Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GCF is a human transcriptional regulator that represses transcription of certain genes and is encoded by a 3-kilobase (kb) mRNA (Kageyama, R., and Pastan, I. (1989) Cell 59, 815-825). The expression of GCF was examined in a variety of clonal cell lines. The 3.0-kb GCF mRNA was found to be expressed at the highest level in HUT 102 cells (derived from a T-cell lymphoma). Elevated levels of the GCF mRNA were also noted in KATO III and AGS (gastric carcinomas), FEM-X (melanoma), and U266B1 (myeloma) cell lines. A human fibroblast cell line (WI38) did not express GCF mRNA, and no cross-hybridization to a mouse cell line (NIH 3T3) or monkey cell line (CV-1) could be detected. The GCF cDNA also hybridizes to RNA species of 4.5 and 1.2 kb. The 4.5-kb RNA has the same general expression pattern as the GCF mRNA. Hybridization of cellular RNA with various probes derived from the 3-kb cDNA revealed that the 4.5-kb RNA species only hybridizes to GCF cDNA probes from the extreme 5' end. By using single-stranded RNA probes, hybridization to the three RNA species was detected with the antisense probe for the 5' end (nucleotides 1-561). The single-stranded antisense probe for the region encompassing nucleotides 561-1692 hybridized to the 3.0- and 1.2-kb RNA species. The sense probes for these regions did not hybridize to these RNAs. The GCF gene was localized to a single locus, the chromosome 2 p11.1-11.2 region, by in situ hybridization. Treatment of human KB epidermoid carcinoma cells with phorbol 12-myristate 13-acetate (PMA) lead to a rapid induction of GCF RNA after 1 h and a decline to lower than control levels after 6 h. Epidermal growth factor receptor mRNAs were not increased by PMA until 2 h after treatment and were at their highest level only after GCF mRNAs were decreased. The 4.5- and 1.2-kb RNAs were also induced by PMA with the same kinetics as the GCF mRNA. These results show that the GCF gene is widely expressed in human tissues and cell lines and that the 4.5- and 1.2-kb RNAs have similar expression patterns.
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PMID:Expression and chromosomal localization of the gene for the human transcriptional repressor GCF. 137 Apr 79

Acquired Robertsonian translocations are considered to be very rare chromosome changes in human malignancy, and only three cases have been described. We report a dic(14;14)(p11;p11) in a patient with myelodysplastic syndromes (MDS) following treatment for multiple myeloma. This patient also had other complex chromosomal abnormalities. The pattern of karyotype evolution in this patient was established by a series of cytogenetic studies. The relationship of the complex chromosomal changes to MDS following treatment for multiple myeloma is discussed.
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PMID:An acquired Robertsonian translocation dic(14;14)(p11;p11) in a patient with a myelodysplastic syndrome following treatment of multiple myeloma. 342 38

An identical chromosome abnormality, which appears to be derived from a 1;7 translocation [+der(1),t(1;7)(p11;p11)], was observed in the bone marrow of 12 patients with various hematologic disorders at the Mayo Clinic from 1980 to 1984. At the time of cytogenetic evaluation, nine of the patients had either a myeloproliferative disorder or a myelodysplastic syndrome, one had an acute leukemia, and two had treated multiple myeloma with no morphologic evidence of evolving myeloproliferative disease. Of the 11 patients for whom information about previous therapy was available, seven had a history of exposure to chemotherapy for a previous malignant disorder; we were unable to establish whether the remaining patient had had prior treatment. This study suggests a possible relationship between +der(1),t(1;7)(p11;p11) and some treatment-induced hematologic disorders. Such chromosome abnormalities may be the result of a reciprocal chromatid translocation and adjacent I segregation of a quadriradial configuration in metaphase.
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PMID:Unbalanced 1;7 translocation and therapy-induced hematologic disorders: a possible relationship. 370 88

