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V Brito-Babapulle

Publications and source records attributed to V Brito-Babapulle.

53 records · Page 3Linked to original sources
PubMed1986

Two new cell lines from B-prolymphocytic leukaemia: characterization by morphology, immunological markers, karyotype and Ig gene rearrangement.

Leukaemic cells from 2 patients with B-prolymphocytic leukaemia were immortalized in vitro by means of Epstein-Barr virus and phorbol-ester TPA. The resulting cell lines, named JVM-2 and JVM-3, have been growing continuously in liquid culture for more than one year. JVM-2 is characterized cytogenetically by t(11;14)(q13; q32), and JVM-3 by trisomy 12. The immunoglobulin (Ig) heavy- and light-chain genes showed the same pattern of rearrangement in both lines as in the original prolymphocytes from each case. The cells from these lines showed a spectrum of morphological and immunological features corresponding to different stages of B-cell maturation. The expression of Ig, IgM-lambda in JVM-2 and IgMD-K in JVM-3, changed from a predominantly membrane pattern in the original cells to a cytoplasmic one in the cell lines. By comparison with their original progenitors, the cells from both lines showed reduced reactivity with the monoclonal antibody (MAb) FMC7, and increased expression of the antigens recognized by the MAbs OKT10, alpha-Tac, FMC53 and Ki-I. The availability of cell lines from this rare type of lymphoid leukaemia offers a potential tool for the study of molecular events associated with the expression of Ig and other antigens by neoplastic cells.

B-Lymphocytes↗
PubMed1986

The 14q+ marker in hairy cell leukaemia. A cytogenetic study of 15 cases.

Leukaemic cells from 19 patients with hairy cell leukaemia (HCL), characterised by morphological, immunological and ultrastructural criteria, were investigated for chromosome abnormalities after stimulation with B-cell mitogens (Pokeweed mitogen (PWM), lipopolysaccharide B and EBV). The cells from all cases had a B-cell phenotype and in each case only a single light chain type was expressed on the membrane of the cells. Only 15 patients with adequate metaphases are included in this study. Clonal chromosome abnormalities were observed in 12 patients of which five had a 14q + involving q32. Of the remaining 3 cases 1 had nonclonal abnormalities and 2 had normal karyotypes. The donor chromosomes were identified in 3 cases and were found to be 9, 18 and 22. An interstitial rearrangement of chromosome 14 involving band q22 was seen in 2 cases and a deletion of chromosome 14 at q24 in 1 case. Amongst other chromosome abnormalities 12p was involved in 4 cases, 12q in 2 cases and chromosomes 7 and 22 in 3 cases each. The significance of the abnormalities has been discussed in relation to sites of cellular oncogenes. Our study demonstrates that chromosome abnormalities common to other B-cell disorders are present in HCL.

B-Lymphocytes↗
PubMed1986

Variant translocation t(8;22) and abnormalities of chromosome 15(q22) and 17(q12-21) in a Burkitt's lymphoma/leukaemia with disseminated intravascular coagulation.

Severe disseminated intravascular coagulation was observed in a patient with Burkitt's lymphoma/leukaemia. Immunological studies on leukaemic blasts from relapsed bone marrow revealed a B-cell phenotype (B4+, B1+, HLA-Dr+, J5+) with membrane bound IgM lambda. Cytogenetic investigation revealed a variant Burkitt's translocation t(8;22)(q24;q11) involving the lambda light chain gene region and abnormalities of chromosomes 15 and 17 with breakpoints at q22 and q12 respectively, similar to those observed in the t(15;17) in acute promyelocytic leukaemia. Transmission electron microscopy of the leukaemic blasts showed crystalline cytoplasmic inclusions which may have had a role in precipitating the disseminated intravascular coagulation.

Adult↗
PubMed1986

Abnormalities of chromosome 7q and Tac expression in T cell leukemias.

