[A case of spontaneous remission in chronic B-cell leukemia with virus infection].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
H Tsuda
Publications and source records attributed to H Tsuda.
Pathogenetic significance of p53 and c-Ki-ras gene mutations and human papillomavirus DNA integration in adenocarcinoma of the uterine cervix and uterine isthmus.
The pathogenetic significance of p53 and c-Ki-ras gene mutations and genomic integration of human papillomavirus (HPV) DNA was examined in surgically resected specimens of adenocarcinomas of the uterine cervix and isthmus using polymerase chain reaction (PCR), single-strand-conformation polymorphism and Southern blotting analysis. Among 25 cervical adenocarcinomas, p53 gene mutations between exons 5 and 8 were detected in 32%, and the incidence of these mutations was higher in cases at advanced clinical stages and with high grades of nuclear and structural atypia both in endocervical and in endometrioid types. HPV DNA type 16 or 18 in cervical adenocarcinomas was detected in 35% of cases by PCR and in 29% by Southern blotting, and, in contrast to the p53 mutations, the majority of cases with the HPV DNA were at a relatively early clinical stage with low-grade histological atypia. c-Ki-ras gene mutation was detected in only 4% of cervical adenocarcinomas. Among 8 isthmus adenocarcinomas, the incidence of p53 and c-Ki-ras gene mutations, and the presence and integration of HPV DNA type 16 or 18 were 38%, 50%, 57% and 25% respectively. The pattern of p53 mutations differed between isthmus and cervical adenocarcinomas: all of the mutations in the former were one-base substitutions of the transition type, whereas in the latter nearly half of the mutations were of the transversion type. Among cervical adenocarcinomas, p53 mutations between exons 5 and 8 were indicated as being mostly involved in the pathogenesis and development of biologically aggressive tumors, whereas HPV type 16 or 18 infection appeared to be involved in less aggressive cases. In isthmus adenocarcinoma, c-Ki-ras gene mutation, apart from p53 mutation and HPV-type-16 or -18 infection, appeared to be involved frequently in cancer development.
Adenocarcinoma↗
Pure red cell aplasia caused by chlormadinone.
Explore the source record for details and available documents.
Aged↗
Enhanced neoplastic lesion development with adenine-induced experimental multicystic nephropathy by adenine--a model system for the analysis of renal tumor generation in long-term hemodialysis patients.
To cast light on the high incidence of renal cell tumors (RCT) in long-term hemodialysis patients, the role of background multicystic nephropathy was studied in a rat model. Group 1 animals were initially given N-ethyl-N-hydroryethylnitrosamine (EHEN) then subjected to adenine feeding until killing during weeks 20-27. Groups 2 and 3 received EHEN and adenine, respectively. All rats receiving adenine developed multicystic nephropathy. The incidence of renal cell hyperplasias (RCH) and multiplicities of both RCH and RCT in Group 1 were significantly increased as compared with Group 2, suggesting multicystic nephropathy provides favorable environment for tumor development.
Adenine↗
Different mutations of the p53 gene in nodule-in-nodule hepatocellular carcinoma as a evidence for multistage progression.
The p53 gene was analysed for mutation in three macro- and micro-scopically different areas of a nodule-in-nodule hepatocellular carcinoma (HCC). Two inner nodules revealed distinct mutations while the surrounding early HCC lesion was negative for mutation. This case clearly demonstrated that the p53 mutation was associated with the progression of HCC from an early to a more advanced stage, and that the primary HCC lesion was composed of genetically heterogeneous subclones. These findings provide direct proof of the involvement of genetic abnormalities in one step of multistage tumor progression.
Carcinoma, Hepatocellular↗
Association among p53 gene mutation, nuclear accumulation of the p53 protein and aggressive phenotypes in breast cancer.
