Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 22-year-old man with a synovial cell sarcoma attained an excellent response to therapy with adriamycin (NSC-123127) and dimethyltriazeno imidazole carboxamide (NSC-45388). Therapy was discontinued at a cumulative dose of adriamycin of 600 mg/m2. Relapse occurred 13 1/2 months later, and therapy with adriamycin was restarted. Because of tumor progression, therapy was discontinued after a cumulative dose of adriamycin of 120 mg/m2. Ten weeks later, severe congestive heart failure developed which ultimately caused the patient's death. Exacerbations of the heart failure were temporally related to the administration of the antitumor antibiotics actinomycin-D (NSC-3053) and mithramycin (NSC-24559). Electron microscopic examination of the heart revealed changes characteristic of adriamycin cardiomyopathy. Thus, even after a long hiatus, it may not be safe to exceed the recommended maximum cumulative dose level of adriamycin. The pathogenic mechanisms involved in the development of adriamycin cardiomyopathy are reviewed, and the possible synergistic effect of other antitumor antibiotics is discussed.
 ...
PMID:Cardiomyopathy after widely separated courses of adriamycin exacerbated by actinomycin-D and mithramycin. 17 14

Hepatocellular carcinoma with a tumor thrombus extending into the right atrium has been considered beyond the reach of resection. These patients usually die within a short period because of pulmonary embolism, heart failure, or cancer progression. The only treatment is hepatic resection with removal of the tumor thrombus. A 38-year-old woman underwent left lobectomy with removal of the tumor thrombus with the use of cardiopulmonary bypass. The patient had an uneventful course and is doing well 15 months after surgery, without signs of recurrence. We have proved that hepatic resection with removal of a tumor thrombus extending into the right atrium can be carried out successfully. The next problem is whether the lives of these patients can be prolonged by this operation.
 ...
PMID:Hepatocellular carcinoma with tumor thrombus extending into the right atrium: report of a successful resection with the use of cardiopulmonary bypass. 184 85

In a prospective study of 103 patients with carcinoid tumors consecutively referred for medical treatment, the most common sites of the primary tumors were the ileum (73%), bronchi (7%), and jejunum (4%). All patients had local metastases, and 96 (93%) also had liver metastases. The most common initial symptoms were diarrhea (32%), ileus (25%), and flush (23%). The overall frequency of diarrhea was 84% and of flush was 75%. Heart insufficiency caused by cardiac valve disease was seen in 33% of the patients. The carcinoid syndrome, including flush, diarrhea, and elevated urinary 5-hydroxyindole acetic acid (5-HIAA) concentrations, was manifested by 69 patients (67%), 64 of whom (93%) had carcinoid tumors of mid-gut origin. Elevated urinary 5-HIAA was found in 91 patients (88%), of which 89 displayed liver metastases. The plasma concentration of the tachykinin neuropeptide K (NPK) was elevated in 67 patients (66%), 63 of whom had tumors of the mid-gut region. Serum pancreatic polypeptide (PP) and human chorionic gonadotrophin alpha levels were elevated in 43% and 28% of the patients, respectively, and the highest levels were found in patients with metastatic bronchial carcinoid tumors. Thirty-nine of the 103 patients are now dead; 18 died of tumor progression, whereas 14 patients died of heart failure secondary to a carcinoid tricuspidal valve insufficiency. The estimated median survival from the time of histologic diagnosis was 14 years, and from the time of carcinoid syndrome was 8 years.
 ...
PMID:Malignant carcinoid tumors. An analysis of 103 patients with regard to tumor localization, hormone production, and survival. 244 Mar 90

The report analyses clinical manifestations, preoperative preparatory procedures, variants and results of urgent and emergency surgical procedures carried out in 47 cases of advanced thyroid cancer. Syndrome of grave lung-heart failure proved a major clinical sign of the disease. It could be compensated by intensive care (in a special ward included). Cervical and cervico-transsternal access was used, and surgery was performed to an extent determined by the pattern and extension of tumor. Thirteen patients died within a few days after operation and 23 at later stages. Among immediate causes of death were lung artery embolism, obstructive tracheobronchitis and tumor progression. Development of emergencies was avoided in many cases by carrying out timely examination and treatment.
 ...
PMID:[Emergency and urgent operations in the treatment of patients with thyroid cancer]. 246 Oct

