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)

The prognosis of doxorubicin-induced congestive heart failure (CHF) is reported to be poor. To define the clinical course of doxorubicin-induced CHF, the authors reviewed their experience with 43 patients with this diagnosis. The median age of the total group was 55 years (range, 23-69); the median cumulative dose of doxorubicin was 450 mg/m2 (range, 200 mg/m2-1150 mg/m2). A majority of the patients had a diagnosis of breast cancer. The median survival of the whole group estimated by means of a Kaplan-Meier plot was 112 weeks. Twelve of 43 patients (28%) died of CHF, 7 of them (16%) because of fulminant failure in less than 8 weeks and the remaining 5 because of a more protracted course with recurrent episodes of cardiac decompensation. Twenty-five of the 43 patients (58%) achieved complete control of CHF. In the remaining 6 patients (14%), CHF had improved but was not completely controlled at the time of death, which was secondary to progressive tumor. Treatment consisted of standard therapy with digitalis and diuretics. Survival was significantly shorter in patients who presented with class IV dyspnea and in those who developed CHF less than 4 weeks after administration of the last dose of doxorubicin. The authors conclude that in a majority of patients, doxorubicin-induced CHF is easily treatable and frequently controlled with digitalis and diuretics.
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PMID:Doxorubicin-induced congestive heart failure in adults. 402 74

43 patients with advanced breast cancer, resistant to conventional therapies, were treated with mitomycin C at a dose of 20 mg/m2 i.v. every 6 weeks. No response was observed. The most common side effect was myelotoxicity. Leukopenia occurred in 63% of the patients, thrombocytopenia in 67%, and anemia in 14%. Two episodes of acute dyspnea were observed which were thought to be pulmonary hypersensitivity reactions. This study does not suggest that mitomycin C is of value as second- or third-line treatment in metastatic breast cancer. It is likely that the drug could play a more important role in combination with other chemotherapeutic agents.
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PMID:Mitomycin C in patients with metastatic breast cancer refractory to hormone therapy and chemotherapy. 640 47

Chemotherapy-related pneumonitis developed in eight patients during treatment for breast cancer. Six were receiving adjuvant therapy and two were being treated for metastatic disease. Fever, chills, dyspnea, and dry cough were the initial symptoms. Observations from chest roentgenograms varied from normal to bilateral interstitial-alveolar infiltrates. Results of pulmonary function tests were markedly abnormal, with a decreased diffusing capacity being the most characteristic abnormality. The pneumonitis developed in six patients while receiving 20 mg or less per day of prednisone and appeared temporarily related to tapering of steroid therapy in four patients. All patients recovered clinically, although prednisone therapy of 60 mg/day or its equivalent was required in three cases. Mild pulmonary function abnormalities persisted. Drug-induced pneumonitis should be considered in the differential diagnoses of patients with breast cancer in whom unexplained fever, dyspnea, or infiltrates develop during multidrug chemotherapy.
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PMID:Chemotherapy-associated pulmonary toxic reactions during treatment for breast cancer. 660 32

Although hypercalcemia is a well-known complication of malignant diseases, hypocalcemia seems to be a rather rare one. A 34-yr-old woman with advanced breast cancer who presented hypocalcemia is described. She had generalized multiple osteolytic bone metastases which were progressive in spite of chemo-endocrine and radiation therapy. She was admitted because of severe bone pain and dyspnea caused by bilateral pleural effusion. Laboratory examination on admission showed that the serum calcium was 9.6 mg/dl, serum total protein 5.9 g/dl, serum inorganic phosphorus 4.6 mg/dl, and serum alkaline phosphatase 29.6 King-Armstrong units. The serum calcium gradually fell to 7.0 mg/dl on the 45th hospital day when the serum total protein was 6.8 g/dl and she complained of paresthesia in the extremities. On the 58th day, severe tachycardia and hypotension developed and she died of congestive heart failure on the 67th hospital day. At that time the serum calcium was 5.4 mg/dl. During her hospital course, the plasma parathyroid hormone levels were examined repeatedly and were 0.4, 0.6, 0.6 and 0.7 ng/ml (normal; less than 0.5 ng/ml). Autopsy revealed that cancer invaded the space between the thyroid and the trachea and no parathyroid glands could be found even in the mediastinum. Microscopically the parathyroid glands were replaced completely by the cancer cells. These observations indicate that metastasis of breast cancer to the parathyroid glands caused relative hypoparathyroidism, resulting in hypocalcemia. In addition, congestive heart failure which was refractory to digitalis and diuretics might have been caused by impaired contractility of the myocardium associated with hypocalcemia.
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PMID:A case of advanced breast cancer associated with hypocalcemia. 688 61

