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A Montaldi

Publications and source records attributed to A Montaldi.

At least 19 recordsLinked to original sources
PubMed1998

Cytogenetic analysis of hepatoblastoma: hypothesis of cytogenetic evolution in such tumors and results of a multicentric study.

Hepatoblastoma is a rare pediatric malignant tumor of the liver. Previous cytogenetic reports are sporadic. We karyotyped nine consecutive hepatoblastomas from the Italian centers participating in a multicentric study on hepatic tumors (SIOPEL 1). Six cases showed abnormal karyotypes. The most common abnormalities were trisomies of chromosomes 2 and 20. Four cases showed abnormalities of chromosome 1. On the basis of findings, we speculate the possibility of a cytogenetic evolutive pattern of hepatoblastomas.

Child, Preschool↗
PubMed1997

Nonrandom gain of chromosome 7 in central neurocytoma: a chromosomal analysis and fluorescence in situ hybridization study.

Central neurocytoma is a benign, slow-growing neoplasm with favourable prognosis. Biomolecular analysis has failed to demonstrate significant alterations, and no cytogenetic alterations have been reported. In this study we demonstrate chromosome 7 gain in three of nine neurocytomas (33%). Traditional cytogenetic analysis performed in four of the nine cases identified trisomy 7 as the sole chromosomal abnormality in one case. Interphase cytogenetics utilizing fluorescent in situ hybridization (FISH) on cell suspensions from formalin-fixed paraffin-embedded tumour tissue performed in all nine cases detected trisomy 7 in two more cases and tetrasomy in another. Our results suggest that chromosome 7 gain is a feature of neuroectodermal tumorigenesis, possibly conferring growth advantage on the neoplastic cells. FISH on interphase nuclei is a valuable adjunct in the genetic evaluation of rare central nervous system neoplasms with low baseline proliferative activity.

Adult↗
PubMed1996

Cytogenetics of pediatric central nervous system tumors.

A cytogenetic analysis was performed on short-term cultures of 43 previously untreated childhood central nervous system neoplasms of various histology. The cells were obtained from pediatric patients, none of whom had received therapy before karyotypic evaluation. Successful chromosome studies were performed on 24 tumors. The most commonly detected structural abnormalities involved chromosomes 1 and 17. Other structural chromosome abnormalities involved chromosomes 3, 6, 8, 9, 11, 12, and 20.

Adolescent↗
PubMed1996

A (15;17) translocation not associated with acute promyelocytic leukaemia.

We report a woman with acute myeloid leukaemia (AML) type M2 according to FAB classification, showing a t(15;17) apparently identical to that of acute promyelocytic leukaemia (APL) on conventional cytogenetic analysis. Fluorescence in situ hybridization (FISH) using cosmidic probes specific for RAR alpha and PML, regions did not show a fusion signal as in APL. The breakpoints were assigned to 15q24.3 and 17q21.1. Detailed molecular analyses did not reveal any involvement of RAR alpha and PML genes. The patient was resistant to several front-line AMI treatments and to all-trans retinoic acid (ATRA). These findings reinforce FISH and RT-PCR as useful tools for the characterization of a t(15;17) as the translocation specifically associated with APL.

Adult↗
PubMed1995

Leiomyosarcoma.

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Adult↗
PubMed1995

Short-term treatment for adult hypergranular and microgranular acute promyelocytic leukemia.

