Biomedical subjects
Publications and source records attributed to S Fukuhara.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Chromosomes were studied in cells from 15 japanese patients with adult T-cell leukemia (ATL). Mitoses were obtained from unstimulated peripheral blood in 12 patients and a lymph node in one patient. In two other patients, mitotic cells were obtained solely from peripheral blood stimulated with phytohemagglutinin (PHA). Chromsomally abnormal cells were seen in 14 of the 15 patients. The abnormal cells had a modal number of chromosomes in near diploid range in 12 patients, and in near triploid and tetraploid range in the remaining 2 patients, respectively. Eight of the nine patients analyzed by Q-banding had clonal chromosome abnormalities. The most common abnormality was trisomy no.7 or 7q, which was seen in 5 cases and has been primarily observed in lymphoid neoplasms. A 14q+ marker chromosome was found in two patients and a Dq+ in one patient; loss of a sex chromosome was found in three patients. Most chromosomes were involved in gains, losses, or structural rearrangements, but abnormalities of no. 11, which have been frequently found in lymphoid malignancies, was not observed in our series. The significance of these chromosome abnormalities is discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In six patients with Epstein-Barr virus (EBV) induced infectious mononucleosis (IM) and in two patients with IM-like syndrome, peripheral blood lymphocytes in the acute and convalescent phase were tested for human la-like antigens as well as other cell surface markers. The major population of T lymphocytes in the acute phase showed la-like antigens, as detected by indirect immunofluorescence with heteroantisera, and the number of la-like antigen-positive T lymphocytes decreased with convalescence. The crossabsorption study indicated that the amount of la-like antigen on the surface of IM T cells was less than that of Raji cells.
Explore the source record for details and available documents.
In three patients with non-Hodgkin lymphomas and in one cell line (HPL-Hod) derived from pleural effusion cells of a patient with Hodgkin's disease, rearrangements of the long arm of chromosome No. 14(14q) were observed. These rearrangements appeared to be consistently associated with a 14q translocation, suggestive of occurrence of a break at 14q13. The translocation in an individual case could occur with 1p, 2q, 4q, and another 14q. A 14q13 translocation may be comparable with a 14q32 translocation, which has often been observed in various types of lymphoid malignancy.
Explore the source record for details and available documents.
Chromosome studies were performed on malignant cells obtained from 22 patients with non-Hodgkin lymphomas. A marker chromosome resulting from a translocation that affected the long arm of No. 14 (14q+) was the single most frequent abnormality and was noted in 14 of these patients. The frequency of the 14q+ marker chromosome varied with the type of lymphoma as defined by Rappaport. When the Lukes and Collins classification was used, the 14q+ marker was consistently associated with lymphomas having a clone of large noncleaved cells, small cleaved cells, and small noncleaved cells, but was absent in lymphomas composed of a clone of large cleaved cells and small lymphocytes. The findings suggest that, in certain groups of lymphoid malignancies, cells with a 14q translocation have a proliferative advantage compared with cells having other chromosome rearrangements, and that these malignant cells could be derived from a common progenitor.
Chromosome studies were performed on malignant cells obtained from 27 patients with non-Burkitt lymphomas. A marker chromosome affecting the long arm of No. 14 (14q+) was the single most frequent abnormality and was noted in 17 of these patients. The frequency of the 14q+ marker varied with the type of lymphoma. For patients with malignant lymphoma, histiocytic, the frequency was 5 of 8; for mixed-cell type, 1 of 3; for poorly differentiated lymphocytic, 8 of 8; for well-differentiated lymphocytic, 0 of 3; for lymphoblastic, 0 of 1; for Hodgkin's disease, 2 of 3; and for mycosis fungoides, 1 of 1. The donor chromosome involved in the 14q translocation was identified in 12 cases; certain chromosomes appeared to be affected more frequently than others. Although the break point was band 14q32 in most cases, the exact location of the receptor site on 14q was not always consistent. The distal part of 14q24 was also involved as a receptor site in at least one translocation. These findings suggest that, in some types of lymphoid malignancy, cells with a 14q translocation have a proliferative advantage over cells with other chromosome rearrangments. The presence of the 14q translocation may be important in the future for the distinction among morphologically different, but functionally comparable, subgroups of lymphoid malignancies.
