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F Lampert

Publications and source records attributed to F Lampert.

At least 109 records · Page 6Linked to original sources
PubMed1990

Multiple methylation-free islands flank a small breakpoint cluster region on 11p13 in the t(11;14)(p13;q11) translocation.

The t(11;14)(p13;q11) translocation is one of the most frequent chromosomal abnormalities in T-cell acute lymphoblastic leukemia (ALL). Ten different leukemias carrying this translocation have been analysed and all 10 breakpoints fall within a region of less than 25 kb on chromosome band 11p13. We have used PFGE and cosmid cloning to assess the presence of potential genes by analysing methylation-free islands in the vicinity. Four methylation-free islands, within 270 kb, flank the t(11;14)-associated breakpoint cluster region (T-ALLbcr), one occurring about 25 kb on the telomeric side and one about 100 kb on the centromeric side of the T-ALLbcr. Evidence for eight further methylation-free islands on both sides of the T-ALLbcr region is also presented. Thus multiple methylation-free islands exist on 11p13 flanking the t(11;14)(p13;q11) translocation-associated breakpoint cluster region, representing multiple potential transcription units whose chromosomal environment is altered by chromosome translocation.

Chromosomes, Human, Pair 11↗
PubMed1990

Neuroblastoma: inverse relationship between expression of N-myc and NGF-r.

12 primary neuroblastomas (NB) of different maturation stages, 2 ganglioneuromas (GN), and 2 neuroblastoma cell lines were analysed for RNA expression of the protooncogene N-myc and the gene encoding the nerve growth factor receptor (NGF-r) by Northern-blots, RNA-dot-blots and for receptor presence by immunohistological procedures. In 4 tumors with strongly elevated RNA expression of N-myc the NGF-r RNA expression was weak or absent. In all 8 tumors with highly increased NGF-r transcription no N-myc expression was detectable. These results, indicating an inverse relationship between N-myc and NGF-r expression, could help in establishing markers for differentiation, and thus prognosis, in neuroblastoma.

Blotting, Southern↗
PubMed1989

Detection of fms-oncogene-specific tyrosine kinase activity in human leukemia cells.

The c-fms protooncogene encodes the receptor for the colony-stimulating factor 1 of macrophages. Its transforming counterpart, the v-fms oncogene has previously been recognized as the transforming gene of the McDonough strain of feline sarcoma virus. We have isolated rabbit antisera against a 115-kDa recombinant polypeptide containing the 926 carboxy-terminal amino acids of the v-fms protein. All antibodies recognized the cytoplasmic domain of the v-fms protein, which is 95% homologous to the corresponding domain of human c-fms proteins. These sera were applied in a survey of various human cancer cell lines, such as peripheral blood mononuclear (HL60) and choriocarcinoma (BeWo) cells, as well as leukemic cells from 58 patients with acute myelocytic, chronic myelocytic or acute lymphocytic leukemias (AML, CML, ALL). Significantly enhanced levels of fms-specific tyrosine kinase activity were detected in 12-O-tetradecanoylphorbol-13-acetate-induced HL60 and in BeWo cells, and in 7 out of 24 samples from AML patients, whereas no activity could be detected in 9 ALL or in 25 CML cell preparations. The AML cells were classified according to the FAB criteria. The highest incidence of increased fms activity was found in cells assigned to the M4 class (four out of five cases). While no activity was found in material belonging to FAB classes M2 or M3, one of the two cases of the M5 class was kinase-positive. Interestingly, two out of seven cases of the M1 class cells exhibited enhanced levels of fms kinase. These data suggest that the determination of the fms kinase may be useful to subdivide the M1 class of the FAB classification into monocytic and non-monocytic precursor leukemia cells.

Animals↗
PubMed1989

[Tumor cytogenetics and prognosis in neuroblastoma].

