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Biomedical subjects

G Rechavi

Publications and source records attributed to G Rechavi.

At least 163 records · Page 9Linked to original sources
PubMed1988

More than two immunoglobulin heavy chain J region genes in the majority of infant leukemia.

Congenital and infant leukemia are rare conditions associated with a very poor prognosis due to the high frequency of adverse clinical and laboratory parameters. As the occurrence of multiple immunoglobulin heavy chain hybridization band in childhood leukemia has been associated with poor prognosis, we studied whether it was present in this type of leukemia as well. Seven cases were examined, 4 of them less than 7 months of age. The immunophenotype was lymphoid in 5 and hybrid in 2. Most had abnormal karyotypes. In 5 of the 7, including all with congenital leukemia, an immunoglobulin heavy chain J region multiband pattern was found by Southern blot. The multiband pattern, whether primary or due to clonal evolution, seems to be associated with poor prognosis.

Adolescent↗
PubMed1987

Undifferentiated leukemia of infancy with t(11:17) chromosomal rearrangement. Coexpressing myeloid and B cell restricted antigens.

It has been suggested that the malignant transformation, in some of the acute leukemias, may involve totipotent stem cells resulting in a biphenotypic leukemia expressing both myeloid, and lymphoid characteristics. We describe here a hybrid cell acute leukemia, in a 16-day-old infant, in whom leukemic cells coexpressed myeloid and lymphoid B cell antigens. Blast cells in the bone marrow showed L2 morphology according to the French American British (FAB) classification, with positive periodic-acid Schiff, and nonspecific esterase staining. Sudan black, and specific esterase were negative. Terminal deoxynucleotidyl transferase, was strongly positive in 5% of blasts, and faintly reactive with the rest. Karyotypic analysis demonstrated a translocation of t(11:17);(q23;p13). Immunoglobulin gene analysis revealed rearrangement of the heavy chain genes. The blasts' phenotype was HLA/DR+ B4+ My7+ My9+ common acute lymphoblastic leukemia antigen (CALLA) B1- T11-. Dual immunofluorescence staining using anti My7, and My9 fluorescein isothiocyanate, and anti B4 pycoerythrin conjugated monoclonal antibodies, and flow cytofluorometry, revealed a labeling pattern of 25% B4+; 10% to 15% My7+; 17% My9+; and 50% of cells coexpressing B4 My7, and My9 antigens. These results provide evidence for a hybrid leukemia with lymphomyeloblasts being part of a single clone, which may indicate the origin of this leukemic clone from a pluripotent (lymphoid/myeloid) stem cell.

Antibodies, Monoclonal↗
PubMed1987

Cerebellar ataxia and opsoclonus as the initial manifestations of myoclonic encephalopathy associated with neuroblastoma.

Cerebellar ataxia and opsoclonus were the initial manifestations of an associated neuroblastoma in a 20-month-old girl. Two months after the initial symptomatology, a physical examination revealed an abnormal mass palpable left to the midline. Urinary catecholamines were within normal limits. The child's neurological findings improved immediately after surgery, and steroid treatment and the follow-up on her after 2 years revealed normal general and neurological development. The syndrome of myoclonic encephalopathy including cerebellar ataxia, myoclonus and opsoclonus, and its relationship to neuroblastoma is reviewed. Failure to recognize this association can result in delays in both diagnosis and treatment and could be fatal.

Abdominal Neoplasms↗
PubMed1987

Molecular analysis of Burkitt's leukemia in two hemophilic brothers with AIDS.

In two hemophilic brothers infected by the human immunodeficiency virus (HIV), Burkitt's leukemia developed within 1 year. Both patients were treated by aggressive chemotherapy, and both are still in complete remission for 23 and 14 months, respectively. Sera from both brothers contained anti-HIV antibodies. However, DNA extracted from the tumor cells, when analyzed by Southern blot using a cloned HIV probe, did not reveal HIV-related sequences. Hybridization experiments with an Epstein-Barr virus (EBV) probe revealed the presence of EBV-specific sequences in the tumors' DNA. In both patients' tumors rearranged c-myc genes were found. The rearrangements occurred in both genes 3' to the third exon of c-myc, thereby suggesting that a variant chromosomal translocation took place in both cases. Indeed, karyotype analysis of the malignant cells of one of the patients revealed the variant t(2:8) translocation. In contrast to the majority of Burkitt's tumors carrying this translocation, which are kappa light-chain producers, cells of our patient expressed lambda chains. Furthermore, in both cases the lymphoblasts carried IgG on the surface, again an unusual finding in Burkitt's tumors. Finally, because both patients had an identical HLA phenotype, the role of genetic factors in the development of such tumors should be considered.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Abnormalities of cellular immunity and natural killer cells in Gaucher's disease.