Clonal chromosome abnormalities were demonstrated in 13 cases of T cell leukemia with a mature membrane phenotype. The cases comprised two adult T cell lymphoma leukemia (ATLL), five Sézary syndrome (SS), three T prolymphocytic leukemia (T-PLL), and three T chronic lymphocytic leukemia (T-CLL). The presence of clonal chromosome abnormalities in the three cases of T-CLL supports the view that although clinically benign, this disorder probably represents a neoplastic process. Cells from six of 11 patients were tested and found to be reactive with monoclonal antibody (McAb) anti-Tac in the absence of mitogens (two ATLL, two SS, and two T-PLL). Only the two ATLL patients were serologically positive for the human T cell leukemia virus I (HTLV-I), and their cells showed a higher anti-Tac reactivity. Chromosome 7 abnormalities were observed in seven cases (two ATLL, three SS, two T-PLL), and a strong correlation was seen between the presence of a 7q abnormality and the expression of the Tac antigen (T cell growth factor receptor). These findings are discussed in relation to the localization of T cell receptor genes on chromosome 7 and possible mechanisms for the activation of the Tac gene.

Antibodies, Monoclonal↗
PubMed1985

Atypical promyelocytic leukemia (M3) with immature primary granules and t(15;17).

An unusual case of acute myeloid leukemia with a standard t(15;17) is described. While light microscopy morphology was suggestive of acute myeloid leukemia M5a and light microscopy cytochemistry showed 80% of blasts to be strongly positive with Sudan Black B--more consistent with a diagnosis of M4--ultrastructural analysis demonstrated that the predominant cells were promyelocytes with immature primary granules hardly visible with the Romanovsky stains by light microscopy. Because typical cytologic and clinical features of M3 or M3 variant were lacking this atypical case would not have been recognized but for the presence of t(15;17) and the demonstration of promyelocytic features by electron microscopy.

Chromosome Banding↗
PubMed1985

Chromosome 1 heterochromatin variants and cancer: a reassessment.

Evidence for a relationship between chromosome #1 heterochromatin polymorphisms and cancer has been reviewed. Eighty-four of 135 (62%) patients with epithelial malignancies were heteromorphic for C-band size compared with 38 of 107 (36%) controls (significant at the 0.1% level). However, only 33 of 67 (49%) patients with nonepithelial malignancies were heteromorphic (not significantly different from controls). Similarly, the incidence of partial inversions of the C-band region in one or both homologs was significantly greater than controls [28 of 107 (26%)] for patients with epithelial [66 of 135 (49%)] but not nonepithelial [25 of 67 (37%)] malignancies. However, when the presence of either or both size heteromorphism and inversions were assessed, the incidence was significantly higher in patients with nonepithelial [46 of 67 (69%), including 11 of 11 patients with leukemia or myeloproliferative disorders] as well as epithelial [112 of 135 (83%)] malignancies compared with controls [52 of 107 (49%)]. Forty-seven of the patients did not differ significantly from controls with respect to the incidence of chromosome #1 heteromorphism as revealed by the Giemsa-11 technique. However, 26 patients assessed for their chromosome #1 lateral asymmetry pattern differed significantly from controls, having a higher incidence of compound asymmetry with a large proximal and small distal block and a lower incidence of simple asymmetry.

Chromatin↗
PubMed1984

Neoplastic kappa and lambda cells in a B-PLL with chromosome translocations of both light chain gene regions.

We describe a chromosome translocation t(2;13) (p11-12;p11) involving the kappa (kappa) light chain gene region (2p11-12), and a subsequent translocation t(11;22) (q23;11) involving the lambda (lambda) light chain gene region (22q11) within the same clone, in a patient with B-cell prolymphocytic leukaemia (B-PLL), of whose peripheral mononuclear cells 82% expressed (kappa) chains and 8% expressed (lambda) chains. Electron microscope (EM) studies using the immunogold method showed that both kappa- and lambda-producing cells were prolymphocytes. Immunoglobulin (Ig) gene analysis by Southern blotting demonstrated rearrangement of both Ig heavy (H) chain genes and one kappa gene. Although a lambda gene rearrangement corresponding to the minor lambda-positive population was not detected, a small monoclonal (M) band of IgM-lambda was present in the serum. The chromosome translocations and the pattern of light chain expression, particularly the lambda-producing cells, are discussed in the light of the restricted light chain expression observed in Burkitt's lymphomas with variant translocations involving the light chain genes.

