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V Buccheri

Publications and source records attributed to V Buccheri.

12 recordsLinked to original sources
PubMed2001

Late diagnosis of HIV infection in women seeking counseling and testing services in São Paulo, Brazil.

We investigated whether women positive for human immunodeficiency virus (HIV) infection were late in seeking an anonymous HIV counseling and testing service, and the factors associated with a low CD4 count, in São Paulo, Brazil. Seventy-one consecutive HIV-1-seropositive women were interviewed by means of a structured questionnaire. Blood samples were collected for CD4+ T-lymphocytes count and determination of HIV-1 subtypes. Hepatitis C, syphilis, human T-cell lymphotrophic virus type I (HTLV-I), and HTLV-II infections were assessed by serologic tests. More than 70% of the women had less than 500 CD4+ cells/mm3 (20% below 200). Low CD4 count was significantly associated with sex work history, condom use in the last 6 months, and seropositivity to HTLV-I and syphilis. There was no relation between low CD4 count and HIV-1 subtypes. These results indicate that in Sao Paulo many women are seeking an anonymous testing service late in the course of HIV infection. The main purposes of anonymous HIV testing services - early diagnosis of infection, and counseling to prevent infection - are not being achieved. Another strategy for reducing the interval between infection and diagnosis in women must be addressed.

Adolescent↗
PubMed1996

Cytogenetic findings in acute biphenotypic leukaemia.

We have studied the immunological and cytogenetic features of 26 patients with acute leukaemia classified as biphenotypic according to a scoring system based on the number and lineage specificity of antigens expressed on the blast cells. The series included 19 adults (age >15 years) and seven children. The cases were distributed in four immunophenotypic groups: (1)coexpression of myeloid and B antigens, 18 cases (69 percent);(2)myeloid and T cell antigens, six (23 percent); (3) one case with trilineage differentiation; and (4) one case with coexpression of both B and T cell antigens. Cytogenetic analysis revealed a normal karyotype in four cases (15 percent) and abnormal clones in 22 (85 percent). Eight patients had the Philadelphia (Ph) translocation, t(9;22)(q34;q11), (31 percent), three cases had structural aberrations of 6q and two had 11q23 rearrangements, one with t(11;19) and a second with t(4;11); the other eight cases had different alterations including t(9;12)(q1;q1), t(8;21)(q22;q22), t(2;7) (p1?3;q3?4), t(7;12)(q11;p11), hyperdiploidy and other structural abnormalities. The chromosomal rearrangements in children were characterised by abnormalities of 11q23 in two cases and the Ph translocation in three. Our data indicate that biphenotypic features are common in cases presenting with t(9;22) as the eight cases included here represent 47 percent of all cases of Ph+ve acute leukaemia studied in our Institution. Biphenotypic acute leukaemias comprise a heterogeneous group of leukaemias involving pluripotent stem cells. Cytogenetic studies are essential in characterising these cases as they will disclose several poor prognosis chromosome aberrations of which the Ph chromosome is the most frequent.

Adolescent↗
PubMed1994

Neonatal mixed lineage acute leukaemia.

We report here an uncommon case of neonatal acute leukaemia that presented concomitant with serological evidence of rubella infection. The clinical course was aggressive and the patient died 5 days after diagnosis from septicaemia. Leukaemic blasts had a mixed lineage immunophenotype co-expressing a constellation of B-lymphoid (CD19, cytCD22, TdT) and myeloid (CD13, CD33, CD14, anti-MPO) markers, as well as multiple adhesion molecules and markers associated with early lympho-myeloid progenitor cells (CD34, CD7, HLA-DR). A previously unrecorded discordant expression of different CD10 and CD34 epitopes was identified using different monoclonal antibodies. The karyotype was 46,XX t(4;11)(q21;q23) and molecular analysis confirmed rearrangement of the trithorax-related oncogene HRX at 11q23. There was a clonal biallelic rearrangement of the immunoglobulin heavy-chain gene. The features of this rare case have implications for possible aetiological events leading to leukaemia.

Acute Disease↗
PubMed1993

mb-1: a new marker for B-lineage lymphoblastic leukemia.

