Search PubMed⌕ Search

Biomedical subjects

B K Hecht

Publications and source records attributed to B K Hecht.

At least 73 records · Page 4Linked to original sources
PubMed1986

Chromosome clues to acute leukemia in Down's syndrome.

Surprisingly few cases of Down's syndrome with acute leukemia have been documented by chromosome banding studies of the leukemia cells. We studied a Down's syndrome child with acute myelomonocytic leukemia and found that, including this case, only 24 cases of Down's syndrome and acute leukemia have been reported with chromosome banding analysis. Twenty-three of the patients had a trisomy 21 chromosome complement, whereas, one had a translocation. The types of acute leukemia included acute myeloblastic leukemia, acute myelomonocytic leukemia, acute monoblastic leukemia, acute lymphoblastic leukemia, and erythroleukemia. Only three cases had chromosomes missing from the leukemic cells. Sixteen of the 24 patients had extra chromosomes in their malignant cells. Chromosomes #8 and #21 were extra in six cases each and chromosomes #19 and #22 were extra in four cases each. Chromosome rearrangements were observed in nine cases. Three of the nine cases had partial deletion of the long arm of chromosome #6. Cases of Down's syndrome with acute leukemia need to be reported with high-resolution chromosome banding of the leukemia cells. There is as yet no clear chromosome clue as to the precise basis of the etiologic association between Down's syndrome and acute leukemia.

Acute Disease↗
PubMed1986

The Philadelphia chromosome: a model of cancer and molecular cytogenetics.

Recent developments in molecular biology related to the Ph chromosome lead us to an evaluation of knowledge regarding this chromosome. The molecular advances are related to two cellular oncogenes, c-abl and c-sis, and also to the identification and molecular cloning of specific areas of DNA (e.g., band 22q11), permitting the isolation of a probe specific for the translocation breakpoint domain. In the preponderant number of cases examined, it was found that the breakpoints at 22q11 occur within a limited region of up to 5-6 kb, for which the term "breakpoint cluster region" (bcr) has been suggested. In contrast, breaks at 9q34 seem to occur within a much larger region at the molecular level. Yet to be established is the exact genetic composition of the bcr and a determination as to whether or not the breaks leading to the disease occur preferentially within specific areas. In spite of this level of knowledge, we do not understand how the Ph chromosome participates in CML. If Ph-positive CML is ultimately associated with a cascade of gene activations, the unraveling of their nature and chronology will undoubtedly tell us much of their contribution to the biology of CML, in particular, and to neoplasia, in general. In this respect, the rather clear description of CML in cytogenetic, clinical, and laboratory terms, the relatively long chronic phase of the disease, and the association of the blastic phase with nonrandom chromosome changes (at least in the initial phases of the disease) make Ph-positive CML an excellent candidate for a model for the study of molecular events in human neoplasia.

Chromosome Banding↗
PubMed1986

Telomeric fusion in pre-T-cell acute lymphoblastic leukemia.

Telomeric fusion, a rare phenomenon, was observed in malignant cells from the peripheral blood of an 18-year-old male with rapidly progressive pre-T-cell acute lymphoblastic leukemia (ALL). Only two comparable cases, both with B-cell ALL, have been reported with telomeric fusion in neoplasia. All of the leukemic cells examined from our patient had two chromosome abnormalities consisting of partial triplication (trp) of chromosome 2 and a derivative chromosome 3. Approximately a third of the leukemic cells showed in addition telomere-telomere fusions. These involved the telomeric regions of 1p, 2p, 4q, 5q, 7q, 10q, 11q, 12p, 15p, 21p, and Xq and 3p of the derivative (3). The findings in this case suggest that telomeric fusion may function as a mechanism for the development of chromosome rearrangements that may play a role, albeit rarely, in human neoplasia.

Adolescent↗
PubMed1986

Chromosomes in kidney, ureter, and bladder cancer.

Although Wilms tumor has been a favored subject for cytogenetic investigation, little is known about chromosomes in adult urinary tract cancers. For this reason, we excluded Wilms' tumor and studied a series of 32 adult urinary tract tumors. Nineteen tumors had detectable autosomal abnormalities. Each of ten renal tumors (consisting of eight renal cell and two transitional cell carcinomas) had three or more chromosome abnormalities. Two candidates for primary chromosome changes in renal cancer are rearrangement of 3p14 and an unbalanced translocation with breakpoints of 5q13 and 14q22. Trisomy 20 is a frequent secondary change. Other nonrandom changes in renal cancer are rearrangements of 1q and +7, -8, -9, -14, -15, +16, and deletions of 17p. Eight bladder and a ureter tumor were all transitional cell carcinomas. Two bladder and the ureter tumor had only one detectable abnormality: deletions of 10q24 and 21q22 and +7, respectively. Other nonrandom bladder changes were -9, +13, +15, and +20. From a cytogenetic standpoint, adult urinary tract tumors appear to be chromosomally complex but critical consistencies are emerging.

