Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tumor suppressor gene APC was recently identified, and the cDNA was cloned from chromosome 5q21. Point mutations affecting APC are seen in the hereditary syndrome familial adenomatous polyposis, and point mutations in APC and a closely linked gene, MCC, as well as loss of heterozygosity involving chromosome 5q have been reported in sporadic colon cancer. To our knowledge, loss of heterozygosity involving APC or MCC or both has not yet been described in any other human cancer besides lung cancer. We used the polymerase chain reaction and DNA content flow cytometric nuclear sorting to examine 30 primary human esophageal cancers for loss of heterozygosity of APC or MCC or both. Loss of one allele was detected in 77% of 26 informative cases. These data suggest that loss of heterozygosity of regions on 5q including the APC and MCC genetic loci is involved in the development and/or progression of most human esophageal cancers. They imply that inactivation of APC, MCC, and/or a linked gene on chromosome 5q plays a role in the pathogenesis of some cancers of the upper gastrointestinal tract, as well as in colon cancer and familial adenomatous polyposis.
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PMID:Loss of heterozygosity involving the APC and MCC genetic loci occurs in the majority of human esophageal cancers. 156 31

In this study, the intensity of exposure to asbestos was evaluated in the residents of Kure City, the site of the Japanese naval shipyard, Kure. The number of asbestos bodies was counted in 728 autopsied cases from those treated surgically in Kure Kyosai Hospital. Five grams of lung tissue was lysed, and the number of asbestos bodies was counted with the use of light microscopic examination. By this method, the number of asbestos bodies detected in men was significantly higher than that in women. There was a peak between 60 and 70 years of age. The number of asbestos bodies in exposed cadavers in Kure City exceeded greatly that found in other districts of Japan. By this criterion, 58 of 109 patients with lung cancer had asbestos exposure, and 39 had a high exposure to asbestos. All 13 patients with malignant mesothelioma had a high exposure to asbestos. Excess asbestos exposure also was found in a large proportion of patients with gastric cancer, colon cancer, and acute leukemia. The crocidolite type of asbestos was detected frequently in patients of malignant mesothelioma or leukemia, and the chrysotile form was found in those with lung cancer.
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PMID:Intensity of exposure to asbestos in metropolitan Kure City as estimated by autopsied cases. 156 84

Of 446 deaths among serving and retired British Airways pilots between 1966 and 1989, 411 were analysed using the Proportional Mortality Ratio (PMR) technique. After removal of the predictable excess of aircraft accidents, excesses of cancer (PMR 1.31) and other accidents (1.60) were balanced by deficits in diseases of the circulatory (0.83) and respiratory (0.49) systems. While lung cancer was close to expectation (1.10), consistent excesses were shown in all analyses for malignant melanoma (6.68), cirrhosis of the liver (2.88), colon cancer (2.30) and brain/CNS cancer (2.68). Consideration of these ratios in relation to pilots' lifestyle and occupation leads to the conclusion that the brain/CNS cancer excess must be studied further.
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PMID:The mortality of British Airways pilots, 1966-1989: a proportional mortality study. 161 Mar 37

The number of bone marrow fibroblast colony-forming cells (CFU-F) were studied in twelve healthy donors, four colon (CP) and nine lung cancer patients (LP). A liquid culture system has been used to characterize human bone marrow CFU-F. The results showed any recognizable CFU-F in three patients with colon cancer and in two patients of the other group. One of the four CP and five of the nine LP presented a CFU-F value of 17 and 2, 8, 22, 29, 32, respectively compared to 65 from normal subjects. Two LP reached normal CFU-F values (normal range = 33-191). These data support the conclusion that the 84.6% of these solid tumor cancer patients study produced less number of proliferative status of fibroblast colony-forming cells.
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PMID:[In vitro formation of fibroblast colony-forming units in the bone marrow of patients with solid malignant tumors]. 162 Nov 82