Gaucher's disease (GD) which is a congenital defect characterized by the accumulation of glucocerebroside in cells of the reticulo endothelial system, is associated with malignancies of the lymphoid system such as multiple myeloma, chronic lymphatic leukemia, as well as acute leukemia of childhood. We report the immunological profile of the T-cell system in GD patients and in GD carriers. We found a variable response to lectins stimulation (PHA, Con A, PWM in various concentrations) which supports the hypothesis that a persistent antigenic stimulation in GD affects all components of the immune system of those patients. A highly significant decrease in the number of NK cells was also found, which might be a predisposing factor to the increase in malignant B and other lymphoid cell proliferations described in patients with GD.

B-Lymphocytes↗
PubMed1987

Common origin of transmissible venereal tumors (TVT) in dogs.

We determined the sequence of the 1.5-kb insert upstream to c-myc in the transmissible venereal tumor (TVT) of dogs. The sequence is highly homologous to the 3' region of the mammalian repetitive LINE element. The insert is bound by a 10-bp repeat indicating DNA transposition by a mechanism involving reverse transcriptase. We analyzed DNA of four TVT tumors from various geographical locations as well as normal canine DNA for the presence of the LINE insert. The results indicate that in all TVT tumors, but not in normal tissues, the same LINE insert was present upstream to c-myc. This result suggests that TVT tumors in various dogs may have a common cellular origin.

Animals↗
PubMed1987

Polymorphism of human immunoglobulin VH genes: a possible marker of autoimmune disease.

Human DNA from 11 individuals was analysed by Southern blot for the immunoglobulin genes coding for the heavy chain variable region (VH). The analysis included two probes detecting the genes of subgroup VHII and VHIII. The VH genes pattern shows very little polymorphism whereas the VHIII genes showed a significant polymorphism. When DNA from four patients with Graves' disease was analysed, a VH band was found in DNA of all patients analysed, and of 50 per cent of SLE patients, whereas only 36 per cent of healthy people contained this VH band. This may serve as a new tool to study genetic markers of autoimmune diseases.

Autoimmune Diseases↗
PubMed1986

Structure and activity of the translocated c-myc in mouse plasmacytoma XRPC-24.

In the mouse plasmacytoma XRPC-24 both c-mos and c-myc are rearranged. We cloned the rearranged c-myc and found that it was translocated to the immunoglobulin C alpha locus. The breakpoint is at the end of exon 1 in c-myc and approximately 0.5 kb upstream from exon 1 of C alpha. The cloned translocated c-myc linked to a strong transcriptional promoter can efficiently transform rat embryo fibroblasts when co-transfected with the activated Ha-ras. The transformed cells are tumorigenic in syngeneic rats.

Animals↗
PubMed1985

"Retroposon" insertion into the cellular oncogene c-myc in canine transmissible venereal tumor.

We examined by Southern blotting the state of the cellular oncogene c-myc in the dog transmissible venereal tumor. The tumor DNA contains a 16.8-kilobase pair (kbp) rearranged c-myc fragment in addition to the normal 15-kbp and 7.5-kbp fragments. We compared the structure of the cloned rearranged c-myc (re-myc) with that of a cloned normal c-myc and found that the rearrangement was due to the insertion of a 1.8-kbp DNA upstream to the first exon of c-myc. The inserted DNA is flanked by 10-base-pair direct repeats and contains a dA-rich tail, suggesting its origin from mRNA. Partial sequence of the inserted element showed 62% homology with the primate interdispersed Kpn I repetitive element. These results provide an example for the behavior of repetitive DNA sequences like the Kpn I family, as movable elements that can transpose nearby to oncogenes or other structural genes and perhaps affect their activity.

Animals↗
PubMed1985

Association of Gaucher's disease and lymphoid malignancy in 2 children.

2 cases of acute lymphoblastic leukaemia (ALL) of childhood in association with Gaucher's Disease (GD) are presented, which are the first to be described. One of them is a common non-B non-T cell ALL and the other is at T-cell ALL. The association of GD with benign and malignant B-cell proliferation has recently been described. It is suggested that chronic stimulation of the immune system by the accumulated glucocerebroside may predispose to B cell proliferation.

B-Lymphocytes↗
PubMed1984

Mechanism of activation of the mouse c-mos oncogene by the LTR of an intracisternal A-particle gene.