Chromosomes from a patient with mycosis fungoides were examined in detail with banding techniques. Hyperdiploid cells from a lymph node had common anomalies of certain chromosomes which formed three similar clones. The abnormalities involved chromosomes No. 1, 2, 5, 8, 9, 10, 14, and 18, in addition to an unkwown small metacentric marker (M3). Although there were a number of mitotic cells in peripheral blood cultured both with and without PHA, none of the few cells with abnormal karyotypes was similar to the clonal cells of the lymph node. One of the abnormalities in the lymph node was a 14q rearrangement, which could be the result of a translocation of Nos. 8 and 14 involving a third chromosome, No. 2. An abnormality in the blood resulted from a translocation between the long arms of Nos. 1 and 14. These findings could be useful for studies in which mycosis fungoides is compared with the Sézary syndrome and other lymphoid malignancies.
Statistical analysis of 361 cases of primary leukemia induced in outbred Long-Evans and Sprague-Dawley rats by 7,12-dimethylbenz[a]anthracene (DMBA) and 7,8,12-trimethylbenz[a]anthracene (TMBA) showed that the incidence of trisomy of chromosome No. 2 was significantly lower with TMBA (17.8%) than with DMBA (29.3%). This tendency was reproducible in both sexes. Another characteristic chromosome abnormality, long No. 2, was found in 10 cases (2.8%). Quinacrine fluorescence analysis revealed that cells with No. 2 trisomy or either of two types of long No. 2 had total and partial No. 2 trisomy, respectively. Other chromosome members of cells with long No. 2, as well as the chromosomes of cells with typical No. 2 trisomy and "normal diploid" leukemia cells, revealed no band abnormality. The phenotype of No. 2 trisomy, severe anemia of the hosts reported in DMBA-induced leukemias, was also noted in leukemias with TMBA-induced No. 2 trisomy but not in leukemias with long No. 2.
Several noncognate tRNA's from Escherichia coli were mischarged with glutamine by E. coli glutaminyl-tRNA synthetase if dimethylsulfoxide was present in the reaction mixture. Kinetic analysis of the mischarging revealed that dimethyl sulfoxide stimulated the misacylation by affecting the maximum velocity. Several noncognate tRNA's were shown to interact with glutaminyl-tRNA synthetase as measured by their ability to protect the enzyme against thermal inactivation or to replace cognate tRNA in stimulating glutamine-dependent ATP-PPi exchange reaction. These tRNA's, however, did not coincide with those which were mischargeable with glutamine.
Chromosomes were studied in cells from tissues primarily involved by diffuse "histiocytic" lymphoma in nine patients. Two of the patients had stage II disease; their tumors were fibrotic and had no mitotic cells. One patient was in stage III, and the remaining six patients had stage IV disease. The modal chromosome number of abnormal cells from these last seven patients was hypodiploid in two, hyperdiploid in four, and near-triploid in one. Complete banding studies of six cases and partial analysis of the seventh indicate that (1) every patient had a distinct cell line with common markers, with a few cells showing minor variants; (2) although certain chromosomes (Nos. 1, 2, 3, 9, 12, and 14) were structurally affected more often than others, no markers with the same banding pattern were noted among them; and (3) the cytologic type of lymphoma could be correlated with the karyotype in all seven patients. When the Lukes and Collins classification was used, three patients whose tumors were composed predominantly of large noncleaved cells showed a 14q translocation leading to the formation of a 14q+ marker chromosome. This marker was not observed in four patients whose tumors had a majority of large cleaved cells. These preliminary results, if confirmed in a larger series of patients, will provide additional evidence that there are consistent chromosome changes associated with specific subtypes of lymphoproliferative disorders analogous to the Ph1 chromosome in chronic myelogenous leukemia.
Explore the source record for details and available documents.
We have previously reported on two patients with acute promyelocytic leukemia (APL) who had what appeared to be a deletion of chromosome No. 17. We now describe a third patient with APL. All three patients had a structural rearrangement involving No. 15 and No. 17. Our current interpretation of the chromosomal abnormality is that it is a reciprocal translocation, t (15;17) (q22; q21). Evidence that this is a consistent rearrangement associated with APL comes not only from our three patients, but also from two other published cases of APL, studied with banding, who also had an identical abnormality.
Explore the source record for details and available documents.