Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We established a human T-lymphoma cell line from the cancerous ascites of a male patient with prostate cancer which was named H-TL90. This cell line was characterized by its histological features, and by chromosomal and immunological analysis. Immunophenotypic analysis revealed that the cells expressed surface antigen CD-3CD-4CD+7CD-8. Biological analysis revealed that the cell can promote lymphocyte proliferation. This suggested that the cell line has an autosecretion function. Cytogenetic analysis revealed that H-TL90 was a hyperdiploid with 47 chromosomes and had characteristic translocation between chromosome 3 and 11, and the deletion of the long arm of chromosome 6. These results demonstrated the H-TL90 cell line can be a useful model for the study of human T-lymphoma.
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PMID:Establishment of a human T-lymphoma cell line (H-TL90) and analysis of its biological characteristics. 858 Apr 90

A subgroup of patients with metastatic carcinomas of unknown origin may benefit from combination chemotherapy. The relevance of immunohistochemistry in detecting such patients was investigated. Immunohistochemical studies with a panel of antibodies were performed on the tissue specimens of 41 patients having a light-microscopic diagnosis of poorly differentiated adenocarcinoma or undifferentiated carcinoma of unknown origin, who had been treated with cisplatin- containing chemotherapy. The study aimed to answer the following questions: (a) Can the tissue type of the tumor be verified? (b) Can a primary organ site be identified? (c) Can a prognostic immunohistochemical profile be recognized? The original diagnosis had to be changed in 2 of the 41 patients, who turned out to have a malignant lymphoma and neuroblastoma, respectively. The primary site was diagnosed in a patient with prostate cancer, whereas in one case the diagnosis could be narrowed down to a neuroendocrine tumor. No certain immunohistochemical profile with prognostic significance could be identified. It was concluded that immunohistochemistry should be routinely used in cases of undifferentiated carcinoma of unknown primary origin to verify the histological diagnosis and to select the appropriate therapy.
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PMID:The value of immunohistochemistry in patients with poorly differentiated adenocarcinomas and undifferentiated carcinomas of unknown primary. 860 68

Deficiency in p53-mediated cell death is common in human cancer, contributing to both tumorigenesis and chemoresistance. In an attempt to restore p53, we evaluated in vitro infectivity and cytotoxicity of a wild type (w.t.) p53-expressing adenovirus (Ad-p53) toward a panel of human cancer cell lines (n = 19). At a multiplicity of infection of 30, both Ad-p53 and adenovirus expressing beta-galactosidase (Ad-LacZ) infected greater than 99% of cells derived from brain, lung, breast, ovarian, colon, and prostate cancer, but failed to infect leukemia or lymphoma cells. Ad-p53, but not Ad-LacZ, infection of cancer cells was followed by nuclear accumulation of the CDK inhibitor p21WAFI/CIPI, cell cycle arrest and loss of viability. Ad-p53 induced apoptotic death in cancer cells that express mutant p53, including multi-drug resistant cells, but fewer deaths were observed in some w.t. p53 expressing cells. Ad-p53-infected SKBr3 breast cancer cells were more sensitive to cytotoxicity of the DNA damaging drugs mitomycin C or Adriamycin, but not the M-phase specific drug vincristine. Our results suggest that Ad-p53 is capable of infecting and killing cancer cells of diverse tissue origins (including multi-drug resistant cancer cells), that p21WAFI/CIPI may be a useful marker of p53 infectivity and that there may be synergy between Ad-p53 and either mitomycin C or Adriamycin induced cell death in tumors with p53 mutations.
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PMID:In vitro evaluation of a p53-expressing adenovirus as an anti-cancer drug. 870 13

A proportionate mortality study of a cohort of golf course superintendents was conducted using death certificates for 686 deceased members of the Golf Course Superintendents Association of America who died from 1970 to 1992. White males were included in the study population from all 50 states. The study objective was to compare mortality from this cohort to the general U.S. white male population. The proportionate mortality ratio (PMR) for all types of cancer was 136 (CI: 121, 152). Significant excess mortality from smoking-related diseases was observed. The PMR for arteriosclerotic heart disease was 140, which was significantly elevated (CI: 127, 155). In addition, the PMR for all respiratory diseases was 176 (CI: 135,230), while the PMR for emphysema was 186 (CI: 101,342). The PMR for lung cancer was 117 (CI: 93, 148). Mortality for four cancer types--brain, lymphoma (non-Hodgkin's lymphoma, NHL), prostate, and large intestine--occurred at elevated levels within this cohort: brain cancer PMR = 234 (CI: 121,454), non-Hodgkin's lymphoma (NHL) PMR = 237 (CI: 137,410), prostate cancer PMR = 293 (CI: 187,460), and large intestine cancer PMR = 175 (CI: 125,245). The PMR for diseases of the nervous system was 202 (CI: 123,333). A similar pattern of elevated NHL, brain, and prostate cancer mortality along with excess deaths from diseases of the nervous system has been noted among other occupational cohorts exposed to pesticides.
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PMID:Proportionate mortality study of golf course superintendents. 913 Dec 18

