Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new monoclonal antibody, 1C5, was produced by fusion of spleen cells obtained from mice immunized with CAC-1, a human cell line of cervical adenocarcinoma of the uterus, and NS-1 myeloma cell. The objectives of this study were to obtain moAb that can be used for routine histology and cytology, and to examine the histogenesis of cervical adenocarcinoma. 1. 1C5 reacted with 88% of cervical adenocarcinoma of the uterus, but did not react with cervical squamous cell carcinoma of the uterus and other squamous cell carcinoma. However, 1C5 reacted with some adenocarcinomas, such as endometrial carcinoma of the uterus and ovarial carcinoma. 2. The staining pattern by 1C5 was different, in cervical adenocarcinoma from that in endometrial carcinoma of the uterus, and also different in the endocervical type from that in the endometrioid type of cervical adenocarcinoma. Therefore, 1C5 is useful in distinguishing between two types of adenocarcinoma of the uterus. 3. 1C5 did not react with normal squamous cells or normal columnar cells of the uterine cervix, or with normal endometrial cells of the uterus. However, the columnar cells in a limited area of the squamocolumnar junction were strongly stained with 1C5. 4. 1C5 reacted with ethanol-fixed, and routine formalin-fixed and paraffin-embedded tissue. Thus, 1C5 may be used for clinical diagnosis. 5. 1C5 was found to be IgG1. 6. The molecular weight of the 1C5-defined antigen was 26,000 daltons, and the epitope of the 1C5-defined antigen was carbohydrate moiety. 7. We examined the histogenesis of cervical adenocarcinoma of the uterus by utilizing the reactivity of 1C5.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The production and characterization of monoclonal antibody, 1C5, reactive with cervical adenocarcinoma of the uterus]. 247 40

A human monoclonal antibody termed HMST-1 was produced by fusing lymphocytes from segments of human pelvic lymph nodes from an endometrial cancer patient with murine myeloma cells. The epitope recognized by HMST-1 was determined to be lacto-series type 1 chain-containing glycosphingolipid (Gal beta 1-3GlcNAc beta 1-3Gal beta 1-4Glc beta 1-1Cer) by isolating the antigen from endometrial cancer cell line SNG-II and analyzing with fast atom bombardment mass spectrometry, permethylation analysis, and exoglycosidase treatment. By the immunohistochemical avidin-biotin-peroxidase complex method, no normal endometrium and benign endometrial hyperplasia were stained with HMST-1, but HMST-1 reacted with about 35% of endometrial cancer cases. These facts indicate that the rate of expression of the antigen increases along with the course of malignancy in the endometrium. By sialidase treatment of the section, the positive rate increased to 57% in endometrial cancers and to 13% in normal endometrium, indicating that the antigen was masked with sialic acid and exposed by neuraminidase treatment. Immunohistochemistry also revealed that the antibody reacted with human fetal alimentary tract epithelium and mesothelium, indicating the oncodevelopmental nature of Gal beta 1-3GlcNAc beta 1-3Gal beta 1-4Glc beta 1-1Cer.
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PMID:Human monoclonal antibody (HMST-1) against lacto-series type 1 chain and expression of the chain in uterine endometrial cancers. 268 63

A murine monoclonal antibody, 1C5, was produced by fusion of spleen cells obtained from mice immunized with CAC-1, a human cell line of adenocarcinoma derived from uterine cervix, and NS/1 myeloma cells. 1C5 can be used for the staining of routine formalin-fixed and paraffin-embedded tissue sections. 1C5-defined antigen was found to have a molecular weight of 26,000. The 1C5-defined antigen was resistant to neuraminidase and trypsin treatment, but sensitive to periodate treatment, indicating that an epitope of the 1C5-defined antigen is a carbohydrate moiety. Immunohistochemical study using immunoperoxidase staining demonstrated that 1C5 reacted with 87% of adenocarcinomas of the uterine cervix, 39% of endometrial carcinomas of the uterus, 100% of ovarian mucinous cystadenocarcinomas, 43% of ovarian serous cystadenocarcinomas, 45% of adenocarcinomas of the colon, and 40% of gastric adenocarcinomas, thus showing the broad reactivity to adenocarcinoma cells of various origins. However, 1C5 did not show any reactivity to ectocervix epithelium, cervical intraepithelial neoplasia, or squamous cell carcinoma of the uterine cervix. In addition, adenocarcinoma of the uterine cervix exhibited strong cytoplasmic reactivity with 1C5, whereas endometrial carcinoma of the uterus showed the luminal reactivity. 1C5 also reacts with 95% ethanol-fixed malignant cells in cervical smears.
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PMID:New monoclonal antibody, 1C5, reactive with human cervical adenocarcinoma of the uterus, with immunodiagnostic potential. 305 7