In order to reveal whether differences in the type and site of p53 gene mutations influence the function of the gene and tumor phenotype, we examined nuclear accumulation of the p53 protein immunohistochemically, loss of the other p53 allele by restriction-fragment-length polymorphism analysis, and histological grade of atypia in 52 breast-cancer tissue specimens in which the position and pattern of the mutation were identified. When mis-sense point mutations or deletions of 3n bases (n = 1, 2, ...), which did not cause a frameshift downstream, occurred within codons 110-180 or 234-285, containing highly conserved regions, the p53 protein was almost always (92%) accumulated in nuclei in a majority of the cancer cells. When these mutations occurred outside these regions, only 46% of the cases showed nuclear accumulation of the protein in a majority of cancer cells. In tumors with non-sense point mutations or deletion of 3n + 1 or 3n + 2 bases (n = 0, 1, 2, ...), which caused a downstream frameshift, nuclear accumulation of the p53 protein was absent in 93% of cases. Irrespective of the mutation site or pattern, a majority of cases showing p53 mutation revealed loss of heterozygosity on 17p13 (83%), which suggested they do not carry wild-type p53 allele, and the highest histological grade of atypia (90%). Regardless of differences in their protein-expression pattern, a majority of the p53 gene mutations were suggested to function in a recessive mode and to be involved in the development of histologically aggressive breast cancer.
Alleles↗
Allele loss on chromosome 16q24.2-qter occurs frequently in breast cancers irrespectively of differences in phenotype and extent of spread.
Loss of heterozygosity on chromosomal arm 16q has been shown to be a frequent event in sporadic breast cancer and is suggested to be involved in cancer development through inactivation of a tumor-suppressor gene. To specify the commonly deleted region in which the unknown tumor-suppressor gene is located, a deletion map of chromosome 16 was constructed for 78 breast cancers, using 27 polymorphic DNA markers. Loss of heterozygosity on chromosome 16q was detected in 38 of the tumors. From the deletion map, the incidence of the loss of heterozygosity was deduced to be > or = 36% in the region distal to 16q12 and was most frequent in the 16q24.2-qter region. Then, association of the loss of heterozygosity in the 16q24.2-qter region with clinicopathological parameters of the tumors was examined for a total of 234 tumors, to reveal its biological significance in breast cancer development. The total incidence of loss of heterozygosity in the 16q24.2-qter region was 52% (118 of 225), and loss of heterozygosity was frequent irrespectively of the presence of invasion and metastasis, differences in clinical stage, tumor size, histological grade, or type, or amounts of estrogen receptor. Inactivation of an unknown tumor-suppressor gene on 16q24.2-qter was thus suggested to be involved commonly in the genesis of sporadic breast cancer, irrespectively of the extent of tumor spread or grade of aggressiveness of the cancer cells. On the other hand, eight cases revealed loss of heterozygosity not at 16q24-qter but in more proximal regions. Therefore, it appears that multiple tumor-suppressor genes are located on chromosome 16q.
Breast Neoplasms↗
Prognostic significance of the overexpression of c-erbB-2 protein in adenocarcinoma of the uterine cervix.
BACKGROUND: The overexpression of c-erbB-2 protein is a prognostic marker in patients with breast cancer. Alteration of the c-erbB-2 oncogene in development of adenocarcinoma of the uterine cervix, an unfavorable gynecologic neoplasm, is unknown. METHODS: To clarify the role of the c-erbB-2 oncogene in adenocarcinoma of the uterine cervix, formalin-fixed, paraffin-embedded tissue sections from 44 cases of cervical adenocarcinoma were immunohistochemically examined for expression of c-erbB-2 protein and for c-erbB-2 gene amplification in DNA by slot blot-hybridization analysis. RESULTS: The expression of c-erbB-2 protein was detected in 34 cases (77%). Strong expression on cell membranes was detected in 11 cases (25%). Most cases with strong membrane expression of c-erbB-2 protein also showed amplification of the c-erbB-2 gene by slot blot-hybridization. Expression of the protein on cell membranes was more often seen at clinical Stage II or III (9 of 23 [39%]) than at Stage 0 or 1 (2 of 21 [9%]) (P < 0.05, Fisher's exact test). Expression of the c-erbB-2 protein was also associated with poorer prognosis of patients with cervical adenocarcinoma by comparison of survival curves (P < 0.005) and by the Cox regression model analysis. CONCLUSIONS: Overexpression of c-erbB-2 protein is associated with amplification of c-erbB-2 gene and frequently occurred in cervical adenocarcinomas of the patients with poor prognoses.
Adenocarcinoma↗
Measurement of fetal urine production in mild infantile polycystic kidney disease--a case report.
