[Prognosis of non-Hodgkin's lymphoma. 3. Clinical and pathological diagnosis of T- and B-lymphoma and its staging].
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Biomedical subjects
Publications and source records attributed to K Minato.
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Although it is not uncommon to find multiple malignant neoplasms in the same organ, the incidence of synchronous malignant lymphoma and colonic adenocarcinoma has been very rare. This a case report involving a 52-year-old woman in whom malignant lymphoma actually arose within the same segment in which colonic adenocarcinoma was present. Under the diagnosis of advanced adenocarcinoma, she had been treated by right hemicolectomy. However, she developed intestinal obstruction about a month later. At the second surgery for this latter condition, cytologic examination of ascitic fluid revealed many malignant lymphoma cells. In spite of antilymphoma chemotherapy, the patient's condition became progressively worse during the subsequent five-month period, and she died of recurrent malignant lymphoma.
We evaluated the occurrence and the type of second malignancies among 74 patients with Hodgkin's disease (HD) and 407 patients with non-Hodgkin's lymphoma (NHL) who were treated at the National Cancer Center Hospital for more than one year. Fifteen patients developed a second malignancy. In 10 of these patients the second cancer was gastric cancer, but no cases of acute nonlymphocytic leukemia were encountered. The observed number of second cancers in females among the HD patients was significantly (p less than 0.005) greater than the expected incidence based upon the number of age-adjusted person-years both for all cancers and for stomach cancer. However, no significant differences between males and females in the NHL patients were found. Furthermore, no significant differences were seen in any of the groups between the observed and expected numbers of second malignancies according to the treatment.
Of those patients with localized (CS I-II) non-Hodgkin's lymphoma of Waldeyer's ring who were treated with radiotherapy or radiotherapy plus chemotherapy and who suffered relapses at the National Cancer Center Hospital over the past 22 years, 24 cases were analyzed on the basis of their response rate and duration of remission with reinduction chemotherapy, and survival time after recurrence. The group [ADM (+)], treated with regimens including adriamycin, was compared with the group [ADM (-)] treated with regimens excluding adriamycin. Complete response was seen in 9 out of 11 cases (81.8%) and in 8 out of 13 cases (61.5%) for the ADM (+) group and the ADM (-) group, respectively (p greater than 0.1). The period of complete response of the ADM (+) and ADM (-) groups was compared using the logrank method. The prognosis of the former was significantly (p less than 0.01) better than that of the latter and the median duration of remission was 30 months and 7 months, respectively. When the survival after recurrence of the ADM (+) and ADM (-) groups was compared, the median survival time was 38 months for the ADM (+) group and 12 months for the ADM (-) group, but no significant difference was observed between the two groups (0.05 less than p less than 0.1).
Prognostic factors in 68 consecutive patients with myeloma treated at the National Cancer Center Hospital from 1962 to 1984 were analyzed. Median survival time from onset was 100 months for stage I, 72 months for stage II, and 26 months for stage III of the Durie and Salmon's clinical staging system. It was 55 months in patients with normal renal function and 18 months in those with abnormal renal function. All early deaths occurred in patients with stage III disease. Hemoglobin level, bone lytic lesions and presence of Bence Jones protein were also significant prognostic factors. On the other hand, heavy chain as well as light chain subtypes of monoclonal immunoglobulin (M-component) and M-component production rate did not influence the survival of myeloma patients. The analysis of chemotherapeutic responses and survival curves according to the chemotherapy used in this study (alkylating agent vs Vinca-alkaloid plus alkylating agent) did not disclose any significant difference between the two groups. The overall response rate was 67%. The survival time from the initial chemotherapy of responding patients was significantly longer than that of nonresponders.