A female infant, born at the gestational age of 29 weeks with a birthweight of 1,350 gm, developed progressive hepatomegaly at 10 days of age. Congestive heart failure gradually developed, and hepatic hemangioendothelioma was diagnosed at 1 month of age by open biopsy. Due to rapid enlargement of the tumor and progressive heart failure, steroid therapy was given from 36 days of age, including methylprednisolone 15 mg/kg/day for 3 days and 10 mg/kg/day for 4 days, then prednisolone 4 mg/kg/day for 20 days followed by tapering till 74 days of age. The tumor regressed gradually and was not detectable by sonography at 33 months of age. We suggest that, even in very-low-birthweight infants, the prognosis of hepatic hemangioendothelioma may be improved with aggressive therapy when symptoms develop during tumor progression, and that steroid should be the initial treatment.
 ...
PMID:Hepatic hemangioendothelioma: successful treatment with steroid in a very-low-birth-weight infant. 893 13

The aim of the present study was to evaluate an intensive chemotherapy regimen in patients with diffuse large B-cell lymphoma and poor prognosis, as presence of high- or high-intermediate clinical risk, bulky disease, high levels of beta 2 microgloblin, and more than two extranodal sites of involvement at diagnosis. One hundred previously untreated patients were treated with an intensive CEOP-Bleo regimen with increased doses of cyclophosphamide (1000 mg/m(2)) and epirubicin (120 mg/m(2)) in each cycle. Granulocyte colony-stimulating factors was employed to ameliorate severe granulocytopenia. Complete response was achieved in 79 cases (79%). With a median follow-up of 32.3 mo (range 10-45 mo) only seven patients have relapsed. Thus, actuarial curves at 3 yr, showed that event-free survival was 72%. Five died secondary to tumor progression, actuarial curves at 3-yr for overall survival were 75%. Toxicity was mild, granulocytopenia grade III or IV were observed in the 46% of the cycles; infection-related granulocytopenia was observed in 17%, but no fatality due to therapy was observed. Cardiac toxicity was mild, only seven patients showed a drop in left ejection ventricular function, but no symptomatic heart failure has been observed. The intensive CEOP-Bleo regimen with increasing doses of cyclophosphamide and epirubicin is a useful and well-tolerated regimen in the treatment of poor prognosis diffuse large B-cell lymphoma.
 ...
PMID:Intensive chemotherapy in the treatment of aggressive diffuse large B-cell lymphoma: malignant lymphoma. 1545 55

Experience is presented of 53 cases of diaphragm plasty of the bronchial stump, tracheobronchial anastomosis, pericardium, and esophagus wall after extended pneumonectomy on account of lung cancer. A pedicled diaphragm flap was used to prevent bronchopleural fistula in 53 patients, as well as heart dislocation after wide resection of the pericardium in 26, and esophagopleural fistula after resection of the muscle coat of the esophagus in 2. In all cases, there was a high risk of these complications. Dehiscence of the bronchial stump or tracheobronchial anastomosis occurred in 9 patients, but due to diaphragm plasty, a bronchopleural fistula formed in only 3. Restoration of the pericardium and the esophageal muscle coat was successful in all cases. Overall morbidity was 22.6%, 30-day mortality was 7.5%, hospital mortality was 11.3%. Causes of death were fulminant pneumonia of the single lung, cerebral hemorrhage, pulmonary embolism, heart failure, early tumor progression, and sepsis, in one case each. The results were compared with those in 49 patients who underwent other methods of bronchial stump or tracheobronchial anastomosis reinforcement. The analysis revealed that the diaphragm flap was highly efficacious as a multipurpose plastic material.
 ...
PMID:Preventive diaphragm plasty after pneumonectomy on account of lung cancer. 1686 97