Between December 1990 and January 1994, bone marrow (BM) samples from 151 patients with multiple myeloma (MM), including 117 patients evaluated at diagnosis, were collected for cytogenetic analysis. A total of 129 patients had assessable metaphases (100 patients at diagnosis). Cytogenetic studies were performed on BM cells after longterm cultures (6 days) with stimulation of cultures by granulocyte-macrophage colony-stimulating factor (GM-CSF), GM-CSF plus interleukin (IL)-6, IL-3 plus IL-6, or GM-CSF plus IL-3 plus IL-6 to improve myeloma cell growth, and 91 patients had an additional unstimulated culture. Sixty-six patients (51%) had cytogenetic abnormalities, including 47 of 100 patients at diagnosis (47%) and 17 of 24 patients at relapse (71%; P = .04). The aberration rate increased with stage (P = .007), BM plasmacytosis (P = .003), beta 2 microglobulin level (P = .001), C-reactive protein (CRP) level (P = .001), and Ki-67 (P = .007). The abnormality detection rate was higher in stimulated than unstimulated cultures, and the difference was statistically significant (P < .01). Hyperdiploidy was observed in 39 patients (30% of patients with an assessable karyotype) and hypodiploidy in 19 patients (15%). Among numeric changes, gains predominantly involved chromosomes 3, 5, 7, 9, 11, 15, 19 and losses, chromosomes 8, 13, 14, and X. The most frequent loss was loss of chromosome 13, observed in 22 patients (15%), including 18 patients at diagnosis (12%). We observed frequent structural changes of chromosomes 1 (15%) and 14 (10%) but also a 5% incidence of 19q13 abnormality and two patients with translocation t(1;16)(p11;p11). By using the proportional hazard univariate model, patients with abnormal karyotypes were demonstrated to have 2.5-fold greater chance of death than patients with normal karyotypes (P < .014). Despite a multivariate approach with the same model, the respective roles of karyotype abnormality, age, stage, and beta 2 microglobulin level could not be clearly ascertained. From these results we conclude that cytogenetic analysis using stimulation of cultures by cytokine(s) may be a promising method to identify about 50% of cytogenetic abnormalities in patients with newly diagnosed MM. Cytogenetic analysis may help to define a high-risk population that would benefit from intensive therapeutic approaches.
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PMID:Improved cytogenetics in multiple myeloma: a study of 151 patients including 117 patients at diagnosis. 753 17

Multiple myeloma (IgG kappa + IgA kappa type, clinical stage IA) was diagnosed in a 82-year-old woman in January 1986. Chemotherapy (melphalan, prednisolone, vindesine, cyclophosphamide), caused prolonged myelosuppression. Therefore she was given other treatment. In October 1992, her peripheral blood examination demonstrated 2% blastic cells and 12% eosinophils. Bone marrow aspiration showed dysplastic features of trilineage blood cells with 4.8% myeloblasts. The karyotype of bone marrow cells from this patients was 47, XX, +der(1)t(1;7) (p11;p11), -7, +8. A diagnosis of therapy-related myelodysplastic syndrome (refractory anemia) was established. Eleven months after diagnosis of myelodysplastic syndrome, she is alive without leukemic transformation.
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PMID:[Multiple myeloma preceding myelodysplastic syndrome with eosinophilia and der (1;7)]. 782 98

Structural chromosomal abnormalities and their break-points were characterized in 17 patients with multiple myeloma (MM) and 4 with plasma cell leukemia by banding. Chromosome 14q32 translocations with a variety of partners were detected in 13 patients, and a variant translocation t(8;22)(q24.1;q11) was detected in 1. Three recurrent 14q32 translocations have been identified: t(6;14)(p21.1;q32.3) occurring in 3 cases, and t(11;14)(q13;q32.3) and t(14;18) (q32.3;q21.3) each occurring in 2 cases. Translocations t(1;14)(q21;q32.3), t(3;14)(p11;q32),t(7;14)(q11.2;q32.3), and t(11;14)(q23;q32.3) were found in each patient, whereas in the remaining 2 patients, partner chromosomes could not be determined. The band 19p13.3 was newly delineated as a recurrent breakpoint involved in translocations in MM. Chromosomes 1 and 6 were also commonly involved in structural abnormalities (14 and 10 patients, respectively), although no particular bands were noted. However, the short arm of chromosome 1 was preferentially involved in deletion, suggesting a certain antioncogene on 1p associated with the development of myeloma. In addition; fluorescence in situ hybridization was successfully applied to determine the nature of the structural abnormalities in a patient with t(8;22) translocation. The present findings suggest that there may be subsets of 14q32 translocations specific to MM.
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PMID:Nonrandom chromosomal rearrangements of 14q32.3 and 19p13.3 and preferential deletion of 1p in 21 patients with multiple myeloma and plasma cell leukemia. 791 47

