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Biomedical subjects

K Minato

Publications and source records attributed to K Minato.

At least 145 records · Page 8Linked to original sources
PubMed1984

[Screening test of antitumor agents by human tumor cell lines in nude mice in ascitic form].

Two kinds of, serially transplantable human tumor cell lines were established in nude mice in ascitic form. One is breast cancer cell line, poorly differentiated adenocarcinoma, Hattori strain, and the other is acute lymphocytic leukemia cell line, T-cell type, Ichikawa strain. There exists a distinct correlation between the survival time of nude mice and the number of tumor cells transplanted. Clinically established antitumor agents which showed over 200% increase in life span were MMC, ADM and 5FU in Hattori strain, and VCR, VLB, VDS, ADM and BH-AC in Ichikawa strain. These results were considered to be consistent with the clinical effect of these drugs in breast cancer or in acute lymphocytic leukemia. Both strains can serve as the reliable screening system of antitumor agents.

Adenocarcinoma↗
PubMed1984

A novel human myelomonocytoid cell line, P39/Tsugane, derived from overt leukemia following myelodysplastic syndrome.

A novel human cultured cell line, P39/Tsugane, was established from leukemic cells in the peripheral blood of a 69-year-old male with overt leukemia following myelodysplastic syndrome (MDS). P39/Tsugane cells were characterized by blastic appearance, presence of NaF-sensitive alpha-naphthyl butylate esterase activity, Fc gamma-receptor, C3-receptor, capacity to phagocytize sensitized erythrocytes, and reactivity with monoclonal antibodies such as OKT4, My4, VIMD5, MCS-2 and My7. These data indicate that P39/Tsugane cells are of myelomonocytoid nature. P39/Tsugane had a hypodiploid chromosome constitution with a gain of a consistent marker, 6q+, the presence of less consistent markers 9q+ and rcp(14;16), and random and non-random losses of autosomes: in accordance with the reported cytogenetic profiles of MDS, a representative karyotype of the present cell line is 45,XY,+del(6)(q15),9q+, t(14;16)-(q24;q21),-16,-17. P39/Tsugane cells were transplantable intraperitoneally into nude mice, and produced abdominal tumors and hemorrhagic ascites. These results indicate that P39/Tsugane is the first cultured cell line of myelomonocytoid nature to be derived from overt leukemia following MDS. Therefore, P39/Tsugane cells should be useful for studies on the differentiation of leukemia cells, the pathogenesis of MDS and in vitro-in vivo experimental chemotherapy.

Aged↗
PubMed1983

Variation of serum prolactin-releasing activity in women with the galactorrhea-amenorrhea syndrome after bromocriptine treatment.

Serum methanol extracts were obtained from nine women with the galactorrhea-amenorrhea syndrome, 24 pregnant women in the third trimester, and 18 normal men and women. The serum extract released prolactin (PRL) in significant amounts from rat anterior pituitary in vitro. The extracts from patients with galactorrhea-amenorrhea released PRL in large quantities. A significant positive correlation was observed between the PRL-releasing activity and serum PRL levels in individual samples from the pregnant women and normal subjects but not from the patients with galactorrhea-amenorrhea. Bromocriptine therapy suppressed serum PRL levels of five patients without tumors but increased the PRL-releasing activity in three out of five patients after treatment for 1 or 2 months. Apparently hypothalamic regulation of PRL secretion was disrupted in these three patients after bromocriptine therapy.

Adult↗
PubMed1983

Non-Hodgkin's lymphoma phenotyping: problems in the use of heterologous and monoclonal antibodies.