A high hemorrhagic risk and a complete response to the differentiative agent all-trans-retinoic acid (ATRA) are the main clinical features of acute promyelocytic leukemia (APL), two distinct subtypes of which have been recognized, the common hypergranular leukopenic form (M3) and a microgranular hyperleukocytic variant (M3v). We analyzed, with emphasis on both disease- and therapy-related prognostic factors, the results from a 9-year trial in 65 adults with M3 and M3v APL, treated homogenously with a short-term therapy (STT) program excluding maintenance. STT comprised a maximum of six courses with doxorubicin, cytosine arabinoside (ara-C), and 6-thioguanine. Sixty-five APL patients formed the study group, M3v accounting for 25% of cases. In M3v, the absolute blast cell count was significantly higher (p < 0.0001) and early hemorrhagic deaths were more frequent (p = 0.05). The blast count correlated inversely with the probability of remission (p = 0.005), poor-risk patients being those with > 10 x 10(9)/l blast cells. During the study, the median survival improved from 0.1 to 2.7 years (p = < 0.005). In first place, response to chemotherapy increased from 42 to 84% (p = 0.006), by giving daily prophylactic platelet transfusions (to > 30 x 10(9)/l) and no heparin (course I), and by avoiding too toxic high-dose ara-C and deferring treatment in infected/neutropenic patients showing the atypical differentiative bone marrow pattern (course II). Secondly, the probability of first unmaintained remission differed significantly between patients given intentionally more than four total chemotherapy courses or intermediate/high-dose ara-C consolidation (0.59 at 5 years) and those treated less intensively (0.21) (p < 0.005). Intensive STT was very effective for the management of adult APL patients at standard hemorrhagic risk and receiving optimal supportive care. In high-risk patients with hyperleukocytosis and M3v, induction results could be improved by the concomitant use of ATRA. M3v in adults must be recognized promptly because of the very high early hemorrhagic risk.

Adolescent↗
PubMed1992

Value of cytogenetics in the differential diagnosis of the small round cell tumors of childhood.

Small round cell tumors are among the most common problems in the differential diagnosis of cancer, even when more sophisticated histological techniques are utilized (Ezinger and Weiss: In Soft Tissue Tumors. St. Louis: CV Mosby, 1988, pp 668-683). Six cases of small round cell tumors are described the diagnosis of which was particularly difficult. Cytogenetic analysis provided useful information in all of them in making the definitive diagnosis. The reported cases stress the value of cytogenetic methods in approaching difficult diagnostic problems.

Adolescent↗
PubMed1992

Large-cell medulloblastomas. A distinct variant with highly aggressive behavior.

We present four cases of infantile cerebellar neoplasms composed of cells with large vesicular nuclei with prominent nucleoli. All four cases were strongly immunoreactive for synaptophysin, and one case showed immunoreactivity for neurofilaments. Filter hybridization for N-myc and c-myc oncogenes showed a 27-fold c-myc amplification in one case. The cytogenetic analysis in this case showed Double-Minutes and isochromosome 17q. An intracerebral xenograft in nude mice obtained from one such tumor showed a similar morphology to that of the original tumor as well as strong immunoreactivity for synaptophysin and neurofilaments. All the neoplasms were characterized by highly aggressive behavior leading to early cerebrospinal fluid dissemination despite radiotherapy and chemotherapy. We conclude that large-cell medulloblastoma represents a distinct and more aggressive variant of medulloblastoma that requires more aggressive therapy.

Blotting, Southern↗
PubMed1990

Recurrent chromosomal aberrations in peripheral T-cell lymphoma.

Histological, immunological, and cytogenetic analysis of the same neoplastic tissues have been performed on seven patients with peripheral T-cell lymphomas (PTCL). Clonal chromosomal abnormalities in five cases are reported. The most common chromosomal aberration, observed in four patients, is a rearrangement of chromosome 14 with a breakpoint in q11.2. Aberrations of chromosome 8 also occurred in four patients, three of whom had an extra 8q. The data indicate that breakpoints of malignant diseases affecting similar cell types might cluster to specific chromosomal regions, which can be helpful in recognition and classification of PTCL.

Adult↗
PubMed1990

Establishment and characterization of a primitive neuroectodermal tumor of bone continuous cell line (LAP-35).