Two patients with multiple myeloma and an unbalanced translocation, t(1;16)(p11;p11), are reported. The fluorescence in situ hybridization (FISH) technique was used in one patient to confirm the translocation. To our knowledge, t(1;16)(p36;q13) and t(1;16)(q21;p13), but not t(1;16)(p11;p11), had been reported previously in multiple myeloma. Our results suggest that FISH is useful to characterize structural abnormalities and identify marker chromosomes in multiple myeloma where analysis with conventional cytogenetics is often difficult.
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PMID:Two cases of t(1;16)(p11;p11) in multiple myeloma: confirmation by chromosome painting. 807 42

A new human myeloma cell line, KMS-18, was established from a 58-year-old male with multiple myeloma associated with hyperammonemia. The original leukemic cells and established KMS-18 cells possessed several of the same chromosomal abnormalities, including add(1)(q32), add(10) (q24) and add(17)(p11). In addition, the KMS-18 cells showed novel t(4;14)(p16.3;q32.3) masked translocation which was determined by the FISH method. Moreover, we compared the ammonia production in culture medium of the KMS-18 cell line with that of non-myeloma hematological malignant cell lines and a hepatocellular carcinoma cell line. KMS-18 produced higher levels of ammonia in medium than the other cell lines examined. This new cell line may prove helpful in analyzing the role and biological mechanisms of the t(4;14)(p16.3;q32.3) translocation in myeloma and also in investigating hyperammonemia in cases with myeloma.
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PMID:Establishment of a new human myeloma cell line, KMS-18, having t(4;14)(p16.3;q32.3) derived from a case phenotypically transformed from Ig A-lambda to BJP-lambda, and associated with hyperammonemia. 947 91

We report here a new case of multiple myeloma (IgG, kappa, stage IIIA) with a variant Burkitt-type translocation (8;22)(q24;q11). Bone marrow plasma cells were morphologically immature with fine nuclear chromatin and nucleoli. Chromosome analysis showed complex aberrations; that is, 53,XX, der(1)add(1)(p11)dup(1)(q12q32),+3,+5,t(8;22)(q24;q11),+9,add(10)( p13), +11,+15,add(19)(q13),+21. Fluorescence in situ hybridization analysis with the yeast artificial chromosome (YAC) clone I2 containing the C-MYC gene at 8q24 and the chromosome-22-specific DNA library pBS22 revealed that 12 was located on the der(8)t(8;22). A fusion signal derived from I2 and the YAC clone B99E1 containing the BCR gene at 22q11 was also observed on the der(8)t(8;22). Our results indicate that the breakpoint at 8q24 in this patient was located far downstream of the C-MYC gene. This breakpoint site is similar to Burkitt lymphoma with t(8;22)(q24;q11). A review of eight cases in the literature and the present case of multiple myeloma with t(8;22)(q24;q11) showed that most of them were of advanced stage and had an immature phenotype. It is suggested that the C-MYC gene may be activated by t(8;22)(q24;q11) and implicated in disease progression in multiple myeloma.
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PMID:A variant Burkitt-type translocation (8;22)(q24;q11) in multiple myeloma. Report of a new case and review of the literature. 966 1

We describe a 58-year-old woman with anaplastic multiple myeloma and multiple chromosomal abnormalities. Her karyotype showed extreme hyperploidy with 77 chromosomes. Some of the aberrations were typical of multiple myeloma (+3, +5, +15, +19, +21, t(11;14)(q13;q32)), others were characteristic of the aggressive anaplastic myeloma (+8), t(11;14)(q13;q32), while three chromosomal abnormalities (t(11;20)(p11;q13); t(4;7)(q31;q11); and t(14;20)(q24;q13)) have not been, to the best of our knowledge, described previously in the literature. The fulminant course of the disease confirms the poor prognosis of multiple karyotypic abnormalities in myeloma.
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PMID:Multiple chromosomal abnormalities in fulminant anaplastic myeloma. 1044 3


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