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)

Creatine kinase BB serum levels were evaluated by radioimmunoassay in patients with benign or malignant breast pathology. Elevated enzyme levels were observed in 6 out of 20 (30%) patients with primary breast cancer. After surgery the levels fell to normal values only in patients without nodal involvement. Six out of 28 (21%) patients with benign breast lesions and 4 out of 38 (13%) patients with metastatic breast cancer also showed increased levels of the enzyme. Most of the patients with high creatine kinase BB serum levels were found to have estrogen and progesterone receptor-positive tumors. These findings suggest that creatine kinase BB can barely be considered a marker of malignancy in breast pathology, but rather an indicator of hormone dependency in breast cancer.
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PMID:Elevated serum levels of creatine kinase BB in breast cancer. 397 93

Thirty-eight evaluable patients with metastatic breast cancer refractory to hormonal therapy and multiple chemotherapy regimens were treated with mitolactol at a dose of 130 mg/m2/day orally for 10 days every 6 weeks. Only one patient, with nodal and chest wall metastases, had a sustained complete regression; two patients had stable disease; and 35 patients had disease progression. The toxicity, which was primarily hematologic, was acceptable.
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PMID:Phase II study of mitolactol in chemotherapy-refractory metastatic breast cancer. 654 36

Twenty-one evaluable patients with metastatic breast cancer received three pulses of intravenous cyclophosphamide, escalating from 1.5 g/m2 to 2.5 g/m2 in the second and third courses. There were eight partial remissions (34.7%), but most were of short duration. All responding patients had soft tissue or nodal disease, but additional sites of response were bone (three cases), liver and lung (one case each). Marked leucopaenia (median WBC 0.7 X 10(9)/L) occurred 10-12 days after the higher doses (2.5 g/m2) and was associated with nine episodes of severe infection in five patients. Marked vomiting and anorexia led to significant weight loss (mean 4.5 kg) in half the patients, and alopecia was universal. In metastatic breast cancer cyclophosphamide seems to have a shallow dose response curve and high intermittent dosage seems to have no advantage over chronic daily administration.
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PMID:Intermediate dose single agent cyclophosphamide chemotherapy of advanced breast cancer. 661

Comprehensive immune function by integrated score was assessed in 158 operable, 55 inoperable, and 52 metastatic breast cancer patients relative to 107 healthy controls. The score was derived from in vivo response to PPD and DNCB and in vitro lymphocyte stimulation by PPD and PHA. Proportion of E-RFC was significantly lower in patients than in controls but was not found to correlate directly with the above functional criteria. Fifty-one percent of the patients with early, operable tumors were shown to be at least partially immunosuppressed by integrated score achievement vs. 11% of controls. This proportion rises to 68% of inoperable and 89% of metastatic patients. Quantitative analysis by graded response revealed an additional, significant degree of immune impairment in the respective patient groups by all testing parameters. Depression of immune function in operable patients was not related to age nor influenced by surgery. Immunocompetence of patients with mammary dysplasia did not differ from controls. Increasing size of primary tumor (T) was not found to be matched by progressive degree of immunosuppression, excepting that associated with large T4 tumors. Patients with lymph node involvement (N+) were not significantly immunologically inferior to those without (N0) where the larger operable T2-3) tumors are concerned. In the smallest, T1 tumors, nodal involvement (N+) is accompanied by remarkable immunosuppression relative to T1N0 cases. This finding suggests a pre-existing immune defect inherent in T1N+ patients. It supports the hypothesis that the immunosuppression associated with early breast cancer is primary, patient related. Secondary tumor-induced depression of immune response characterizes advanced and metastatic human breast cancer.
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PMID:Immunocompetence, immunosuppression, and human breast cancer. II. Further evidence of initial immune impairment by integrated assessment effect of nodal involvement (N) and of primary tumor size (T). 737 Sep 52

