Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay for a plancental glycoprotein, beta1SP1, capable of detecting 2 microgram/l of the glycoprotein in serum was used to measure concentrations of beta1,SP1 in patients with choriocarcinoma, teratoma, colonic cancer, breast cancer, and ovarian cancer. 12 out of 94 (13%) healthy men and health non-pregnant women had detectable serum-beta1SP1 concentrations. Concentrations up to 50 000 microgram/l were found in the sera of patients with hydatidiform mole, invasive mole, choriocarcinoma, and malignant teratoma. beta1-glycoprotein concentrations were generally much lower than corresponding concentrations of chorionic gonadotrophin which is the most reliable marker for trophoblastic tumours. In a few cases, however, beta1-glycoprotein measurements may be useful in the detection of minimal residual tumour. The slightly raised values found in some patients with carcinoma of the colon, breast, or ovary seem unlikely to be useful for diagnostic purposes of for monitoring the course of these cancers.
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PMID:Serum-SP1-pregnancy-specific-beta-glycoprotein in choriocarcinoma and other neoplastic disease. 7 23

Eighty one patients (59 females, 22 males) with advanced solid tumors were treated with Adriamycin in doses of 40 mg/m2 body surgace daily, in two days cycles, with resting periods of 3 weeks. Overall response rate was 46% (37/81). In breast cancer response rate was 56% (13/23) and in ovarian cancer 48% (13/27). In various other tumors remission was observed in soft tissue sarcomas (3/8), thyroid cancer (1/7), osteogenic sarcoma (1/4), oesophageal cancer (2/4), lung cancer (2/4), bladder cancer (1/2) and hepatoma (1/2). In breast cancer patients, 2-7 month remission duration was observed (M equal to 4.5 month) and in ovarian cancer 1.5-5 month (M equal to 3.2 month). Adriamycin was also applied intrapleurally in 31 patients with malignant pleural effusions with a low response rate (26%). This modified schedule of Adriamycin administration showed a high antitumor activity in breast and ovarian cancer and in soft tissue sarcomas. Squamous cell carcinoma of the esophagus was also sensitive to Adriamycin therapy. The very low rate of myelosuppression and oral ulceration showed the decreased toxicity of this Adriamycin administration schedule.
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PMID:Modified administration schedule of adriamycin in solid tumors. 14 May 42

A clinical trial of the oral form of VP 16-213 (NSC-141540), a semisynthetic podophyllotoxin, was undertaken. In 20 patients, treatment was started at 200 mg/day p.o. for 5 days; courses were repeated after a rest period of 16 days. Five patients were treated at the same dose, repeated with only 9-day rest periods. Subsequently, 65 patients were given 300-400 mg/day for 5 days, with rest periods of 9 days between courses. The side effects encountered included anorexia, nausea and vomiting, stomatitis, diarrhea, leukopenia, thrombocytopenia, alopecia, and pruritus. Substernal discomfort with or without palpitations was reported by 18 patients; no explanation for this symptom could be found. No complete remissions (CR) were observed. Parital remissions (PR) and improvement (IMP) were seen as follows: small cell carcinoma, lung (10 patients)--2 PR, 3 IMP; adenocarcinoma, lung (4 patients)--1 PR; alveolar cell carcinoma, lung (1 patient)--1 IMP; mesothelioma (4 patients)--1 IMP; ovarian cancer (12 patients)--3 PR, 3 IMP; breast cancer (20 patients)--4 IMP; colon cancer (8 patients)--2 IMP; bladder cancer (4 patients)--2 IMP; histiocytic lymphoma (7 patients)--2 PR, 3 IMP; chronic myeloid leukemia (1 patient)--1 IMP.
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PMID:A clinical trial of the oral form of 4'-demethyl-epipodophyllotoxin-beta-D ethylidene glucoside (NSC 141540) VP 16-213. 16 75

Frequencies of 25 HLA antigens in 526 Caucasian patients were compared to those in 629 healthy controls who were HLA-typed between September 1975 and February 1977. Haplotypes were compared for 711 patients and 549 controls typed between September 1974 and December 1976. Frequency deviations were found in those with ALL, AML, breast cancer, lymphoma and ovarian cancer, but only the increase in A29 in AML patients was statistically significant when corrected for the number of specificities. Interesting associations, when compared with earlier studies, include elevation of AW24 in both ALL and AML patients and increased B27 in ALL patients. Significant haplotype differences were increased A3-B8 and absence of A1-BW17 in ALL patients and increased A11-B5 and A2-BW40 as well as absence of A2-B5 in AML patients.
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PMID:HLA frequencies in cancer: a third study. 28 33