Hypoxia exists in solid tumor tissues due to abnormal vasculature, vascular insufficiency, treatment or malignancy related anemia, and low intratumor blood flow. Hypoxic status in solid tumor promotes accumulation of hypoxia-inducible factor-1 alpha which is promptly degraded by proteasomal ubiquitination under normoxic conditions. However, under hypoxic conditions, the ubiquitination system for HIF-1 alpha is inhibited by inactivation of prolyl hydroxylase which is responsible for hydroxylation of proline in the oxygen-dependent degradation domain of HIF-1 alpha. HIF-1 alpha is an important transcriptional factor that codes for hundreds of genes involved in erythropoiesis, angiogenesis, induction of glycolytic enzymes in tumor tissues, modulation of cancer cell cycle, cancer proliferation, and cancer metastasis. Hypoxia and accumulation of HIF-1 alpha in solid tumor tissues have been reported to associate with resistance to chemotherapy, radiotherapy, and immunotherapy and poor prognosis. Production of vascular endothelial growth factor (VEGF) in cancer cells is regulated by the activated HIF-1 mediated system. An increase in VEGF levels subsequently induces HIF-1 alpha accumulation and promotes tumor metastasis by angiogenesis. Recently, angiogenesis targeting therapy using humanized VEGF antibody and VEGF receptor tyrosine kinase inhibitors have been used in solid cancer therapy. Nitric oxide (NO) is a unique chemical gaseous molecule that plays a role as a chemical messenger involved in vasodilator, neurotransmitter, and anti-platelet aggregation. In vivo, NO is produced and released from three different isoforms of NO synthase (NOS) and from exogenously administered NO donors. In cancer science, NO has been mainly discussed as an oncogenic molecule over the past decades. However, NO has recently been noted in cancer biology associated with cancer cell apoptosis, cancer cell cycle, cancer progression and metastasis, cancer angiogenesis, cancer chemoprevention, and modulator for chemo/radio/immuno-therapy. The presence and activities of all the three isoforms of NOS and were detected in cancer tissue components such as cancer cells, tumor-associated macrophages, and vascular endothelium. Overexpression of iNOS in cancer tissues has been reported to associate with poor prognosis in patients with cancers. On the other hand, NO donors such as nitroglycerin have been demonstrated to improve the effects of cancer therapy in solid cancers. Nitroglycerin has been used safely for a long time as a potent vasodilator for the treatment of ischemic heart diseases or heart failure. Therefore, we think highly of clinical use of nitroglycerin as a novel cancer therapy in combination with anticancer drugs for improvement of cancer therapeutic levels. In this review article, we demonstrate the unique physiological characteristics of malignant solid tumors, several factors in solid tumors resulting in resistance for cancer therapies, and the effects of NO from NOS or exogenous NO-donating drugs on malignant cells. Furthermore, we refer to promising therapeutic roles of NO and NO-donating drugs for novel treatments in solid tumors.
 ...
PMID:Solid tumor physiology and hypoxia-induced chemo/radio-resistance: novel strategy for cancer therapy: nitric oxide donor as a therapeutic enhancer. 1850 79

The extracellular matrix molecule tenascin-C is highly expressed during embryonic development, tissue repair and in pathological situations such as chronic inflammation and cancer. Tenascin-C interacts with several other extracellular matrix molecules and cell-surface receptors, thus affecting tissue architecture, tissue resilience and cell responses. Tenascin-C modulates cell migration, proliferation and cellular signaling through induction of pro-inflammatory cytokines and oncogenic signaling molecules amongst other mechanisms. Given the causal role of inflammation in cancer progression, common mechanisms might be controlled by tenascin-C during both events. Drugs targeting the expression or function of tenascin-C or the tenascin-C protein itself are currently being developed and some drugs have already reached advanced clinical trials. This generates hope that increased knowledge about tenascin-C will further improve management of diseases with high tenascin-C expression such as chronic inflammation, heart failure, artheriosclerosis and cancer.
 ...
PMID:The role of tenascin-C in tissue injury and tumorigenesis. 1983 19

Cancer growth and metastasis are often driven by activating mutations in, or gene amplications of, specific tyrosine or serine/threonine kinases. Kinase inhibitors (KIs) promised to provide targeted therapy-specifically inhibiting the causal or contributory kinases driving tumor progression while leaving function of other kinases intact. These inhibitors are of 2 general classes: (1) monoclonal antibodies that are typically directed against receptor tyrosine kinases or their ligands and (2) small molecules targeting specific kinases. The latter will be the focus of this review. This class of therapeutics has had some remarkable successes, including revolutionizing the treatment of some malignancies (eg, imatinib [Gleevec] in the management of chronic myeloid leukemia) and adding significantly to the management of other difficult to treat cancers (eg, sunitinib [Sutent] and sorafenib [Nexavar] in the management of renal cell carcinoma). But in some instances, cardiotoxicity, often manifest as left ventricular dysfunction and/or heart failure, has ensued after the use of KIs in patients. Herein we will explore the mechanisms underlying the cardiotoxicity of small-molecule KIs, hoping to explain how and why this happens, and will further examine strategies to deal with the problem.
 ...
PMID:Why do kinase inhibitors cause cardiotoxicity and what can be done about it? 2072 98


1 2 3 Next >>