Sixty breast cancer patients with hormone-resistant metastatic disease who had progressed after chemotherapy with low-dose cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) or with L-phenylalanine mustard underwent treatment with a low-dose Adriamycin regimen,i.e., 20 mg/m2, intravenously on days 1 and 8 every 28 days. Two percent of patients had complete responses; 25%, partial responses; 38%, stabilization; and 35%, progression. The time to progression for the responders was similar to that of the stabilized patients, while the responders and stabilized patients survived significantly longer than did the progressors. Responses were seen in nodal, hepatic, dermal/subcutaneous, bone, pulmonary, and peritoneal metastases. The toxicity was mild: 18% of patients had leukocyte counts of less than 3,000/mm3; 10% had platelet counts of less than 90,000/mm3, 22% experience vomiting; and 33% had hair loss. No patient experienced local venous/subcutaneous toxicity or heart failure. Since this regimen of low-dose Adriamycin appears to be as effective as, but less toxic than, the secondary standard-dose of Adriamycin at 60--75 mg/m2 every three weeks, a randomized trial of low-dose Adriamycin vs. standard-dose Adriamycin should be conducted in metastatic breast cancer patients who have previously undergone chemotherapy.
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PMID:An effective low-dose adriamycin regimen as secondary chemotherapy for metastatic breast cancer patients. 739 18

Paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) administered by a 3-hour infusion causes a rapid decline to and recovery from the hematologic white blood cell nadir. This suggests that biweekly administration of paclitaxel alone or in combination with drugs that have limited hematologic toxicity may be possible. The first study discussed in this report tried to determine the tolerability and activity of biweekly paclitaxel administered in combination with cisplatin in patients with metastatic breast cancer. Subsequently, after an impressive response rate, a second study of biweekly paclitaxel alone was initiated to attempt to discern which activity spectrum and which toxicities were due to paclitaxel and which were due to cisplatin. Patients with metastatic breast cancer who received up to one prior adjuvant chemotherapy regimen were eligible for both studies. Paclitaxel was administered intravenously by a 3-hour infusion followed by intravenous cisplatin biweekly in the ambulatory setting. In the second study, paclitaxel was administered alone. Twenty-nine patients have been entered in the combination study, of whom 27 had received prior adjuvant therapy and 23 had received prior anthracyclines. Dose-limiting toxicity for the phase I study of paclitaxel and cisplatin proved to be a failure to recover neutrophil counts greater than 750 cells/microL by day 14. The maximum tolerated dose was paclitaxel 90 mg/m2 and cisplatin 60 mg/m2 every 2 weeks. Nonhematologic toxicities were mild and included fatigue, arthralgias, and nausea and vomiting. At this time, the 27 patients evaluable for response have achieved an 85% response rate and an 11% complete response rate. Complete responses have been seen in soft tissue, lung, and nodal disease. All patients with complete responses have had previous anthracyclines. The biweekly paclitaxel-alone study is still accruing patients. The current paclitaxel dose level is 150 mg/m2. It is still too early to evaluate response; however, response rates appear to be less impressive than those seen with combined paclitaxel/cisplatin. The final results of these studies are pending.
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PMID:Biweekly paclitaxel in the treatment of patients with metastatic breast cancer. 748 53

Both chemotherapy and hormonal therapy have been used in the adjuvant therapy of breast cancer to treat micrometastatic disease before it is clinically detectable. Several prospective, randomized trials consistently have demonstrated that disease-free survival can be significantly prolonged by the use of adjuvant chemotherapy. In some of these trials overall survival was increased as well. Premenopausal nodal-positive patients should receive adjuvant chemotherapy e.g. six cycles of CMF. Tamoxifen reduces overall tumor recurrence and mortality in postmenopausal estrogen receptor positive patients and to a lesser extent in estrogen receptor poor or negative patients. The effect of GnRh-analog for premenopausal patients with is currently investigated in multicentric studies. A response related strategy for management of metastatic breast cancer by hormonal manipulation and cytotoxic chemotherapy is outlined.
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PMID:[Chemotherapy and hormone therapy in breast carcinoma]. 770 19

