Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human lung, ovarian, colonic, and renal carcinomas have been grown in mice artificially deprived of T-lymphocytes. All grew slowly and were shown to have a human karyotype even after several transplant generations. Their responses to chemotherapy were similar to the expected clinical response with the important exception of hexamethylmelamine which caused complete regression of two lung carcinomas (even when weighing up to 2.5 g at the start of treatment) and a renal carcinoma, while completely inhibiting the growth of an ovarian carcinoma and another lung carcinoma. Measurement of plasma carcinoembryonic antigen levels proved to be of value in assessing drug efficacy.
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PMID:Chemotherapy of human tumors in T-lymphocyte-deficient mice. 40 45

The cell-mediated immune (CMI) response to tumor-associated antigens present in 3 M KCL extracts of renal cell carcinoma tissue was measured in patients with renal cell carcinoma (RCC) by the leukocyte migration inhibition (LMI) test. Of 30 patients with histologically proved RCC, 19 (63%) gave a positive LMI test; whereas, 2 of 28 (7%) of the normal donors, 13 of 43 (30%) patients with other cancers, and 5 of 14 (36%) benign kidney disease patients gave positive tests. Thirteen per cent of RCC patients reacted to a normal kidney extract. Although 33% gave a positive response to a lung carcinoma extract, the incidence of reactivity was less than that observed with the lung cancer patients. These results suggest that a CMI response to a renal carcinoma-associated antigen was measured by the LMI test. Correlation of the LMI data with the stage of disease and clinical status indicated that 71% of patients that had a localized tumor and were clinically free of disease one year postnephrectomy lost their tumor-directed CMI response. Patients with distant metastasis (Stage D) were LMI positive provided they had not received radiation or hormone therapy at the time of testing. These results suggest that the demonstration of CMI, as measured by the leukocyte migration inhibition test, correlates with the presence of active disease.
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PMID:Cell-mediated immunity in patients with renal cell carcinoma as measured by leukocyte migration inhibition test. 72 70

One hundred and nine adult patients with metastatic carcinoma were treated at 3-4-week intervas with a combination of adriamycin (40 mg/m2 given iv on Day 1) and cyclophosphamide (200 mg/m2/day given orally in divided doses on Days 3-6). Ninety-two of 96 patients who had an adequate trial (minumum of two courses or progression of disease after one course) had follow-up observations of tumor sites and were considered evaluable for response. Overall objective response rates by tumor type were as follows: stage III or IV ovarian adenocarcinoma, 61% (14 of 23 patients); endometrial adenocarcinoma, 67% (four of six patients); cervical adenocarcinoma, 33% (one of three patients); prostatic adenocarcinoma, 18% (two of 11 patients); testicular carcinoma, 33% (one of three patients); lung carcinoma, 21% (four of 19 patients); renal adenocarcinoma, 14% (one of seven patients); gastrointestinal adenocarcinoma, 18% (two of 11 patients); melanoma, 25% (one of four patients); and miscellaneous tumors, no responses in five patients. In patients with ovarian adenocarcinoma who had not previously received any cytotoxic chemotherapy the response rate was 80% (12 of 15 patients) with 33% five of 15 patients achieving complete clinical remission. CRs in these patients have now been maintained for periods ranging from 7 to 12 months. The major toxic effects were mild to moderate leukopenia, alopecia, and nausea with vomiting. Hemorrhagic cystitis was observed in three patients. The combination of adriamycin and cyclophosphamide is an effective treatment for carcinoma of the breast (reported elsewhere), ovary, and endometrium and should be considered for initial chemotherapy in patients with these tumors. Further investigations of its use for melanoma and carcinoma of the lung, prostate, kidney, and gastrointestinal tract are also warranted.
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PMID:Combination chemotherapy with adriamycin (NSC-123127) and cyclophosphamide (NSC-26271) for solid tumors: a phase II trial. 100 May 20

