Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278488 (metastatic breast cancer)
 7,812 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-one of 62 consecutive premenopausal women with primary cancer of the breast completed a 1-year investigation period, receiving either 30 mg tamoxifen daily (15 patients) or placebo (16 patients). They were examined at the operation (t0) and at 3-month intervals (t1, t2, t3, and t4). Bone mineral content (BMC) was measured at operation and after 12 months. Fifty-six patients with benign tumors were included as healthy controls. All values of both cancer treatment groups and of the benign tumor group were comparable at the time of operation. BMC decreased significantly in both cancer patient groups when 12-month values were compared to the initial level (tamoxifen, -3.2%, P less than 0.001 and placebo -2.5%, P less than 0.01). However, no significant difference in BMC changes was noted between tamoxifen and placebo treatment. The serum phosphate was significantly decreased in the tamoxifen treatment group at each examination. In the placebo group, the alkaline phosphatase level increased significantly at each examination, whereas the serum magnesium fell at the 6- and 12-month examinations. All other biochemical indices of calcium metabolism were basically unchanged. It is concluded that BMC is reduced in metastatic breast cancer through osteolytic metastatic bone foci. Tamoxifen also decreases the BMC. It is, however, unclear if this effect is due to a progression of the disease in spite of the treatment or if it is caused by a direct action of tamoxifen on bone.
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PMID:The effect of tamoxifen on bone mineral content in premenopausal women with breast cancer. 669 87

Serum CEA levels were determined in 2095 patients following mastectomy for breast cancer by means of a double antibody 125 I-CEA-radioimmunoassay. 91% of 1462 patients free of metastases had normal levels less than or equal to 3 ng/ml (98% less than or equal to 5 ng/ml). In contrast, 54% of 633 patients with overt metastases had raised values greater than 3 ng/ml (43% greater than 5 ng/ml). The incidence of pathological levels was dependent on tumour burden and metastatic location rising from solitary lymph node disease (6% greater than 5 ng/ml) to skin, lung, bone, liver and multiple organ involvement (60%). CEA levels correlated weakly with total alkaline phosphatase and gamma-GT activities, but not with ESR or bilirubin levels. Of 531 patients followed after surgery and who had 3-18 serial determinations in 3-51 months, 46% without metastases had normal CEA levels as did 41% of 285 patients with metastases. Of the remaining 168 patients with elevated CEA levels, most showed a correlation between rising levels and disease progression, decreasing levels with remission and persistence of fluctuating levels with stationary disease. The CEA test is recommended as a valuable adjunct to monitor the clinical response to chemo/hormo/radiotherapy in metastatic breast cancer.
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PMID:Serial carcinoembryonic antigen (CEA) determinations in the management of metastatic breast cancer. 727 99

Peripheral blood progenitor cells (PBPCs) are increasingly used for autografting after high-dose chemotherapy. One advantage of PBPCs over the use of autologous bone marrow would be a reduced risk of tumor-cell contamination. However, the actual level of tumor cells contaminating PBPC harvests is poorly investigated. It is currently not known whether mobilization of PBPCs might also result in mobilization of tumor cells. We evaluated 358 peripheral blood samples from 46 patients with stage IV or high-risk stage II/III breast cancer, small cell (SCLC) or non-small cell (NSCLC) lung cancer, as well as other advanced malignancies for the detection of epithelial tumor cells. Monoclonal antibodies against acidic and basic cytokeratin components and epithelial antigens (HEA) were used in an alkaline phosphatase-anti-alkaline phosphatase assay with a sensitivity of 1 tumor cell within 4 x 10(5) total cells. Before initiation of PBPC mobilization, circulating tumor cells were detected in 2/7 (29%) patients with stage IV breast cancer and in 2/10 (20%) patients with extensive-disease SCLC, respectively. In these patients, an even higher number of circulating tumor cells was detected after chemotherapy with VP16, ifosfamide, and cisplatin (VIP) followed by granulocyte colony-stimulating factor (G-CSF). This approach has previously been shown to be highly effective in mobilizing PBPCs. In the 42 patients without circulating tumor cells during steady state, tumor cells were mobilized in 9/42 (21%) patients after VIP+G-CSF induced recruitment of PBPCs. The overall incidence of tumor cells varied between 4 and 5,600 per 1.6 x 10(6) mononuclear cells analyzed. All stage IV breast cancer patients and 50% of SCLC patients were found to concomitantly mobilize tumor cells and PBPCs. Kinetic analyses showed two patterns of tumor cell recruitment depending on the presence or absence of bone marrow disease: (1) early after chemotherapy (between days 1 and 7) in patients without marrow infiltration, and (2) between days 9 and 16 in patients with marrow infiltration, ie, within the optimal time period for the collection of PBPCs. We show that there is a high proportion of patients with circulating tumor cells under steady-state conditions, and in addition a substantial risk of concomitant tumor cell recruitment upon mobilization of PBPCs, particularly in stage IV breast cancer patients with bone marrow infiltration. The biologic and clinical significance of this finding is unknown at present.
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PMID:Mobilization of tumor cells and hematopoietic progenitor cells into peripheral blood of patients with solid tumors. 790 97