Phenesterin was evaluated in 222 patients with two different dosage regimens, one by daily treatment and the other with an intermittent schedule. Toxicity was moderate with both programs. The largest group of patients treated had breast cancer; they experienced a 10% response rate. Of interest was a higher percentage of responses in ovarian cancer (36%). An expanded study of patients with ovarian cancer would be of interest.
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PMID:A phase II study of phenesterin (NSC-104469). 35 20

Data on the etiology of hormone-associated cancers are reviewed. Although for breast cancer many risk factors point to the relevance of hormonal factors, findings are not uniform. Evidence points to the importance of dietary factors, and one study appears to confirm an association with high total fat intake. Dietary factors, although possibly mediated through a hormonal mechanism, may eventually be found to play a major role in the etiology of breast cancer. Studies of both endometrial and ovarian cancer also show the importance of hormonally associated factors, although not always in the same way as for breast cancer. In addition, both for these sites and for cancer of the prostate, dietary factors may also be relevant in their etiology. As yet, no direct assessment of the importance of diet has been attempted for these sites, but this could be rewarding.
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PMID:An overview of hormone-associated cancers. 35 31

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

An overview of the risk of developing cancer related to oral contraceptive (o.c.) use is presented. A committee of experts affiliated with WHO studied the problem of developing cancer related to o.c. use. O.c. use for more than 2 years prevents the formation of benign breast tumors, even after discontinuing o.c. use. The effect is due to the progestin component. There is no clear indication that o.c. use increases the risk of breast cancer. A higher risk of endometrial cancer is associated with sequential preparation use, but not with the use of combination preparations. Cervical neoplasms and pituitary adenoma may be more frequent among predisposed women who use o.c.s. Studies show a reduced risk of ovarian cancer with o.c. use, but more studies are necessary. There is a marked increase in the relative risk of developing hepatocellular adenoma among women who use o.c.s for longer than 3 years. The risk increases with the hormone dosage, the duration of treatment, and the age of the patient. There is no reliable data to indicate that the risk of malignant melanoma increases with o.c. use. More study is needed to determine the possible cancer risks of injection preparations. Combination preparations can cause an increased risk of vaginal epithelial metaplasia. Diethylstilbestrol taken during early pregnancy can cause vaginal neoplasms in the offspring. More epidemiological studies and clinical and laboratory studies on the carcinogenic effects of o.c.s and the endocrinological effects of o.c.s on younger women should be undertaken. It is recommended that o.c.s with the lowest possible hormone dosages be used. O.c.s should not be prescribed to women with vaginal adenosis.
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PMID:[Oral contraceptives and the risk of neoplasms]. 44 57

We compared age-adjusted mortality rates for cancer of selected sites for Chinese, Japanese, and native Indian residents of British Columbia during the years 1964-73 to the corresponding rates for the white population. Mortality from all cancers of the Chinese did not differ significantly from that of whites. Elevated rates are seen for cancer of the nasopharynx in both sexes, of the liver and esophagus in males, and of the lung in females. Chinese males had a lower mortality than whites from stomach, prostate, and bladder cancer and brain tumors, whereas females had a lower mortality from tumors of the colon, breast, and ovary; both sexes had a lower mortality from leukemia. For Japanese males and females, the mortality rates for all cancers combined were similar to those of the white population. The rates for cancer of the stomach and gallbladder were higher in both sexes; males also showed a higher rate of liver cancer. Prostate and breast cancer mortality rates were lower. Native Indian males had a lower mortality rate from all cancers combined; the difference was significant for stomach, colon, lung, and prostate cancers, and for leukemia. Native Indian females showed a lower rate for ovarian cancer and a higher rate of tumors of the gallbladder and uterine cervix, but their overall cancer mortality was similar to that of whites.
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PMID:Cancer mortality among Chinese, Japanese, and Indians in British Columbia, 1964-73. 53 37

Following a report of several relatives suffering from breast cancer, the occurrence of neoplasms in 3 generations of a large family was carefully checked. Members of one out of 8 branches were found to have a high incidence of breast cancer with 6 women affected, 4 of them under the age of 40. As well as early onset, these women presented other features typical of "breast cancer families": bilateral breast cancer, other second primary tumours, ovarian cancer in the daughter of one affected patient, and benign breast disease in the sister of another.
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PMID:Familial breast cancer: report of a family pedigree. 62 64


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