It is generally recognized that the sonographic findings of infantile polycystic kidney disease (IPKD) are bilaterally enlarged kidneys, oligohydramnios, an absent fetal bladder, and the typical kidney texture. Since there is a broad spectrum of renal compromise with IPKD, in utero diagnosis is thought to be limited to the severe forms. This paper reports a mild case of IPKD, where the in utero diagnosis was established by measuring fetal urine production and amniotic fluid volume serially during pregnancy, and by ultrasonographic examination of fetal kidneys.
Adult↗
Abrogation of suppressor cells activity by cis-diamminedichloroplatinum (CDDP) treatment using therapeutic doses in ovarian cancer patients.
We examined the activity of natural killer (NK) cells and suppressor cells and the population of peripheral blood lymphocytes before and after cis-diamminedichloroplatinum (CDDP) treatment using therapeutic doses in 15 ovarian cancer patients. CDDP did not decrease NK cell activity but selectively abrogated suppressor cell activity up to 7 days after treatment (P < 0.05). The CD56+CD16+ cell and CD8+CD11+ T cell populations significantly decreased; however, the CD4+2H4+ T cells, showed a significant increase after treatment (P < 0.05). We conclude that CDDP treatment using therapeutic doses could selectively abrogate suppressor cell activity.
Adult↗
Effect of penicillin on GABA-gated chloride ion influx.
To investigate the mechanism of penicillin-induced convulsions, we have studied the effects of penicillin G (PC-G) on GABA-gated chloride ion influx in brain 'microsac' preparations of mice. In the presence of 10(-4) M GABA, PC-G inhibited GABA-gated chloride ion influx in a dose-dependent manner. The dose-response curve for GABA in the presence of 10(-3) M PC-G was shifted rightward and there was a decrease in maximum response. The inhibitory effects of PC-G were not reversed by RO 15-1788, an antagonist of benzodiazepine (BZ) receptors, but were reversed by washing the 'microsac' membranes. Therefore, PC-G probably exerts its proconvulsant effect by inhibiting GABA-gated chloride ion influx. However, it appears not to act through the BZ receptor of the GABA/BZ receptor complex.
Animals↗
Plasminogen activator and hemorrhage in brain tumors.
Explore the source record for details and available documents.
Brain↗
Bilateral malignant lymphoma of the breast in patients with a familial history of cancer: a report of three cases.
We report three cases of bilateral malignant lymphoma of the breast in patients with a familial history of cancers. All the patients had B-cell malignant lymphoma and were treated by a radical mastectomy and polychemotherapy. Bilateral tumors were detected synchronously in one case, whereas the second tumors in the other cases occurred 4 years and 8 years after the initial treatment. Although the patients had no relevant past history, these cases were notable for the fact that all were associated with a familial history of cancers. One patient had a definite familial history of breast cancer, that is to say, her mother, sister and brother all suffered from this disease. The brother of another patient died of gastric cancer while two of her uncles each suffered from sarcoma of the lower extremities and a brain tumor, respectively. As for the remaining patient, one of her maternal uncles and an aunt also died of prostate cancer and leukemia, respectively. However, only one out of seven patients with unilateral malignant lymphoma of the breast used for comparison had a familial history of cancer. A possible relationship between bilateral primary malignant lymphoma of the breast and a familial history of cancer is suggested.
Adult↗
Enhanced therapeutic effects of anti-tumour agents against growth and metastasis of colon carcinoma 26 when given in combination with interferon and interleukin-2.
Chemoimmunotherapy of pulmonary metastases was investigated in a protocol of combined anti-tumour agents and interferon-beta and/or interleukin-2. The combination of interferon-beta and interleukin-2 after treatment with etoposide or cisplatin exerted profound therapeutic effects in an experimental model (lung colonization) using colon carcinoma 26, which was resistant to interferon-beta or to interleukin-2 alone. Cured mice treated with anti-tumour agents and cytokines rejected re-implanted tumours. Moreover, this approach also had profound effects on spontaneous pulmonary metastases, together with the effect on primary tumours. However, this combination of cytokines did not enhance the anti-tumour activity of etoposide in athymic mice with pulmonary metastases. Injections of tumour-bearing BALB/c mice with a combination of etoposide and these cytokines resulted in a marked increase in CD8+, asialo-GM1+ cells. Thus the combined treatment with interferon-beta and interleukin-2 after administration of cytotoxic drugs may induce specific anti-tumour immunity, and such combinations may offer a new approach to the development of effective therapy for cancer metastases.