Adult↗
PubMed1985

Use of novel chemical supplements in the establishment of three human malignant lymphoma cell lines (NU-DHL-1, NU-DUL-1, and NU-AMB-1) with chromosome 14 translocations.

Three new cell lines have been established from patients with malignant lymphoma utilizing a human diploid feeder layer, pooled human serum, and the chemical supplements L-cysteine, iron-saturated transferrin, and bathocuproine disulfonate, a copper chelator. After a short period of growth, the 3 cell lines were successfully weaned from the feeder layers but continued to require human serum and the chemical supplements for up to 9 months of culture. The cell lines are currently grown in RPM1-1640 medium and fetal calf serum without further supplementation. The NU-DHL-1 cell line was established from the involved lymph node of a 73-year-old White male with diffuse large-cell lymphoma. The cell line expresses cytoplasmic IgM/lambda heavy and light chains, is Epstein-Barr virus (EBV)-negative, and is positive for several B-cell markers, indicating that it is derived from a mature-B-cell neoplasm. The NU-DUL-1 cell line was established from the cerebrospinal fluid of a 42-year-old White male with undifferentiated lymphoma, non-Burkitt's type, who initially presented with a mediastinal mass and had subsequent involvement of the central nervous system. The cell line is EBV-negative, but surprisingly it is positive for early B-cell markers. The NU-AmB-1 cell line was established from the abdominal mass of a 12-year-old Hispanic male with undifferentiated lymphoma, Burkitt's type. The cell line is EBV-positive and expresses early B-cell markers. All 3 cell lines are aneuploid or pseudodiploid and contain chromosome 14q+ abnormalities including a newly described complex translocation t(?;1;8;14) in the NU-AmB-1 cell line. The establishment of these cell lines was made possible by refinements in the cell culture of the human malignant lymphomas. The availability of well-characterized lymphoma cell lines with specific chromosomal translocations will aid molecular and cellular studies designed to identify the biological significance of genomic rearrangements.

Cell Line↗
PubMed1985

Histiocytic lymphoma cell lines: immunologic and cytogenetic studies.

Cell lines were established from 15 patients with diffuse histiocytic lymphoma (DHL) of the intermediate grade, diffuse large cell (class G), and high-grade, large cell immunoblastic (class H) types. Immunologic studies indicated that 11 of the 15 DHL cell lines were B cell in origin, 2 were histiocytic, and 2 were null cell. Cytogenetic studies revealed 1 hypodiploid, 11 hyperdiploid, and 3 near-tetraploid cell lines. Chromosome #7 was trisomic in 3 lines, chromosomes #12 in 4 lines, and chromosome #13 in 3 lines. Chromosome #2 was monosomic in 3 lines, chromosome #8 was monosomic in 5 lines, chromosome #14 in 4 lines, and chromosome #22 in 6 cell lines. This is of special interest, as chromosomes #2, #8, #14, and #22 are clearly concerned with rearrangements in Burkitt's lymphoma and immunoglobulin expression. The most common rearrangement in the DHL cell lines involved chromosome #14 at band 14q32. However, in contrast to Burkitt's lymphoma, the pattern of translocation in DHL is between chromosome #14 and usually chromosome #11 or chromosome #18. The 14;18 translocation is not restricted to patients with low-grade follicular, small cleaved cell lymphomas, as has been reported. The 14q+ chromosome is characteristic of lymphoid malignancies in general. It is due, invariably, to a translocation with the breakpoint in band 14q32, which is the locus of the immunoglobulin heavy chain genes. We propose that in each translocation, for example, chromosomes #11 or #18, an oncogene may be transposed onto chromosome #14, and that each 14q+ translocation in DHL represents an event that transposes an oncogene from another chromosome to chromosome #14.

Cell Line↗
PubMed1985

The Philadelphia (Ph) chromosome in leukemia. II. Variant Ph translocations in acute lymphoblastic leukemia.

Nearly 20 patients with a masked Philadelphia (Ph) translocation have been described in chronic myelocytic leukemia. We report two instances of acute lymphoblastic leukemia (ALL) with variant Ph translocations. One case, involving a 26-year-old male, was associated with a variant t(14;22)(q32;q11) translocation. The second case involved a 36-year-old male with a more complex translocation, t(9;15;22)(q12;q26;q11). In each case, cells with a masked Ph translocation were observed. These appear to be the first ALL cases reported with a masked Ph chromosome. The findings are discussed in relation to recent knowledge regarding the genesis of the Ph chromosome.

Adult↗
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

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

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↗