The expression of the Ig-linked mb-1 polypeptide was analyzed by immunocytochemistry (alkaline phosphatase anti-alkaline phosphatase technique) using a specific monoclonal antibody in 165 cases of acute leukemia, with 88 being lymphoblastic (ALL) and 77 myeloid (AML). The purpose of the study was to investigate the specificity of this reagent for B-lineage cases and its reactivity on leukemias that coexpress myeloid and B-cell antigens (biphenotypic). The majority (89%) of 72 B-cell precursor ALL patients were positive. Of these, mb-1 was expressed in all 9 patients with early-B-ALL (CD10-, c mu-), in all 11 patients with pre-B-ALL (c mu+) and in the single case of B-ALL (smIgM+). Forty-three of 51 patients with common-ALL (CD10+, c mu+) were also positive. All 16 T-lineage ALL patients and 72 (93.5%) of the AML patients examined were mb-1 negative. Four of the 5 mb-1-positive AML patients were considered biphenotypic and expressed other B-cell antigens such as CD10, CD19, and/or cCD22 and all showed rearrangement of the Ig heavy chain genes. Within the AML cases, mb-1 and cCD22 were more useful than other B-cell antigens in detecting biphenotypic cases, and mb-1 showed the highest correlation with the clonal rearrangement of Ig heavy chain genes. These results indicate that mb-1 is a sensitive and specific reagent for B-lineage blasts that will aid in the classification of B-cell precursor ALL and in the identification of biphenotypic leukemia presenting as AML.

Antibodies, Monoclonal↗
PubMed1993

Unusual deletions within the immunoglobulin heavy-chain locus in acute leukemias.

We have investigated the structure of the Ig heavy (IGH) chain locus in 309 cases of acute leukemia. Seventy-one cases of B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) were analyzed: in six cases deletion of joining (JH) segments in the presence of cytogenetically normal chromosome 14 was observed. Similar deletions were seen in 1 out of 8 cases of biphenotypic acute leukemia analyzed: this case exhibited t(9:22)(q34;q11) and coexpressed both myeloid and B cell differentiation antigens. Five of the 7 cases analyzed had deleted the JH segments from both chromosomes. Because these deletions may have contributed to the pathogenesis of the disease we have attempted to define their boundaries. Using probes that map both 5' and 3' of JH, the 3' (centromeric) boundary of the deletions was mapped to an approximately 30-kb central region of the 60 kb between C delta and C gamma 3 in 10 of the 12 deleted chromosomes. In the remaining two chromosomes, the 3' boundary mapped to S mu. The 5' (telomeric) boundary could not be defined. However, three cases with biallelic deletion of JH showed biallelic deletion of the most proximal variable (VH) (VH6 and VH5-B2) genes, indicating that the deletions spanned over 500 kb. VH5-B1 and VH5-B3 were retained in germline configuration and no gross deletions were observed using a VH3 subgroup-specific probe, indicating that the 5' boundary mapped within the VH locus. Unusual deletions of the portion of the IgH locus including JH segments and the C mu and C delta genes may occur in acute leukemias with immunophenotypic evidence of commitment to the B cell differentiation pathway. The possible consequences of the deletions remain to be determined. However, the clustering of the centromeric boundary of the deletions to S mu and to a region between the C delta-C gamma 3 genes, a known "hot spot" for recombination, may indicate the operation of a distinct pathogenic mechanism.

Acute Disease↗
PubMed1993

Immunological and ultrastructural studies in acute biphenotypic leukaemia.

AIMS: To compare the sensitivity of the ultrastructural method to detect myeloperoxidase (MPO) with light microscopy and immunocytochemistry using an anti-MPO antibody; to examine the expression of lymphoid antigens in relation to MPO activity in blast cells from cases of biphenotypic leukaemia. METHODS: Blast cells from 14 cases of biphenotypic acute leukaemia were analysed. Immunological markers were performed by single or double immunofluorescence staining on a flow cytometer. The presence of MPO was determined by light microscopy, electron microscopy on fixed and unfixed cells, and by immunoalkaline phosphatase with an anti-MPO antibody. The immunogold method was applied at the ultrastructural level to assess the expression of lymphoid and myeloid antigens at the same time as the MPO activity. RESULTS: Six of the 14 cases were initially classified as acute lymphoblastic leukaemia (ALL) and eight as acute myeloid leukaemia (AML). MPO activity was shown at the ultrastructural level in 4-99% blasts from all cases. Six of the 14 were MPO negative by light microscopy and three of these were negative with the antibody anti-MPO. Coexpression of lymphoid antigens (CD19, CD10, or CD2) and MPO was shown by the immunogold method in four out of 11 cases; in seven cases the blasts coexpressed myeloid antigens (CD13, CD33) and MPO. CONCLUSIONS: Electron microscopy is more sensitive for showing MPO than light microscopy and immunocytochemistry; the immunogold method combined with MPO used at the ultrastructural level can help to define the cell lineage involved in biphenotypic leukaemia by highlighting the myeloid component defined by MPO.