B-Lymphocytes↗
PubMed1984

Adult T-cell lymphoma/leukemia in a Caribbean patient: cytogenetic, immunologic, and ultrastructural findings.

Cytogenetic findings on immunologically and morphologically characterized leukemic cells from a Caribbean patient with adult T-cell lymphoma/leukemia (ATLL) (HTLV+) are reported. Marker studies on peripheral blood lymphoid cells showed a mature postthymic phenotype: TdT-, OKT3+, OKT4+, OKT6-, OKT8-, 3A1-, anti-HLA-DR-. Light and electron microscopic analysis revealed a great cellular pleomorphism with respect to nuclear features. Three main types of leukemic cell were observed: typical multilobed ATLL lymphocytes, Sézary's syndrome (SS) cells, and cells intermediate between those two. Chromosome studies on PHA-stimulated cultures revealed three clones. The predominant clone was hyperdiploid; significant abnormalities were 1q+, 14q+, and 6q- (breakpoint q21), which are known to occur in lymphoid malignancies, together with trisomy 7q and i(17q), which have been reported previously in Japanese ATLL and the small variant of SS, respectively. The 14q+ marker was t(11;14)(q13;q22-24). The incidence of 6q-, trisomy 7q, and i(17q) varied within the main clone, and it is speculated that these chromosome abnormalities might be related to the variation observed in the cell types of this patient. Two minor clones had 6q- (breakpoint q25) and 13q+ markers, respectively. It was not possible to unequivocally establish the relationship between these three clones. The chromosomal, morphologic, and immunologic findings in this case support a close relationship between ATLL in Japan and in the Caribbean basin, as well as between the proliferating cells of ATLL and SS.

Antigens, Surface↗
PubMed1984

Clinical, immunological, ultrastructural, and cytogenetic studies in black patients with adult T-cell leukemia/lymphoma.

We describe studies in 14 black patients with adult T-cell leukemia/lymphoma (ATLL) born in the Caribbean (13) and west Africa (1). Lymphadenopathy, hypercalcemia, and a leukemic blood picture were seen in the majority. The clinical course was short with a median survival of 5 months. Serum antibodies to human T-cell leukemia virus (HTLV) were detected in all the 10 cases investigated. Marker studies showed a mature (post-thymic) T4+ T-cell phenotype. Functional studies in 3 cases demonstrated that the cells did not provide help but rather suppressed B-cell differentiation. Cells from 2 cases of T4+ prolymphocytic leukemia (T-PLL) were shown to have helper function. Type C viral particles were identified by electron microscopy (EM) on cultured cells from 4 ATLL patients and these were shown to react with the monoclonal antibody (McAb) to the HTLV proteins p19 and p24. Such findings were not observed in HTLV negative T-cell leukemias except for cells of a T-PLL which showed evidence of budding and extracellular release of C-type particles after 5 days culture with phytohemagglutinin (PHA). A close association between the localization of the receptor for T-cell growth factor, demonstrated by McAb anti-Tac, and areas of the cell membrane showing release of HTLV viral particles was documented at EM level by the immunogold method. This technique also demonstrated the specific binding of anti-p19 to HTLV. Cytogenetic studies on PHA stimulated cultures from 2 ATLL revealed trisomy for 7q and this was also observed in 1 of 2 T-PLL and 2 of 4 Sezary syndrome cases. The clinical, morphological, immunological, and cytogenetic features of ATLL in black patients diagnosed in the U.K. are identical to those reported from Japan and the U.S.A. There is also strong evidence that the disease is caused by HTLV-I.

Adult↗
PubMed1983

Chromosome 1 C-band heteromorphisms in patients with carcinoma in situ and invasive carcinoma of the cervix uteri.

