficiency, amyloid polyneuropathy, Duchenne/Becker muscular dystrophy, and CML. About one third of the cloned genes show RFLPs (restriction fragment length polymorphisms). In addition "random" DNA fragments have been cloned, many of them can also be used to detect RFLPs. An RFLP study has proven very useful in the preclinical/prenatal diagnosis of hereditary diseases even though gene-action is unknown (e.g., Huntington disease and von Recklinghausen disease). DNA diagnosis has also been found to be very useful in the detection of microorganisms, minute chromosome changes (e.g., XX males) and for forensic purposes. The techniques and understanding of DNA diagnosis have become mandatory in many areas of medicine.
Rinsho Byori 1990 Sep
PMID:[DNA diagnosis in medicine]. 197 43

The efficacy of ultrafiltration (UF) in the attempt of total bloodless open heart surgery using membrane oxygenator (MO) was investigated in two groups. Group I (GI) consisted of 6 ASD operations between Dec. 1983 and Feb. 1987, which cardiopulmonary bypass (CPB) were performed without UF and with non-hemic priming of Capiox II MO. (Age; 18 +/- 2 (SD) years old, Body Weight; 53 +/- 6 kg, CPB; 77 +/- 24 min.) Group II (GII) consisted of 11 cases (4ASD, 1VSD, 4MS/MR (2MVR), 2AR (2AVR] between Mar. 1987 and Sep. 1988, which CPB were performed with UF in 9 cases and with non-hemic priming of CML/VPCML MO. (Age; 34 +/- 20 yo, Body Weight; 52 +/- 12 kg, CPB; 112 +/- 54 min). Total bloodless surgery were successful in 9 cases (82%) of GII against in only one case (17%) of GI (p less than 0.05). The hematocrit values of successful 9 cases in GII were 40 +/- 2% before operations, more than 19 +/- 3% during CPB, 33 +/- 4% just after operations, and more than 29 +/- 3% through the postoperative course. Blood loss during operations were 1013 +/- 586 ml in GI, and 659 +/- 388 ml in GII (NS). Blood loss after operations were 696 +/- 283 ml in GI and 478 +/- 284 ml in GII (NS). In successful 9 cases of GII, blood loss after operations were 387 +/- 215 ml, significantly less than that in GI (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bloodless open heart surgery using membrane oxygenator--the efficacy of ultrafiltration]. 205 Nov 2

Necrotizing fasciitis of the vulva developed in an immunocompromised patient with chronic myelogenous leukemia, apparently from secondarily infected herpes simplex lesions. In addition to surgical debridements and broad-spectrum intravenous antibiotic therapy, the wound was treated using specially prepared amniotic membranes as a wound dressing. The patient died on hospital day 65 because of complications of her immunocompromised state, with autopsy findings of disseminated cytomegalovirus. However, use of amniotic membranes as a wound dressing appeared to be beneficial.
Obstet Gynecol 1990 Sep
PMID:Amniotic membranes in the treatment of necrotizing fasciitis complicating vulvar herpes virus infection. 216 65

Until recently, T cells were believed not to be involved in chronic myeloid leukemia. We describe an example of CML in T lymphoblastic crisis with massive generalized lymphadenopathy in which the blasts were CD2(+), CD5(+), and CD7(+), variably CD1(+) and CD3(+), and both responded to and could be induced to produce the T cell growth factor, interleukin-2. Additionally, the blasts were shown to contain the CML-related tyrosine kinase P210bcr-abl rather than the smaller kinase associated with Ph1(+) ALL. Finally, the participation of the T lymphoid lineage in the CML clone was proven by the presence of the same BCR rearrangement in blasts as in granulocytes, suggesting the existence of a bone marrow progenitor common to the T cell and myeloid lineages.
Leukemia 1990 Sep
PMID:Chronic myeloid leukemia arising in a progenitor common to T cells and myeloid cells. 216 6

Based on in vitro evidence of time-dependent synergistic kill of HL-60 leukemia cells exposed to Ara-C and mitoxantrone, 44 patients with relapsed or refractory AML and 3 with blastic CML were treated with a timed sequence of both drugs. There were 25 females and 22 males, with a median age of 53 (range 21-75). Of 31 patients with relapsed AML, 24 had one prior remission, 6 had two and 1 had three. Of these, 15 had failed a second reinduction attempt. Thirteen patients were primarily refractory to induction with Ara-C plus daunorubicin. Each dose of Ara-C, 500 mg/m2, was followed after 6 hr by mitoxantrone, 5 mg/m2, and the sequence was repeated four to six times (44-68 hr) in different cohorts of patients. All but two patients (one with blastic CML and one in relapse and refractory) are evaluable for response and toxicity. Of 16 patients in relapse without prior reinduction 7 achieved CR and 3 PR (62% response rate); there were 3 CR in the 14 patients who were in relapse and refractory (21% response rate) and 4 CR and 1 PR (35% response rate) in the 14 patients with primary anthracycline resistance. Five of seven patients previously exposed to mitoxantrone achieved CR. Response lasted from 2 to 42 months, with two patients alive and in continuing remission at 34 and 42 months. Average marrow recovery was seen after 25 days and time to remission was 30 days. Six patients died in induction (four from sepsis and two from the tumor lysis syndrome) and 21 had progressive disease. Chemotherapy was well tolerated with minor nausea and vomiting in 13 patients, moderate in 20, and severe in 2. Most patients did not have evidence of drug-induced mucositis: it was minor in 9 and moderate in 2. Renal dysfunction was attributable to the use of nephrotoxic antibiotics. Hepatic dysfunction was reversible and was minor in 10 patients, moderate in 13, and severe in 3. Sequential, timed administration of intermediate-dose Ara-C and mitoxantrone is an active and well-tolerated antileukemic regimen.
Am J Hematol 1990 Sep
PMID:Sequential intermediate-dose cytosine arabinoside and mitoxantrone for patients with relapsed and refractory acute myelocytic leukemia. 220 4