We identified a large French-Canadian family with 21 cases of breast cancer, including two affected brothers. Segregation of markers from chromosome 13q in this family showed linkage to the BRCA2 gene locus (lod = 3.67 at D13S289). A number of cancers of other types occurred in this family, including three cases of prostate cancer and two cases of lymphoma. The penetrance of breast cancer among BRCA2 carriers is estimated to be 75% to the age of 70.
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PMID:A large multisite cancer family is linked to BRCA2. 882 30

Conventional cytogenetics of breast and other solid tumors has been hampered by a number of factors. An analysis of breast tumor tissues was therefore undertaken using fluorescent in situ hybridization (FISH). A total of 34 specimens were analyzed using a chromosome 8-specific alpha-satellite probe. Various approaches were tested and compared. Among 30 informative samples, 11 infiltrating ductal carcinomas, not otherwise specified (NOS), 5 ductal carcinomas in situ, 5 lobular carcinomas, 3 papillary carcinomas, and 6 benign lesions were studied. Of the 11 cases of infiltrating ductal carcinomas (NOS) analyzed, four cases showed 3 signals, one case showed 4 signals, and the rest showed 2 signals. Of the 5 cases of ductal carcinoma in situ samples, 1 showed 3 signals and the other 4 cases showed 2 signals. All cases of lobular carcinomas, papillary carcinomas, and benign lesions showed 2 signals. We inferred from these data that 36% of the infiltrating ductal carcinomas (NOS) were trisomic and 9% were tetrasomic, whereas 20% of the ductal carcinomas in situ were trisomic. All samples from lobular carcinomas, papillary carcinomas, and the benign lesions were disomic. From our preliminary data, it can further be concluded that a subset of breast cancer is characterized by chromosome 8 trisomy. These data are consistent with an ever-increasing database on the association of chromosomal 8 trisomy with other cancers such as leukemia, lymphoma, prostate cancer, ovarian carcinoma, salivary gland tumor, malignant melanoma, desmoid tumors, and recently gestational trophoblastic disease. It is also noted that the ability to analyze formalin-fixed, paraffin-embedded archival material will enable a more comprehensive cytogenetic study of breast cancer than is currently available.
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PMID:Fluorescent in situ hybridization assessment of chromosome 8 copy number in breast cancer. 886 38

N-(4-Hydroxyphenyl)retinamide (4-HPR, Fenretinide) is a retinoid derivative with antineoplastic activity in various tumor types including prostate carcinoma. The mechanism of action of 4-HPR toxicity is unknown. 4-HPR induces apoptosis in leukemia- and lymphoma-derived cells, neuroblastoma, and small cell lung cancers. The present study was designed to investigate: (a) the mechanism of 4-HPR cytotoxicity in prostate cancer cells; and (b) correlate increased expression of transforming growth factor beta 1 (TGF beta 1) with induction of apoptosis. 4-HPR exposure to PC-3 cells in vitro was associated with apoptosis as evidenced by increased incidence of hypodiploid nuclei in propidium iodide fluorescence histograms and DNA fragmentation. An increase in the percentage of nuclei in the G1 phase of the cell cycle preceded induction of apoptosis. TGF beta 1-increased expression was noted in mRNA levels and in secretion of active TGF beta 1 into culture media. TGF beta 1 and TGF-beta receptor type II detected immunohistochemically were increased in 4-HPR-treated PC-3 cells. Furthermore, 4-HPR-induced cytotoxicity in PC-3 cells was abrogated by the addition of anti-TGF beta 1 antibody. In BT-20 cells, a 4-HPR-resistant breast carcinoma cell line, apoptosis was not observed after exposure to 4-HPR nor was TGF beta 1 expression enhanced in stained cells or in conditioned media. It is concluded that 4-HPR induces the expression of TGF beta 1 in association with the induction of apoptosis.
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PMID:Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells. 899 39