Circulating blood cell counts, serum cortisol, proteins, alkaline phosphatase, carcinoembryonic antigen and CA15.3 displayed significant circadian rhythms in a group of 13 women with metastatic breast cancer. Statistical significance (P < 0.05) was assessed with both analysis of variance and cosinor analysis. All patients had been previously treated with chemo-and/or radiotherapy and/or antiestrogens. All patients had been treatment-free for 1 month prior to the study. Each patient had blood drawn every 4 h for 48 h. Circadian rhythms were examined as a function of performance status, graded according to the World Health Organization, liver involvement and number of metastatic sites. Group circadian rhythms in serum cortisol or proteins were abolished in patients with liver metastases, and were altered in cases of poor performance status. Circulating leukocytes, neutrophils or platelets did not exhibit synchronized circadian rhythmicity in patients with poor performance status or liver metastases. The number of metastatic organs had a minor influence on circadian rhythmicity. These results suggest that rhythm alteration may be associated with both poor performance status and liver metastases in patients with advanced breast cancer. Such alteration of the normal circadian time structure may favor and/or result from cancer spread.
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PMID:Rhythm alteration in patients with metastatic breast cancer and poor prognostic factors. 771 90

The CA 15-3 and CEA concentrations and the alkaline phosphatase (ALP) and gamma-glutamyl transferase (Gamma GT) activities of serum from 78 patients with breast cancer have been measured. The patients included 27 with localised breast cancer, 19 who had been treated for breast cancer but were now disease-free, 17 with liver metastases, 8 with bone metastases, and 7 with disseminated breast cancer but with neither metastases to the liver or bone. As an indicator of localised breast cancer the predictive value of an increase in CA 15-3 concentration was 93%. As an indicator of metastatic breast cancer the predictive value of an increased CA 15-3 was 62%, whereas the predictive values of an increase in both CA 15-3 and CEA and an increase in CA 15-3, CEA, and ALP 88% and 100%, respectively. A normal CA 15-3 excluded metastatic breast cancer and a normal gamma-GT excluded liver metastases. The four tests together provide a set of markers for use in the follow-up of patients with breast cancer.
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PMID:A profile of serum CA 15-3, carcinoembryonic antigen, alkaline phosphatase, and gamma-glutamyl transferase levels in patients with breast cancer. 809 32

Because of their high affinity for bone, bisphosphonates are used both in the treatment of benign and malignant bone disease and in radiopharmaceutical bone imaging. A prospective study was undertaken to evaluate whether intravenous clodronate (dichloromethylene bisphosphonate) therapy might affect the results of bone scintigraphy with 99mTc-labeled methylene diphosphonate (MDP). In 11 female patients with breast cancer and metastatic bone disease, quantitative bone scans were obtained using a region of interest (ROI) method on Days 0 and 22. After intravenous clodronate therapy from Day 1 to Day 21, all metastatic bone lesions were still detectable, and median ROI ratios did not differ to a statistically significant extent from baseline values. Serum calcium levels decreased (p = 0.0449), whereas parathyroid hormone concentrations showed an increase (p = 0.0053). Mean serum levels of creatinine, inorganic phosphorus, osteocalcin, gamma glutaminyl-transpeptidase and alkaline phosphatase remained unchanged. However, a more than twofold rise in the serum activity of alkaline phosphatase was measured in three patients. We conclude that 3 wk of intravenous clodronate treatment did not impair the sensitivity of 99mTc-MDP bone scintigraphy in detecting bone lesions in patients with metastatic breast cancer.
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PMID:Effect of clodronate treatment on bone scintigraphy in metastatic breast cancer. 866 85

The evaluation of contaminating breast cancer cells in hematopoietic grafts is of considerable importance for monitoring the efficiency of purging procedures. We report a comparison of three systems for the in vitro detection and enumeration of metastatic breast cancer cells. Breast cancer cells from established cell lines were mixed with Daudi cells at dilutions ranging from 1:10 to 1:1,000,000, and a predetermined number were fixed in defined areas on microscope slides coated with one of the following attachment factors: (i) Cell-Tak Cell and Tissue Adhesive, (ii) 0.1% solution of Poly-L-Lysine, or (iii) Cel-Line HTC Super Cured slides. We employed a specificity-proven pancytokeratin antibody (A45-B/B3) and the alkaline phosphatase-antialkaline phosphatase (APAAP) staining technique. In multiple experiments, one breast cancer cell in 1,000,000 Daudi cells could reliably be detected in the Cell-Tak and Cel-Line systems and 1 in 100,000, with the Poly-L-Lysine system. The observed number of seeded cells showed a highly significant correlation with the number of cells seeded (p < 0.0001 in all cases). Finally, we used the Cell-Tak method to evaluate clinical material from various sources: from patients with primary carcinomas of the breast, prechemotherapy, and during various chemotherapeutic regimens, as well as from patients with metastatic disease. The system consistently detected tumor cells in bone marrow samples from these patients. All peripheral blood samples from patients with metastatic disease tested positive at incidences ranging from 5 to 19/10(6) peripheral blood mononuclear cells. This is a simple and reliable technique that allows rapid screening of large cell numbers with high resolution of positive cells.
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PMID:Immunocytochemical detection of breast cancer cells: a comparison of three attachment factors. 911 15

