Search PubMed⌕ Search

Biomedical subjects

M J Bello

Publications and source records attributed to M J Bello.

At least 55 records · Page 3Linked to original sources
PubMed1989

Cytogenetic follow-up from direct preparation to advanced in vitro passages of a human malignant glioma.

In order to evaluate which cytogenetic evolutionary patterns take place during the in vitro establishment of a permanent glioma cell line, cytogenetic follow-up was performed on direct preparations and primary cultures from a malignant astrocytoma and on serial passages for more than 2 years of in vitro propagation. Sixteen passages were studied, and the presence of a marker chromosome in direct preparations and after in vitro growth permitted us to identify the clonal evolution of the resulting permanent cell line. Near-triploid cells present in the direct study became the main cell population in vitro; chromosomal losses and the acquisition of a few new marker chromosomes were also characteristic features, leading to a stable modal number of around 60 chromosomes in the last passages analyzed. The results provide new evidence of the existence of more than one pattern of chromosomal evolution during the in vitro establishment of human gliomas.

Chromosome Aberrations↗
PubMed1989

Precise in situ localization of NCAM, ETS1, and D11S29 on human meiotic chromosomes.

In order to sublocalize NCAM, ETS1, and the anonymous DNA fragment D11S29 within 11q23, in situ hybridization was performed on pachytene bivalents. Analysis of the grain distribution within the band 11q23 indicated that the chromosomal sublocalization of both NCAM and D11S29 was in 11q23.1, whereas ETS1 was found to be localized in 11q23.3. These results clearly demonstrate the usefulness of in situ hybridization applied to pachytene bivalents to obtain accurate gene sublocalization.

Chromosome Mapping↗
PubMed1989

Cytogenetic analysis of metastatic effusions from breast tumors.

Chromosome analysis was performed on direct and in vitro cultures of 30 effusions from breast carcinoma. Although in 14 samples normal diploid stem-lines were found, chromosome abnormalities were present in stem- or side-lines of all cases. Recurrent numerical deviations were only verified as gains of Nos. 6 and 7. Rearrangements were seen involving almost all chromosome pairs (except No. 18 and gonosomes), however, Nos. 1, 3, 6 and 11 were those most frequently related to the genesis of markers. Double minutes (DMs) were found in seven samples, and there was a homogeneously staining region (HSR) in one.

Breast Neoplasms↗
PubMed1988

Incidence and origin of dicentric chromosomes in cultured meningiomas.

Based on the cytogenetic findings in 32 human meningiomas, an analysis of dicentric chromosomes, usually present in cultures from meningiomas, has been performed. The incidence and origin of such markers have been analyzed and the chromosomal composition of the stem line in the corresponding sample established (i.e., normal karyotype, -22 as the sole chromosomal deviation, or complex karyotypes in addition to #22 abnormalities). More than 10 dicentric chromosomes were found in 12 of 32 meningiomas (37.5%). Sixty-eight of the markers could be identified individually or as belonging to a chromosome group. Fifty-three percent of the meningiomas characterized by a complex stem line karyotype also displayed dicentric chromosomes in variant cells, whereas only 12.5% of meningiomas with a normal diploid stem line showed such chromosomal aberrations. Chromosomes of groups C and D participated most frequently in the genesis of dicentrics; however, chromosomes 19, 20, 3, 6, and 13 were the most frequently involved. Thus, the existence of a nonrandom pattern of involvement supports the fact that dicentrics might play a biologic role in the progression of human meningiomas.

Centromere↗
PubMed1988

Chromosomal involvement secondary to -22 in human meningiomas.

Cytogenetic analyses have been performed on cultures in vitro from 32 human meningiomas, seeking chromosomal anomalies in addition to characteristic monosomy 22. Eight cases showed stem lines with normal karyotype, whereas, monosomy 22 as the only chromosomal deviation characterized the stem line of ten tumors. In 14 samples stem lines or modal numbers displaying numerical deviations (other than -22) and/or structural rearrangements were found. A hyperdiploid modal number was present in three, whereas, it was hypodiploid in the remainder. Numerical deviations in these tumors involved mainly #14 by losses, and also #22; recurrent structural rearrangements involving 1p and 11p were also characteristic features. Thus, these results could imply that involvement of #14, 1p, and 11p would be a form of clonal evolution secondary to monosomy 22 in certain meningiomas.