Acute Disease↗
PubMed1993

Lineage commitment in biphenotypic acute leukemia.

Acute leukemias (ALs) with phenotypic and genotypic features of several hematopoietic lineages are difficult to classify and may represent the transformation of multipotent stem cells. We have studied immunological features of 200 cases of acute leukemia (109 acute myelogenous leukemia, AML, and 91 acute lymphoblastic leukemia, ALL, according to FAB criteria), including 17 (8.5%) classified as biphenotypic by a scoring system based on the number and specificity of unexpected lineage antigens and which gives more weight to cytoplasmic markers such as myeloperoxidase, CD3, and CD22, and less to other membrane markers. Sixty-eight AML and 42 ALL cases were also examined for rearrangements of the immunoglobulin (Ig) and T-cell receptor (TCR) beta, gamma, and delta genes, and these included 12 biphenotypic AL. The expression of myeloid antigens in ALL was seen in 25% of the cases. All B-lineage ALL had rearrangements and/or deletions of the Ig genes whereas TCR beta, gamma, and delta genes were rearranged in 21%, 52%, and 71%, respectively. TCR delta, gamma and/or beta were rearranged in T-ALL and four out of 13 cases had Ig gene rearrangement. Lymphoid-associated antigens were expressed in 40% of AML cases; those most frequent expressed were CD7 (17%), CD2 (15%), CD19 (10%), and CD10 (7.5%). Evidence of Ig and/or TCR gene rearrangements was detected in 12% of AML cases. There was no correlation between the isolated expression of terminal deoxynucleotidyl transferase (TdT), B, and T-cell antigens with Ig and TCR gene rearrangements. However, in cases of AML defined as biphenotypic because they expressed two or more lymphoid antigens there was a statistically significant correlation between gene rearrangements and lymphoid score (p < 0.001). Our findings support the concept of biphenotypic leukemia as a distinct entity in which there is frequent correspondence between phenotypic and genotypic changes.

Acute Disease↗
PubMed1992

The role of an anti-myeloperoxidase antibody in the diagnosis and classification of acute leukaemia: a comparison with light and electron microscopy cytochemistry.

The enzyme myeloperoxidase (MPO) is the hallmark of the myeloid lineage. We have analysed the presence of MPO in blasts from 180 cases of acute leukaemia (103 acute myeloid leukaemia (AML) and 77 acute lymphoid leukaemia (ALL) by means of monoclonal antibodies anti-MPO and immunocytochemistry (alkaline phosphatase anti-alkaline phosphatase method). The aim of the study was to investigate the specificity and sensitivity of this marker compared with MPO cytochemistry by light (LM) and electron microscopy (EM), and with the expression of myeloid antigens. Anti-MPO was positive (greater than 3% blasts) in all but one of the 90 AML positive by LM cytochemistry. Of 13 AML cases negative by MPO cytochemistry, six showed 3-10% blasts reactive with anti-MPO and were also positive with antibodies to CD13 and/or CD33. The presence of MPO was confirmed in four of these by EM. The overall positivity of anti-MPO in AML was 92%. Anti-MPO was negative in all but two ALL (6% and 8% positive blasts). The blasts in these two cases were also CD13, CD33 and MPO positive by EM; both were thus reclassified as biphenotypic. Another two ALL reinterpreted as biphenotypic were negative by MPO cytochemistry and anti-MPO but were MPO positive by EM and with CD13 and/or CD33. We conclude that anti-MPO is a sensitive and specific early marker of myeloid blasts and should be incorporated in the routine immunophenotyping of acute leukaemia.

Acute Disease↗
PubMed1991

A classification of acute leukaemia for the 1990s.

The need for reproducibility in the classification of acute leukaemia has made it necessary to incorporate information derived from new techniques which have become essential for the study of these disorders. In addition to classic morphology and cytochemistry (FAB proposals), it is necessary to add immunology and cytogenetics (MIC proposals), as well as to investigate further the biological and diagnostic significance of molecular events. As a result of these investigations a new group of leukaemias merit recognition as distinct entities. These include three types of ALL with specific chromosome abnormalities, namely, i) t (9;22), ii) t (4;11) and iii) t (1;19) and four subtypes of AML, i) with minimal differentiation or AML-M0, ii) with basophilic precursors or M2Baso, iii) AML (M4/M5) with t (8;16) and iv) AML with trilineage myelodysplasia. Biphenotypic acute leukaemia constitutes also a distinct entity with features of ALL and AML and represents a malignancy probably affecting multipotent stem cells. We propose an objective evaluation system for biphenotypic leukaemias based on a score in which the various lineage markers are graded according to their known specificity.

Humans↗