Osteopontin (OPN) is a secreted, integrin-binding phosphoprotein that has been implicated in both normal and pathological processes; qualitative increases in OPN blood levels have been reported in a small number of patients with metastatic tumors of various kinds. We measured plasma OPN levels in 70 women with known metastatic breast carcinoma, 44 patient controls who were on follow-up after completion of adjuvant treatment for early breast cancer, and 35 normal volunteers. The median plasma OPN of patients with metastatic disease was 142 microgram/liter (range, 38-1312 microgram/liter) and was significantly different (P < 0.0001, Mann Whitney U test) from both control groups (medians, 60 and 47 microgram/liter; ranges, 15-117 and 22-122 microgram/liter). Furthermore, we found that increasing plasma OPN is associated with shorter survival (P < 0.001) when patients were grouped in terciles for plasma OPN. This was also demonstrated when using a Cox proportional hazards model. Median plasma OPN levels were significantly increased for three or more sites of involvement (median, 232 microgram/liter; n = 13) versus 1 or 2 metastatic sites (medians, 129 and 130 microgram/liter; n = 29 and 28, respectively). Plasma OPN levels were correlated with other biochemical markers related to the extent of disease, such as serum alkaline phosphatase, aspartate succinate aminotransaminase, and albumin (r = 0.81, 0.62, and -0.56, respectively; all P < 0.001). This study demonstrates a statistically significant elevation in plasma OPN in the majority ( approximately 70%) of a large series of patients with metastatic breast cancer when compared (95th percentile) to healthy women or patients who had completed adjuvant treatment for early-stage breast cancer. Furthermore, this is the first study to demonstrate that higher OPN levels in patients with metastatic breast cancer may be associated with an increased number of involved sites and decreased survival.
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PMID:Elevated plasma osteopontin in metastatic breast cancer associated with increased tumor burden and decreased survival. 981 27

Concentrations of soluble c-erbB-2 were determined in the sera of 64 patients with distant metastasis from advanced breast cancer receiving second-line hormone or chemotherapy in comparison to 35 breast cancer patients without detectable recurrent disease and 17 healthy blood donors. The sera of non-metastatic breast cancer patients contained s-erbB-2 concentrations similar to those of healthy blood donors. Patients with distant metastasis from advanced breast cancer had significantly higher values of s-erbB-2 in comparison to patients with non-disseminated disease (mean: 59.6 vs. 11.6 U/ml; p = 0.022). A significant correlation was observed between s-erbB-2 serum levels and serum LDH concentrations (p < 0.001), levels of alkaline phosphatase (p < 0.001), and the presence of hepatic metastasis (p = 0.001). Time to tumor progression was significantly shorter in patients with s-erbB-2 levels above 40 U/ml (mean: 23.4 vs. 56.7 months; p = 0.002). Furthermore, breast cancer patients with hepatic metastasis and those with elevated s-erbB-2 serum levels above 40 U/ml had limited response to hormone or chemotherapy. Non-responders had significantly higher s-erbB-2 levels (mean: 270.3, range: 42-500 U/ml;) compared with the responder group (mean: 23.1, range: 0-149 U/ml; p < 0.001). Logistic regression analysis indicated that elevated s-erbB-2 serum levels above 40 U/ml independently predicted an unfavorable response to second-line hormone or chemotherapy in patients with advanced metastatic breast cancer.
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PMID:Clinical relevance of soluble c-erbB-2 for patients with metastatic breast cancer predicting the response to second-line hormone or chemotherapy. 1206 44

A 47-year-old woman with metastatic breast cancer developed acute pancreatitis while receiving capecitabine. She had been receiving capecitabine 2000 mg/m2/day; however, when the dosage was increased to 2500 mg/m2/day (the maximum dosage approved by the Food and Drug Administration) she experienced abdominal pain and cramping. These symptoms were followed by nausea and vomiting, palmar-plantar erythrodysesthesia (hand-foot syndrome), and mucositis, resulting in admission to the hospital. Laboratory tests for liver function showed elevated levels of alkaline phosphatase and lactate dehydrogenase. The patient's lipase and amylase levels were also elevated, but an abdominal ultrasound was normal. After bowel rest and intravenous hydration, the patient's liver function tests and lipase and amylase levels returned to normal. Many chemotherapeutic agents have been documented to cause pancreatitis; however, we found no previously described reports of capecitabine-induced pancreatitis. Clinicians should be aware of this potential adverse effect, particularly in patients with preexisting risk factors for pancreatitis who are prescribed capecitabine.
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PMID:Capecitabine-induced pancreatitis. 1292 Dec 54


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