A significantly higher incidence of heteromorphism for the size of the C-band regions of the chromosome 1 homologues was found in the lymphocytes of patients with carcinoma in situ and invasive carcinoma of the cervix uteri than in controls (15 out of 19 and 12 out of 18 patients, respectively, as compared with 13 out of 38 controls). There was also a higher incidence of partial inversions of this region in patients with carcinoma in situ and invasive carcinoma although the differences from that found in the controls were not statistically significant. C-band variants of chromosome 1 may play a part in the cytogenetic events that determine the early stages of some forms of malignancy.

Adenocarcinoma↗
PubMed1981

Break points in chromosome #1 abnormalities of 218 human neoplasms.

A survey of 343 break points that lead to chromosome #1 abnormalities in 218 human neoplasms showed that 49.9% were located in or immediately adjacent to the centromeric heterochromatin. Amongst rearrangements with breaks in bands p 12-q21 were 27 isochromosomes, 22 translocations of the long arm, and four translocations of the short arm to the heterochromatic regions of other chromosomes, and 35 deletions resulting in chromosomes consisting mainly or solely of one arm. Deletions following breakage at various sites in the short arm of chromosome #1 are frequent in malignancies and are quite often found in cells that are trisomic for the long arm. It is suggested that fragility of chromosomes generated as a result of early events in carcinogenesis may be one source of chromosome rearrangements, including those of chromosome #1, on which selection can operate and give rise to progressively more malignant clones.

Chromosome Aberrations↗
PubMed1981

Three or four copies of a dicentric 17q isochromosome in an acute myeloproliferative disorder.

The majority of metaphases in the bone marrow of a male patient aged 72 with a rapidly evolving aleukemic erythremic myelosis had 48 chromosomes with three copies, or 49 chromosomes with four copies, of an i(17q), which was seen to be dicentric in C-banded and Giemsa-11-banded preparations. There was also loss of a chromosome No. 5 and the addition of a chromosome resembling a No. 22. The presence of multiple copies of the isochromosome is postulated to be related to the acuteness of the condition.

Acute Disease↗
PubMed1981

Lateral asymmetry in human chromosomes 1, 3, 4, 15, and 16.

Chromosomes 1, 3, 4, 15, and 16 show lateral asymmetry after replication in the presence of BrdU and staining with Giemsa at pH 10.4. Lateral asymmetry is thought to result from an unequal interstrand distribution of thymine in regions of repetitive DNA. Compound lateral asymmetry in 1 may be due to the presence of two segments of DNA differing in base composition and with different strands rich in thymine. Polymorphism for lateral asymmetry is observed in the AT-rich quinacrine-positive centromeric regions of 3 and 4, even though none of the four satellite DNAs are demonstrable by in situ hybridization there. Other workers have shown that a satellite fraction isolated using Hoechst 33258 and an EcoRI restriction fragment of human satellite DNA map on 3. There is no evidence for the presence of satellite DNA on 4. Since 20% of the DNA in the human genome reassociates at a C0t of less than or equal to 1 and only 4% is satellite DNA, 4 may have repetitive nonsatellite sequences; on the other hand the lack of an appropriate satellite probe may be the limiting factor. Lateral asymmetry in the Y has been demonstrated using the Hoechst method by other workers but cannot be observed with BrdU-Giemsa staining at pH 10.4.

Chromosome Aberrations↗
PubMedDate not supplied

Immunophenotype changes and loss of CD52 expression in two patients with relapsed T-cell prolymphocytic leukaemia.

T-cell prolymphocytic leukaemia (T-PLL) is an aggressive disease often resistant to conventional chemotherapy. Long lasting remissions with the monoclonal antibody CAMPATH-1H (anti-CD52) have been documented. We describe two unusual T-PLL patients treated successfully first with CAMPATH-1H in whom, at the time of relapse, the cells underwent a phenotypic switch with loss of CD52 expression. In one of them, cytogenetic analysis demonstrated the same chromosome abnormalities in the cells at diagnosis and relapse. The reasons for the immunophenotypic changes are unknown but it is likely that loss of CD52 antigen expression contributed to the resistance to CAMPATH-1H in one of the patients when re-treated.

Adult↗