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)

Lipotropin (LPH) has been evaluated as a potential tumor marker using a sensitive beta melanocyte-stimulating hormone (beta MSH) radioimmunoassay. All 79 acetic acid extracts of carcinomas of lung, colon, stomach, esophagus and breast contained LPH in concentrations greater than blood; 61 of 79 extracts contained LPH in larger amounts than control tissues from patients without cancer. In a blind prospective study, plasma LPH was quantified in 107 patients admitted for work-up because of an abnormality on a chest roentgenogram. Thirty-one of 33 patients subsequently diagnosed as having benign lesions had plasma LPH within the 95 per cent confidence limits of normal subjects whereas 28 (36 per cent) of the 74 patients subsequently diagnosed histologically as having primary lung carcinoma had elevated levels. In control studies, 13 of 100 patients with chronic obstructive pulmonary disease had elevated plasma LPH levels; three of the 13 with elevated levels and four with normal levels have been diagnosed, during the two years of follow-up, as having lung carcinoma. In control studies of 23 patients with granulomatous lung disease, 22 had normal levels of LPH. In those with carcinoma of the colon elevated plasma LPH levels were observed in two of 21 untreated patients and in 11 of 61 patients receiving noncurative chemotherapy. Elevated plasma LPH levels were also observed in 10 of 59 patients with breast cancer, eight of 28 with pancreatic cancer, eight of 22 with gastric or esophageal cancer, six of 16 with renal cancer, four of eight with prostatic cancer, one of seven with cervical cancer and one of six with ovarian cancer. We conclude, an elevated LPH level is frequently observed in blood and tumor tissue from patients with various types of carcinoma.
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PMID:Ectopic production of lipotropin by cancer. 43 67

The cytotoxicity and cardiotoxicity of benzoyl mustard (FCE 24517) and epoxamido (FCE 24561) synthetic derivatives of distamycin A were reported in the present study. The 50% inhibiting concentration (IC50) of colony formation of FCE 24517 on human SNB-19 glioblastoma, A2780 ovarian cancer and DU 145 prostate cancer was at least three times lower than that of FCE 24561; on the same cell lines the IC50 of DXR was up to 14 and 240 times higher than that of FCE 24561 and FCE 24517, respectively. Isolated rat hearts perfused with concentrations of both derivatives equivalent to their respective IC50 values did not show any significant change in ECG parameters, contractility and coronary flow. Compared to control hearts, FCE 24517 10(-6) M induced a significant increase in PR interval, reduction in + dF/dtmax, heart rate and coronary flow, while FCE 24561 10(-6) M produced a modest but significant increase in S alpha T segment and decrease in + dF/dtmax. Rats treated with FCE 24561 3, 6 or 12 mg/kg, intravenously (i.v.), once weekly for 3 weeks had a modest increase in S alpha T segment and QRS complex duration, while a slight alteration of S alpha T segment and QRS complex duration were observed in rats given FCE 24517 1 or 2 mg/kg i.v. once weekly for 3 weeks. No cardiac histologic alterations were found in hearts from rats receiving FCE 24517 or FCE 24561. For comparison, the cardiotoxicity of doxorubicin (DXR) was evaluated in the same experimental models; perfusion of hearts with DXR 10(-6) M induced severe alterations in all parameters of the isolated hearts; the administration of DXR 3 mg/kg i.v. once a week for 3 weeks was associated with a widening of the S alpha T segment and QRS complex and cardiac histologic picture was markedly altered. In conclusion, distamycin A derivatives display elevated cytotoxicity while no substantial cardiotoxicity was observed.
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PMID:Characterization of the toxicity of distamycin derivatives on cancer cell lines and rat heart. 145 30