The present study was designed to analyse the cytotoxic effects of the combination of fotemustine with 5-fluorouracil (5-FU) plus folinic acid (FA). Two human tumor cell lines were used; one line was derived from colon cancer (WIDR) and the other, from a non-small-cell lung cancer (CAL 12). Cytotoxic effects were assessed using the MTT (tetrazolium bromide) semi-automated test in 96-well incubation plates. The effects of various drug combinations were evaluated by the isobologram method. The drug combinations tested included fotemustine concentrations of 20, 30, 40, 50 and 70 micrograms/ml, 5-FU concentrations of 5, 15 and 30 micrograms/ml, and a constant FA concentration of 10(-5) M. A total of 180 different experimental conditions were tested. When cells were exposed to fotemustine prior to treatment with 5-FU, the final cytotoxic effects on both cell lines were additive or synergistic in the majority of cases (P less than 0.001). The 5-FU concentration was a determinant factor that modified the effects of the drug combination from antagonism (at low 5-FU concentrations) to synergism (high 5-FU concentrations; P less than 0.001). The addition of FA (10(-5) M) resulted in a significant shift towards synergistic associations in both cell lines. Administration of 5-FU prior to treatment with fotemustine caused marked antagonism, which 10(-5) M FA could not significantly shift towards simple additivity.
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PMID:Sequence-dependent cytotoxic effects of the combination of a new nitrosourea, fotemustine, with 5-fluorouracil plus folinic acid. 165 24

Analogues of somatostatin (SS) and luteinizing hormone-releasing hormone (LH-RH) activate tyrosine phosphatases in MIA PaCa-2 human pancreatic cancer cell line membranes and inhibit growth. We compared the substrates phosphorylated by epidermal growth factor (EGF) to those dephosphorylated by the SS analogue RC-160 (D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2) and [D-Trp6]LH-RH in cancer cell lines such as MIA PaCa-2 (human pancreatic cancer), HCPC (hamster cheek pouch carcinoma), A-549 (human lung cancer), HT-29 (human colon cancer), and R3230AC (breast cancer). EGF phosphorylated proteins of 170, 65, and 60 kDa and analogues of SS and LH-RH promoted the dephosphorylation of these proteins in MIA PaCa-2 and HCPC cell lines. The EGF receptor is 170 kDa. pp60src (60 kDa) is known to be a substrate for EGF receptor. The LH-RH receptor is also 60 kDa. The effects of RC-160 and [D-Trp6]LH-RH were quantitatively different. Examinations of HT-29, A-549, and R3230AC cancer cell lines revealed no phosphorylation by EGF or dephosphorylation by RC-160 and [D-Trp6]LH-RH. In addition to the 170-, 65-, and 60-kDa proteins, 35-kDa proteins were also phosphorylated in some cancer cell lines. This work demonstrates that analogues of SS and LH-RH can reverse the effects of EGF biochemically as well as functionally.
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PMID:Effects of epidermal growth factor and analogues of luteinizing hormone-releasing hormone and somatostatin on phosphorylation and dephosphorylation of tyrosine residues of specific protein substrates in various tumors. 167 42

Efforts to diminish the overall morbidity and mortality of malignancy have required a variety of strategies and a balanced national research agenda. The design of curative regimens against leukemia, lymphomas, testis cancer, and childhood malignancies is a tribute to the interactions between laboratory and clinical scientists. Laboratory models illustrated the importance of dose and the need for combinations to avoid the emergence of drug resistance in heterogeneous tumors. In addressing the incurability of common epithelial cancers in adults once disseminated, again laboratory models suggested that regimens which produced responses in advanced disease might be curative in patients with micro-metastases. Such proved to be the case in adjuvant therapy for breast cancer involving lymph nodes and for osteogenic sarcoma. Recent studies have extended this strategy to less advanced breast cancer and to locally advanced colon cancer. Lung cancer has required a different strategy. A coalition has developed to support the strongest possible public position against smoking. For the first time lung cancer incidence has leveled off in white males. Women and minorities continue to be a major target for smoking cessation programs. While large randomized trials are expensive (and to some scientists, unexciting), they are our most reliable means of detecting treatment differences of 10 to 15%. Because lung, breast, and colon cancer kill almost 250,000 Americans each year, such "small" differences represent thousands of Americans. There are also a number of interesting current studies that may impact in the longer term on the care of patients with cancer. Research of three different groups of investigators has recently converged. Over the past 3 decades several groups of basic laboratory investigators had been studying and cloning hematopoietic growth factors. Large randomized trials now confirm that myelosuppression after intensive chemotherapy can be substantially ameliorated, reducing infections and decreasing hospital days, risks, and costs. Another cohort of clinical pharmacologists and clinicians were studying bone marrow transplantation, developing combinations of agents that can be given at high dose to overcome resistance, albeit with considerable toxicity. Other groups in blood banks and those interested in the regulation of hematopoiesis recognized that early hematopoietic progenitor cells circulate in the peripheral blood. Their number were increased after certain chemotherapy regimens, by growth factors and most remarkably, with growth factors given after chemotherapy. Patients supported with peripheral blood progenitor cells reengraft both platelets and granulocytes more rapidly than those given marrow, in the time frame of recovery after standard doses of chemotherapy (i.e., 21 days).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New developments in clinical oncology: the interdependence of bench and bedside. 167 75

