PubMed Health⌕ Search

Biomedical subjects

N Uike

Publications and source records attributed to N Uike.

70 records · Page 4Linked to original sources
PubMed1993

[A case of primary non-Hodgkin lymphoma of the adrenal gland presenting with Addison's disease].

A 69-year-old male was admitted to our hospital complaining of skin pigmentation. Masses in bilateral adrenal glands were noted on computed tomography. An exploratory laparotomy revealed malignant lymphoma confined to the bilateral adrenal glands. Histological diagnosis was diffuse mixed-cell type, B-cell lymphoma. Laboratory tests disclosed an elevated ACTH level and decreased urinary 17KS and 170HCS secretion. Based on hypofunction of adrenal glands and skin pigmentation, the patient was diagnosed as having Addison's disease. After complete remission with combination chemotherapy, adrenal function recovered normal and pigmentation disappeared, Addison's disease is an extremely rare complication of primary malignant lymphoma of the adrenal gland.

Addison Disease↗
PubMed1992

[i(17q) appearing in acute phase in Ph1-negative, BCR-negative CML].

A 36-year-old woman was referred to our hospital because of splenomegaly in February 1989. The leukocyte count was 55,500/microliter without hiatus leukemicus. The leukocyte alkaline phosphatase score was low (29). The bone marrow showed myeloid hyperplasia (24.8% myeloblasts) but no dysplastic change. The karyotype of the bone marrow cells was 46, XX and a diagnosis of Ph1 (-) CML was made. Treatment with VCR, 6MP and prednisolone made 7-month duration chronic phase, but the abnormal karyotype.[46, XX, i(17q)] gradually increased to 100% of bone marrow cells. The patient died in June 1990. The evidence that not only a BCR rearrangement but also messages of BCR/ABL fusion gene were negative made us able to differentiate this case from Ph1(-), BCR(+) CML. The addition of an i(17q) results in partial monosomy of 17q (17q13;p53 gene) and partial trisomy of 17q (17q11.2-12;G-CSF gene). We examined the rearrangement of p53 gene and G-CSF-dependent tumor cell growth in vitro, demonstrating one allelic loss of p53 gene and independent cell growth on G-CSF respectively. It is thought that in Ph1 (-), BCR (-) CML as well as in Ph1 (+) CML, an i(17q) is related to the progression but not to the initiation of these leukemias. However the precise mechanism, including p53 gene inactivation by point mutation, is still to be elucidated.

Adult↗
PubMed1991

Genotypic and cytogenetic study of acute myelocytic leukemia and chronic myelocytic leukemia in blast crisis: specific delta rearrangement pattern does not involve J delta gene locus.

We have analysed the configuration of immunoassociated genes and the karyotypes of 30 patients with acute myelocytic leukemia (AML) and 10 with chronic myelocytic leukemia in blast crisis (CML-BC). In AML, the frequencies of T-cell receptor (TcR) beta, gamma, and delta chain and immunoglobulin heavy and light chain gene rearrangements were 4.2%, 19%, 8%, 10.7% and 10.5%, respectively. In CML-BC, they were 10%, 20%, 40%, 50% and 0%, respectively. Nine patients had abnormalities in chromosome 2, 7 or 14, upon which immunoassociated genes are located. There seems to be no apparent relationship between these chromosome abnormalities and gene rearrangements. In all patients but one (5/6), the delta rearrangement was accompanied by other immunoassociated gene rearrangements. Molecular size analysis revealed specific delta rearranged band(s) (19.5 kb-BamHI and/or 6.9 kb-EcoRI), as commonly detected in B-acute lymphocytic leukemia (ALL). All the patients with the delta rearranged band, however, had a germline configuration of J delta gene loci, suggesting a DD or V(D)D (probably V delta 2(D)D) pattern. This study also indicates that the delta rearrangement is specific in AML or CML-BC and distinct from that in early T leukemia/lymphoma.