In ten human malignant T-cell lines (HPB-ALL, HPB-MLT, CCRF-CEM, RPMI-8402, MOLT-4, JM, P12/Ichikawa, TALL-1, SKW-3, HUT-102), the expression of the antigen defined by OKT-4 or Leu-3A monoclonal antibody was remarkably decreased after a short incubation (1 hr) with 12-0-tetradecanoylphorbol-13-acetate (TPA) (1.6 nM). This phenomenon was also observed in all types of cells tested, including two lymphoblastoid cell lines with B-cell properties (RPMI-6410 and RPMI-8392), thymus cells from three children, peripheral blood lymphocytes from four normal individuals, and fresh neoplastic T cells from a case of T-cell acute lymphoblastic leukemia (ALL) and a case of T-cell lymphoma. The presence of puromycin (10 microM), cycloheximide (35 microM), or retinoic acid (1.0 microM) had no effect on the TPA-induced loss of OKT-4 defined antigen. Incubation at 4 degrees C or with lidocaine (4 mM) partially prevented this effect of TPA, and the presence of sodium azide (150 mM) did so totally. Recovery of antigen expression occurred 24 hours after cessation of TPA treatment. Comparative study using several phorbols other than TPA showed that this effect accorded with the tumor promotor activity of the compounds, but the phenomenon appears to be at the membrane level, not necessarily as a result of TPA-induced cellular differentiation.
To depict the three-dimensional distribution of 99mTc-pyrophosphate in the heart, emission computed tomography (ECT) was performed, following the conventional planar imaging, in 32 cases with suspected acute myocardial infarction (AMI). There were 23 cases with evidence of AMI, 7 with unstable angina (UA), and 2 with dilated cardiomyopathy (DCM). While the planar images showed discrete cardiac activity in only 11 of the 23 cases (48%) with AMI, the ECT images delineated focal myocardial uptake clearly in 20 of them (87%). On the other hand, the ECT images revealed cardiac blood-pool activity without significant myocardial uptake in all cases with UA and DCM in which the planar images showed diffuse activity. Thus, the ECT imaging of 99mTc-pyrophosphate seems to be a valuable technique for assessing the presence and localization of myocardial necrosis, especially in cases showing diffuse cardiac activity in the planar imaging.
To estimate tricuspid regurgitation (TR) quantitatively, a curve fitting method by computer has been employed. Transport in the right cardiac chambers after intravenous bolus injection of macro-aggregated albumin labeled with technetium 99m (99mTc-MAA) was recorded in anterior view by a gammacamera system. Disturbance of the dilution curves from the left heart can be avoided by using 99mTc-MAA injection. To know the radioisotope activity during the transport, time-activity curves are recorded for the superior vena cava, right atrium, and right ventricle. Parametric differential equations, obtained from compartmental analysis, interpret these curves mathematically. The rate of regurgitation is determined by comparison, using an iterative process, between the original and simulated curves. The whole process is performed automatically by computer. The calculated regurgitation value correlated well with the value from the analog simulation. The method clearly separated those with TR from those without TR. This digital simulation for estimating parameters using a compartmental model is a feasible tool in detecting and quantifying TR.
A cephalexin and penicillin G resistant strain of Rothia dentocariosa was clinically isolated from pus of infected postoperative maxillary cyst. The strain contained multiple plasmids. Plasmid curing tests with rifampicin eliminated cephalexin and penicillin G resistant phenotypic functions and 47 megadalton plasmids from the strain. Beta-Lactamase isolated from the strain hydrolyzed cephalosporin more efficiently than penicillin.