In the mouse myeloma XRPC-24 the DNA of an intracisternal A-particle (IAP) is inserted within the coding region of c-mos. This insertion splits the c-mos into a 3' rc-mos and a 5' rc-mos separated by approximately 4.7 kb of IAP DNA. The insertion is in a head-to-head orientation and brings the 5' LTR of the IAP in juxtaposition to the 3' rc-mos such that the IAP and the 3' rc-mos are transcribed in opposite directions. The intact c-mos gene is usually dormant, whereas the 3' rc-mos is actively transcribed and is capable of transforming NIH3T3 cells. In an effort to understand the nature of this activation we mapped the 5' ends of the 3' rc-mos mRNA present in XPRC-24. We found two main mRNA start sites, one mapping to the junction of the 3' rc-mos and the 5' LTR, and the other located 10 nucleotides upstream to this junction, within the 5' LTR. This result indicates that the 3' rc-mos in XRPC-24 was activated by insertion of a promoter provided by the LTR of an IAP genome. Furthermore, the 5' LTR appears to possess promoter activities in two directions. This conclusion was confirmed by the fact that this 5' LTR, in both orientations, was able to activate the bacterial gene coding for chloramphenicol acetyltransferase (CAT) in the modular vector pSVOCAT.

Acetyltransferases↗
PubMed1983

Homology between an endogenous viral LTR and sequences inserted in an activated cellular oncogene.

Recently, some of us reported the detection and molecular cloning of a rearranged cellular oncogene, designated rc-mos, from a non-virally-induced mouse myeloma, XRPC24. Recombinant lambda phage DNA containing the rc-mos gene was active in transforming NIH 3T3 cells in a transfection assay, whereas recombinant DNA containing the unrearranged c-mos gene was not. In rc-mos, coding sequences from the 5' end of c-mos were found to have been displaced by a novel cellular element whose nucleotide sequence was reported. We now document the fact that a 349-base pair (bp) segment of the novel DNA immediately adjacent to the retained c-mos sequences in rc-mos has close homology with the long terminal repeat (LTR) of a known intracisternal A-particle gene. This homology was mentioned in Nature recently after it had been brought to the attention of the editors (N. Hozumi and R. Hawley, personal communication).

Base Sequence↗
PubMed1983

Retention and loss of immunoglobulin heavy chain alleles in helper T cell hybridoma clones.

Retention or loss of immunoglobulin heavy chain genes was studied in 20 functional T cell hybridoma clones. DNA probes representing C mu, C alpha and JH genes, as well as VH subgroups II and III were hybridized with restriction enzyme fragments of hybridoma DNA by the Southern filter hybridization technique. Parental alleles of the hybridoma cells were distinguished on the basis of polymorphism of the lengths of restriction enzyme fragments. All clones retained the alleles of the lymphoma parent cell BW-5147 at all four loci. Thirteen clones lost both CH and VH alleles of the immune partner cell, whereas seven retained both VH alleles, and at least C alpha of the antigen-specific partner. Hence, T cell function in these cells is compatible with the loss of most immunoglobulin heavy chain alleles. This is interpreted to indicate either gene rearrangement and deletion, or chromosome loss. Accordingly, the T cell receptor is either controlled by two split gene loci in chromosome 12, at the two respective (5' and 3') ends of the mouse heavy chain gene family, or by a gene(s) outside chromosome 12.

Alleles↗
PubMed1983

Analysis of recombinant DNA clones specific for the murine p53 cellular tumor antigen.

Three cDNA clones, corresponding to two non-overlapping regions of the mRNA coding for the mouse p53 cellular tumor antigen, were isolated and characterized. In hybridization-selection assays, these clones were capable of selectively binding p53 mRNA, as demonstrated by in vitro translation and immunoprecipitation with anti-p53 monoclonal antibodies. The p53 mRNA appeared to be the only messenger species specifically selected by these clones. The size of the p53 mRNA was found to be approximately 2 kb, and its levels to vary substantially among different types of transformed cells. Evidence was found for the existence of two distinct p53-specific genes in mouse genomic DNA. Two partially overlapping recombinant phage clones were obtained, both derived from the same p53-specific genomic DNA region. The orientation of the various cDNA clones relative to that of the p53 mRNA was established by S1 analysis and the relationship between the cDNA clones and the genomic ones was determined by comparative restriction enzyme mapping and nucleic acid hybridization.

Animals↗
PubMed1983

Activation of the c-mos oncogene in a mouse plasmacytoma by insertion of an endogenous intracisternal A-particle genome.

The activation of the cellular oncogene c-mos in mouse plasmacytoma XRPC24 was found to result from the insertion of a 4.7-kilobase-pair cellular DNA element, within the c-mos coding region. The element terminates on both sides with a direct repeat of around 335 nucleotides. The repeat as well as internal sequences of the element show strong homology to endogenous intracisternal A-particle (IAP) genes. The IAP genome integrated within c-mos in a head-to-head (5' to 5') configuration. This juxtapositioned the IAP 5' long terminal repeat next to the bulk of the oncogene's coding region and shifted c-mos 5' coding and flanking sequences to a position further upstream. The significance of several aspects of this activation and transposition event is discussed.

Animals↗