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Biomedical subjects

F Hecht

Publications and source records attributed to F Hecht.

At least 91 records · Page 5Linked to original sources
PubMed1987

Establishment and characterization of a common acute lymphoblastic leukemia cell line with a deletion of chromosome 3 band q26.

This paper describes the establishment and characterization of a new cell line (SUP-B7) which was established from a child with "common" acute lymphoblastic leukemia. The SUP-B7 cells (and the patient's tumor) have been characterized by cytochemical staining, monoclonal antibodies, enzyme analyses, gene rearrangement studies, and karyotype analysis. The SUP-B7 cells are periodic acid-Schiff positive, common acute lymphoblastic leukemia antigen positive, and terminal deoxynucleotidyl transferase positive, and they lack the Epstein-Barr virus genome. In addition, the SUP-B7 cells lack cytoplasmic and surface immunoglobulins, and the immunoglobulin gene rearrangement studies showed rearranged heavy chain genes with germ line light chain genes. Concordance between the cell line and the patient's tumor was established by the immunoglobulin gene rearrangement studies. Using Southern blot analysis of the DNA from the patient's tumor and the SUP-B7 cells, there was comigration of the bands representing the rearranged immunoglobulin heavy chain gene. In addition, the SUP-B7 cells possess a single chromosome abnormality: del(3)(q26q28), with the chromosome breakpoint at or near the transferrin receptor gene. Since the SUP-B7 cell line is concordant with the patient's malignancy and since these cells possess a single chromosomal abnormality, the SUP-B7 cell line may be a useful tool in determining the biological significance of the chromosome deletion: del(3)(q26q28).

Antigens↗
PubMed1987

Lymphocyte subpopulation profiles and mitogen kinetics in immunological deficiency testing.

The correlation between lymphocyte proliferative responses to mitogens and T4/T8 ratios was analyzed in a cross section of patients who either were in a high-risk group for HTLV-III infection or fulfilled clinical criteria for acquired immune deficiency syndrome (AIDS). The patient results showed that, correlated with decreased T4/T8 ratios, there was a decrease in mitogen responsiveness first to pokeweed mitogen (PWM), followed by concanavalin A (Con A) and then phytohemagglutinin (PHA). Parallel to this decrease there was a shift toward higher concentrations of mitogens needed for optimal proliferation. In comparison, depletion of T4+ lymphocytes from normal healthy controls also decreased lymphocyte proliferative responses to all three mitogens but shifted the amount of mitogen needed for optimal proliferation toward lower concentrations. The differences in mitogen-induced proliferation between patients and healthy controls suggest a model whereby there is a functional defect(s) in mitogen responsiveness of the remaining T4- lymphocyte population that can be overcome when higher concentrations of mitogen are used.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Cytogenetic analyses in 89 patients with secondary hematologic disorders--results of a cooperative study.

Eighty-nine patients who developed a secondary hematologic disorder and were studied with chromosome analysis were collected from nine institutions. The results of the study confirmed previous findings, in particular, -5/5q-, -7/7q-, -17, and +21 were the most frequently encountered aberrations. Moreover, a t(1;7)(p11;p11) was reported in four cases and consistent chromosome abnormalities were observed in a small group of patients who had been treated only with surgery, but not with chemo- or radiotherapy for a previous tumor.

Acute Disease↗
PubMed1987

Fragile sites limited to lymphocytes: molecular recombination and malignancy.

