Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We treated a 43-year-old man with recurrent malignant fibrous histiocytoma in right distal femur with intra-arterial infusion of cisplatin and caffeine 5 years after wide excision and chemotherapy. At the time of the first recurrence in the lateral aspect of thigh, intra-arterial infusion of CDDP (120 mg/m2) was ineffective. We treated him with radiation (7000 rad), and there was no evidence of tumor by radiological evaluation. The second local recurrence was treated with intra-arterial infusion of CDDP (120 mg/m2/1 hour) and caffeine (1.2 g/m2/24 hours x 3 days), and the tumor disappeared, radiologically and histologically. Caffeine did not increase the nephrotoxicity of CDDP, and no insomnia nor palpitation was seen. Intra-arterial infusion of CDDP and caffeine could be useful to increase the effect of CDDP for regional chemotherapy.
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PMID:[Intra-arterial infusion of cisplatin and caffeine for a recurrent malignant fibrous histiocytoma]. 215 70

Human malignant melanoma cells (G-361) were irradiated with X-ray for different irradiation times. The amount of DNA damage was much increased by the treatment of the cells with HpO before X-ray irradiation. Furthermore, it was found that the caffeine inhibited effectively the repair of the damaged DNA. Furthermore, HpO was administered before X-ray irradiation of transplantable skin tumor in C3H mice and/or caffeine+ was to be given the mouse after X-ray irradiation. The growth of the tumor irradiated with HpO and/or caffeine was more inhibited and the necrotic area was more expanded than that of the tumor irradiated X-ray only. Labeling Index utilizing bromodeoxyuridine (BrdU) in the viable area of the treated tumor decreased when HpO and/or caffeine were administered. The amount of DNA damage more increased in the tumor cells irradiated with HpO than that irradiated only. And, the repair of the damaged DNA was more delayed in the tumor cells irradiated with HpO and caffeine than that irradiated with the other treatments. In conclusion, it was considered that HpO might be a radioactive sensitizer and caffeine enhanced the inhibition of the repair of DNA damaged. We hope that the treatment of X-ray radiation with HpO and caffeine is useful for clinical treatment of human malignant tumor.
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PMID:[A sensitization effect of hematoporphyrin oligomer (HpO) and caffeine for X-ray radiation of skin cancer]. 221 35

The diagnosis of polycythemia requires an accurate and independent assessment of both plasma volume and red blood cell mass. Patients with an increased red cell mass (absolute polycythemia) may be hypoxic or have an erythropoietin-secreting tumor or space-occupying lesion compressing the kidney. Those with a reduced plasma volume (relative polycythemia) most often are tobacco smokers, are taking diuretic or cardiac medications, or ingest increased quantities of caffeine-containing beverages. On the other hand, polycythemia vera is a systemic disease with multiple complications, which is best diagnosed through a complex of findings as outlined by the Polycythemia Vera Study Group.
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PMID:Polycythemia vera and other polycythemic states. 227 78

The effects of two methylxanthines, caffeine and isobutylmethylxanthine (IBMX), on the response to radiation given at two low dose rates were studied in a human hepatoma cell line, HepG2. These dose rates are in the range to which tumor cells are exposed in radiolabeled immunoglobulin therapy of primary hepatoma. At the higher dose rate (0.3 Gy/hr for 24 hr), the radiation completely inhibited growth, and cells accumulated in the G2 phase of the cell cycle. Caffeine (1 mM), given either continuously or during the last 4 hours of the radiation exposure, counteracted the growth inhibition and G2 accumulation and enhanced cell killing. The 0.5-mM dose of IBMX had little effect on cells. For a lower dose rate and longer exposure period (0.06 Gy/hr for 3 days), the radiation partially inhibited growth and the accumulation of cells in G2 was small. Continuous, but not short, exposure to caffeine enhanced killing at this dose rate and counteracted the G2 accumulation. At the lower dose rate, IBMX enhanced the growth inhibition, G2 accumulation, and killing above that with radiation alone.
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PMID:Effects of methylxanthines on cell-cycle redistribution and sensitization to killing by low-dose-rate radiation. 245 Nov 34

We reviewed 49 patients with urothelial tumors of the ureter: 33 male and 16 female patients with a mean age of 64.8 and 66.3 years, respectively. Median followup was 83 months. Gross hematuria was present in 29 patients and a silent kidney was found in 21. The majority of the tumors were in the distal ureter and approximately 50 per cent of the patients had synchronous or asynchronous urothelial tumors. The majority of the patients had low grade, low stage tumors (75 per cent). A total of 21 patients underwent local resection and none died of tumor. Only 1 of these 21 patients had an ipsilateral recurrence. Nephroureterectomy was performed in 24 patients and 5 of them died of ureteral tumor, including 4 in whom periureteral tumor growth initially was recorded. The prognosis of patients with papillomas or grades 1 to 3, stages Pa to P1 ureteral tumors was excellent and a conservative approach is recommended for these patients. Abuse of combination analgesics containing phenacetin, phenazone and caffeine may be a risk factor for development of ureteral tumors.
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PMID:Carcinoma of the ureter: a clinicopathologic study of 49 cases. 248 33