Progesterone receptor (PR) from a human endometrial carcinoma (EnCa 101) grown in nude mice consists of two hormone-binding proteins with mol wt around 116,000 and 85,000. To generate monoclonal antibodies against this receptor, PR was partially purified from EnCa 101 and used to immunize Robertsonian mice. Immune mouse spleens were fused with HL-1 Friendly myeloma-653 cells, and hybridomas were screened by solid phase dot-blot assay and double antibody precipitation. Seven stable hybridomas were obtained, designated hPRa 1-7. Subisotyping revealed that hPRa 1 and 6 were immunoglobulin G2b, while the remainder were immunoglobulin G1. Ultracentrifugation in high salt sucrose gradients showed that six of the seven antibodies effected a shift of [3H]progestin-labeled PR from EnCa 101; only hPRa 4 was ineffective in this regard. Protein blots of EnCa 101 cytosols and DEAE eluates revealed that hPRa 1, 3, 4, 5, and 7 recognized both PR proteins equally. hPRa 2 recognized principally the 116,000 mol wt PR protein; it recognized the lower mol wt PR protein very poorly if at all, whereas hPRa 6 recognized only the 116,000 mol wt protein. Interestingly, the latter was consistently detected as a closely migrating triplet. Immunolocalization of PR by hPRa 1-7 in tissue sections was confined to nuclei of target tissues and varied in intensity: hPRa 7 greater than 3 = 5 greater than 6 = 2 greater than 1 greater than 4. In proliferative phase uterus, the intensity of staining was ranked: endometrial gland nuclei (3+) greater than myometrial cell nuclei (2-3+) greater than endometrial stromal cell nuclei (0-1+). Thus, seven monoclonal antibodies directed against human PR have been prepared, and their suitability for the study of PR by biochemical and immunohistochemical techniques has been demonstrated.
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PMID:Monoclonal antibodies to human progesterone receptor: characterization by biochemical and immunohistochemical techniques. 330 78

A series of drug combination sequence studies was conducted in vitro using HEC-1A human endometrial carcinoma cells or 8226 myeloma cells. Four drugs were evaluated for schedule-dependent and sequence-dependent inhibition of human tumor colony formation in soft agar. Six different two-drug combinations were analyzed using the median dose effect method, and three different three-drug combinations were examined using the cumulative surviving fraction method. The results show that the specific sequence and method of drug exposure significantly influenced the production of antagonistic, additive, or synergistic cytotoxicity patterns. Drug combinations that were consistently synergistic included bleomycin or mitomycin C and cisplatin in 8226 cells, and etoposide plus bleomycin in human endometrial cancer (HEC-1A) cells. Most other two-drug combinations of bleomycin, etoposide, cisplatin, and mitomycin C were antagonistic in vitro, irrespective of the sequence of exposure. Among the three-drug combinations tested, consistent synergism was noted with cisplatin, etoposide, and bleomycin when either of the latter two agents was tested as a continuous exposure in vitro. Within individual two- and three-drug combinations, it was possible to observe synergism, additivity, or antagonism based on the particular exposure sequence tested. These results suggest that antitumor agent cytotoxicity in vitro can be radically influenced by the sequence of drug administration, a feature commonly overlooked in many clinical combination drug regimens.
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PMID:The effect of anticancer drug sequence in experimental combination chemotherapy. 767 39

In 1976, an accident in a plant near Seveso, Italy, exposed the local population to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Persons residing in three zones of decreasing TCDD contamination (A, B, and R) and a reference population were followed up for cancer occurrence in 1977-1986. The most exposed subgroup (A) was small, and only 14 cancer cases were observed. In zone B, hepatobiliary cancer was elevated, especially for those living in the area for > 5 years [relative risk (RR) = 2.8; 95% confidence interval (CI) = 1.2-6.3]. Men exhibited an increase in hematologic neoplasms, most notably lymphoreticulosarcoma (RR = 5.7; 95% CI = 1.7-19.0). Women experienced an increased incidence of multiple myeloma (RR = 5.3; 95% CI = 1.2-22.6) and myeloid leukemia (RR = 3.7; 95% CI = 0.9-15.7). In zone R, the incidence of soft tissue tumors and non-Hodgkin's lymphomas was elevated, particularly among persons living in the area for > 5 years (RR = 3.5; 95% CI = 1.2-10.4 for sarcomas, and RR = 2.0; 95% CI = 1.2-3.6 for non-Hodgkin's lymphomas). Breast cancer among females was below expectations in the most contaminated zones, and a clear deficit for endometrial cancer was observed in zones B and R.
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PMID:Cancer incidence in a population accidentally exposed to 2,3,7,8-tetrachlorodibenzo-para-dioxin. 839 84

