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Biomedical subjects

G Manolov

Publications and source records attributed to G Manolov.

At least 19 recordsLinked to original sources
PubMed1991

Chromosomal alterations in lymphocytes of patients with Balkan endemic nephropathy and of healthy individuals after incubation in vitro with ochratoxin A.

The possible involvement of mycotoxins in chromosomal alterations in patients with Balkan endemic nephropathy (BEN) was investigated cytogenetically. Lymphocyte cultures from patients with BEN and from individuals from a nonendemic region were examined and compared with cultures from healthy people which had been incubated in vitro with noncytotoxic doses of ochratoxin A. Significantly increased numbers of various numerical and structural anomalies were found in patients with BEN. Chromosome X in female patients occurred in both monosomic and polysomic forms. A 'prosomization' effect was seen along the entire length of supernumerary X chromosomes, manifested by retarded contraction resembling early mitotic stages, with a comparably detailed band pattern. No other specific numerical or structural change was found consistently in BEN patients. Incubation of the lymphocytes of healthy people with ochratoxin A induced similar aberrations and prosomization. These findings may support the hypothesis that ochratoxin A is involved in the pathogenesis of BEN.

Balkan Nephropathy↗
PubMed1990

Induction of characteristic chromosomal aberrations, particularly X-trisomy, in cultured human lymphocytes treated by ochratoxin A, a mycotoxin implicated in Balkan endemic nephropathy.

Ochratoxin A (OA), a mycotoxin which induces nephropathy and kidney tumours in rats and mice, is a contaminant of food consumed by a population with a high incidence of endemic nephropathy (EN). It was therefore tested in vitro for its ability to induce chromosomal aberrations in human peripheral lymphocytes in a small number of subjects, in the presence or absence of a kidney microsomal metabolic activation system. OA was found to induce aberrations on X chromosomes of similar types to those previously detected in lymphocytes from patients suffering from endemic nephropathy.

Animals↗
PubMed1986

Alternative involvement of two cytogenetically distinguishable breakpoints on chromosome 8 in Burkitt's lymphoma associated translocations.

The chromosomes of 16 Burkitt's lymphoma (BL) derived cell lines were submitted to high-resolution G-band analysis. They included seven lines with t(8;14), three with t(2;8), and four with t(8;22). The translocation breakpoint in chromosome #14 was located in 14q32.3, in chromosome #2 in 2p11.1, and in chromosome #22 in 22q12.12. In chromosome #8, the translocation breakpoint was located in two cytogenetically distinct subbands: 8q24.1 in cell lines with t(8;14) and t(2;8) and 8q24.22 in cell lines with t(8;22). In the light of recent molecular findings, these results indicate that the distance between the c-myc gene, located in 8q24, and the Ig sequences might be much larger in BL lines with t(8;22) than in those with t(2;8).

Burkitt Lymphoma↗
PubMed1986

Satellite DNA in the three C-bands of an unusual mouse marker chromosome. A model of chromosomal evolution.

A marker chromosome in the stemline of a new murine cell line is described on the basis of different stainings and in situ hybridization. The marker was characterized originally by three C-bands, one from each centromeric region of the three chromosomes constituting the marker. In the course of stemline evolution, two of the C-bands have been lost and the marker has developed into a monocentric chromosome, phenotypically and functionally normal.

Animals↗
PubMed1986

High resolution chromosome analysis of constitutional and acquired t(15;17) maps c-erbA to subband 17q11.2.

High resolution chromosome analysis was performed on bone marrow cells from four patients with acute promyelocytic leukemia and t(15;17), and in lymphocytes from two unrelated, phenotypically normal persons with an apparently identical constitutional translocation. Scrutiny of prophase-prometaphase chromosomes localized the breakpoints in all six cases to subbands 15q22.3 and 17q11.2. Molecular genetic studies have localized the oncogene c-erbA to chromosome #17 between the breakpoints of the constitutional and the acquired anomaly. The present results, therefore, map c-erbA to subband 17q11.2.

Chromosome Aberrations↗
PubMed1985

Small noncleaved B cell Burkitt-like lymphoma with chromosome t(8;14) translocation and Epstein-Barr virus nuclear-associated antigen in a homosexual man with acquired immune deficiency syndrome.

This case report describes new manifestations of the acquired immune deficiency syndrome (AIDS) in a promiscuous homosexual man. Investigation of upper gastrointestinal bleeding in the patient lead to discovery of a high-grade, small, noncleaved cell (Burkitt-like) gastroduodenal lymphoma with visceral and extralymphatic extension. Specific phenotyping of the lymphoma revealed that it was a monoclonal B cell lymphoma of mu kappa isotype. An in vitro cell line was established that was Epstein-Barr virus nuclear-associated antigen-positive. The lymphoma cells displayed a t(8;14) translocation similar to endemic African Burkitt lymphoma. Epstein-Barr virus genomes were identified in the lymphoma and an axillary lymph node biopsy specimen by molecular hybridization. These data strongly suggest that Epstein-Barr virus actively infected this patient. However, he showed normal Epstein-Barr virus-specific serologic responses, indicating an immune defect against the virus.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Chromosome aberrations in peripheral lymphocytes of male homosexuals.

Karyotypes of peripheral lymphocytes of 19 male homosexuals showed increased hypodiploidy. Chromosomes #19 and #20 were most frequently lost. Also, structural chromosome aberrations frequently occurred consisting chiefly of translocations and simple chromosome breaks. Terminal deletions, inversions, and isochromosomes occurred less commonly. In three of the cases, 100% of the cells were involved in a pericentric inversion of a chromosome #9. Chromosomes #3 in p21.1 and 1 in p32.3 were repeatedly affected. Structural aberrations were seen less frequently in men with acquired immunodeficiency syndrome(AIDS) and AIDS-related complex than in asymptomatic homosexuals. The hypodiploidy with preferential loss of chromosomes was constantly present. The marker chromosomes and simple breaks at repeated sites are another manifestation of damage to the immune system in these male homosexuals from Greenwich Village in New York City. The chromosomal damage was potentially the result of exposure to amyl and butyl nitrites, viral infections, or immunologic reactions to sperm, which crossreact with lymphocytes.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Role of Epstein-Barr virus in the etiology of Burkitt's lymphoma.

Although Epstein-Barr virus (EBV) was discovered in cultured Burkitt's lymphoma (BL) cells, its exact role remains unclear. Viral genome is found in 95-98% of endemic BL and 15-20% of non-endemic BL. Children destined to develop BL in Africa show elevated titres of viral capsid antibodies one to two years preceding emergence of BL. A multistep process follows early EBV infection during early childhood. Immune deficiency probably permits continuation of the infections, with smouldering polyclonal B-cell proliferation proceeding. Final steps in the pathogenesis consist of cytogenetic and molecular conversion to monoclonal BL. Reciprocal chromosomal translocations involve breakpoints containing c-myc, heavy- and light-chain Ig loci. Activation of oncogenes, c-myc and B-lym, may be essential in the molecular pathogenesis of BL. A spectrum of EBV-induced pathological entities is found in individuals with X-linked lymphoproliferative and acquired immune deficiency syndromes. Lymphoma identical to endemic BL occurs in these immune-deficient patients. Non-endemic BL is possibly due to immune defects, initiators and promoters of B-cell proliferation, which may not be identical to factors in endemic BL; however, cytogenetic events and activation of oncogenes may be pathways of both endemic and non-endemic BL.

Acquired Immunodeficiency Syndrome↗