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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A multi-institutional prospective study for the analysis of prognostic factors for patients with osseous metastasis was performed. From February 1986 through June 1988, a total of 216 patients were included in this study. Cox's regression model made it clear that the most significant overall prognostic factor was primary site (p = 0.0002). In the lung cancer group, performance status (p = 0.0036) and metastasis of organs than bone (p = 0.0105) were also significant prognostic factors. In the breast cancer group, no significant factors were obtained. In the hepatoma group, the values for alkaline phosphatase (ALP) (p = 0.0021), lactate dehydrogenase (LDH) (p = 0.0195), and sex (p = 0.0264) proved significant. In the group of other cases, the most significant prognostic factor was the value for urinary hydroxyproline/creatinine ratio (p = 0.0001), followed by the pain score of RTOG (p = 0.0018). These factors and actual survival periods obtained in this study will be useful for the future stratification of patients for individualized optimal radiation schedules.
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PMID:Prognostic factors for patients with osseous metastasis: a multi-institutional prospective study. 219 3

We have previously reported that physiological levels of progestins alone stimulate lactate dehydrogenase in a dose-responsive manner in the progesterone-receptor-rich human breast cancer cell line T-47D. Using isozyme electrophoresis, we have not found that lactate dehydrogenase isozyme 5 is the only isozyme detectable in these cells, as has been reported for other human breast cancer cells in long-term tissue culture. Upon treatment with progestins, isozyme 5 remains the only isozyme detectable. T-47D cells were plated in charcoal-stripped serum-containing medium and grown for 2 days before treatment with progestin. Lactate dehydrogenase stimulation then plateaued after around 2-3 days of treatment with progestin and was maintained until around day 5, following which a decline in enzyme activity occurred. The effect is specific for progestins, and inhibited by the anti-progestin RU-38486 (17 beta-hydroxy-11 beta-(4-dimethyl-aminophenyl-1)-17 alpha-(prop-1-ynil)-estra-4,9-dien-3-one). Experiments using actinomycin D and cycloheximide suggests that the effect is dependent on RNA and protein synthesis, respectively. Lactate dehydrogenase stimulation occurs regardless of the presence of the estrogenic pH indicator Phenol red, and of whether it was analyzed per mg DNA or per mg protein.
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PMID:Progestin stimulation of lactate dehydrogenase in the human breast cancer cell line T-47D. 244 61

We have previously reported progestin stimulation of growth and lactate dehydrogenase (LDH) in the human breast cancer cell line T47D. Our further findings now show that growth stimulation by progestins occurs in a dose-responsive manner at physiological concentrations and is inhibited by the antiprogestin RU486. 17 beta-Estradiol (E2) also stimulates proliferation and LDH, and these stimulations are inhibited by tamoxifen. In addition, tamoxifen alone slightly stimulates proliferation. Surprisingly, RU486 also inhibits stimulation by E2. Thus, RU486 acts not only as an antiprogestin, but also as an antiestrogen. While combined promegestone (R5020) and E2 substantially stimulate proliferation, when RU486 is added to this combination it does not further inhibit, but leads to enhanced stimulation. However, the same addition of RU486 to combined E2 and R5020 diminishes LDH stimulation. This suggests that LDH stimulation and growth stimulation are dissociated. Finally, tamoxifen inhibits growth stimulation by combined R5020 and E2, but addition of the antiprogestin RU486 to this combination does not lead to a further inhibition of proliferation. Even so, this same combination reduces LDH levels to control values, further suggesting that stimulation of growth and LDH are dissociated. All of these findings occurred in the absence of the estrogenic pH indicator phenol red. These results emphasize the potential of LDH as an end point for studying the mechanism of female steroid hormone action. They also reveal antiestrogenic activity in RU486. Further, they shed light on the interaction among estrogens, progestins, antiestrogens, and antiprogestins in their effects on growth. Further understanding of this complex interplay may be helpful in treatment of human breast cancer.
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PMID:Effects of progestins, estrogens, and antihormones on growth and lactate dehydrogenase in the human breast cancer cell line T47D. 273 55