Adult↗
PubMed1987

Cytogenetic findings in an effusion secondary from pleural mesothelioma.

Cytogenetic analysis was performed on cells from pleural effusion secondary to an epithelial mesothelioma. Although chromosomal findings (pseudodiploid stemline, including marker chromosomes involving chromosomes #1, #3, #5, and #6) suggested the neoplastic origin of the effusion, routine cytologic diagnosis was negative.

Adult↗
PubMed1987

Cytogenetic clones in a recurrent neurofibroma.

Chromosome studies were performed on a plexiform neurofibroma arising in a probable von Recklinghausen's disease patient, who also showed a de novo constitutional reciprocal translocation, t(1;22)(p32;q11). Banding analysis of the metaphases obtained from two primary cultures in vitro showed the presence of five cytogenetic clones, characterized by different chromosomal rearrangements. In addition to t(1;22), marker chromosomes involved pairs 1, 2, 3, 5, 8, 9, 10, 12, 16, and X. These findings suggest a possible polyclonal evolution in this neurofibroma.

Adult↗
PubMed1987

Deletion 3p in two lung adenocarcinomas metastatic to the brain.

Cytogenetic analysis by direct and in vitro preparation of brain metastatic lesions from two lung adenocarcinomas have shown the presence of a recurrent chromosomal abnormality, del(3p). These results add new evidence about the presence of 3p- marker chromosomes in adenocarcinoma of the lung.

Adenocarcinoma↗
PubMed1987

Chromosomal patterns in human malignant astrocytomas.

Cytogenetic analysis by direct and/or in vitro preparations was performed on 34 malignant astrocytomas. Thirty tumors showed near-diploid chromosome numbers, whereas, tritetraploid chromosome complements were present in four tumors. The most frequent chromosomal changes implied numerical deviations by a gain of chromosomes #7, #19, and #20, and by losses of #10, #22, and Y. Structural rearrangements were present in stem- or side lines of 24 tumors. Although no common chromosomal rearrangement seems to exist among those tumors, chromosomes #1, #6, #7, and #9 were predominantly involved. Polysomy and structural rearrangements of chromosome #7 could be related to the overexpression of epidermal growth factor gene, previously observed in some malignant gliomas.

Adult↗
PubMed1987

Chromosomal composition of a series of 22 human low-grade gliomas.

G-banded chromosomal analysis was performed on direct and/or in vitro cultures of 22 low-grade gliomas, including nine grade I-II astrocytomas, nine oligodendrogliomas, one mixed tumor oligodendroglioma-astrocytoma, and three ependymomas. Normal diploid stem lines were present in most astrocytomas and oligodendrogliomas, whereas, all three ependymomas displayed polyploid modal numbers. However, secondary cell lines showed the presence of clonal recurrent numerical abnormalities, mainly polysomy 7, monosomy 10 and 22, and loss of the Y chromosome. Clonal structural rearrangements were present with a low incidence; they mainly involved chromosomes #1 and #7. These patterns of chromosome involvement seem to correlate with the scarce previous cytogenetic banding data available from low-grade gliomas. They are also similar to the chromosome alterations found in high-grade gliomas.

Adolescent↗
PubMed1986

A case of pituitary adenoma with 58 chromosomes.

Chromosome analysis was performed on a growth hormone secreting pituitary adenoma. G-banding analysis showed a stem line with 58 chromosomes including numerical deviations of pairs #3, #5, #7, #9, #11, #12, #13, #17, #19, #20, and gonosomes was found. These findings add new evidence of the nonrandom involvement of C and F group chromosomes in numerical deviations in this tumor type.

Adenoma↗
PubMed1985

Cytogenetic findings in a human malignant melanoma metastatic to the brain.

Cytogenetic analysis by G-banding of direct and preparations of a malignant melanoma metastatic to the brain in vitro showed a pseudodiploid modal chromosome number, including five marker chromosomes, one of which was an i(6p). These results agree with those recently reported about the preferential involvement of chromosome #6 in malignant melanoma.

Brain Neoplasms↗