A case of endobronchial metastasis from breast cancer is presented. The anatomopathological findings suggested the presence of another primary site with metastatic pleural effusion. It is imperative, however, to consider intrathoracic metastasis in patients with breast carcinoma and presenting symptoms such as cough, dyspnea with radiological findings of pulmonary nodules, pneumonitis, atelectasis, pleural effusion and hilar lymphadenopathy. Endobronchial metastasis is extremely rare: it may be the result of carcinomatous emboli through the blood stream or direct invasion of the bronchus by the adjacent carcinomatous lymphadenopathy. Pleural effusion in patients with intrathoracic metastasis does not necessarily evidence pleural metastasis.
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PMID:Endobronchial metastasis from breast carcinoma. 727 10

To evaluate the efficiency of pleurodesis (PD) in the management of symptomatic malignant pleural effusion (PE) in breast cancer, we reviewed 46 patients undergoing 49 PDs. When radiotherapy was part of the initial treatment, 41% of PEs were ipsilateral to the primary, if not, 85% of PEs were ipsilateral (P < 0.0075). Six percent of patients presented dyspneic with exertion, 32% during daily routine; 61% at rest. All except 1 were improved after PD; 74% had no dyspnea, 23% had exertional dyspnea. PD relieved chest pain in 4 and cough in 5 patients. With 31 Talc/Iodine PDs, 2 mortalities and 2 minor complications occurred. Of 17 tetracycline PDs, 1 was complicated by bronchopleural fistula and 1 failed. 1 Mustine PD was uncomplicated. Survival at 6, 12, and 24 months was 58%, 40%, and 13%, respectively. Primary local radiotherapy may prevent ipsilateral PE. Talc/Iodine and tetracycline PD reliably provide relief from the distressing symptoms of malignant PE.
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PMID:Breast cancer complicated by pleural effusion: patient characteristics and results of surgical management. 789 13

An animal model for breast cancer, brain and bone metastasis was developed using ENU1564, a cell line established from a metastatic mammary adenocarcinoma induced by N-ethyl-N-nitrosourea in a female Berlin-Druckrey IV rat. The original tumor isolate (designated FP1) spontaneously metastasizes to regional lymph nodes and lung following orthotopic inoculation into mammary fat pad (mfp) and metastasizes widely following left cardiac ventricle (LV) inoculation. From FP1, two sublines were selected from brain metastases (designated Br7-C5) or from slowly growing colonies in vitro (FP2-A11), then cloned and compared in assays of spontaneous and experimental metastasis. After inoculation of 10(5) cells into mfp, Br7-C5 formed large tumors at the inoculation site (9.4 +/- 3.3 g) and spontaneously metastasized to lung and lymph node by 55 days post-inoculation (dpi). In contrast, FP2-A11 produced much smaller tumors within mfp (0.6 +/- 0.3 g) and failed to metastasize by 55 dpi. Rats inoculated via the LV with 10(4) Br7-C5 cells developed signs of weight loss, head tilt, and dyspnea by 24 +/- 1.4 dpi with consistent colonization of brain, bone, lung, heart, kidney, and stomach. Rats inoculated similarly with FP2-A11 showed no signs until 53 +/- 12.3 dpi, when all developed rear limb paresis. There was significant colonization of only brain and bone, with only minor lung involvement. These ENU1564 sublines thus differ in their apparent rates of tumor growth and lesion development in vivo, their capacity to metastasize from orthotopic implantation sites, and in the spectrum of tissues colonized in experimental metastasis assays. Both clones provide reproducible models of breast cancer metastasis in syngeneic hosts, particularly to brain and bone.
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PMID:Characterization of brain and bone-metastasizing clones selected from an ethylnitrosourea-induced rat mammary carcinoma. 803 3