Fragile sites on chromosomes are points at which rearrangements tend to occur nonrandomly. Because translocations between chromosomes #7 and #14 occur nonrandomly in normal cultured lymphocytes, we analyzed chromosomes #7 and #14 in 53,580 cultured lymphocytes and 109,300 other human cells. We found one rearrangement per 1,218 lymphocytes. These rearrangements were not restricted to translocations but included inversions and hitherto undetected duplications and deletions. In lymphocytes cultured for only 48 hours, rearrangements were seen indicating their presence in vivo. The breakpoints were exclusively in chromosome bands 7p13, 7q35, 14q11, and 14q32. The predisposition to form these rearrangements appeared nonrandom and inherited. These four bands act as if they contain fragile sites limited to lymphocytes. Fragility was not observed in these bands in cells from amniotic fluid, bone marrow, skin, or chorionic villi. Bands 7p13, 7q35, and 14q11 contain T-cell receptor (TCR) genes, whereas, band 14q32 contains the immunoglobulin heavy (IgH) chain locus. Rearrangements of these bands may result from molecular recombination between TCR or between TCR and IgH genes forming TCR/TCR and TCR/IgH chimeric genes important to understanding lymphocyte development and neoplasia. TCR/IgH chimeric genes have been found in T- and B-cell malignancy.

Chromosome Fragile Sites↗
PubMed1987

Trisomy 4: an entity within acute nonlymphocytic leukemia.

Trisomy 4 is a newly recognized primary chromosome change in leukemia. Five cases of acute nonlymphocytic leukemia (ANLL) are described from the United States and France. As in cases from Belgium, the only chromosome abnormality detected in the leukemic cells was trisomy 4. This was associated preferentially with ANLL of the M4 type (by FAB classification): acute myelomonocytic leukemia.

Acute Disease↗
PubMed1987

An acquired Robertsonian translocation in prolymphocytic leukemia: a case presentation and review.

Robertsonian translocations between the acrocentric autosomes are the most common type of constitutional chromosome rearrangement in humans. However, Robertsonian translocations are very rarely acquired in cancer cells. We report a patient with prolymphocytic leukemia and an acquired Robertsonian translocation in the leukemic cells. The translocation was between chromosomes #13 and #15; t(13;15)(q11;p12). Two other cases of malignancy with an acquired Robertsonian translocation have been found, one being of the t(13;15) type, which accounts for only 1% of constitutional Robertsonian translocations. We propose, therefore, that although Robertsonian translocations are occasionally observed in cancer cells, they are very rarely acquired.

Chromosomes, Human, Pair 13↗
PubMed1987

Chromosome changes connect immunodeficiency and cancer in ataxia-telangiectasia.

Ataxia-telangiectasia (AT) is a primary genetic immunodeficiency disease predisposing to cancer. Approximately 40% of patients with AT develop malignancy, usually of the lymphoid system. Increased chromosome breakage in AT leads to rearrangements such as translocations and inversions. The preferred chromosome breakpoints in AT involve genes in the immune system: the immunoglobulin (Ig) gene loci in chromosome bands 2p12, 14q32, and 22q11 and the T cell receptor (TCR) gene loci in chromosome bands 7p13, 7q35, and 14q11. Identical chromosome breakpoints are observed in chromosome rearrangements in normal T cells, Burkitt's lymphoma, and adult T cell leukemia. Molecular analysis of these chromosome rearrangements reveals recombination between an oncogene and Ig or between Ig and TCR. In AT, chromosome rearrangements connect the immune system to lymphoid cancer.

Adult↗
PubMed1987

Genetic history: II. The Cohens of London.

The genetic history in contemporary pedigree form is a useful tool for historical reading and study. The pedigree provides a guide to related personages and a data base for analysis. These points are illustrated by the family of Levi Barent Cohen, who came to London in the 18th century. There have been comparatively few consanguineous matings in the Cohen family. The family members have played central roles in Anglo-Jewish life in their own right and through marriage to other families such as the Montefiores and Rothschilds.

Female↗
PubMed1987

Gene for incontinentia pigmenti maps to band Xp11 with an (X;10) (p11;q22) translocation.

Incontinentia pigmenti (IP) is a genetic disease that is usually lethal in males. We report finding an X;10 translocation in a girl with IP. Three other X/autosome translocations have been observed in females with IP: two involving chromosome 9 and one involving chromosome 17. The breakpoint in all four cases in the X chromosome was in band Xp11. The IP gene locus can therefore be confidently assigned to the X chromosome and, specifically, to band Xp11. The IP gene is most likely to subband Xp11.2. We propose that IP may prove to be a submicroscopic deletion.

Abnormalities, Multiple↗