In 40 children with neuroblastoma of different clinical stages the tumorkaryotype was determined at onset (n = 30) or at relapse (n = 10) of disease after short-term culture of tumor tissues or bone marrow aspirates. None of the 10 stage I, II, and IVs tumors revealed a chromosome 1p aberration, in contrast to stage III and IV tumors where this abnormality was encountered in 25 (=83%) of 30 patients. Amplification of the proto-oncogene N-myc in the tumor-DNA could not be detected in stage I, II and IVs, was however present in 53% of stage III and IV tumors. Cytogenetic phenomena of gene amplification such as Double minutes (DMs) and Homogeneously Staining Regions (HSRs) correlated with N-myc amplification. About 50% of stage III and IV tumors had chromosome numbers in the neardiploid range whereas prognostically favourable tumors were characterized by hyperploid chromosomal numbers mainly in the triploid range. Life-table analysis according to Kaplan-Meier showed a probability of surviving in about 80% of patients with a normal morphology of chromosome 1 in their tumor cells, compared to about 60% in the absence of N-myc oncogene amplification and of about 50%, if aneuploidy is detected. Thus, we think, the presence or absence of chromosome 1p aberration in the tumorkaryotype is the most sensitive discriminator for outcome in children with neuroblastoma.

Aneuploidy↗
PubMed1988

T-cell acute childhood lymphoblastic leukemia with chromosome 14 q 11 anomaly: a morphologic, immunologic, and cytogenetic analysis of 10 patients.

Ten patients with T-cell acute lymphoblastic leukemia (ALL) and a chromosome anomaly involving band 14 q 11 are described. Mitotic index of bone marrow blasts was high in all patients (average 3.0%). Lymphoid morphology of the leukemic blasts, however, varied somewhat among the patients. The leukemic cells of 5 patients showed an immunophenotypic profile corresponding to early or common thymic differentiation stages whereas 5 children showed strong expression of CD 3 suggesting a more mature thymic phenotype. Leukemic karyotypes revealed a modal chromosome number of 46 in 9 cases, 92 in one case. A chromosome translocation t(11; 14) (p 13; q 11) was found in 5 cases, a t(1; 14) (p 32; q 11) in 2 cases, a t(10; 14) (q 24; q 11) in one case, a (hitherto undescribed) t(12; 14) (q 22; q 11) in one case, and an inv (14) (q 11 q 32) in one patient. Additional abnormalities were t(3; 10), t(7; 9), dup(7 q), del(6 q), del(10 q), and del(1 q). Of 32 cases with T-cell ALL successfully karyotyped in our laboratory 15 (= 47%) had structural aberrations involving chromosomes 1, 3, 6, 7, 9, 10, 12, 14. Ten of these 15 patients (= 67%) had a chromosome 14 q 11 anomaly. It is concluded that chromosome band 14 q 11, the gene locus of the T-cell receptor alpha-chain, is the most common site for structural chromosome aberrations in T-cell ALL.

Acute Disease↗
PubMed1988

N-myc amplification at chromosome band 1p32 in neuroblastoma cells as investigated by in situ hybridization.

Chromosome deletion at the short arm of one chromosome 1 (1p32)--the most common aberration in neuroblastoma cells--was found to be combined with the generation of a homogeneously staining region at this specific site in a newly established neuroblastoma cell line (GI-LI-N) from a stage IV neuroblastoma. By in situ hybridization this homogeneously staining region was shown to contain multiple copies of the proto-oncogene N-myc. This 30-fold oncogene amplification was confirmed by Southern-blot and DNA-dot-blot analyses. In two additional cell lines from children with stage IV neuroblastoma (GI-ME-N and GI-CA-N) N-myc amplification was not detected. Chromosome 1, however, was involved in a structural rearrangement in one cell line (GI-ME-N).

Child, Preschool↗
PubMed1988

Chromosome translocation (2;13)(q37;q14) in a disseminated alveolar rhabdomyosarcoma.

Chromosome analysis of tumour cells in the bone marrow of a 13.5-year-old girl (without a primary tumour) revealed a pseudo-diploid or pseudo-tetraploid karyotype with a translocation involving the long arms of chromosomes 2 and 13: t(2;13)(q37;q14). This finding enabled the diagnosis of a disseminated alveolar rhabdomyosarcoma (RMS) to be established. The patient was treated by cytotoxic chemotherapy, went into complete remission, but died of relapse 14 months after diagnosis. As several cases with this translocation have been described recently, this additional report confirms that t(2;13) is specific for the alveolar subtype of RMS.

Adolescent↗
PubMed1988

Fragile sites and neuroblastoma: fragile site at 1p13.1 and other points on lymphocyte chromosomes from patients and family members.

