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)

Cells from spontaneous adenocarcinomas of the prostate (Pollard, M.: J. Natl. Cancer Inst. 51: 1235, 1973) in aged Lobund Wistar rats were examined by electron microscopy. Cytologic structures of the rat prostate tumor cells resembled analogous structures from human prostate tumor cells. These findings support the prospect that the rat prostate tumor will provide a model system of prostate cancer in man.
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PMID:Ultrastructural cytology of prostate carcinoma cells from Wistar rats. 18 62

In a preliminary report on a small fraction of the projected subject population, some evidence in support of both sexual activity and venereal transmission hypotheses is accumulating. Prostatic cancer cases, in contrast to hospitalized and/or neighborhood controls, are beginning to show greater proportions of selected sexual activities compatible with venereal transmission of an infectious agent, such as number of sexual partners, use of prostitutes, prior venereal disease, and genital infections in the spouse. Patients with prostatic cancer also appear to have had higher fertility and more prostatic cancer in blood relatives than controls. Age at first intercourse and at first marriage are lower among the cancer patients than among the controls. Antibody titrations for herpesvirus and cytomegalic virus, although currently not revealing striking disparities in positivity, tend to show higher titers among the cancer cases.
Cancer Treat Rep
PMID:Epidemiologic study of prostatic cancer: preliminary report. 19 89

Cells cultured from human urogenital cancer and other cancers as well as cells from noncancerous tissues were examined by immunofluorescent staining with antibodies to T-antigens and capsid antigens of papovaviruses BK virus (BKV), JC virus, and simian virus 40(SV40), and to capsid antigens of herpes simplex virus types 1 and 2 and human cytomegalovirus (CMV). Cells from early passage cultures of 123 primary tissues and from 14 continuous lines derived from transitional or renal cell carcinoma were tested. None of the cell preparations was specifically stained with any of the antisera. A serologic comparison of patients with bladder cancer, patients with prostate cancer, and normal control groups of BKV hemagglutination-inhibiting and SV40-neutralizing antibodies showed no differences among the 3 groups. None of the sera in the 3 groups had SV40 or BKV T-antibodies. In tests of supernatants of 35 primary cultures for presence of virus, a single isolation, that of a cytomegalovirus, was made. The study revealed no evidence that infection with papovaviruses of the SV40-polyoma subgroup has any part in the production of bladder and prostate cancer.
J Natl Cancer Inst 1978 Mar
PMID:Investigation of human urogenital tract tumors of papovavirus etiology: brief communication. 20 10

Most humans in the United States have been infected with BK virus (BKV), a human papovavirus. Because BKV has oncogenic properties, we have investigated whether it may be a cause of human cancer. Basic principles of tumor virology imply that BKV-induced tumors should contain BKV DNA sequences. Therefore, we assayed (by molecular hybridization) DNA from human tumors and malignant cell lines for BKV DNA, using BKV [(32)P]DNA as probe. The BKV [(32)P]DNA was labeled in vitro (nick translation) to specific activities of 1 to 2 x 10(8) cpm/mug. The BKV DNA used to prepare our probes had the properties expected of authentic BKV genomes, including density of superhelical DNA, sedimentation velocity in alkaline and neutral sucrose gradients, production of one fragment by endonuclease EcoRI cleavage and four fragments by endonuclease Hin II + III cleavage and reassociation properties. From these studies we conclude that our BKV probes hybridized well, and represented bona fide BKV DNA. Using three different BKV [(32)P]DNA probes, i.e., from three distinct plaque isolates, we have analyzed DNA from BKV-transformed cells, normal human tissues, and a large number of human tumors. All human DNAs (cell lines, normal tissues, tumors) hybridized 5% with BKV DNA. Hybridization analysis of BKV-transformed hamster cell DNA indicated 5-6 copies of at least 88% of the BKV genome per cell. No BKV DNA sequences were detected (above the normal 5% hybridization to all human DNAs) in the following normal human tissues: 10 kidney (BKV is usually isolated from urine), 3 spleen, 13 lung, 23 colon, 2 rectum, 1 ileum, and 1 skin. No BKV-specific DNA was found in 166 tumors, including 5 carcinomas (Ca) of stomach, 3 Ca small intestine, 26 Ca colon, 9 Ca rectum, 31 Ca lung, 9 adenocarcinomas and 5 oat cell carcinomas of lung, 17 melanomas, 5 Ca prostate, 4 Ca bladder, 6 Wilms tumors, 4 hypernephromas, 15 Ca kidney, 7 brain tumors, 5 Hodgkin lymphomas, 10 lymphomas (immunosuppressed patients have a high incidence of lymphomas), 2 reticulum cell sarcomas (spleen), and 3 skin tumors. We have also analyzed 7 human malignant cell lines (melanoma, lung, rhabdomyosarcoma, and glioblastomas), including several clones of a lung melanoma line; no BKV DNA sequences were detected. Because our probes could detect one copy of BKV DNA if only 10% of the cells were tumor cells, our results are very strong evidence that the tumors we analyzed did not have a BKV etiology. The tumors we tested represent about 50% of all cancers in the United States; there is no evidence that BKV is involved in the etiology of these types of tumors.
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PMID:Analysis of human tumors and human malignant cell lines for BK virus-specific DNA sequences. 20 40