Hormonal therapy for breast cancer began more than a century ago with the observation that bilateral oophorectomy caused tumor regression in selected premenopausal patients. In the first half of this century, besides extending ablation of ovarian function to photon irradiation, surgical adrenalectomy and hyophysectomy were introduced, and hormonal additive therapy was established. Regression rates for advanced breast cancer with all types of endocrine therapy at this point did not exceed 35%. The demonstration that adjuvant systemic therapy can prolong the disease-free interval and improve overall survival has been a major advance in the management of breast cancer, the rationale was to control or eliminate micrometastases before tumor recurrence. The nonsteroidal antiestrogen tamoxifen was chosen for the majority of studies since the mid-1970s. Since the first report of successful treatment of metastatic breast cancer, the number of treated women worldwide has reached over 3,000,000. Objective response rate (CR+PR following UICC) in unselected patients is 34%. Tamoxifen has been used successfully to treat both pre- and postmenopausal women with all stages of the disease. In an overview analysis of 30,000 patients from 40 trials of adjuvant tamoxifen, a significant increase was found in both disease-free and overall survival. When patients were separated by nodal status, statistically significant increases were observed in disease-free and overall survival for both node-positive and node-negative patients. Women over 50 appear to benefit most from tamoxifen treatment experiencing highly significant increases in disease-free and overall survival regardless of nodal status. However, since tamoxifen primarily acts as a cytostatic and not cytotoxic agent, most patients ultimately experience disease recurrence or progression during or after therapy. Newer antiestrogens include trioxifene, toremifene, and droloxifene (3-OH-tamoxifen). Randomized, prospective studies are still under way to establish their clinical superiority (or lack of it). Progestins exert direct antiproliferative effects on human breast cancer cell lines. They may also exert direct antiestrogenic action by increasing the oxidative activity of 17 beta-hydroxy-steroid-dehydrogenase, thereby facilitating the conversion of estradiol to estrone. Progestins may exert additional antiestrogenic effects by suppressing estrogen receptor levels. As they also cause estrogen deprivation indirectly through suppression of pituitary ACTH secretion, resulting in reduced production of adrenal androgen precursors, both low- and high-dose regimens have been studied. Aromatase inhibition in premenopausal women interrupts estrogen biosynthesis; the reflex rise in FSH then stimulates production of new aromatase enzyme, and the LH increment results in enhanced ovarian steroidogenesis, counteracting the inhibitory action of aromatase-blocking drugs on the ovary.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endocrine management of breast cancer. 787 88

Chemotherapy is a major tool for metastatic breast cancer treatment. In this study, a series of 316 patients have been analyzed to evaluate the time needed to reach tumor response by means of combination chemotherapy. Twenty-five percent of patients responded within 3 months and virtually all responses occurred within 7.5 months. The time curves of response (any) and best response are superimposable. A subset analysis has shown that the following pretreatment characteristics predict a significantly longer time to response: prior exposure to adjuvant chemotherapy, nodal positivity at diagnosis, no previous endocrine treatment and osseous metastases.
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PMID:Analysis of time to response to chemotherapy in 316 metastatic breast cancer patients. 823 88

Identification of multiple clinical and pathologic prognostic factors in differentiated thyroid cancer has permitted some degree of risk stratification. However, these clinical indices fail to distinguish potential intrinsic differences in tumor virulence. The nm23 gene has been identified as a potential metastasis suppressor gene that is homologous to nucleoside diphosphate kinases. Studies in human breast cancer have shown a significant inverse correlation between nm23 levels and nodal involvement/tumor recurrence. Given the possible clinical utility of a marker of metastatic potential in the management of thyroid carcinoma, we examined 34 thyroid neoplasms and a human medullary thyroid cancer (MTC) cell line (TT) for nm23 expression. Normalized nm23 expression was assessed by Northern analysis of tumor RNA. nm23 Expression (tumor expression/TT cell expression, mean +/- SE) was 1.14 +/- 0.15* in MTCs (n = 5), 0.70 +/- 0.10* in follicular cancers (n = 6), 0.51 +/- 0.11 in papillary cancers (n = 19), and 0.31 +/- 0.03 in follicular adenomas (n = 4) (*p < 0.05 when compared to adenomas). Within histologic groups, we found no correlation between nm23 expression and nodal involvement of distant metastases. Our results indicate that thyroid neoplasms of different histologies express varying levels of the nm23 transcript. Although nm23 expression seems diminished in metastatic breast cancer, it appears not to be the case in metastatic thyroid cancer. The nm23 gene may therefore have different roles in the evolution and metastases of different neoplasms.
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PMID:Expression of a potential metastasis suppressor gene (nm23) in thyroid neoplasms. 827 82


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