Blast Crisis↗
PubMed1991

Missing Y chromosome in Ph1-negative chronic myeloid leukemia with bcr rearrangement. Evidence for a bcr-abl recombination on chromosome 22 by in situ hybridization.

In a case of Philadelphia chromosome (Ph1)-negative chronic myeloid leukemia (CML) without the Y chromosome, we investigated the differences, at the molecular level, from Ph1-positive CML. Using Southern blot analysis and in situ hybridization studies, we could demonstrate a rearrangement within the breakpoint cluster region (bcr), and the location of a bcr-abl fusion gene on chromosome 22. To our knowledge, this is the first case of Ph1-negative CML with a loss of the Y chromosome in which the molecular abnormalities are shown to be identical with those in Ph1-positive CML.

Chromosome Aberrations↗
PubMed1991

Interleukin 4 suppresses the spontaneous growth of chronic myelomonocytic leukemia cells.

We studied the effects of IL-4 on the spontaneous proliferation of chronic myelomonocytic leukemia (CMMoL) cells in vitro. IL-4 (100 U/ml) suppressed the spontaneous DNA synthesis by approximately 50% in 5 of 8 cases examined. IL-4 (100 U/ml) also inhibited the spontaneous colony formation by CMMoL cells in a methylcellulose culture by 50-97% in all of the 10 cases in which spontaneous colonies were formed. This IL-4-mediated suppression of the growth of CMMoL cells was completely abolished by the addition of anti-IL-4 neutralizing antibodies. The spontaneous CMMoL colonies were substantially suppressed by the addition of either anti-IL-6 or anti-granulocyte/macrophage colony-stimulating factor (GM-CSF) antibodies to the colony assay system: the addition of both anti-IL-6 and anti-GM-CSF antibodies resulted in greater than 80% inhibition of the colony formation by CMMoL cells. On the other hand, none of anti-IL-1-beta, anti-granulocyte-CSF, anti-macrophage-CSF, or anti-tumor necrosis factor-alpha antibodies affected the CMMoL colony formation. In the supernatants from 24-h cultures of CMMoL cells, high levels of IL-6 and GM-CSF were demonstrated in 9 of 9 and 2 of 9 cases examined, respectively. IL-4 (100 U/ml) almost completely inhibited the secretion of IL-6 and GM-CSF by CMMoL cells. These observations suggest that IL-4 suppresses the spontaneous proliferation of CMMoL cells by inhibiting their production of IL-6 and/or GM-CSF, both of which could act in vitro as an autocrine growth factor for CMMoL cells.

Adult↗
PubMed1989

The possible mode of escape of adult T-cell leukaemia cells from antibody-dependent cellular cytotoxicity.

Antibody-dependent cellular cytotoxicity (ADCC) was measured using 51Cr-labelled ATL derived cell lines as the target, peripheral mononuclear cells (PMNCs) from disease-free persons as the effector cells and heat-inactivated serum from patients with ATL or the IgG purified from this. The release of 51Cr was not usually demonstrated in the HTLV-1 non-producing ATL derived cell line (MT-1), but was evident in the HTLV-1 producing ATL derived cell lines (KT 252 and IT 607). The 51Cr-labelled MT-1 cells after induction of HTLV-1 retrovirus by 5-iodo-2'-deoxyuridine (IdUr), showed a remarkable target sensitivity in the ADCC assay. On the other hand, the 51Cr-labelled MT-1 cells after culture with IdUr and ATL patient's serum, had no ADCC sensitivity. The fresh ATL cells immediately separated from ATL patient's blood did not express HTLV-1 virus in the cell and had no ADCC sensitivity as the target. Based on these findings, an antigenic modulation on the ATL cell surface by ATL patient's serum is considered to be the possible mode of escape of ATL cells from ADCC.

Adult↗
PubMed1989

Dual rearrangement of immunoglobulin and T-cell receptor genes in blast crisis of CML.

