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)

A pilot phase II study of a hybrid chemotherapy for SCLC has been conducted between October 1986 and March 1988. Dose and schedule of the regimen were as follows: CTX, 700 mg/m2, on day 1; ADM 30 mg/m2, on day 1; VCR, 1.4 mg/m2, on day 1 (CAV); and CDDP, 60 mg/m2, on day 8; VP-16, 100 mg/m2, on days 8 and 9 (PVP). Courses were repeated q. 4 weeks up to 6 cycles. Patients with LD received chest irradiation at a dose of 50 Gy when maximal response was achieved. Thirty-six patients were fully evaluated for tumor response and toxicity. All 18 patients with LD responded to the regimen including 11 CRs (61%); there were 7 CRs (39%) and 9 PRs (50%) in patients with ED. Fourteen of the 18 patients with LD have survived for 7 to 22 months, against 12.8 months in ED patients. The major toxicity was myelosuppression, but it was well tolerated. These results indicate that hybrid chemotherapy is highly effective for SCLC, and warrants further clinical trials.
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PMID:[Pilot phase II study of hybrid chemotherapy of CAV-PVP in small cell lung cancer (SCLC)]. 254 49

Primary sarcomas of the liver are rare malignant neoplasms. Only four cases of Malignant fibrous histiocytoma (MFH) of the liver have previously been reported in the literature. The authors report a 64-year-old man of MFH of the liver, complained of epigastric discomfort. Laboratory values revealed raised ESR and positive CRP. An abdominal computed tomographic scan disclosed 7.4 x 7.6 cm low density area in the posterior segment of the right lobe. Selective angiography of the celiac artery revealed hypovascular tumor. The diaphragm was involved in the tumor and right hepatectomy with partial resection of diaphragm was performed. Microscopically, the tumor cells were arranged with a storiform pattern and electron microscopic studies demonstrated fibroblast like cells and histiocyte like cells. Although systemic chemotherapy with ACR, CPM and VCR was performed, he died of peritoneal and pleural dissemination on the 142nd day after.
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PMID:[Malignant fibrous histiocytoma of the liver]. 254 36

A rare case is reported of pineal metastasis from lung cancer initially caused by neurological abnormalities of pineal tumor. A 70-year-old female suffering from headache and deterioration of consciousness for 1 week was admitted. She also had a tumor on both sides of her neck. On admission, neurological examination revealed disturbance of upward gaze, and CT scans showed hydrocephalus and pineal tumor. The tumor was seen as a slightly high density mass on non-contrast CT, and was homogeneously enhanced after administration of contrast material. Right V-P shunt and excision of the left neck tumor were performed at the same time. Pathological diagnosis of neck tumor was undifferentiated carcinoma metastasized to cervical lymph nodes. Extensive study was made, by bronchial fiberscope and biopsy, in order to find the origin of the malignancy and disclosed a small cell lung cancer of left lower lobe. The patient took radiation therapy for both the whole brain (60 Gy) and for the bilateral cervical regions (45 Gy). Two courses of chemotherapy using CDDP, ADR, VCR and CY were administered. Both the neck and the pineal tumors were markedly reduced in size at the termination of radiation therapy. However, she was readmitted 3 months later because of dyspnea. Chest X-P revealed enlargement of the left-lung tumor. She died on April 22, 1987. General autopsy disclosed invasive enlargement of left lung cancer, however, no remote metastasis was found. Examination of pineal region showed only necrotic pineal tissue, and no tumor cell was seen in either macroscopic or microscopic study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pineal metastatic tumor from lung cancer initially caused by neurological abnormalities of pineal body tumor]. 255 Aug 31

A 53 year old male was admitted with cough, chest pain and bloody sputa for one month. His admission chest radiography revealed a tumor shadow in right hilus. The patient was diagnosed as small cell lung cancer (oat cell type) by transbronchial biopsy. Clinical staging was IIIA and performance status was 1. The patient was treated by combined chemotherapy (CPA, ADM and VCR) for 3 courses and chest irradiation (5,000 rad). After such therapy, the primary site was regressive until 2 months prior to death. One month after irradiation, abdominal CT showed multiple liver metastases. Though CDDP 100 mg/body and etoposide 100 mg/body X5 were administered systemically, improvement of metastases of the liver was not revealed by abdominal CT. However, after hepatic arterial infusion of ADM (10 mg/body) suspended in a lipiodol (3 ml/body) and CDDP (100 mg/body) was performed, liver metastases were remarkably regressive by abdominal CT. The patient died of a systemic relapse about 14 months after liver involvement.
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PMID:[A case of intra-arterial infusion chemotherapy in small cell lung cancer with liver metastases]. 255 17