Cyclophospamide was given in two dose schedules to 25 patients with a variety of nonlymphoid solid tumors. Eleven patients were given 18 courses of cyclophosphamide at a total dose of 60 mg/kg. Sixteen patients received 26 courses at a total dose of 100 mg/kg. Two patients were treated with both regimens. Partial responses were achieved in two patients treated with 60-mg/kg dose of cyclophosphamide. One of these patients had osteogenic sarcoma and the other had renal carcinoma. The higher dose also produced two partial responses, one in a patient with anaplastic carcinom a of the lung and the other in a patient with anaplastic carcinoma of the lung and the other in a patient with embryonal testicular carcinoma. Mean leukocyte counts fell to a nadir of 1400 cells/mm after 60 mg/kg while they dropped to below 1000 cells/mm for 5 days after 100 mg/kg of cyclophosphamide. Mean platelet counts remained above 150,000 platelets/mm after both cyclophosphamide schedules. In fective complications were documented aftter three of the 18 courses at 60 mg/kg and after ten of the 26 courses at 100 mg5kg. In the latter group, there were three episodes of bacteremia, including one death from pseudomonas sepsis. Nonhematologic toxicity noted with the 100-mg/kg dose of cyclophosphamide included rare instances of electrocardiogram changes and serum enzyme alterations compatible with myocardial toxicity. The intensive cyclophosphamide therapy did not appear to result in an increased antitumor response in malignancies usually considered to be refractory to alkylating agents.
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PMID:Intensive cyclophosphamide (NSC-26271) therapy for solid tumors. 109

Virtually any malignancy may lead to hypercalcemia, but carcinoma of the breast, myeloma, and carcinoma of the lung are especially frequent offenders. A more difficult diagnostic problem is posed by the "silent" tumor which secretes a substance causing hypercalcemia. Foremost in this category are bronchogenic carcimona and hypernephroma.
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PMID:Hypercalcemia and malignant disease. 111 72

Dominant rearrangements of T-cell receptor (TCR) beta-chain genes are reported among tumor-infiltrating lymphocytes (TIL). After interleukin-2 expansion of TIL from renal and lung carcinoma and melanoma biopsy tissues, rearrangements of TCR beta-chain genes were analyzed by Southern blotting. Nongermline restriction fragments, indicating dominant rearrangements, were detected among the TIL from all 6 patients with renal cell carcinoma, 17 of 20 patients with melanoma, and 3 of 6 patients with lung tumors. The restriction-fragment sizes of these dominant rearrangements were heterogeneous among the various patients. Rearrangements into C beta 1 were more common than C beta 2 rearrangements. Phenotypic analyses indicated that dominant rearrangements occurred in both CD4 and CD8 predominant TIL populations. The TIL populations that were extracted were expanded to derive large cell numbers suitable for in vivo transfer in an interleukin-2 and TIL immunotherapy program. The data indicated that the cells delivered to these patients usually were characterized by dominant populations of T-cells with selective TCR gene rearrangements. The significance of selective TCR use requires evaluation of the function and specificity of the TIL comprising these dominant populations both in their native in vivo setting and in the context of therapeutic transfer.
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PMID:Dominant rearrangements among human tumor-infiltrating lymphocytes. Analysis of T-cells derived from 32 patients with melanoma, lung, and renal cell carcinoma. 131 29

A patient was referred to our hospital for resection of a large renal cell carcinoma with invasion of the inferior caval vein, diagnosed as such with CT, angiography and cavography. The history mentioned partial resection of the left lung for lung carcinoma 16 months before. At operation the tumor could not be removed, the patient died because of postoperative pulmonary complications. Autopsy and histopathological examination revealed a large metastatic tumor of the previous lung carcinoma in the left adrenal gland. The clinical implications and some diagnostic methods are discussed.
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PMID:Involvement of the inferior caval vein in adrenal metastasis. 133 28

