RESUMO
Histologically normal and neoplastic human breast tissues obtained from 25 patients at the time of mastectomy were homogenized (200 mg/ml) in distilled water and 5-microliter aliquots dried on Formvar films for trace element analysis by energy-dispersive X-ray fluorescence. The elements measured were calcium, vanadium, copper, zinc, iron, chromium, manganese, nickel, selenium, molybdenum, bromine, rubidium, strontium, mercury, arsenic, and lead. In general, significantly large increases (p less than 0.001) in calcium, vanadium, copper, zinc, selenium, and rubidium were found in breast tumors, with a less significant increase (p less than 0.05) for nickel. When a comparison was made between histologically normal and neoplastic tissues from the same individual, zinc and rubidium were found to be consistently higher in the tumor, whereas calcium, copper, and vanadium levels varied from normal to high. In no instance were the tissue changes in calcium, copper, zinc, or rubidium reflected in the blood levels, which were within normal limits. The distribution of calcium, copper, and zinc in urine varied among individuals with primary tumors; however, rubidium levels tended to be consistently elevated. An attempt is being made to correlate these various differences with the extent of the primary disease at the time of surgery, the postoperative tumor-free interval, and subsequent therapy.
Assuntos
Neoplasias da Mama/análise , Mama/análise , Oligoelementos/análise , Cálcio/análise , Cobre/análise , Microanálise por Sonda Eletrônica , Feminino , Humanos , Mastectomia , Valores de Referência , Rubídio/análise , Selênio/análise , Zinco/análiseRESUMO
C-reactive protein (CRP) is an acute-phase reactant whose serum level rises rapidly in response to tissue injury. C-reactive protein binding to cells can activate the classical complement pathway, and enhance opsonophagocytosis. The polycation poly-L-arginine (PLA) can artificially fix CRP to target cells. The effects of CRP and PLA on tumor growth were evaluated, both independently and synergistically, using the V X 2 tumor line in the rabbit host. Ten normal animals and seven acute-phase animals were bilaterally inoculated with V X 2 cells (control side) and PLA-treated V X 2 cells (experimental side). Tumor growth was significantly retarded on the treatment side (P less than 0.005), in both animal groups. It is concluded that topical PLA is a potent inhibitor of V X 2 tumor growth. Comparison of normal and acute-phase animals revealed no persistent difference in tumor growth for either cell inoculum. Similarly, cell treatment with topical CRP did not inhibit tumor growth, whether PLA was present or not. Thus, circulating and topical CRP did not alter the rate of V X 2 tumor growth. PLA cytotoxicity remains to be evaluated when the agent is administered orthotopically, selectively, or systemically.
Assuntos
Antineoplásicos/uso terapêutico , Proteína C-Reativa/uso terapêutico , Neoplasias Experimentais/terapia , Peptídeos/uso terapêutico , Animais , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Proteína C-Reativa/administração & dosagem , Proteína C-Reativa/análise , Linhagem Celular , Avaliação Pré-Clínica de Medicamentos , Imunoterapia , Neoplasias Experimentais/patologia , Peptídeos/administração & dosagem , Coelhos , Fatores de TempoRESUMO
Elevated creatine phosphokinase (CPK) MB isoenzyme has become accepted as a highly specific criterion for the diagnosis of myocardial infarction (MI). A patient with metastatic neuroendocrine carcinoma of the colon who had marked and persistent elevation of CPK-MB isoenzyme, in the absence of clinical and cardiographic evidence for MI, is described. The CPK-MB level was 25 percent (normal, less than 3 percent) on admission, 39 percent postoperatively, and 57 percent on discharge. A prompt decline in serum CPK-MB activity (11 percent, less than 3 percent) paralleled chemotherapy-induced tumor regression. Resurgence of the isoenzyme heralded recurrent disease. These findings suggest that CPK-MB may be a valuable adjunct marker in the diagnosis and monitoring of neuroendocrine carcinomas.