Data on the association of ovarian cancer with other cancers in families are limited, and no data are available on the involvement of specific morphological types. The nationwide Swedish Family-Cancer Database on 10.2 million individuals and 19175 invasive ovarian cancers was used to calculate standardised incidence ratios (SIRs) and 95% confidence intervals (CIs) for familial ovarian cancer in 0-66-year-old daughters when mothers or sisters were affected. The SIR for concordant ovarian cancers was increased. When the mother or sister had breast cancer, the SIRs were 1.21 and 1.48, respectively; when they had endometrial cancer, the SIRs were 1.45 and 2.53. Multiple myeloma in the mother was associated with a risk of ovarian cancer in the daughter. The risk of endometrioid ovarian cancer was 3.40 in the daughter when the mother presented with endometrial cancer. Our data show a strong familial coupling of ovarian and endometrial cancers, which appears to be specific to the endometrioid morphology.
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PMID:Familial clustering of ovarian and endometrial cancers. 1468 94

Asthma is an increasingly common disorder, affecting 5-10% of the population. It involves a dysregulated immune function, which may predispose to subsequent cancer. We examined cancer risk among Swedish subjects who had hospital admission once or multiple times for asthma. An asthma research database was created by identifying asthma patients from the Swedish Hospital Discharge Register and by linking them with the Cancer Registry. A total of 140 425 patients were hospitalised for asthma during 1965-2004, of whom 7421 patients developed cancer, giving an overall standardised incidence ratio (SIR) of 1.36. A significant increase was noted for most sites, with the exception of breast and ovarian cancers and non-Hodgkin's lymphoma and myeloma. Patients with multiple hospital admissions showed a high risk, particularly for stomach (SIR 1.70) and colon (SIR 1.99) cancers. A significant decrease was noted for endometrial cancer and skin melanoma. Oesophageal and lung cancers showed high risks throughout the study period, whereas stomach cancer increased towards the end of the period. The relatively stable temporal trends suggest that the asthmatic condition rather than its medication is responsible for the observed associations.
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PMID:Cancer risk in hospitalised asthma patients. 1917 22

A low vitamin D status and inadequate calcium intake are important risk factors for various types of cancer. Ecological studies using solar UV-B exposure as an index of vitamin D3 photoproduction in the skin found a highly significant inverse association between UV-B and mortality in fifteen types of cancer. Of these, colon, rectal, breast, gastric, endometrial, renal and ovarian cancer exhibit a significant inverse relationship between incidence and oral intake of calcium. In addition, lung and endometrial cancer as well as multiple myeloma are considered calcium and vitamin D sensitive. Studies on tissue-specific expression of the CYP27B1-encoded 25-hdroxyvitamin D-1alpha-hydroxylase and of the extracellular calcium-sensing receptor (CaR) have led to an understanding how locally produced 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Thus, impairment of antimitogenic, proapoptotic and prodifferentiating signaling from the 1,25(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency has been implicated in the pathogenesis of the aforementioned types of cancer. 1,25(OH)2D3 and calcium interact in modulating cell growth in different ways: (i) Signaling pathways from the VDR and the CaR converge on the same downstream elements, e.g. of the canonical Wnt pathway; (ii) high extracellular calcium modulates extrarenal vitamin D metabolism in favor of higher local steady-state concentrations of 1,25(OH)2D3; (iii) 1,25(OH)2D3 may up-regulate expression of the CaR and thus augment CaR-mediated antiproliferative responses to high extracellular Ca2+. This can explain why combined supplementation is required for optimal chemoprevention of cancer by calcium and vitamin D.
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PMID:Calcium, vitamin D and cancer. 1966 66

Epidemiological studies have provided convincing evidence that obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colon, pancreas, breast (post-menopausal), endometrium and kidney. The magnitude of the increase in risk varies between cancer sites. For an increase in BMI of 10 kg/m2 relative risks are approximately 2.3 for adenocarcinoma of the oesophagus, 1.5 for colon cancer in men, 1.2 for colon cancer in women, 1.4 for post-menopausal breast cancer, 2.9 for endometrial cancer and >1.5 for kidney cancer, while the size of the effect on cancer of the pancreas is uncertain. There is also evidence that obesity increases the risks for cancers of the gallbladder, malignant melanoma, ovary, thyroid, non-Hodgkin lymphoma, multiple myeloma and leukaemia. Estimates of the percentage of cancers that can be attributed to excess body weight suggest that in the UK and similar countries approximately 5% of all cancers are attributable to overweight and obesity.
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PMID:Symposium 1: Overnutrition: consequences and solutions. Obesity and cancer risk. 1995 65


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