Chronic GnRH analogs (GnRH-A) administration has proven to be effective for the control of some hormone-dependent tumors. GnRH-A are now in the standard treatment of prostatic cancer. In the present paper experimental and clinical data on the use of GnRH-A in gynecologic oncology are reviewed in order to identify a possible role in the therapy of breast, endometrial and ovarian cancer. Besides the indirect hormonal effect of GnRH-A, mediated by the suppression of gonadal steroidogenesis, in vitro evidence suggests a direct anti-proliferative action involving autocrine-paracrine regulation of cellular function. In advanced or recurrent breast cancer objective responses were observed in 157 out of 378 premenopausal patients (41%) and in 18 out of 166 postmenopausal women (10%). In ovarian cancer complete and partial responses were observed in 14 out of 121 (11%). At present, data on advanced endometrial carcinoma are limited: only 18 treated patients are reported, of whom 7 responded (38.8%). However, in general, most of the responses observed were transient. Thus, so far, the use of GnRH-A in gynecologic oncology has to be considered for palliation, after the failure of other better understood treatment modalities. The possible use of GnRH-A as an adjuvant is still under investigation.
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PMID:GnRH analogs in gynecological oncology: a review. 147 22

10 patients with ovarian cancer, whose disease had progressed while receiving platinum-based therapy, were entered onto a phase II clinical trial of the antiproliferative agent suramin. Suramin was administered in a fashion that is associated with durable objective disease response in patients with hormonally resistant metastatic prostate cancer. No individual had an objective response to therapy in this study, but 3 of 9 evaluable patients (33%) experienced disease stabilisation and subjective clinical improvement for periods ranging from 2 to 5 months. Disease stabilisation was associated with prolonged periods of comparatively high plasma levels of drug, which appeared to be determined primarily by reduced drug clearance. We conclude that suramin has potential activity in platinum-resistant ovarian cancer, and we have initiated a second clinical trial using pharmacological information derived from this study.
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PMID:Suramin in advanced platinum-resistant ovarian cancer. 152 10

Unknown primary malignancy (UPM) is not a disease entity. Rather, it represents a variety of different metastatic, malignant neoplasms all presenting with either an occult primary or having such a highly undifferentiated histologic appearance that an accurate pathologic classification on routine hematoxylin-eosin section is not possible. UPM is a spectrum of malignancies that includes those that are treatable and curable and those for which no specific treatment exists. For the physician, a diagnosis of UPM represents a beginning rather than an end. The minimal workup of such patients includes a thorough history and physical examination, complete blood counts, urine analysis, multichannel chemistries, a chest radiograph, and computed tomography of the abdomen and pelvis. Having completed this workup, further tests are unnecessary and unwarranted unless specific symptoms or physical signs exist. Once the aforementioned workup is completed, the physician must communicate frequently and freely with the pathologist as further diagnostic tests will be laboratory based and include electron microscopy, histochemical stains, and immunocytochemistries. Immunocytochemistries are relatively new laboratory procedures which have made a significant contribution in the accurate pathologic diagnosis of a tissue specimen that in years past would have been classified as an unidentified malignant neoplasm. An initial panel of immunocytochemistries (vimentin, cytokeratin, CEA, and common leukocyte antigen) should be performed on the tissue block in patients with UPM as they provide direction in the accurate classification of the malignant neoplasm. Chromosomal analysis of tissue is useful in the recognition of lymphomas or soft-tissue sarcomas which would otherwise be classified as UPM. In years to come, when specific DNA probes capable of identifying specific chromosomal rearrangeaments are widely available, pathologic classification of UPM will be performed on a molecular level. Some unknown primary malignancies are treatable and potentially curable. These include large cell lymphoma, extragonadal germ cell malignancies, squamous cell carcinoma metastatic to cervical lymph nodes without an obvious primary, metastatic adenocarcinoma to axillary lymph nodes in women (invariably on occult breast primary), and malignant ascites in women, which usually represents ovarian cancer. Metastatic adenocarcinoma of unknown primary origin, with the exception noted above and the rare presentation of an occult prostate cancer as UPM, is an ultimately fatal malignancy with a relatively shor clinical course.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Malignancies of undetermined primary origin. 154 98

Case-control studies have been carried out in Alberta in the last seven years to investigate possible risk factors for cancer of the prostate, skin and ovary. For each study, controls were randomly selected from an age- and sex-matched population. The information obtained from each control that agreed to participate in each study (n = 1236) included name, sex, date of birth, address and date of participation as well as the specific questions for each study. A review of these controls was carried out in 1988 by checking the number of deaths through death certificate listings from Vital Statistics (n = 142) and cancer incidence through the population-based Alberta Cancer Registry (n = 134). Of the 619 controls interviewed for the prostate cancer case control study in 1982 and 1983, 25 have been diagnosed with cancer of the prostate. From the non-melanoma skin cancer study, 15 cases from the 409 controls interviewed in 1983-1984 have been diagnosed with non-melanoma skin cancer. As for the 208 controls for ovarian cancer interviewed in 1985-1986 no new cases have been diagnosed. This possible ascertainment bias should be taken under consideration when case-control study analyses are carried out.
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PMID:Follow-up of controls participating in case-control studies for cancer risk factors. 195 70