Nude mice, inoculated with LAX 83 in bilateral subrenal capsules, were used in experimental therapy with 8 antitumor drugs. Treatment was initiated 2 d after tumor inoculation. All the drugs were ip to the nude mice daily for 7 d. At the daily doses VCR 0.4, MMC 2, CCNU 16, cis-DDP 2, AdM 2.5, 5-Fu 30, CTX 40 and MTX 2-6 mg/kg, the inhibition of the tumor growth were 100, 95.8, 91.3, 79.2, 65.2, 60.7, 62.3 and 0%, respectively. The results indicated that the effects of the drugs on nude mice inoculated with LAX-83 in subrenal capsule not only exhibited a good correlation to those in sc, but also shortened the period of experiment from 22 to 11 d. Furthermore, when LAX-83 was inoculated into the subrenal capsule of Swiss +/+ mice, the tumor tissues degenerated and disintegrated 2 d after the inoculation and replaced by inflammatory granuloma tissues 6 d later.
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PMID:[Effects of 8 antitumor drugs against the growth of human lung adenocarcinoma (LAX-83) transplanted under the kidney capsule of nude mice]. 261 35

A new method to test the sensitivity of human tumor cells has been developed. A suspension of mechanically dissociated tumor cells is kept in continuous incubation for 24h, in cultures with antineoplastic agents. Drug induced cell cycle perturbations are monitored by flow cytometric computer analysis and DNA distributions of the cells stained with propidium iodide are expressed in percentage. The test is used in 15 head and neck human solid tumors. The drugs tested were: VCR, EpiDx, CDDP, MTX, 5-FU, CPM, BLM. The results obtained reveal that tumor sensitivity varies independently from the stage and malignity grading. Therapeutic combinations are assigned by selecting the drugs on the basis of the individual in vitro response.
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PMID:In vitro short-term chemosensitivity test in head and neck tumors. 272 14

For the characterization of membrane changes related to Adriamycin resistance in tumor cells, we have developed monoclonal antibodies against Adriamycin-resistant human myelogenous leukemia K562 (K562/ADM). In addition to the monoclonal antibodies which recognize P-glycoprotein, we have obtained two monoclonal antibodies (designated MRK4 and MRK20) which recognize an Mr 85,000 membrane protein. Using MRK20 as a probe, we have studied the expression of the Mr 85,000 protein in various human multidrug-resistant and -sensitive cell lines. The Mr 85,000 protein was overexpressed in K562/ADM and in a human ovarian cancer cell line resistant to Adriamycin, 2780AD. The protein, if any, was not detected in other drug-resistant human cell lines such as colchicine-resistant KB cells (KB-C4), vinblastine-resistant CEM cells (CEM/VLB100), and vincristine-resistant K562 cells (K562/VCR). We have isolated subclones of K562/ADM cells which express different amounts of the Mr 85,000 protein. The expression of the Mr 85,000 protein diminished when the cells were not kept in Adriamycin, and increased when the clones were kept in the presence of Adriamycin. In contrast, the expression of P-glycoprotein remained constant whether in the presence or absence of Adriamycin during these experiments. These findings suggest that the Mr 85,000 membrane protein is closely related to the resistant mechanism specific to Adriamycin resistance, which is different from that of the pleiotropic drug resistance.
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PMID:Mr 85,000 membrane protein specifically expressed in adriamycin-resistant human tumor cells. 290 93