Determinations of estradiol receptor (ER), progesterone receptor (PR), total lactate dehydrogenase activity (LDH) and electrophoretic separation of LDH isoenzymes were performed in cytosols from 118 samples of primary infiltrating ductal mammary carcinoma. ER + PR+ tumors demonstrated a significant increase in the proportion of the LDH muscle-type isoenzyme (LDH5) as compared to ER-PR- samples (p less than 0.002). Tumors lacking one of the receptors presented intermediate LDH5 percentages. As total LDH activity bore no relation to either the presence or absence of receptors, the increased proportion represents an absolute elevation of LDH5, suggesting that LDH5 may be a promising hormone-dependence marker. As an in vitro model to study whether LDH5 was induced by estradiol via ER, we have used two human breast cancer cell lines, MCF-7 and T47D. In both cell lines LDH5 was the sole isoenzyme. Total ER and PR have been determined by a whole-cell method. In MCF-7 cells (with high ER levels), after incubation with 10(-10) M estradiol, maximal induction of LDH had already been achieved. In relation to T47D (low ER levels) estradiol did not evoke an induction of LDH5 at any concentration examined. In MCF-7 cells, the level of LDH5 induction paralleled processing of ER. The processing effect was rapid, beginning within 5 min of estradiol addition, and was completed within 1 hr. With 10(-6) M tamoxifen, LDH5 induction was suppressed and this effect was reversed by estradiol. Such antiestrogenic effects of tamoxifen on LDH5 have not been observed in T47D cells. Agonistic effects of low doses of tamoxifen on LDH5 were not observed. Our studies suggest that estrogen stimulation of LDH5 involves ER.
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PMID:Estrogen control of lactate dehydrogenase isoenzyme-5 in human breast cancer. 282 42

The effects of 17 beta-estradiol (estradiol), synthetic progestin R5020 and their antagonists, tamoxifen (Tam) and synthetic RU38486 on lactate dehydrogenase (LDH) activity in MCF-7 human breast cancer cells during the growth period were studied. A specially developed quantitative cytochemical assay was used; LDH activity is expressed per cell, and is thus independent of the positive and negative growth effects of the hormones and antagonists. Estradiol and R5020 stimulated LDH activity after similar exposures (6-48 h) and the stimuli were concentration dependent over the range 10(-7) M to 10(-10) M. As for the antagonists, RU38486 stimulated LDH activity in much the same way as estradiol and R5020; Tam alone, on the other hand, does not stimulate LDH, but when added to estradiol, Tam inhibits estradiol mediated LDH activation. When present at half-stimulant concentration, estradiol + R5020 and estradiol + RU38486 exhibit additive effects on LDH activity. Thus LDH appears to be an interesting tool for the study of hormone and antagonist effects in MCF-7 breast cancer cells.
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PMID:Comparative effects of 17 beta-estradiol, progestin R5020, tamoxifen and RU38486 on lactate dehydrogenase activity in MCF-7 human breast cancer cells. 292 68

Between June 1973 and November 1980, 1,171 patients with metastatic breast cancer were treated with various doxorubicin-containing regimens at our institution (M.D. Anderson Hospital and Tumor Institute, Houston). Retrospective analysis of all 233 cases (20%) with liver metastases was done to correlate various clinical and biochemical characteristics with response to treatment, survival, and causes of death. A similar analysis was performed for 58 consecutive patients with liver metastases treated at this hospital between December 1955 and December 1957 with hormone therapy or single-agent chemotherapy. Objective responses were observed in 132 of 233 patients (57%) treated with combination chemotherapy. The median survival was 14 months in the 1970s and 5 months in the 1950s. Among patients who had liver metastases at the time of initial diagnosis of breast cancer, survival was longer for the group treated with combination chemotherapy. All cases were classified according to the number of organ sites involved by metastases. Patients with only liver metastases, or liver plus bone lesions had the longest survival. Other clinical and biochemical factors that correlated significantly with longer survival were: no prior chemotherapy, performance status of 1 to 2, absence of ascites, normal bilirubin and lactic dehydrogenase (LDH), SGOT less than or equal to 2 times normal and albumin greater than 4.5 g/dL. The main cause of death was multiorgan failure, with only 20% of patients dying of liver failure. The present study shows that the presence of liver metastases in breast cancer is not by itself an ominous factor. Most patients respond to therapy, and significant palliation with extended survival is possible for several prognostic subgroups. Further improvement in length and quality of survival is expected with earlier diagnosis.
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PMID:Clinical course of breast cancer patients with liver metastases. 310 83