Dual rearrangement of immunoglobulin and T-cell antigen receptor (beta, delta) genes was demonstrated in a case of Philadelphia chromosome-positive chronic myeloid leukemia (CML) in blast crisis. The blast cells, showing L2 morphology and high activity of TdT, expressed pre-B cell (CD19+, Ia+) and myeloid (CD13+, CD34+) surface antigens but lacket T-cell antigens (CD2-, CD7-). Cytogenetic studies on bone marrow and peripheral blood revealed the Phl chromosome in all metaphases analyzed, majority of which also had the additional chromosome changes, +8, +10, +21. Furthermore, molecular analysis of the breakpoint cluster region (bcr) on chromosome 22 showed a rearrangement, confirming the CML origin of the blast cells.

Blast Crisis↗
PubMed1989

[Impaired superoxide production by neutrophils in myelodysplastic syndrome: correlation with bone marrow karyotype].

Superoxide (O2-) production by neutrophils was examined in 21 patients with myelodysplastic syndrome (MDS), including 13 with primary MDS (p-MDS) and 8 with therapy-related MDS (t-MDS). O2-production of MDS patients was significantly less than that of healthy controls (2.81 +/- 3.51 vs 6.19 +/- 2.41 nmol/min/10(6) PNMs, p less than 0.005). Although no relationship between pathogenesis (primary or therapy related), FAB type and levels of O2- production was observed, O2- production of 11 patients with abnormal bone marrow karyotypes was significantly reduced than that of 10 other patients with normal karyotypes. Furthermore, five t-MDS patients with monosomy for all or part of chromosome no. 7 (-7 or 7q-) showed the lowest level of O2- production, which was significantly different from the level in the patients with other abnormal karyotypes (0.61 +/- 0.29 vs 1.80 +/- 0.31, p less than 0.001). These results suggest that the long arm of chromosome no. 7 may in part play an important role for O2- production by neutrophils.

Adult↗
PubMed1986

[Clinical investigation of the therapeutic effects of cefmenoxime in the treatment of infections complicated by hematological diseases].

Therapeutic effects on cefmenoxime hemihydrochloride (CMX, Bestcall), a new synthetic cephem antibiotic, were examined in the treatment of various infections complicated with hematological diseases. The number of patients treated with CMX was 37 including 5 cases of sepsis or suspected sepsis, 14 cases of pneumonia or suspected pneumonia, 5 cases of upper respiratory diseases, 2 cases of urinary tract infections and 11 cases of other infections. All of these infections were complicated with hematological diseases: Acute leukemia, 13 cases; chronic myelocytic leukemia, 1 case; adult T cell leukemia, 3 cases; malignant lymphoma, 8 cases; Hodgkin's disease, 2 cases and myeloma, 3 cases. CMX were administered by a single intravenous injection or by a drip infusion. The dose was between 2 and 6 grams per day. Good to excellent clinical results were obtained in 25 out of 37 cases, total effective rate of 67.6%. No clinical side effects or abnormal laboratory findings attributable to CMX were observed except for light diarrhea in 2 cases. By the clinical investigation, it was demonstrated that CMX was one of safe and effective antibiotics for treating infections in the compromised hosts complicated with hematological diseases.

Acute Disease↗
PubMed1983

Case report of adult T-cell leukemia with preceding long-standing cutaneous involvement.

This report documents an unusual case of adult T-cell leukemia (ATL) with a preceding phase of long-standing cutaneous involvement. After nine months of an aleukemic phase, characteristic leukemic cells of ATL, possessing inducer/helper phenotype without helper function, had appeared. In addition, antibodies to ATL virus-associated antigen (ATLA) were found in the serum of the patient and her family. The patient died after an 18-month clinical course due to generalized cytomegalovirus infection in spite of strong chemotherapy. At autopsy, leukemic involvement was restricted to the skin. We postulate that ATL may originate not only from the lymph nodes but also from the skin.

Aged↗