We retrospectively evaluated the computed tomography (CT) findings in 20 patients with pulmonary drug toxicity that followed high-dose chemotherapy and autologous bone marrow transplantation (ABMT). Eighty-five patients with Stage II or III breast cancer that involved > or = 10 axillary lymph nodes were enrolled in a treatment protocol that included four cycles of standard-dose therapy (CAF) followed by one cycle of high-dose treatment (CPA/cDDP/BCNU). After chemotherapy, ABMT was performed. Twenty-six patients (31%) developed pulmonary drug toxicity. Serial thoracic CT studies were available in 20 of these 26 patients. All 20 patients exhibited clinical symptoms (i.e., dyspnea, nonproductive cough, and fever) and abnormal pulmonary function following transplantation. Thirteen patients had pathologically proven drug toxicity, and seven patients had clinical features and treatment responses highly suggestive of this diagnosis. Multiple sputum and blood cultures were negative in all patients. CT scans of 13 patients (65%) demonstrated scattered, predominantly peripheral ground-glass or consolidated opacities that occasionally looked nodular or masslike. Two patients (10%) had CT scans suggestive of pulmonary edema and in five patients (25%), the CT examinations revealed no significant abnormalities. Pleural effusions and adenopathy were uncommon. Pulmonary drug toxicity after high-dose chemotherapy and ABMT should be suspected in the appropriate clinical and radiographic setting, and therapy may be initiated on the basis of these observations.
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PMID:Pulmonary drug toxicity following high-dose chemotherapy with autologous bone marrow transplantation: CT findings in 20 cases. 820 80

We reported a 51-yr-old female with radiation-induced chronic constrictive pericarditis. At age 29, she had received a mastectomy and postoperative irradiation because of left breast cancer. At age 45, she had syncope and was diagnosed with complete atrioventricular block and a pacemaker was implanted. At that time, pericardial thickening with effusion was noted. The following year, tricuspid regurgitation was noted. On catheter study, a dip and plateau pattern of the right ventricular pressure curve appeared. At age 50, tricuspid regurgitation worsened due to the lead wire of the pacemaker compressing the leaflet, and the pacemaker was reimplanted. However, the following year, she complained of general fatigue and dyspnea and was admitted to our hospital. On 67Ga study, diffuse accumulation in the cardiac region appeared. There was no perfusion defect detected in the left myocardium, but right myocardial damage was suspected by thallium study. In 99mTc-HSA RI angiography, right atrium dilatation appeared and a pericardial halo around the ventricles was seen. She underwent pericardectomy, tricuspid replacement and pacemaker reimplanted, but she died. On autopsy, pericardial thickening and adhesion, right myocardial fibrosis, the fibrotic change of the bundle branches were seen. We reported a case of radiation-induced constrictive pericarditis. Radionuclide studies were useful in diagnosing and following the patient.
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PMID:[A case of radiation-induced chronic constrictive pericarditis developing 16 years after irradiation]. 823 Aug 30

A protocol consisting of standard-dose adjuvant chemotherapy, high-dose combination alkylating agent chemotherapy, and autologous bone marrow transplant (ABMT) used at our institution for patients with primary breast cancer and extensive axillary lymph node involvement has been associated with a clinical syndrome of pulmonary drug toxicity in 23 of 59 patients (39%). In 10 patients in whom open-lung biopsies or transbronchial lung biopsies were obtained, we correlated the pulmonary pathology with the clinical features of the syndrome. These 10 patients presented with dyspnea, cough, fever, and hypoxemia at a mean time of 48 +/- 14 days after initiation of high-dose chemotherapy. Chest radiographs and CT scans showed interstitial and alveolar opacities. Pulmonary function tests revealed restrictive lung disease and reduced diffusing capacities. Open-lung and transbronchial lung biopsies showed alveolar septal thickening with fibrosis, atypical Type II pneumocytes, and pulmonary endothelial cell injury characteristic of drug toxicity. Corticosteroid therapy resulted in clinical improvement in 7 of 10 patients, but significant pulmonary function abnormalities remained. Local radiation therapy to the chest wall and regional lymph nodes appeared to exacerbate preexisting pulmonary drug toxicity in 4 patients. Two agents in the protocol, cyclophosphamide and carmustine (BCNU), can be implicated in the pathogenesis of this syndrome, and these agents most likely act synergistically to deplete reduced glutathione and impair antioxidant defenses. Since these drugs appear to contribute to the protocol in prolonging disease-free survival, prophylactic therapy of the lung should be investigated to reduce the high incidence of pulmonary toxicity.
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PMID:Pulmonary drug toxicity in patients with primary breast cancer treated with high-dose combination chemotherapy and autologous bone marrow transplantation. 848 41


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