The effect of concomitant treatment with different antibiotics on the cytotoxicity of epirubicin, bleomycin, estramustine and cisplatin was studied in vitro on fibroblasts (V79) and two cancer cell lines (colon cancer HT29 and lung cancer P31). The cell lines were propagated under standard tissue culture conditions and evaluated as the number of surviving cell clones in comparison to untreated controls. Fifteen commonly used antibiotics were tested and thirteen of these were found to modify the cytotoxic effect in one or several of the combinations tested. One antibiotic agent could affect the toxicity of different cytostatics in opposite directions and there were marked differences between the cell lines tested. Only in one of the situations, the combination of bleomycin and ceftazidim, did the antibiotic cause opposite effects on the toxicity of a cytostatic when comparing fibroblasts and carcinoma cells. A most impressive observation was the pronounced increase in cisplatin-induced cytotoxicity by amphotericin B. In conclusion, the results suggest that antibiotics can interact with the cytotoxicity of antitumoral drugs but that the feature of this interaction is seemingly an erratic phenomenon. Further studies are certainly justified, especially regarding the effects of amphotericin B and its mechanisms in enhancing the cytotoxicity of cisplatin.
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PMID:Effects of antimicrobial drugs on the cytotoxicity of epirubicin, bleomycin, estramustine and cisplatin. 171 83

Thirty-seven patients with tracheobronchial lesions by malignant tumor were treated with Nd-YAG laser. Thirty-seven patients were twenty-three males and fourteen females and ages ranged from 34 to 79 years. Diseases included were primary tracheal tumor in 3 cases, lung cancer in 16 (8 squamous cell carcinoma, 5 adenocarcinoma, 2 large cell carcinoma, 1 small cell carcinoma), cancer of adjacent organs in 9 (5 thyroid cancers, 4 esophageal cancers), and metastatic cancer to the lung or mediastinal lymph nodes in 9 (4 renal cell carcinoma, 2 thyroid cancer, one patient respectively, colon cancer and breast cancer). Intermittent irradiation of YAG laser was done for 0.5 second at 30-40 Watt through flexible bronchoscope under local anesthesia. It was repeated 1 to 41 times (mean 4.1 times) and energy amount was 148 Joules to 18,513 Joules (mean 3,305 J). The result was; stenosis disappeared in 22 cases (59.4%), improved in 14 (37.8%), and in one case YAG laser therapy discontinued due to intractable bleeding. The Nd-YAG laser therapy for tracheobronchial lesions by malignant tumor is very useful to improve dyspnea or atelectasis.
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PMID:[Nd-YAG laser therapy of tracheobronchial lesions by malignant tumor]. 173 32

The pineal hormone melatonin (MLT) is able to exert an oncostatic action. Its possible use in the treatment of human tumors, however, has not yet been investigated. The present study was carried out to evaluate the effects of MLT in patients with metastatic solid tumors resistant to conventional therapies. The study included 54 patients, most of them were affected by lung cancer or colorectal carcinoma. MLT was given intramuscularly at a daily dose of 20 mg at 3.00 p.m. for 2 months; this induction phase was followed by a maintenance period at a dose of 10 mg orally in responder patients or in those with an improvement in performance status (PS). The clinical response was as follows: 1 partial response (cancer of pancreas), 2 minor responses (colon cancer and hepatocarcinoma) and 21 with stable disease. The remaining 30 patients rapidly progressed within the first 2 months of therapy. An evident improvement in PS was achieved in 18 of 54 (33%) cases. These results, by showing an apparent control of the neoplastic growth and an improvement in the quality of life in a reasonable number of cancer patients for whom no other standard therapy is available, would justify further clinical trials to better define the impact of MLT therapy on the survival and quality of life of untreatable advanced cancer patients.
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PMID:Clinical results with the pineal hormone melatonin in advanced cancer resistant to standard antitumor therapies. 174 79


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