Plasma lipid-bound sialic acid (LSA) was assayed in normal volunteers, patients with non-malignant diseases, and a variety of cancer patients. Mean plasma LSA in 50 normal volunteers, 16 patients with non-malignant diseases, 54 breast cancer, 17 lung cancer, 15 colon cancer, 7 ovarian cancer, 5 prostate cancer, 4 leukemia, 4 gastrointestinal, 3 thyroid cancer, 3 pancreas cancer and 2 adrenal cancer patients were 17.7, 23.2, 58, 85, 56.7, 46.2, 56.7, 53.3, 31.1, 33.2 and 119.5 mg/dl, respectively. None of the normal volunteers had elevated plasma LSA values. Plasma LSA level was not significantly different in male and female volunteers. Two out of 114 different cancer patients had plasma LSA levels within normal range exhibiting 98.2% sensitivity of the assay. Plasma LSA, which is relatively simple to assay, may be used as a tumor marker in wide variety of neoplastic diseases.
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PMID:Plasma lipid-bound sialic acid alterations in neoplastic diseases. 229 88

Frequency of nausea was investigated during the last six months of life of 342 patients who died from cancer in 1987. 44% received antiemetic treatment, but only 2% obtained complete relief. There was a close connection between opiate treatment, cytostatic treatment and nausea. The highest frequency of nausea was found among patients with gastrointestinal and ovarian cancer, whilst the lowest frequency was found in the prostate cancer group. We discuss antiemetic treatments in this connection.
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PMID:[Nausea in cancer patients. An analysis of its frequency and an evaluation of the treatment of nausea]. 230 Sep 42

In order to project trends in mortality from 11 major cancer sites in Switzerland to the end of the current century, a log-linear Poisson age/period/cohort model with arbitrary constraints on the parameters was used, fitted to the observed rates for the period 1950-84. One projection was based on the assumption of a total absence of change in the effect of period, the second was based on a linear extrapolation of the logarithms of the seven known periods, and the third was related to a series of a priori external epidemiological hypotheses, whenever available. For instance, coefficients below unity were used for lung and other tobacco-related neoplasms in men, since some decline in exposure to tobacco carcinogens was observed among Swiss men, and above unity for women since the prevalence of smoking has risen among successive generations of women. Although the method has limitations and uncertainties, several qualitative indications could be derived from this exercise. For instance, the various models suggest that the age-standardized mortality from oral cancer in men will probably increase up to the end of the century, even under the optimistic assumption of an appreciable decline in smoking, while cancer of the oesophagus is likely to level-off around current values, as other tobacco-related neoplasms, prostate cancer in men, and breast cancer in women will probably do. Some steady decline is predicted by various models fitted to the incidence of stomach and intestinal cancer in both sexes, and to ovarian cancer. Lung cancer will continue to rise in women but will stop rising in men, and it will possibly fall if the hypothesis of a decline in exposure to tobacco carcinogens proves correct. Although any prediction has, by definition, substantial difficulties and uncertainties, projections of cancer mortality in the near future are based on a substantial amount of information already available, and may offer valuable information for epidemiological inferences and health planning purposes.
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PMID:The application of age, period and cohort models to predict Swiss cancer mortality. 232 65

A number of biological markers have been recently introduced in clinical use as an aid for diagnosis and monitoring of malignant tumors. Some of them are relatively tumor-specific, i.e. CA 125 for non-mucinous ovarian cancer, CA 15.3 for breast cancer, PSA for prostate cancer, CA 19.9 for colo-rectal and pancreatic cancers. The clinical usefulness, the sensitivity and specificity of these tumor markers and of a few others (CA 50, SCC and TPA) are commented in this review.
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PMID:[Critical study of current tumoral markers]. 245 33


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