Age-adjusted rates of mortality from prostate cancer during 1950-69 were correlated by race with demographic, industrial, and agricultural data from 3,056 U.S. countries. Mortality among nonwhites was 50% higher than that among whites in all parts of the country where blacks comprise most of the nonwhite population. The rising rate associated with population density among nonwhites, but not whites, suggested that environmental exposures related to urban living may account for the predisposition of American blacks to prostate cancer. Despite a clustering of counties with elevated mortality in certain North Central and Northeastern States, the geographic variation among whites with prostate tumors was considerably less than that among whites with other tumors. Mortality was elevated in counties with a high percentage of residents of Scandinavian descent, in counties with metal-using and textile industries, and in regions with high consumption of high-fat foods.
J Natl Cancer Inst 1978 Dec
PMID:Geographic patterns of prostate cancer in the United States. 28 45

In 1976, the toll of cancer in Denmark (5 million inhabitants) was 12,481 deaths, or 23% of deaths from all causes. Seven manifestations accounted for more than half of the cancer deaths, namely lung (19%), breast (9%), stomach (7%), colon (9%), rectum (5%), pancreas (6%) and prostate (5%). The median age of the cancer patients was 70 years, ranging from 65 years for breast cancer patients to 75 years for those with prostate cancer. Cancer caused a reduction in the patients' normal life-span; it totalled 182,486 years for all the dead patients, 37% of which were in productive age. The future caseload was projected from the time trend for the years 1968-76. During the following five years an annual increase by 200 deaths is expected. The trend differs between the seven major manifestations, since some will increase and others will stabilize or decrease. When case reports are combined with mortality data, survival tables can be produced. Follow-up surveys of the patient's health, combined with modern data processing, can produce a detailed description of the impact of cancer on the patient's life. These health tables, which illustrate the natural history of the disease, can also be used to assess new therapeutic regimens.
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PMID:Public health aspects of cancer deaths. 29 1

We used delayed hypersensitivity skin testing, in vitro lymphocyte blastogenesis, and lymphocyte surface markers to examine the relationships among host immunologic competence, tumor type, tumor stage, prognosis, and the effects of cancer treatments in patients with genitourinary cancer. We found correlations between host immune competence and both tumor stage and prognosis among patients with bladder cancer, renal cell cancer, and those with advanced prostate cancer not receiving endocrine therapy, but not among patients with prostate cancer receiving endocrine therapy. Radiation and chemotherapy suppressed T-lymphocyte levels, but a chemotherapy-induced tumor remission resulted in a rebound of T-cell counts to above normal levels. In tissue sections of bladder cancers, regions of mononuclear infiltration were virtually devoid of cells with complement receptors or receptors for cytophilic antibody, which suggested that lymphocytes infiltrating bladder cancers are predominantly T-lymphocytes.
Natl Cancer Inst Monogr 1978 Dec
PMID:Host immunocompetence in genitourinary cancer: relation to tumor stage and prognosis. 31 91

