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Biomedical subjects

F Hecht

Publications and source records attributed to F Hecht.

At least 163 records · Page 9Linked to original sources
PubMed1985

Translocation (1;7)(p11;p11): a new myeloproliferative hematologic entity.

Four cases with myeloproliferative syndromes or acute nonlymphocytic leukemia associated with t(1;7)(p11;p11) are presented. In each case, as in all cases published in the literature, the karyotypes of the affected cells contained two normal chromosomes #1, but only one chromosome #7, with the result that the basic karyotype was 46, -7, +t(1;7). This chromosome change is not geographically restricted, and appears to characterize a group of patients with myeloproliferative disorders and acute nonlymphocytic leukemia, including myeloproliferative syndromes, in whom exposure to previous chemotherapy, x-rays, or drugs is in the background history. The t(1;7) in secondary leukemia and myeloproliferative syndromes serves to duplicate the long arm of a chromosome #1 and to rescue the short arm of a chromosome #7.

Acute Disease↗
PubMed1985

Deletion of chromosome band 13q14: a primary event in preleukemia and leukemia.

Chromosome abnormalities were analyzed in 200 consecutive patients with preleukemia and leukemia, and four patients were found with a deletion of 13q14 for an incidence of 2%. Together with data on chromosome aberrations in cancer from the literature, our results indicate clearly that deletion of band 13q14 is a nonrandom chromosome anomaly in premalignant and malignant blood disorders. Deletion of 13q14 appears specifically to constitute a primary event in the initiation of preleukemia. An additional rearrangement involving another chromosome must occur for progression of the preleukemia to acute nonlymphocytic leukemia.

Acute Disease↗
PubMed1985

Unexpected lambda chain expression in lymphocytic malignancy.

Specific chromosome changes occur in the initiation and progression of cancer. A translocation between chromosomes 14 and 18 arises as a primary cytogenetic event in the formation of non-Hodgkin, non-Burkitt lymphomas (BL), while a translocation between chromosomes 2 and 8 is seen in BL and BL-type acute lymphocytic leukemia (ALL-L3) with expression of kappa (kappa) light immunoglobulin chains. These two translocations were detected in a lymphocytic malignancy expressing not kappa, but lambda (lambda) light chains. The anomalous light chain expression, it appears, provides the key clue indicating that the translocation between chromosomes 14 and 18 arose first during lymphoma formation in a cell committed to lambda chain synthesis and the translocation between chromosomes 2 and 8 occurred in the transformation to ALL. This sequence of cytogenetic events is consistent with the clinical course from lymphocytic lymphoma to ALL, the immunologic phenotype of the malignancy, and the concept of a cascade of chromosome changes eventuating in aggressive cancer.

Breast Neoplasms↗
PubMed1985

Leukemia with Down's syndrome: translocation between chromosomes 1 and 19 in acute myelomonocytic leukemia following transient congenital myeloproliferative syndrome.

A girl with Down's syndrome was born with a myeloproliferative disorder. The child had spontaneous regression of the myeloproliferation, with acute leukemia developing at a later date. Morphologic, cytochemical, immunologic, and immunoglobulin gene configuration studies all supported the diagnosis of acute nonlymphocytic leukemia. High-resolution chromosome studies revealed that the leukemic cells consistently contained a translocation between chromosomes 1 and 19: der(19)t(1;19)(q25;p13). Spontaneous regression of the transient myeloproliferative syndrome of the newborn with Down's syndrome may not always be permanent, and the transient myeloproliferative syndrome may sometimes represent an early sign of acute nonlymphocytic leukemia.

Antibodies, Monoclonal↗
PubMed1985

Ataxia-telangiectasia breakpoints in chromosome rearrangements reflect genes important to T and B lymphocytes.

The AT cell fails to pause sufficiently after X-ray or similar radiomimetic insults to repair damage. Rather, it launches with undue speed into DNA replication. It may incorporate errors into DNA that lead to the chromatid and chromosome breaks. Breakpoints have been noted at 7p13, 7q33-35, 14q11-12, and 14q32. The regions at 7q33-35, and 14q11-12 are specific to T cells and include T cell receptor genes. The region at 14q11-12 is involved in T-cell malignancies. The region at 14q32 contains immunoglobulin heavy-chain genes and is involved in B-cell malignancies.

Ataxia Telangiectasia↗
PubMed1984

Common region on chromosome 14 in T-cell leukemia and lymphoma.