Cell suspensions or frozen sections of lymph node biopsies from 32 patients with non-Hodgkin's lymphoma (NHL) were studied for sheep erythrocyte (E)-binding under three conditions (Estandard, EAET, Egravity), Fc and C receptors, immunoglobulin (Ig) heavy and light chain class and reactivity with heterologous antisera to T cells (T-LCL), HLA-D (Ia-like) and common acute lymphocytic leukemia (c-ALL) antigens. Selected B and T cell lymphomas were also tested for reactivity with the monoclonal antibodies OKT 3, OKT 4, OKT 6, OKT 8, OKT 11A, Leu-1, Leu-2a, Leu-3a, Leu-4 and Leu-7. There were 26 B and 6 T lymphomas. Most B lymphomas were mu+ (81%), kappa+ (77%) and 31% were mu+ delta+. One of the T lymphomas arose in a patient with antecedent follicular small-cleaved (B) cell lymphoma. The most accurate marker for characterizing the immunologic phenotype in NHL was the clonal excess of kappa+ or lambda+ cells. Neither Estandard, EAET, Egravity or T-LCL were consistently reliable as sole reagents in identifying T-cell lymphomas, their individual scores often being lower than those of monoclonal pan-T cell reagents. HLA-D (Ia-like) antigen was noted in 89% of B and 50% of T lymphomas. The corresponding values for c-ALL antigen were 12 and 33%, respectively. The comparative scores in T-lymphomas between OKT 4 and Leu-3a for "helper-inducer" (HE) cells and OKT 8 and Leu-2a for "suppressor-cytotoxic" (SU) cells were not uniformly consistent. Four T lymphomas had a mixed HE/SU cell phenotype, one was HE, and another SU. Anti-T reactivity was detected in the neoplastic follicles of six of seven follicular lymphomas. The percentage of anti-T reactive cells within positive neoplastic follicles was usually small (5-15%) and of the same order as that noted within reactive lymphoid follicles (5-30%). High numbers (50-100%) of cells from five small lymphocytic B, three diffuse small cleaved cell B and six T cell lymphomas were also positive with one or more anti-T reagents, suggesting the presence of cross-reactive antigens that make phenotyping of lymphomas with monoclonal antibodies problematic. Reactivity with the monoclonal antibody Leu-7 (HNK-1), a putative NK-specific reagent, was seen in one of five B and three of five T lymphomas.

Antibodies, Monoclonal↗
PubMed1983

Establishment and characterization of 10 cell lines derived from patients with adult T-cell leukemia.

By using human T-cell growth factor (TCGF), 10 cell lines were established from tissue samples of 10 patients with adult T-cell leukemia (ATL). Three cell lines were adapted to growth in medium lacking TCGF. The surface markers of all cell lines were characteristic of inducer/helper T cells, i.e., OKT3+, OKT4+, OKT6-, OKT8-, OKIa1+, and human Lyt2+ and Lyt3+, except that one cell line was OKT3-. The expression of the viral antigen was examined during establishment of 8 of the 10 cell lines. The viral antigen was not expressed in leukemic cells before cultivation. In 5 lines, the viral antigen was detected by immunofluorescent staining after a short period of cultivation. However, 3 cell lines, ATL-6A, ATL-9Y, and ATL-1K did not express the viral antigen during short-term culture: the ATL-6A and ATL-9Y cell lines became positive for the viral antigen after 5 and 2 months of cultivation, respectively; the ATL-1K cell line remained antigen-negative throughout a culture period of 13 months. Southern blot hybridization assay showed that all of the cell lines, including the viral antigen-negative ATL-1K cell line, contained the viral genome. Thus, the retrovirus was associated with all 10 cell lines established from ATL patients, but there was a heterogeneity in the expression time of the retroviral antigen in leukemic cells maintained in vitro. Our findings suggested that the expression of the viral antigen was not required for maintenance of the leukemic state in vivo and for growth of leukemic cells in vitro.

Antigens, Surface↗
PubMed1983

Evidence for prolactin-releasing and release-inhibiting effects of melatonin, serotonin and arginine vasotocin.

Adult female Wistar rats (in 12 hr light/12 hr dark) were pinealectomized (PX) or sham-operated (SO) either 21 days after ovariectomy or on the 15-17th day of pregnancy. Ovariectomized (OVX) rats were injected with estrogen and progesterone (EP) 48 hr before decapitation. Melatonin, serotonin or arginine vasotocin (AVT; 50, 100 or 200 micrograms) were administered intravenously into OVX-EP rats 9 days after pineal removal. In PX and SO groups, the same study was done 3 days after delivery. Sera and pituitaries were collected 30 min after injection in order to determine prolactin (PRL) levels. Fifty micrograms melatonin significantly suppressed serum PRL levels in PX-OVX-EP rats and PX postpartum rats, but had not significant effect in SO-OVX-EP or PX postpartum rats. After administration of AVT, serum PRL levels markedly rose in PX and SO rats. These results suggest that melatonin may act not only to stimulate but also to inhibit rat PRL secretion and that the stimulatory function would be superior to its inhibitory function when the pineal gland is intact.

Animals↗
PubMed1983

Monoclonal antibody studies in B(non-T)-cell malignancies.