Anesthesia, stress, trauma or the operation per se have been reported to result in alterations of host resistance in a wide range of diseases. The effect of such changes on the thymolymphatic system of patients with prostatic cancer is not known. While evaluating in vitro parameters of cellular immunologic responsiveness in patients with prostatic cancer, we have observed a depression two to seven days following cryosurgery or transurethral resection (TUR) of the proliferation of phytohemagglutinin (PHA)-stimulated peripheral blood lymphocytes (PBL). Contrary to the reduced proliferation of PBL cultured in autologous and homologous serum from patients receiving TUR, patients receiving cryosurgery, while also showing reduction in autologous serum, showed increased responsiveness when cultured in homologous serum. Although transient, depression of lymphocyte proliferation, particularly if involving tumor-cloned T-cells, may provide reduced surveillance to potential metastatic tumor cells leading to an alteration of tumor-host homeostasis. The potential of reduced surveillance, at least in the case of TUR, appears to be supported by observations that patients dying from prostatic cancer at our institution had an antecedent TUR. Identifying those patients with changes in responsiveness before surgery, as well as those prone to develop or undergo further reductions in responsiveness after surgery, would appear to be relevant in the management of patient with prostatic as well as other malignancies. Pre- and/or postoperative immunotherapy in such patients may be indicated.
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PMID:Alterations in host responsiveness in patients with prostatic cancer following cryosurgery or transurethral resection. 32 Sep 26

Cancer chemotherapy has developed rapidly over the last twenty years. The majority of patients with cancer die from metastatic disease, so the major therapeutic advance now must be better systemic therapy. From its early beginning in the 1940's with oestrogen therapy for prostatic cancer, nitrogen mustards in the lymphomas, and folic acid antagonists in childhood leukaemia, there are now between thirty and forty active anti-cancer agents in clinical use. The main clinical pharmacological points of the major agents are briefly reviewed, together with their main dose-limiting toxic effects and their activity as single agents. Clinical chemotherapy has developed by the introduction of newer agents from the drug screening programmes and a better understanding of the scheduling to avoid serious toxicity. Although drug-resistance is still a major problem, by combining different active agents there has been a dramatic improvement in survival of patients with selected tumours. More recently, treatment of patients early, before they have gross clinical recurrence, has already shown some benefit in pre-menopausal patients with carcinoma of the breast and in patients with osteosarcoma. The limitations of clinical measurements in monitoring therapy are clear, and a major improvement could well be realised if therapy could be monitored on the basis of quantitative markers. The clinical impact of cancer chemotherapy has already been dramatic in drug-sensitive tumours, but these only contribute a small proportion of the total. Some of the common tumours fall into the group that are relatively drug sensitive where the lives of patients can be prolonged, but there is still a significant fraction of tumours which are insensitive to existing drugs and which will probably require the development of newer agents before chemotherapy can make any impact on the survival of patients with these tumours.
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PMID:The current role of cancer chemotherapy. 36 Nov 39

Twenty-seven patients with a diagnosis of metastatic adenocarcinoma of the prostate were treated in a randomized, prospective trial with either Cyclophosphamide or a combination of Adriamycin, 5-Fluorouracil, and Cyclophosphamide. Doses were either Cyclophosphamide alone (800-1200 mg/m2 iv q 3 weeks) or Cyclophosphamide (150-200 mg/m2 po Day 3-6) plus 5-FU (400-500 mg/m2 iv Day 1, 8) plus Adriamycin (30-50 mg/m2 iv Day 1) given as a 4 week treatment cycle. Patients with compromised bone marrow reserve initially received the lower dose level. Objectively stable disease as defined by a modification of the National Prostatic Cancer Project criteria was seen in 53% of the 15 Cyclophosphamide treated patients and in 50% of the 12 combination treated patients. Survival was not significantly different in the two arms. However, the survival of patients responding to Cyclophosphamide was significantly longer than that of patients responding to the combination (median 18.6 months versus 8.1 months, p less than 0.05). Gastrointestinal and hematologic toxicity was moderate with both regimens. Therefore, in the present study, Cyclophosphamide alone was as effective as the combination of Cyclophosphamide, 5-FU and Adriamycin for patients with disseminated prostatic carcinoma. The moderate hematologic toxicity noted with both regimens suggests further evaluation of drug combinations utilizing higher dosages of active agents in this disease.
Cancer 1978 Dec
PMID:Cyclophosphamide (NSC 26271) versus the combination of adriamycin (NSC 123127), 5-fluorouracil (NSC 19893), and cyclophosphamide in the treatment of metastatic prostatic cancer: a randomized trial. 36 13


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