Animals↗
Preoperative diagnosis of a rudimentary uterine horn.
Two cases of rudimentary uterine horn were able to be diagnosed prior to operation. The case of rudimentary horn with cavity non-communicating to unicornuate uterus was easy to diagnose. Transabdominal ultrasonography and computed tomography (CT) demonstrated the uterus to have binodular structure and two uterine lumina. However, the case with pregnancy was difficult to diagnose. In this case, thick myometrium could be seen by ultrasonography to enclose the sac. In both cases hysterosalpingography revealed unicornuate uterus.
Adult↗
Treatment of adult T-cell leukaemia-lymphoma with irinotecan hydrochloride (CPT-11). CPT-11 Study Group on Hematological Malignancy.
A late phase II study of a new camptothecin analogue, irinotecan hydrochloride (CPT-11), was conducted to evaluate the anti-tumour effect and toxicity in patients with refractory leukaemia and lymphoma including adult T-cell leukaemia (ATL)-lymphoma, in a multi-institutional cooperative study. All the patients with ATL had been previously treated with various conventional combination chemotherapies and were refractory to these therapies or had relapsed. CPT-11 was administered at a dose of 40 mg m-2 day-1 for three consecutive days repeated weekly until evidence of disease progression. One complete remission and four partial remissions were achieved in 13 assessable patients with ATL. The median total dose to achieve remission was 240 mg m-2 and the median duration of response was 31 days. The major toxicities were leucopenia (83%), diarrhoea (62%) and nausea/vomiting (69%). These were relatively severe, but they were generally tolerable and reversible. However, one patient died probably as a result of this therapy. No effective chemotherapy for adult T-cell leukaemia-lymphoma has yet been established, and the prognosis for patients with this disease is very poor. Our results suggest that CPT-11 may be a promising agent for this disease. Further combination therapy with CPT-11 is needed to improve the therapy for ATL.
Adult↗
Antigen-specific human monoclonal antibodies from mice engineered with human Ig heavy and light chain YACs.
We describe a strategy for producing human monoclonal antibodies in mice by introducing large segments of the human heavy and kappa light chain loci contained on yeast artificial chromosomes into the mouse germline. Such mice produce a diverse repertoire of human heavy and light chains, and upon immunization with tetanus toxin have been used to derive antigen-specific, fully human monoclonal antibodies. Breeding such animals with mice engineered by gene targeting to be deficient in mouse immunoglobulin (Ig) production has led to a mouse strain in which high levels of antibodies are produced, mostly comprised of both human heavy and light chains. These strains should provide insight into the adoptive human antibody response and permit the development of fully human monoclonal antibodies with therapeutic potential.
Adult↗
DNA methylation adduct formation and H-ras gene mutations in progression of N-butyl-N-(4-hydroxybutyl)nitrosamine-induced bladder tumors caused by a single exposure to N-methyl-N-nitrosourea.
After receiving 500 p.p.m. N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in their drinking water for an initial 10 weeks, rats were given a single i.p. injection of N-methyl-N-nitrosourea (MNU) at a dose of 50 mg/kg body wt at week 20 (at a stage when bladder tumor development had already occurred), and then maintained until they were killed at week 40. Three and six hours after the MNU injection, the DNA methylation adducts, O6-methyldeoxyguanine (O6-medG) and 7-methyldeoxyguanine (7-medG), were immunohistochemically revealed to be markedly more frequent in urothelial preneoplasias or neoplasias than in normal cells. These adducts were rapidly repaired, and although 7-dmeG in tumor cells still persisted after 72 h, they appeared essentially to have returned to normal levels. At the termination, conversion of transitional cell carcinomas (TCC) to squamous cell carcinomas (SCC) of the urinary bladder was significantly increased in the BBN+MNU group. The extent of invasion was also significantly greater with the additional MNU treatment. Expression of p21 protein, detected by immunohistochemistry, was comparable between the groups. Mutations in the H-ras gene were observed in one case each of the BBN and BBN+MNU groups, and both cases showed a G:C to A:T transition at codon 12. The present study thus suggested that while an additional single treatment with MNU of rats bearing BBN-induced bladder neoplasias is associated with significant, possibly mutation-dependent tumor progression, H-ras mutations are not necessary events.
Administration, Oral↗