The anatomical and temporal patterns of recurrence were studied in 401 patients with first recurrence of breast cancer. All patients underwent the same scheduled investigation program: history, physical examination, blood tests, bone scanning, bilateral iliac crest biopsy, radiologic bone survey, chest x-rays, and ultrasound scanning of the liver. The current article focuses on the diagnosis of intrathoracic (ITH) recurrence. Most patients recurred in a single site and 50% of the recurrences were diagnosed within the first 2 years from initial diagnosis. Chest x-ray revealed ITH recurrence in 27% (109 patients), and in 8% the lung, pleura, and/or mediastinum were the only signs of recurrence. Generally, the status of primary demographic, clinical, and pathoanatomical characteristics were not predictive as to the development of ITH recurrence, although patients with pleural recurrences often had centrally located primary tumors, locally advanced disease, and often received adjuvant radiotherapy. Clinical symptoms and signs of ITH recurrence were present in only one third of the patients, and the diagnostic specificity and sensitivity of serum lactate dehydrogenase were only 33% and 85%, respectively. Since ITH recurrences often are silent, and since recurrence in this site may have both prognostic and therapeutical implications, routine chest x-ray is indicated in all patients with first recurrence of breast cancer.
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PMID:Metastatic pattern in recurrent breast cancer. Special reference to intrathoracic recurrences. 317 37

Concentrations of total serum N-acetyl-neuraminic acid, carcinoembryonic antigen, ferritin, lactate dehydrogenase, creatine phosphokinase and total proteins were measured in both tumor drainage blood (axillary vein) and in peripheral blood taken during surgery from 44 breast cancer patients. There were no significant differences in any of the markers between mean values in peripheral and tumor drainage blood, between cancer patients and healthy controls, between patients with or without axillary lymph node metastases, or according to the site of breast mass.
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PMID:Sialic acid, ferritin and CEA levels in peripheral blood and blood draining from the tumor in breast cancer. 323 52

The clinical efficacy of four laboratory tests in detecting leptomeningeal metastases in 57 patients with breast carcinoma was assessed. The sensitivity and specificity of beta-glucuronidase, beta 2-microglobulin, carcinoembryonic antigen and lactate dehydrogenase in cerebrospinal fluid were determined. As a single test beta-glucuronidase was the most sensitive (93%) and specific (93%) for discriminating between leptomeningeal metastases and other CNS metastases from breast cancer. Lactate dehydrogenase was the next most useful marker. Both beta 2-microglobulin and carcinoembryonic antigen had a sensitivity of 60%. More specific results were achieved by combining beta-glucuronidase and lactate dehydrogenase. CSF beta-glucuronidase may be useful by itself and in combination with lactate dehydrogenase in the detection of leptomeningeal metastases from breast carcinoma.
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PMID:Sensitivity and specificity of single and combined tumour markers in the diagnosis of leptomeningeal metastasis from breast cancer. 972 63

The occurrence of liver metastases was evaluated by ultrasonic scanning and correlated with prognostic factors, pattern of metastases, clinical examination, biochemical liver function tests from serum, and liver biopsy specimens in 394 consecutive evaluable patients with first recurrence of breast cancer. Fifty-nine patients (15%) had a positive scan, and liver metastases were the only sign of recurrent disease in 11 of these patients. The presence of liver metastases was not associated with age, menopausal status, size of the primary tumor, regional lymph node status, or the length of the recurrence-free interval; but patients with liver metastases were significantly closer to the menopause than those without (P = 0.02). The diagnostic value of clinical examinations was comparable to that of serum bilirubin and serum aspartate aminotransferase (ASAT) analyses, but was significantly better than alkaline phosphatase (AP) and lactate dehydrogenase (LDH) analyses. Analysis of serum AP was not a valuable diagnostic tool in the diagnosis of liver metastases, since it was elevated in 58% of the patients with bone metastases, and since metastases in this site were found in one third of the patients without liver metastases. If all four tests were negative, liver metastases were excluded in 99% of the patients, and if more than two of the four tests were positive, liver metastases were found in 95%. Valid (greater than 80%) diagnosis of liver metastases by serum LDH or serum ASAT alone, required an elevation of three or five times the upper normal limits, respectively. Thirty-nine patients with positive ultrasonography results underwent biopsy. The ultrasonographic diagnosis could not be confirmed histologically in three patients (8%). If ultrasonic scanning had not been performed routinely, only one of 213 patients (0.5%) with soft tissue metastases would have been offered local therapy rather than systemic treatment. These data suggest that ultrasonic scanning of the liver should not be a routine diagnostic tool in examination of patients with first recurrence of breast cancer. However, whenever indicated by clinical signs or elevated blood tests, scanning should be performed to confirm the presence of liver metastases, particularly in patients entering therapeutical trials, since liver metastases demonstrated by ultrasound examinations may serve as a measurable parameter.
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PMID:Incidence and methodologic aspects of the occurrence of liver metastases in recurrent breast cancer. 354 42


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