Cultured murine leukemia P388 cell populations were derived from P388 cells resistant to vincristine (P388/VCR), adriamycin (P388/ADR), and 1-beta-D-arabinofuranosylcytosine (P388/ARA-C) that were developed in vivo and to the parental drug-sensitive cells (P388/O) that were passaged in vivo. The doubling times of the cultured cell populations (mean +/- SD) between cell densities of 5 x 10(4) and 1 x 10(6) cells/ml were 14.2 +/- 2 h (P388/O), 16.5 +/- 1.9 h (P388/VCR), 16.9 +/- 1.2 h (P388/ADR), and 15.0 +/- 1.4 h (P388/ARA-C). Exponentially proliferating cultured cell populations were exposed to selected homoharringtonine (HHT) concentrations for 24 h and the surviving cell fractions were determined by colony formation in semisolid medium. The results, based on differential sensitivity of the cell populations to HHT, indicated that cultured P388/VCR cells were cross-resistant to 0.018-1.8 micrograms/ml HHT, P388/ADR cells were cross-resistant to 0.058-1.8 micrograms/ml HHT, and P388/ARA-C cells were collaterally sensitive to 0.09-0.36 micrograms/ml HHT. The results with the cultured P388/VCR, P388/ADR, P388/ARA-C, and P388/O cell populations were confirmed in animal experiments. CD2F1 mice bearing intraperitoneal (i.p.) implants of 1 x 10(6) P388/VCR, P388/ADR, P388/ARA-C, or P388/O leukemia cells were given HHT i.p. qd on days 1-9 postimplantation. Optimal treatment (less than or equal to LD10) produced in vivo cell kills of 2 to 3 log10 units in P388/O and about 7 log10 units in P388/ARA-C, whereas P388/VCR and P388/ADR cells actually increased by 1-2 log10 units during treatment. The results of this study indicate that cross-resistance (P388/VCR and P388/ADR) or collateral sensitivity to HHT (P388/ARA-C) is a function of the cellular properties of the target tumor cell populations that is independent of host factors.
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PMID:Effect of homoharringtonine on the viability of murine leukemia P388 cells resistant to either adriamycin, vincristine, or 1-beta-D-arabinofuranosylcytosine. 292 72

26 patients with astrocytoma grade II-III, and 36 with malignant glioma (astrocytoma grade IV or glioblastoma) were submitted three days after surgery to a cycle of combination chemotherapy, including BCNU, VCR, PCZ (BVP). Eighteen days after surgery, patients received 40 Gy (astrocytoma grade II-III) or 45 Gy (malignant glioma) of megavoltage whole-brain irradiation, with an additional boost to the 'tumor' bed of 20 Gy, delivered in 6 weeks. Vincristine was injected weekly during radiotherapy. At the end of radiotherapy, patients received BVP every 6 weeks for at least 8 cycles or until a recurrence or progressive disease. Performance status of grade 1 or 2 was achieved in 15 (60%) and in 5 (20%), respectively, of patients with astrocytoma grade II-III after 6 months, and in 6 ps. (29%) and in 9 ps. (42%) after 12 months of follow-up. Only 2 (5.5%) and 18 (64%) patients with malignant glioma achieved a performance status of grade 1 or 2 after 6 months, and these proportions are 6% and 35%, respectively, after 12 months. After a 5-year follow-up, 59% of patients with astrocytoma are still alive, with a median survival time of 60+ months, whereas only 4% of patients with malignant glioma are alive, with a median of 11.2 months.
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PMID:Radiotherapy and combination chemotherapy with carmustine, vincristine, and procarbazine (BVP) in primary brain tumors. 298 23

From April 1981 to February 1983, 116 untreated patients (ECOG PS 0-3) with histologically or cytologically proven small cell lung cancer were randomly allocated to chemotherapy regimen using CPA.ACNU.VCR (CNV, n = 64) or ADR.ACNU.VCR (ANV, n = 52). The objective tumor response was 29.7% (19/53) for the CNV regimen and 48.1% (25/48) for the ANV regimen, but there was no statistically significant difference in these groups. Median survival time was 22.9 w for the CNV regimen (n = 64) and 42.4 w for the ANV (n = 52) regimen. The survival rate was statistically significantly higher for the ANV regimen compared to that of the CNV regimen (P greater than 5%). The toxicity showed no difference between these groups. Addition of ADR to ACNU + VCR was effective, but addition of CPA to these two drugs was not effective.
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PMID:[A randomized trial of 3-drug combination chemotherapy in small cell lung cancer--CPA/ACNU/VCR vs ADR/ACNU/VCR]. 299 77


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