Fragile sites on lymphocyte chromosomes of 20 patients with neuroblastoma of different clinical stages and histologic differentiation were studied. A hitherto unknown break in the band p13.1 of chromosome #1 was found in a frequency of 3%-15% in nine cases. The same phenomenon was observed in three members of a neuroblastoma family. In another instance, this fragile site was also seen in the mother of a patient. Fragile sites were expressed when cells were cultured in folate-deprived medium and could be slightly enhanced in frequency by aphidicolin. Additional aphidicolin induced possible fragile sites hitherto unknown or not yet accepted by the HGM 8 were detected.

Child, Preschool↗
PubMed1988

Identical chromosome 1p breakpoint abnormality in both the tumor and the constitutional karyotype of a patient with neuroblastoma.

A 4-year-old boy with a stage III abdominal neuroblastoma was studied. Direct chromosome preparation revealed a t(1;?)(p36;?) in three tumor metaphases (one with a chromosome number of 64). After partial resection of the tumor and further tumor shrinkage by intensive combination chemotherapy, the residual tumor mass was removed by a "second-look" operation, and the patient received postoperative radiotherapy to the tumor area. Chromosome analysis from the peripheral blood taken at that time showed tetraploidy in 14% and hypodiploidy in 66% of 50 available metaphases. Structural abnormalities, mainly involving the distal short arm of chromosome 1, could be identified in seven metaphases. A t(1;?)(p36;?) in a diploid blood cell looked identical to the translocation found in the hyperdiploid tumor metaphase. A del(1)(p36) was also found in a blood cell. It is suggested that an association exists between a chromosome fragility at 1p36, in this case postoperatively induced in vivo by chemoradiotherapy, and the development of neuroblastoma.

Abdominal Neoplasms↗
PubMed1988

Tumour karyotype discriminates between good and bad prognostic outcome in neuroblastoma.

In 28 patients with neuroblastoma of different stages the karyotype was determined in the primary tumour and/or in the metastases by direct chromosome preparation or short term cell culture. In addition, DNA analysis for the proto-oncogene N-myc was performed for comparison in 10 cases. Abnormalities (deletions, translocations, derivations) of the short arm of chromosome 1 with the most frequent breakpoint at 1p32 (besides rarer aberrations in other chromosomes) were found in the tumour karyotype of 15 of 18 (83%) patients with metastatic disease (stage IV) and in 2 of 3 patients with stage III, but in none of the 7 patients with stages I, II, IV-S who are all alive with no evidence of disease. These 7 surviving patients with good prognosis had a hyperploid tumour karyotype, mainly in the triploid range. Eleven of the 18 (61%) patients with stage IV and 1 of 3 patients with stage III also contained double minutes (DMs) and/or homogeneously staining regions (HSRs) in their tumour karyotypes. N-myc amplification (30 to 60 copies) in the tumour DNA was detected in 2 of 6 (33%) examined cases with stage IV, in 1 out of 2 examined cases with stage III, and correlated with the presence of DMs/HSRs. Life table analysis showed a 90% probability of surviving in patients lacking the 1p abnormality as compared to less than 10% in patients with an aberrant 1p chromosome in the tumour cells. We conclude that tumour karyotype, in particular the structure of the short arm of chromosome 1, is the most important factor in determining the different outcome in children with neuroblastoma.

Chromosome Aberrations↗
PubMed1988

The T-ALL specific t(11;14)(p13;q11) translocation breakpoint cluster region is located near to the Wilms' tumour predisposition locus.

A breakpoint cluster region (T-ALLbcr) has been previously described on 11p13 for T-ALL carrying t(11;14)(p13;q11). One further T-ALL breakpoint is described bringing to 5 out of 6 such translocations which are found to break within a maximum of 6.7 kb on chromosome 11p13. Studies of somatic cell hybrids derived from t(11;14)(p13;q11) T-ALL placed the T-ALLbcr between the genes for catalase (CAT) and the beta-subunit of follicle stimulating hormone (FSHB). This suggested a link between the T-ALLbcr and the Wilms' tumour predisposition locus (WT) since constitutional 11p13 deletions predispose to Wilms' tumour. Utilising somatic cell hybrids from patients with Wilms' tumours and aniridia, we show that while the T-ALLbcr maps distal to the catalase gene at 11p13, it maps outside the shortest region of overlap of a series of 11p13 deletions associated with Wilms'-Aniridia. The data suggest the order of genes at 11p13 to be: centromere-CAT-T-ALLbcr-WT-aniridia-FSHB-telomere. Therefore, the T-ALLbcr must lie very close to but may be distinct from the Wilms' predisposition locus at 11p13.

Aniridia↗