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H Christiansen

Publications and source records attributed to H Christiansen.

67 records · Page 4Linked to original sources
PubMed1987

Evolution of tumor cytogenetic aberrations and N-myc oncogene amplification in a case of disseminated neuroblastoma.

Chromosome analyses including in situ hybridization with the protooncogene N-myc were carried out at diagnosis and several times at relapse in the bone marrow cells of a girl with disseminated neuroblastoma (stage IV) at ages 9, 23, 24, and 26 months, respectively. The tumor karyotype was pseudodiploid exhibiting partial monosomy for the short arm of chromosome #1, an aberration of the short arm of chromosome #2, and double minutes at diagnosis. Further structural aberrations of chromosomes #4, #6, and #17, and homogeneously staining regions could be demonstrated at relapse. In particular, the following structural aberrations were encountered: t(1;?)(p22;?),t(2;?)(p24;?), t(4;6)(q31;q25), and a der(17q). All tumor metaphases without homogeneously staining regions contained double minutes. N-myc, normally positioned within bands 2p23-24, was found to be amplified in a homogeneously staining region on the short arm of chromosome #15 by in situ hybridization. It is speculated that the translocation t(2;?)(p24;?) might be related to N-myc oncogene activation and subsequent amplification.

Bone Marrow↗
PubMed1987

[Specific chromosome aberrations in leukemias and tumors in childhood].

Non-random, specific chromosome aberrations can be found by direct preparation in the karyotype of the malignant cell populations of the various leukemias and solid tumors in childhood. These chromosomal deletions in neuroblastoma, Wilms-Tumor, reticlassification and prognosis. There are mainly chromosomal deletions in neuroblastoma, Wilms-Tumor, retinoblastoma whereas translocations predominate in leukemias and lymphomas.

Chromosome Aberrations↗
PubMed1986

Tumour karyotype may be important in the prognosis of human neuroblastoma.

When comparing clinical and tumour cytogenetic data on 14 neuroblastoma patients in different stages of disease we found a high incidence of 1p abnormalities (12/12), homogeneously staining regions/double minutes (9/12) and 2p abnormalities (4/12) in 12 unresectable and metastatic tumours (clinical stages III and IV). In contrast, these features were absent in clinical stage II tumours (2/2) with good prognosis. The coincidence of 1p aberrations with poor outcome of disease will be discussed.

Child, Preschool↗
PubMed1984

Treatment of recurrent endometrial adenocarcinoma with a combination of doxorubicin and cisplatin.

Nineteen patients with recurrent endometrial carcinoma and one patient with Stage IV endometrial carcinoma not previously treated with chemotherapy were treated with a combination of doxorubicin and cisplatin. The dose schedule was doxorubicin, 50 mg/m2 on day 1, and cisplatin, 50 mg/m2 with hyperhydration on day 1, with a new course every 4 weeks. Objective response 60% was obtained in 12 out of 20 patients (two with complete remission and 10 with partial remission). Furthermore, four patients had stationary disease. The two patients with complete remission both had distal vaginal metastases, and they are still alive after greater than 21 and greater than 40 months. The median survival period for those with partial remission was greater than 11 months (range of 4 to 26); for those with stationary disease, 7 months (range of 4 to 10), and for those with progressive disease, 4 months (range of 3 to 7). The response rate was higher for well-differentiated tumors. No serious side effects were noticed. To our knowledge no other reports have been published so far with the use of the same regimen in patients with recurrent endometrial adenocarcinoma with no prior chemotherapy. We find the objective response rate, the survival time, and the quality of life for the responding patients in our study so encouraging that we shall continue with a larger trial.

Adenocarcinoma↗
PubMedDate not supplied

Traditional and emerging molecular markers in neuroblastoma prognosis: the good, the bad and the ugly.