Study of growth factor RNA levels in the stromal cells derived from the adherent layer of long-term bone marrow culture demonstrated constitutive expression of transforming growth factor beta 1 (TGF-beta 1) and macrophage colony-stimulating factor. These cells did not express granulocyte colony-stimulating factor, granulocyte-monocyte colony-stimulating factor, interleukin (IL) 1 alpha, IL-1 beta, IL-3, and IL-6. However, granulocyte colony-stimulating factor expression could be induced by recombinant human IL-1 beta; while IL-6 could be induced by both IL-1 beta and tumor necrosis factor-alpha. No differences could be detected between adherent layers established from normal and benign phase Ph1 chronic myelogenous leukemia bone marrow. The uninduced expression of TGF-beta 1, a potent hematopoietic cell growth inhibitor, suggests that stromal cells play an inherent role in regulating the proliferation of adjacent bone marrow hematopoietic progenitor cells. However, a defect in stromal TGF-beta 1 production cannot account for the profoundly expanded myeloid compartment in chronic phase chronic myelogenous leukemia. In contrast to the constitutive expression of TGF-beta 1 and macrophage colony-stimulating factor, hematopoietic growth factors are only expressed following a proper stimulation.
Cancer Res 1990 Sep 15
PMID:Constitutive and induced expression of growth factors in normal and chronic phase chronic myelogenous leukemia Ph1 bone marrow stroma. 220 22

The v-abl gene in Abelson virus induces pre-B-cell lymphoma in mice while the BCR/ABL oncogene is associated with chronic myelogenous leukemia and some cases of acute lymphocytic leukemia in humans. Understanding the mechanisms by which these oncogenes affect various cell types has been hampered by a paucity of experimental systems that reproduce the range of biological effects associated with them. We have developed an experimental system in which murine hematopoietic stem cell populations are infected with either v-abl or BCR/ABL retroviruses and are used to reconstitute lethally irradiated mice. Irrespective of the form of activated abl, greater than 90% of the animals reconstituted with such cells develop tumors. About 50% of them develop a myeloproliferative syndrome that shares several features with the chronic phase of chronic myelogenous leukemia; the remaining animals succumb to pre-B-cell lymphomas. The myeloproliferative syndrome is characterized by large numbers of clonally derived, infected myeloid cells. This model will allow study of the mechanism by which activated abl genes affect hematopoietic precursors in chronic myelogenous leukemia. Furthermore, our results demonstrate that introduction of an activated abl gene into the appropriate target cell, not the structure of the gene, is the major determinant in myeloid cell specificity.
Proc Natl Acad Sci U S A 1990 Sep
PMID:Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL. 220 61

We studied two cases of chronic myelogenous leukemia (CML) with unusual variant Philadelphia (Ph) translocation (22;22)(q11;q13). Southern blot analysis showed a chromosomal break in the BCR gene within the 5.8-kilobase (kb) breakpoint cluster region (bcr), between bcr exons 2 and 3 and between bcr exons 3 and 4, respectively. Chimeric bcr-abl mRNA was detected using polymerase chain reaction (PCR) which amplified, according to the respective bcr breakpoints, bcr exon 2-abl exon II and bcr exon 3-abl exon II junction products. These results further support the involvement, even when not cytogenetically detectable, of the 9q34 chromosomal region in all variant Ph translocations and that BCR-ABL gene fusion products are causally involved in the development of Ph positive CML.
Cancer Genet Cytogenet 1990 Sep
PMID:Chronic myeloid leukemia with unusual variant Ph translocation (22;22)(q11;q13). Two cases with chimeric BCR-ABL transcripts. 220 77

Previous reports have indicated that mutations of the RAS oncogenes are not associated with the chronic phase of Philadelphia chromosome-positive chronic myelogenous leukemia (Ph1+ CML). However, further studies were needed to determine their association with Ph1- CML and chronic myelomonocytic leukemia (CMML). Therefore, 6 patients with Ph1- CML who were also negative for BCR rearrangements (Ph1-/BCR- CML) and 30 patients with CMML were analyzed for the presence of RAS oncogene point mutations to determine the similarities of these diseases at the molecular level. The assay used the polymerase chain reaction for amplification of the target RAS sequences and panels of specific synthetic oligonucleotide probes for hybridization to wild type and/or mutated sequences. None of the six Ph1-/BCR- CML patients had mutations in the RAS oncogenes, while 17 of 30 (57%) of the CMML patients had RAS oncogene mutations. Eighty percent of the mutations involved substitution of aspartic acid for glycine (G----A) in the 12th or 13th codons of N-ras or K-ras. Furthermore, although not statistically significant, survival studies raise the possibility of shortened survival in patients with RAS oncogene point mutations, with the average survival being 33 months for Ph1-/BCR- CML, 35 months for CMML without point mutations, and 11 months for CMML with RAS mutations. Thus, RAS mutations appear to be associated with CMML and not Ph1-/BCR- chronic phase CML, there is a high propensity for the K-ras or N-ras mutations to involve an G----A substitution in the 12th or 13th codons, and RAS mutations in CMML may relate to prognosis and require further studies.
Blood 1990 Sep 15
PMID:RAS mutations are rare events in Philadelphia chromosome-negative/bcr gene rearrangement-negative chronic myelogenous leukemia, but are prevalent in chronic myelomonocytic leukemia. 220 9


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