Tumor cells suspensions prepared from 129 B- or non-T cell malignancies were investigated with a panel of 10 monoclonal antibodies and conventional surface marker techniques. Surface immunoglobulin (sIg) and B1 antigen proved to be the most useful markers for B-cell lineage. Six major subtypes of acute lymphoblastic leukemia (ALL) of non-T cell nature are now recognized by these immunological techniques, including null-ALL, Ia-ALL, lymphoid stem cell ALL, pre-pre-B ALL, pre-B ALL and B-ALL. In cases of chronic leukemias and lymphomas of non-T cell nature, 80% of the tumor was defined by sIg and 88% by B1 antigen as definitely of B-cell lineage. The clonal character was also defined in 68% of the tumor on the basis of the detection of predominant single light chain in sIg. Ia-like antigen was detected in almost all cases (96%). Leukemic cells from all cases of chronic lymphocytic leukemia (CLL), chronic lymphosarcoma cell leukemia (CLsCL) and hairy cell leukemia (HCL) reacted with OKIa1 and anti-B1, and leukemic cells from most of them with anti-pan T monoclonal antibody (10.2). In more than half of CLL and CLsCL, leukemic cells were reactive with J5, OKM1, 9.6 and OKT8, but not with OKT3, OKT4 and OKT6. HCL cells had almost the same reactivity with these monoclonal antibodies as CLL and CLsCL cells except that J5 remained unreactive. These results indicated that Japanese CLL, CLsCL and HCL were different from Western ones at least with respect to surface marker characteristics. In cases of lymphomas, heavy chains of sIg were expressed in polyclonal fashion, especially in follicular lymphoma and diffuse lymphomas of medium sized cell type and large cell type, indicating that lymphomas of these types may originate from follicular center cells of the heavy chain switching stage. Anti-T monoclonals were also reactive with lymphoma cells. In about half of follicular lymphomas and diffuse lymphomas of the medium sized cell type, lymphoma cells reacted with 10.2, and less frequently with 9.6, OKT4 and OKT3. On the other hand, only in one or two cases of diffuse lymphoma of the large cell type and of immunoblastic sarcoma (IBS), did tumor cells react with 10.2 and 9.6, but this was exceptional. In more than 25% of IBS, tumor cells also reacted with OKT8, but not with OKT4 and OKT3. These results indicated that anti-T monoclonals are no longer specific for T-cell lineage.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1983

Two novel cultured cell lines, A3/Kawakami and A4/Fukuda, derived from malignant lymphoma of B(non-T)-cell nature of the gastrointestinal tract.

A3/Kawakami was derived from ascitic lymphoma cells of a 68-year-old female patient with malignant lymphoma (non-Hodgkin's lymphoma, diffuse, large cell type) of the stomach and A4/Fukuda was derived from ascitic lymphoma cells of a 52-year-old female patient with double cancer of the colon (well-differentiated papillary adenocarcinoma and non-Hodgkin's lymphoma, diffuse, large cell type). The fresh ascitic lymphoma cells in the case of A3/Kawakami were surface immunoglobulin-positive, but the cultured A3/Kawakami cells no longer expressed any distinct markers. In the case of A4/Fukuda, the fresh ascitic lymphoma cells and cultured cells did not express any specific surface markers. Only 20% of A4/Fukuda cells were reactive with OKI1. However, a small amount of IgM could be detected in the cell extract and concentrated culture supernate of A4/Fukuda. In addition, A4/Fukuda cells heterotransplanted into anti-thymocyte sera-treated newborn hamster or athymic nude mice with a BALB/c genetic background were found to have weak surface immunoglobulin and distinct cytoplasmic immunoglobulin (gamma, mu). These data suggest that A4/Fukuda cells share the characteristics of the late differentiation stage of B-cell lineage (intermediate between mature B-cells and plasma cells). It was found that monoclonal antibodies, OKT4 and anti-Leu 3a, which are known to react specifically with inducer/helper T-cells, reacted to both A3/Kawakami and A4/Fukuda cells. The karyotypes of both A3/Kawakami and A4/Fukuda cells were very complicated but included some marker chromosomes such as 14q+.

Aged↗
PubMed1983

Atypical adult T-cell leukemia-lymphoma: diverse clinical manifestations of adult T-cell leukemia-lymphoma.