Wistar female rats housed under conditions of 12 hr dark/12 hr light were pinealectomized (PX) or underwent sham-operation (SO) 21 days after ovariectomy, on the 7th or on the 15-17 th day of pregnancy. Serum and pituitary prolactin (PRL) levels in ovariectomized (OVX) rats were determined 9 days after pinealectomy. In the case of OVX rats receiving estrogen and progesterone injections (OVX-EP), PRL levels were determined 48 hr after injection administered 7 day after pinealectomy. PRL levels in pregnant rats were determined on the 20th day of pregnancy and in postpartum rats, on the 3rd day following parturition. As compared with the SO control, pinealectomy resulted in a significant decrease in the serum PRL level in the OVX-EP rats but in a significant increase in that level in the OVX, pregnant and postpartum rats. In OVX-EP rats, exogenous estrogen raised the serum PRL level less in PX than in SO rats, probably because the pineal gland is closely related to the facilitation of PRL secretion by estrogen. The high estrogen level in OVX-EP rats seemed to trigger pineal stimulation of PRL release, but low estrogen levels in OVX and postpartum rats or markedly high levels of progesterone in pregnant rats on the 20th day are thought to cause pineal inhibition.
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Abnormally large lymphocytes with Pelger-like nuclear lobulation have been found in peripheral blood of smoldering adult T-cell leukemia-lymphoma (ATL) patients. They are also found in quite low percentage in peripheral blood of healthy HTLV carriers. Therefore, it has become difficult to discriminate smoldering ATL having only abnormal lymphocytes from a healthy human T-cell leukemia virus (HTLV) carrier only by morphology and serology. We found that patients with smoldering ATL with visceral organ involvement such as skin or lung lesions had much higher titer (about 1 : 1,000) of anti-HTLV antibodies than those with other subtypes of ATL (about 1 : 250); the difference was highly significant (p less than 0.001). In addition, the period of survival of patients with smoldering ATL having antibody with high titer was much longer than that of patients with other subtypes of ATL, suggesting the role of a host immune response. Four cases of HTLV-negative ATL were found to have the same chromosomal abnormality as that has been seen in HTLV-positive typical ATL; the situation was quite similar to Burkitt's lymphoma. Since it has been considered that HTLV does not include oncogenes, a common oncogenic mechanism, ATL specific cellular oncogenes, might exist: they might be activated by HTLV or a mechanism other than a virus.
The modulation of cell surface antigens in 2 myeloblastic cell lines (ML-1 and KG-1), a promyelocytic cell line (HL-60), and a monoblastic cell line (THP-1-0) by the presence of 12-O-tetradecanoyl-phorbol 13-acetate [(TPA) CAS: 16561-29-8] was investigated by indirect membrane immunofluorescence with the use of three monoclonal antibodies (MoAb) (OKM-1, 63D3, and MCS-2) reacting with myeloid-monocyte antigens (expressed by cells of both granulocyte and monocyte lineages) and two MoAb (1/12/13 and MCS-1) reacting with myeloid antigens (expressed by cells of the granulocyte lineage). Functionally mature macrophage properties, such as adherence, morphologic character, and phagocytosis, were induced by the presence of TPA in each of the cell lines except for adherence in the HL-60 cells. After 3 days in culture, the expression of the OKM-1-defined antigen was markedly augmented in all 4 cell lines. The expression of the 63D3-defined antigen was also markedly augmented in the ML-1, KG-1, and THP-1-0 cells, but it was not significantly altered in the HL-60 cells. The MCS-2-defined antigen was amplified in expression in the ML-1 and HL-60 cells, but it showed minimum decrease in the KG-1 and THP-1-0 cells. The MCS-1-defined antigen expression was suppressed in ML-1, HL-60, and THP-1-0 but was enhanced in KG-1. The suppressed expression of My-1 antigen (detected by the MoAb 1/12/13) was noted in all 4 cell lines. Thus in the ML-1 cells, expression of the myeloid-monocyte antigens was augmented, whereas myeloid antigen expression was inhibited in the presence of TPA, a result that parallels antigenic expression in terminal macrophage differentiation. The trend was true, except for the 4 cell line-antigen combinations (MCS-2-defined antigen and MCS-1-defined antigen in KG-1, 63D3-defined antigen in HL-60, and MCS-2-defined antigen in THP-1-0). The heterogeneous attitude of some antigens to TPA found in these cell lines may result from the fact that they represent different points in the myeloid-monocyte differentiation scheme.
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