Chromosome 14 breakpoints in malignant human lymphocytes cluster on the long (q) arm near bands q11 and q32. An inversion of chromosome 14 due to breaks in q11.2 and q32.3 has now been found in a newly established childhood T-cell lymphoma cell line and confirmed in T-cell chronic lymphocytic leukemia. A translocation was also found between chromosomes 10 and 14 with a breakpoint at 14q11.2 in another T-cell lymphoma cell line. It is proposed that a proximal region on chromosome 14 in or near sub-band q11.2 is related to T-cell function. Rearrangements in this region may affect the growth of T lymphocytes and be involved in the development of T-cell malignancies.

Cell Line↗
PubMed1984

Chromosome analysis in hematologic disorders. The leukemias.

For two decades, cytogenetic studies have been used to rule in (or out) the Philadelphia (Ph1) chromosome associated with chronic myeloid leukemia. Beyond this single purpose, chromosome studies have generally not been utilized in or applied to the practice of hematology-oncology. This report presents male and female patients, teens to 70s in age, with representative hematologic disorders, in whom the cytogenetic findings were useful clinically. These cases illustrate the following principles: (1) hematologic disorders can be characterized by chromosome analysis; (2) chromosome findings help in the diagnosis, prognosis, and treatment of blood diseases; (3) blood and bone marrow samples can be processed routinely for cytogenetic analysis; (4) these samples can be transported long distances from clinic to laboratory; and (5) the contemporary practice of hematology and oncology requires chromosome analysis for fuller evaluation and understanding of hematologic conditions.

Adult↗
PubMed1984

Cis-trans position effect in cancer translocations.

Translocations of chromosomes occurring in human cancer cells appear specific to the type of cell from which the cancer arises. To explain the action of these translocations, we propose dual position effect: Position effect of the cis type transforms the cell to malignancy, while position effect of the trans type permits the normal homologous chromosome to express a normal gene product. Thus, the translocation itself has to do with malignant transformation, while the normal homologous chromosome performs its normal function. This dual concept is illustrated by t(8;14) in Burkitt's lymphoma. The concept can be tested with t(2;18) and t(8;22) in lymphoid malignancies and with other translocations and chromosome rearrangements marking human cancer cells.

Ataxia Telangiectasia↗
PubMed1984

Cancer chromosome breakpoints and common fragile sites induced by aphidicolin.

A new class of fragile sites termed common fragile sites is induced by aphidicolin, an inhibitor of DNA polymerase alpha. Analysis of these common fragile sites and cancer chromosome breakpoints indicates that eight fragile sites are in bands with cancer breakpoints. This is unlikely to be due to chance (p less than 0.01). Common fragile sites are in both bands where breaks occur in carcinoma of the lung and in carcinoma of the ovary. Common fragile sites are in bands with breaks leading to constitutional chromosome abnormalities associated with cancer: hereditary renal cell carcinoma and aniridia-Wilms' tumor complex. Common fragile sites, thus, may predispose to chromosome breaks and rearrangements in cancer.

Aphidicolin↗
PubMed1984

Direct prenatal chromosome diagnosis of a malignancy.

A fetal tumor was suspected at 31 weeks of gestation. The occurrence of polyhydramnios led to an ultrasound examination, which revealed deformation of the fetal head, face, eye, and neck. This was confirmed by computerized tomography. Amniocentesis yielded cells with an inverted duplication of chromosome #1. This abnormality of chromosome #1 marked the malignant teratoma cells in the amniotic fluid. Cytogenetic analysis of tumor tissue and of normal tissue obtained postnatally confirmed that the abnormality of chromosome #1 observed in amniotic fluid cells was confined to the tumor. The constitutional karyotype was normal. To our knowledge, this is the first report of the direct chromosomal detection of malignancy before birth.

Adult↗
PubMed1984

Fragile sites and cancer breakpoints.

To determine whether there might be a statistically significant association between fragile sites and cancer breakpoints, we examined the locations of the 21 fragile sites and the 50 cancer breakpoints recently accepted by the Seventh Human Gene Mapping Workshop. Nine of the 21 fragile sites appeared to be located at or near a cancer breakpoint. The chi-square test for association gives a value of 15.8 (p less than 0.001) indicating that there is a very highly significant statistical association between human fragile sites and cancer breakpoints. This association is not narrowly limited to one class of fragile site, such as those sensitive to folate or to one type of cancer, but appears to extend to leukemia, lymphoma, and solid cancer. To more fully understand the meaning of this intriguing association between fragile sites and cancer breakpoints, future research will need to locate additional fragile sites and cancer breakpoints with precision, record their concurrence in individuals and families, determine if fragile site families are predisposed to cancer, and prove that a fragile site and a cancer breakpoint that appear to be coincident are at the same point on the DNA level.

Chromosome Fragile Sites↗