BACKGROUND: Neuroblastomas (NB) are a heterogeneous group of childhood tumours with a wide range of likelihood for tumour progression. As traditional parameters do not ensure completely accurate prognostic grouping, new molecular markers are needed for assessing the individual patient's prognosis more precisely. PATIENTS AND METHODS: 133 NB of all stages were analysed in blind-trial fashion for telomerase activity (TA), expression of surviving, and MYCN status. These data were correlated with other traditional prognostic indicators and disease outcome. RESULTS AND CONCLUSIONS: TA is a powerful independent prognostic marker for all stages and is capable of differentiating between good and poor outcome in putative "favourable" clinical or biological subgroups of NB patients. High surviving expression is associated with an adverse outcome, but is more difficult to interprete than TA because survivin expression needs to be accurately quantified to be of predictive value. We propose an extended progression model for NB including emerging prognostic markers, with emphasis on telomerase activity.

Biomarkers, Tumor↗
PubMedDate not supplied

Assessment of molecular genetic detection of chromosome translocations in the differential diagnosis of pediatric sarcomas.

BACKGROUND: Recent studies have shown that many types of soft-tissue sarcomas are characterized by specific chromosomal translocations, which are likely to be of etiologic significance. In order to evaluate their diagnostic impact, a panel of 129 sarcomas comprising 78 Ewing's tumors (ET), 19 rhabdomyosarcomas (RMS), 20 neuroblastomas (NB), 9 synovialsarcomas, 2 esthesioneuroblastomas, and 1 desmoplastic small-round-cell tumor (DSRCT) were analysed for the occurrence of the major recurrent translocations, such as t(11;22)(q24;q12), t(21;22)(q22;q12), t(11;22)(p13;q12), t(2;13)(q35;q14), t(1;13)(p36;q14), and t(X;18)(p11;q11). METHODS: Nitrogen-frozen tissue material was analysed by means of Reverse Transcription followed by PCR (Polymerase-Chain Reaction) and nested PCR (RT-PCR). Specificity of the PCR products obtained was confirmed by non-isotopic Southern-Blot analysis with gene-specific probes and/or automated direct sequence analysis. RESULTS: 75 ETs have been shown to carry either a t(11;22) or t(21;22) translocation by identification of chimeric EWS-FLI-1 or EWS-ERG gene-fusion transcripts respectively. 3 ETs were lacking EWS/FLI-1 or EWS-ERG fusion products. 2 of these tumors were shown on review to have unusual morphological features for ETs. 8/19 RMS were initially diagnosed as alveolar RMS. These tumours were shown to carry either a t(2;13) translocation exhibiting chimeric PAX3-FKHR fusion transcripts or a t(1;13) translocation with PAX7-FKHR chimeric gene products. One RMS of the embryonal group also carried a t(1;13) translocation. Reevaluation demonstrated a partly alveolar morphology. In 8/9 synovial sarcomas a t(X;18) translocation was identified. Expression of a EWS-WTI gene-fusion product associated with a t(11;22) translocation was found in the DSRCT. None of these rearrangements were detected in the NBs and 2 esthesioneuroblastomas. CONCLUSIONS: Our results support the concept that the major recurrent translocations are histogenetically specific for a subset of sarcomas. Thus, the detection of tumor type-specific translocations represents an extremely useful diagnostic modality as an adjunct to surgical pathology.

Base Sequence↗
PubMedDate not supplied

[Expression of CD44-standard in 182 primary neuroblastomas].

182 untreated neuroblastomas were examined for the expression of the adhesion molecule CD44s by immunohistochemistry; all tumors were also tested for amplification of the oncogene N-myc by conventional Southern blot analyses. Positive CD44s immunoreactivity correlated not with a more favorable prognosis in contrast to an absence of CD44s expression in stage dependent or independent evaluations. All patients with stage 4S disease (n = 16) expressed CD44s on a high level and had an event-free survival probability of 82%. In undifferentiated neuroblastoma subgroups could be defined, depending on the expression of CD44s (p < 0.01). In 93% of N-myc non-amplified tumors CD44s expression was detected, whereas only 62% of N-myc amplified tumors were positive for CD44s expression. These results point to CD44s expression as a new histological marker in neuroblastoma, having prognostic impact in tumors of undifferentiated morphology.

Biomarkers, Tumor↗