A continuous tumor cell line (LAP-35) was established from a primitive neuroectodermal tumor of bone from the right tibia of a 12-year-old female. The neural character of the cell line was documented by the spontaneous growth of neurites and by the presence of several neural markers, including neuron-specific enolase (NSE), S-100 protein, neurofilaments, chromogranin A, synaptophysin and positivity to monoclonal antibodies UJ127.11, UJ13A, UJ181.4. Cell-sorter analysis showed a high expression of nerve growth factor receptor (NGFr) and major histocompatibility complex class I-related molecules. A unique cytogenetic profile was observed, including a reciprocal chromosomal translocation (rct) 11:22 (q24;q12), typically associated with Ewing's sarcoma and neuroepithelioma, and deletion of the short arm of chromosome 1 (lp-), otherwise a feature of neuroblastoma. N-myc proto-oncogene was neither amplified nor expressed, whereas the expression of c-myc was documented by northern blot analysis. These features distinguish this new cell line from previously reported neuroectodermal cell lines, identifying LAP-35 as a unique model of a group of neural bone tumors that share characteristics of neuroblastoma as well as neuroepithelioma.

Animals↗
PubMed1989

Cytogenetic and clinical studies in acute promyelocytic leukemia (M3) and cytologic M3 variant (M3V).

Cytogenetic specimens were obtained from bone marrow 24-hour cultured cells in 22 patients with acute promyelocytic leukemia, including six with microgranular variant. A t(15;17) was identified in 10-100% of metaphase cells from 13 patients. We have found no correlation between complete remission percentage and karyotype. Our data suggest that each laboratory, as far as M3 and M3V are concerned, must study its own culture time as it relates to numerous parameters involving tumoral cell kinetics.

Adolescent↗
PubMed1988

Nitrilotriacetic acid (NTA) does not induce chromosomal damage in mammalian cells either in vitro or in vivo.

We used human lymphocyte cultures to repeat the experiments under the very particular conditions of nitrilotriacetic acid (NTA) treatments (high doses: up to 10(-2) M; very long exposure times: up to 5 days) which have been described as being able to induce chromosomal aberrations, and we also performed the more conventional treatments (24-48 h of exposure) as suggested in the protocols adopted by the EEC-OECD. Mitomycin C was routinely used as a positive clastogenic control. NTA did not significantly increase the frequency of chromosomal aberrations in any of the different experimental conditions adopted. Furthermore, no induction of micronuclei was observed in mouse polychromatic erythrocytes after treatment in vivo for up to 48 h with NTA (200-400 mg/kg b.w.), whereas the frequency of micronuclei was significantly increased by mitomycin C (1 mg/kg b.w.).

Acetates↗
PubMed1988

Sister chromatid exchanges and chromosomal aberrations in mouse cells infected with the Abelson and Moloney leukemia viruses.

'Spontaneous' and mitomycin C (MMC)-induced sister chromatid exchanges (SCE) and chromatid breaks were scored in ANN-1 fibroblasts, a non-producer mouse cell line transformed by the Abelson murine leukemia virus (A-MuLV), a replication defective retrovirus whose genome contains the v-abl oncogene. Normal, non-transformed NIH3T3 fibroblasts were used as control. SCE and chromatid break frequencies in untreated or MMC-treated ANN-1 and NIH3T3 cells were compared with those observed in the same cells after infection with the helper murine Moloney leukemia virus (M-MuLV), which rescues the ability of A-MuLV to replicate in ANN-1 cells. The frequency of spontaneous and MMC-induced SCE were not significantly different in both ANN-1 and NIH3T3 cells, independently of M-MuLV infection. After M-MuLV infection, however, increased 'spontaneous' frequency of SCE and altered susceptibility to the induction of SCE by MMC was observed in both cell lines compared to M-MuLV-uninfected cells. In the case of chromatid breaks, the baseline frequency was not significantly different between the two cell lines both in the presence or in the absence of M-MuLV infection, nor was it significantly increased by M-MuLV, with respect to the value observed in uninfected cells. These results indicate that, at variance with what occurs with SCE, viral replication is not needed to increase the frequency of chromosomal aberrations and that the portion of A-MuLV genome alone is sufficient to increase chromatid breaks but not SCE in ANN-1 cells. Thus, in mouse cells carrying retroviruses, SCE and chromosomal aberrations seem to be independently generated, and influenced by different viral genes.

Abelson murine leukemia virus↗