We have investigated the ability of several drugs commonly used in the treatment of human cancer to induce bcl2 phosphorylation and cell death in human cell lines derived from acute leukemia, lymphoma, breast cancer, and prostate cancer. The results of this analysis indicate that drugs affecting the integrity of microtubules induce bc12 phosphorylation, whereas anticancer drugs damaging DNA do not. Comparison of the effects of taxol and its analogue, taxotere, indicates that taxotere is capable of inducing bcl2 phosphorylation and apoptotic cell death at 100-fold lower concentrations than taxol. Induction of cancer cell death through phosphorylation of bcl2 thus provides an opportunity not only for more refined targeting of therapeutic drugs but for understanding of an important pathway leading to apoptosis. Phosphorylation of bcl2 in drug-treated cancer cells occurs in G2-M, the phase of the cell cycle in which this class of drugs is active. No induction of bcl2 phosphorylation occurs in chronic lymphocytic leukemia cells that overexpress bcl2 but are blocked at G0-G1. Thus, prevention of polymerization or depolymerization of cellular microtubules by this class of cancer therapeutic drugs causes phosphorylation of bcl2, abrogating the normal antiapoptotic function of bcl2 and initiating the apoptotic program in the cycling cancer cells; these results are consistent with a normal physiological role of bcl2 as "guardian of microtubule integrity."
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PMID:Bcl2 is the guardian of microtubule integrity. 900 May 60

A prospective survey was conducted of patients who began radiotherapy in Sweden during 12 weeks in the autumn of 1992. All hospitals that provided radiotherapy participated. The goal was to study the most common diagnoses, corresponding to approximately 80% of the patients. A special analysis involving all patients who started radiotherapy in 1992 at Sweden's largest unit, Radiumhemmet in Stockholm, revealed that the goal had been achieved. Overall, the assessment showed the data to be representative and of good quality. The analysis included 2988 patients, of whom 2776 received external radiotherapy alone, 63 received both external radiotherapy and brachytherapy, and the remaining 149 received brachytherapy alone. As expected, the two most common diagnoses were breast cancer and prostate cancer. To evaluate the total number of patients receiving radiotherapy in Sweden in 1992, the results of the study were related to the results of the economic assessment from 1991 described in Chapter 8. The assessment shows that approximately 13000 patients began radiotherapy in Sweden in 1992, ie, almost one third of cancer patients receive radiotherapy at some time during the course of their disease. The mean age of radiotherapy patients was 64 years, and 55% of all patients were women. Half of the patients received curative treatment, and the other half palliative treatment. The proportion of curative treatments varied considerably among the departments, from 23% to 86%. The proportion was 39% at county departments, compared to 52% at regional departments, and 76% at the gynecologic oncology departments. Palliative treatment was usually provided by less complicated methods, using fewer fractions and fewer fields. The proportion of curative fractions was 68%, and the proportion of curative fields was 72%. The proportion of curative treatments also varied greatly among different diagnostic groups, from 82% for head and neck cancer to 17% for lung and prostate cancer. Of patients receiving primary treatment, one third received radiotherapy alone and the remainder received a combination of radiotherapy and other treatment, usually surgery. Thirty-three percent of the patients were treated in accordance with clinical protocols or studies, with a somewhat higher proportion of these patients at the gynecologic oncology departments. The figures varied between 82% for gastrointestinal cancer and 11% for prostate cancer. Curative treatment was delivered, on average, using 23 fractions, 2.6 fields, and 49 Gy. The highest dosage, most fractions, and most fields were delivered for prostate cancer and head and neck cancer. The lowest doses were given for malignant lymphoma. Corresponding figures for palliative treatment were 11 fractions, 2.0 fields and 30 Gy. Of patients receiving palliative therapy, 60% were treated for bone metastases. These patients were treated with 8 fractions, 1.7 fields, and 27 Gy. With regard to curative and palliative treatment alike, there was a tendency for regional departments to give more fractions and higher doses than the county departments. No differences in sex or age appeared regarding the number of fractions, the number of fields, and the dose, except in patients over age 85 years where lower figures reflected a higher proportion of palliative treatments. With one exception only, patients with gynecologic cancer were the ones who received brachytherapy. Seventy percent of the patients had cancer in the body of the uterus. They received an average of four treatments, three for those who also received external radiotherapy. The number of brachytherapy treatments varied widely by department. This can be explained by two different therapeutic traditions: one tradition uses agents with low radiation intensity per time unit, resulting in fewer and longer treatments, and the second tradition involves agents with high radiation intensity per time unit, resulting in more, although shorter, treatments.
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PMID:A prospective survey of radiotherapy in Sweden. 915 85

We report a case of prostate cancer in 34 year old man presenting with generalized lymphadenopathy mimicking malignant lymphoma without any urinary symptoms. Lymph node biopsy revealed metastatic adenocarcinoma and immunohistochemical stain was strongly positive to prostate antigen (PSA). Serum PSA level was also markedly elevated. Transrectal ultrasonogram showed mild enlargement in right lobe of prostate. Needle biopsy finding of prostate also was consistent with adenocarcinoma. Bone scan revealed multiple metastatic lesions including vertebrae, ribs, pelvis, and both femurs. Generalized lymphadenopathy and elevated PSA level was decreased after bilateral orchiectomy.
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PMID:A case of prostate cancer in 34 year old man presenting with generalized lymphadenopathy mimicking malignant lymphoma. 925 Sep 26


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