It is necessary to find modifiers which enhance the effects of known anticancer agents in order to improve both survival rate and local curability of patients with high-grade sarcomas. In this study, the effect of anticancer agents combined with caffeine was examined on cultured sarcoma cells and fresh human sarcoma specimens, utilizing the human tumor clonogenic assay technique. The combination of cisplatin and caffeine showed a synergistic inhibition of the growth of two strains of cultured sarcoma cells tested, and 14 of 18 fresh human sarcoma specimens (77.8%). This synergistic effect of caffeine was also observed with cyclophosphamide (44.8%), mitomycin C (44.8%) and adriamycin (27.8%). The combination of vincristine or methotrexate with caffeine, however, did not exhibit a synergistic effect. Caffeine, therefore, enhanced the effect of four cytotoxic DNA damaging agents. No antagonistic effects were seen in our series. This study suggests that caffeine may be useful in enhancing the tumoricidal effect of anticancer drugs, especially DNA-damaging agents, and possibly may aid in overcoming natural drug resistance.
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PMID:Caffeine enhancement of the effect of anticancer agents on human sarcoma cells. 249 63

While having no antitumor effect per se, caffeine substantially enhanced the antitumor effects of the phleomycins PLM-CHP and PLM-PEP, and the bleomycins BLM-CHP and Blenoxane in rats carrying Walker 256 carcinosarcoma and/or mice carrying Ehrlich ascites tumor, even at doses of phleomycin and bleomycin below the minimum effective level. Positive but less conclusive results were also obtained with PLM-A4A4G and PLM-G.
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PMID:Amplification of the antitumor activity of phleomycins and bleomycins in rats and mice by caffeine. 258 Jun 23

In a phase I-II study, 28 patients with advanced pancreatic adenocarcinoma were treated with cisplatin, high-dose cytarabine (ARA-C), and caffeine. This clinical trial was based on a nude mouse-human tumor xenograft model, which demonstrated synergism of these agents by inhibiting the growth of human pancreatic tumors. Toxic effects noted in the clinical study included myelosuppression, moderate nausea and vomiting, and mild renal insufficiency. No toxic effects were directly attributable to caffeine. Eighteen of the 28 patients had measurable or assessable disease; seven (39%) had partial responses (95% confidence intervals, 18%-63%). The median response duration was 6.2 months. Median survival for responders was 9.5 months with two patients surviving for more than 18 months. Median survival for all patients was 6.1 months. The combination of cisplatin, ARA-C, and caffeine is an active and tolerable regimen in the treatment of advanced pancreatic cancer. A phase III trial in which this regimen is being compared with standard therapy is in progress.
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PMID:Advanced pancreatic cancer: a phase I-II trial of cisplatin, high-dose cytarabine, and caffeine. 268 96

A nontoxic dose of caffeine enhanced the cytotoxicity of cisplatin in human osteosarcoma cells (OST strain). Synergistic cytotoxicity was seen in vitro in OST cells when 2 mmol caffeine was added to a nontoxic dose of cisplatin (2 micrograms/ml). Caffeine reduced S-phase, G2/M-phase, and S-and-G2/M-phase accumulation by cisplatin on the DNA histogram, and nuclear fragmentation of tumor cells was frequently observed. Flow cytometric analysis appeared to be useful in assessing the efficacy of the combination of cisplatin and caffeine. The antitumor effect of the combination of cisplatin and caffeine was examined in OST transplanted to BALB/C athymic mice. Regression of the tumor was observed when cisplatin was given at a dose of 10 mg/kg. When 4 mg of caffeine was given once a day for three days after the administration of cisplatin, marked regression of the tumor was observed in groups treated with 5 or 10 mg/kg of cisplatin, without significant weight loss. These results indicate that caffeine enhances the antitumor effect of cisplatin on transplanted osteosarcoma in BALB/C athymic mice.
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PMID:Enhancement of cytocidal and antitumor effect of cisplatin by caffeine in human osteosarcoma. 272 Jul 27

In a molecular epidemiological study of lung cancer cases (n = 81) and noncancer controls (n = 67), polycyclic aromatic hydrocarbon (PAH)-DNA adducts were evaluated in peripheral blood leukocytes from all subjects and in a smaller number of lung tissue specimens collected prior to or at surgery. Sister chromatid exchanges (SCE) in lymphocytes were also studied in a subset of cases and controls. Questionnaire, medical record, or tumor registry data provided a family history of cancer, as well as information on cigarette smoking, dietary and occupational exposure to PAHs, and other factors related to SCEs. In both cases and controls PAH-DNA adducts in leukocytes measured by an enzyme-linked immunosorbent assay were not significantly related to age, sex, ethnicity, amount of cigarette smoking, passive smoking, dietary charcoal, or caffeine consumption. Nor did family history of cancer or histological type of cancer significantly affect adduct levels. However, when subjects were stratified by smoking status (current, former, and nonsmoker), lung cancer cases who were current smokers had significantly higher levels of covalent adducts than current smoker controls. A seasonal variation was observed in PAH-DNA binding, with a peak in adduct levels during July-October. This peak corresponds to that seen in a prior study of aryl hydrocarbon hydroxylase inducibility by other investigators. The finding of significant levels of PAH-DNA adducts in former smokers and non-smokers supports an earlier observation that this marker is not smoking specific but reflects a pervasive and variable "background" exposure to PAH. These results are consistent with a genetically determined enhancement of PAH-DNA adduct formation in leukocytes of lung cancer cases which is evident in current smokers. The results in lung tissue are limited by the small number of samples. Adduct levels were not significantly increased in lung tissue of smokers compared with nonsmokers. An inverse linear correlation was seen between adduct values in lung tissue and age of the donors. SCEs were significantly related to pack years of smoking. However, there was no difference in the frequency of SCE between cases and controls; nor were SCE and DNA adducts significantly correlated in this small sample.
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PMID:Comparison of DNA adducts and sister chromatid exchange in lung cancer cases and controls. 274 34


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