The diverse clinical manifestations of 10 cases of so-called adult T-cell leukemia-lymphoma (ATL)-related T-cell malignancies are described. These cases were anti-ATLA [antibody to ATL virus (ATLV)-associated antigen (ATLA)] positive, and tumor cells had the inducer/helper T-cell phenotype and expressed ATLA when cultured, indicating that these diseases are the same as typical ATL, even though their clinical diagnoses were different from ATL. Accordingly, they are called atypical ATL. Clinically, they could be divided into two subtypes, smoldering type and lymphoma type. In the smoldering type, the disease usually started with skin lesions and rarely with lung lesions. After a prodromal stage of several years, the disease progressed insidiously to the leukemic stage without additional manifestations. The flower cells characteristic of typical ATL were observed in only a small percentage of peripheral lymphoid cells. In two of the five patients the disease progressed to typical ATL after several years from onset. All five patients are alive with a long survival time, more than 6 yr in four, and had high titers of anti-ATLA, suggesting that anti-ATLA might have some role in regulating the proliferation of ATL cells in vivo. In the lymphoma type, morphological diagnosis was not always specific for discriminating ATL-related from ATL-unrelated T-cell lymphomas. Detection of anti-ATLA in the patient's serum and of ATLA in cultured tumor cells, examination of the sera of members of the patient's family for anti-ATLA, and observation of typical flower cells in the peripheral blood though the patients had neither lymphocytosis nor leukemic changes, seem to be useful for the discrimination, especially in an ATL-nonendemic area. Members of the family of a patient with anti-ATLA positive T-lymphoma in an ATL-nonendemic area were also anti-ATLA positive, indicating that healthy ATLV carriers in an ATL-nonendemic area exist as a family colony. This is responsible for sporadic outbreaks of ATL in an ATL-nonendemic area. In summary, the disease entity of ATL is considered, at present, to be a malignancy of inducer/helper T-cells transformed by ATLV or HTLV (human T-cell leukemia virus). In this sense, diverse clinical manifestations of ATL should be recognized as events of viral oncogenesis and host immune response.

Adult↗
PubMed1983

Anti-ATLA (antibody to adult T-cell leukemia virus-associated antigen), highly positive in OKT4-positive mature T-cell malignancies.

Serum or plasma specimens from 252 patients with lymphoid malignancies were screened for reactivity with adult T-cell leukemia virus-associated antigen (ATLA), and the relationship between the immunologic phenotype of the tumor cells and ATLA reactivity was determined. Anti-ATLA antibodies were found in 24 (29.3%) of 82 patients with T-cell malignancy. In contrast, the antibodies were found in none of the 106 patients with B-cell malignancy and only rarely in patients with other lymphoid malignancies without blood transfusions. Among the patients with T-cell malignancy, anti-ATLA antibodies were found in 23 (45.1%) of the 51 patients with OKT4-positive mature T-cell (inducer/helper T-cell) malignancy, but in none of the patients with T-cell malignancy of pre-T, thymic T-cell or OKT8-positive mature T-cell (suppressor/cytotoxic T-cell) phenotype. Furthermore, among the OKT4-positive mature T-cell malignancies, the antibodies were found in 16 (84.2%) of 19 patients with ATL and in 5 (27.8%) of 18 patients with mature (peripheral) T-cell lymphoma, in none of four with typical T-chronic lymphocytic leukemia, in one of nine with mycosis fungoides and in the one patient with small-cell variant of Sézary's syndrome. These results suggest that anti-ATLA positive T-cell malignancies with OKT4-positive mature T-cell phenotype must be the same disease, because it is highly possible that they have the same etiology and the same cellular origin. In the atypical cases, it seems necessary to demonstrate monoclonal integration of proviral DNA of ATLV or HTLV into the tumor cells in order to establish the final diagnosis of ATL.

Antibodies, Viral↗
PubMed1983

Anti-ATLA (antibody to adult T-cell leukemia-lymphoma virus-associated antigen)-negative adult T-cell leukemia-lymphoma.

Five cases of adult T-cell leukemia-lymphoma (ATL) having typical clinicohematologic and morphologic features but negative for anti-ATLA [antibody to ATL virus (ATLV)-associated antigen (ATLA)] are presented. Some differences in immunologic, epidemiologic, and serologic data between anti-ATLA-positive and -negative ATLs are also described. Expression of ATLA in early primary cultured leukemic cells was found to be negative in three patients tested (Cases 1, 2 and 4), however, a long-term cultured cell line, ATL-6A, derived from peripheral blood leukemia cells from Case 1, was found to express ATLA. Mother of Case 1 and a daughter of Case 2 were anti-ATLA negative. These results indicate that ATLV was involved in certain anti-ATLA-negative ATL patients, at least in Case 1, and that the patient had no detectable immune response against ATLV and ATLA. However, in other cases in which no ATLA reactivity of serum and no ATLA expression in cultured leukemic cells were observed, another possibility such as activation of an unknown cellular oncogene specific for ATL without ATLV involvement may be considered. In order to prove these possibilities definitely, it is necessary to elucidate whether or not proviral DNA of ATLV is integrated into chromosomal DNA of ATL cells and to find a cellular oncogene specific for ATL in the future.

Adult↗