Synergy, when it can be convincingly established, is an effective strategy for the development of novel drug combinations. We have evaluated the interaction between 2'-deoxy-5-azacytidine (DAC) and 9-dimethylaminomethyl-10-hydroxycamptothecin (topotecan) based on our hypothesis that DAC, through DNA hypomethylation, might increase the transcription of topoisomerase I (topo I) leading to increased sensitivity to topotecan. Five human tumor cell lines, A375 melanoma, DX-3 melanoma, DMS4C non-small cell lung carcinoma, UP-1 unknown primary adenocarcinoma, SN12C renal carcinoma, and the murine CT-26 tumor cell line, were studied. Drug interactions were assessed using the multiple drug effect analysis of Chou and Talalay (Chors, T-C, and Talalay, P. Adv. Enzyme Regul., 22:27-54, 1984.). A synergistic interaction was documented in four human cell lines and the murine CT-26 line. An antagonistic interaction was observed with the SN12C cell line. The toxicology and efficacy of this combination were analyzed using CT-26 in BALB/c mice. Various treatment schedules were studied, including: single doses of each agent; single sequential combination treatments where DAC was administered followed by topotecan 24 h later; and multiple sequential treatments where DAC and topotecan were administered on days 1, 2, 8, and 9. Efficacy studies showed that the single sequential combination of DAC (50 mg/kg) and topotecan (10 mg/kg) resulted in tumor growth delay as compared to single doses of DAC (50 mg/kg) or topotecan (10 mg/kg). When the multiple sequential combination schedule was used, the antitumor effect was more pronounced. In that experiment 50% of the control animals had tumors of 20 mm by day 28. For animals receiving a single sequential treatment with DAC and topotecan, the median time until the mean tumor size reached 20 mm was 38 days, and for the group with multiple sequential combination treatments the time was 51 days. Studies of the mechanism of the interaction showed that the activity of topotecan versus each cell line correlated with the topo I activity in nuclear extracts However, there was no correlation between topo I levels and synergy and no reproducible increase in topo I activity following exposure to DAC. Thus, while the exact mechanism of the interaction remains unclear, DAC can be effectively combined with topotecan to enhance antitumor activity.
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PMID:Synergistic cytotoxicity with 2'-deoxy-5-azacytidine and topotecan in vitro and in vivo. 137 5

A 54-year-old woman who had undergone radical nephrectomy for renal cell cancer nine months before was admitted to our hospital because of difficulty in breathing. X-ray films of the chest showed massive pleural effusion on the left side and cytological examination of the effusion revealed malignant cells which may have originated from renal cell cancer. Intrapleural instillations of interleukin-2 and of tumor infiltrating lymphocytes isolated from the pleural effusion were performed. After the initiation of the treatment, the pleural effusion decreased and malignant cells disappeared from the pleural fluid. Partial response defined by the criteria provided by the Japan Lung Cancer Society was achieved. No serious side effects were observed. This would be a useful treatment for pleuritis carcinomatosa by renal cell cancer.
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PMID:[Successful local adoptive immunotherapy for pleuritis carcinomatosa due to renal cell cancer. A case report]. 143 78

Fluorescent in situ hybridization (FISH) is a powerful technique for gene mapping and multi-color FISH allows us to determine directly the order of two or more probes on both metaphase and interphase chromosomes. We report the physical ordering of three DNA markers by three-color FISH using two fluorochrome dyes, fluorescein isothiocyanate (FITC; green) and rhodamine (red). The third color was visualized as a pseudo-color (yellow) generated by optical interference with FITC and rhodamine. Using this system we could rapidly determine the order of three polymorphic DNA markers located on the 3p23-p21.2 bands which span a tumor suppressor gene for renal cell carcinoma, lung carcinoma, and several other types of tumors.
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PMID:Physical ordering of three polymorphic DNA markers spanning the regions containing a tumor suppressor gene of renal cell carcinoma by three-color fluorescent in situ hybridization. 148 39


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