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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hexavalent chromium [Cr(VI)] is a known etiological factor in human lung cancer. Cr(VI) exposure-related lung cancer has a high mutation incidence in the p53 gene. Upon intake in human cells Cr(VI) is reduced to Cr(III), which is able to conjugate with amino acids and consequently form either binary Cr(III)-DNA or ternary Cr(III)-amino acid-DNA adducts. Both binary and ternary Cr(III)-DNA adducts are mutagenic. We have found that the Escherichia coli nucleotide excision enzyme UvrABC nuclease is able to incise Cr(III)- and Cr(III)-histidine-modified plasmid DNA and the extent of incision is proportional to the amount of Cr(III)-DNA adducts in the plasmid. In order to determine the role of Cr(III)-DNA adducts in the mutagenesis of the p53 gene in human cancer using the UvrABC nuclease incision method, we have mapped the Cr(III)-DNA distribution in PCR DNA fragments amplified from exons 5, 7 and 8 of the p53 gene. We have found that the sequence specificities of Cr(III)-DNA and Cr(III)-histidine-DNA adducts in the p53 gene sequence are identical and that both types of adducts are preferentially formed at -NGG- sequences, including codons 245, 248 and 249, the mutational hotspots in human lung cancer. It has been found that Cr(III)-DNA adducts induce mainly G to T mutations. Therefore, these results suggest that Cr(III)-DNA adduct formation contributes to the p53 gene mutations in lung carcinogenesis.
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PMID:Sequence specificity of Cr(III)-DNA adduct formation in the p53 gene: NGG sequences are preferential adduct-forming sites. 1625 Dec 6

The two-kringle domain of tissue-type plasminogen activator (TK1-2) has been identified as a novel angiogenesis inhibitor. In the previous study, purified Pichia-derived TK1-2 has been shown to suppress in vivo growth of human lung and colon cancer cells. Here, we demonstrate that E. coli-derived non-glycosylated TK1-2 suppresses tumor growth more potently than Pichia-derived TK1-2 and prolongs the survival of tumor bearing mice. The recombinant TK1-2 prepared through E. coli expression, His-tag affinity chromatography and in vitro refolding was injected intraperitoneally once daily into nude mice 7 days after subcutaneous implantation with PC14 lung cancer cells (n=10). Measurement of tumor volumes indicated that low-dose TK1-2 treatment (10 mg/kg) suppressed tumor growth by approximately 85.2% (p<0.01), while high-dose TK1-2 treatment (50 mg/kg) even more potently inhibited tumor growth (>93.8%) (p<0.005). Treatment of TK1-2 also prolonged the survival of tumor-bearing mice in a dose-dependent fashion. In an independent HCT116 xenograft model, E. coli-derived TK1-2 was more effective in suppressing tumor growth than Pichia-derived TK1-2. Immunohistochemical analysis of tumor tissue also revealed that the expression of VEGF, SMA-alpha, TNF-alpha and angiogenin was less positive in the E. coli-derived TK1-2-treated group than in the Pichia-derived TK1-2-treated group. These results suggest that E. coli-derived refolded, non-glycosylated TK1-2 can be used more effectively as an anti-cancer agent.
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PMID:Potent anti-tumor and prolonged survival effects of E. coli-derived non-glycosylated kringle domain of tissue-type plasminogen activator. 1639 90

We here describe a case of multiple pyomyositis in a 62-year-old man who had systemic chemotherapy for recurrent lung cancer. His initial symptoms consisted of fever and general fatigue, followed by progressive pain and swelling in his extremities, which mimicked deep venous thrombosis along with bacterial infection. He was admitted to the hospital for intravenous administration of antibiotics. MRI appeared very useful to find the intramuscular fluid collections with circumferential inflammatory changes, which confirmed diagnosis of the multiple pyomyositis. Surgical drainage as well as intravenous administration of antibiotics worked very well and improved clinical symptoms in a few weeks after the treatments. He could resume normal activities with minimum functional impairments in the extremities. Pyomyositis should be kept in mind as one of the adverse effects after chemotherapy for malignant tumors.
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PMID:[A case of multiple pyomyositis after chemotherapy for lung cancer]. 1677 Jan 9

Therapy and the handling of dyspnea in the last period of one's life is described and discussed from a case report. A patient with lung cancer and a distinct chronic obstructive pulmonary disease is presented. His coping with increasing dyspnea and the therapeutic strategies are described. Problems with the side effects of therapy and coping strategies are dealt with, too.
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PMID:[Dyspnea in the last period of one's life]. 1683 Feb 39

Ernst Wynder did not believe that environmental tobacco smoke (ETS), also known as secondhand smoke, was a cause of lung cancer because his own data did not support this. His view on the issue may have begun to change with our initial studies, carried out at the American Health Foundation, showing that metabolites of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were present in the urine of non-smokers exposed to ETS. The metabolites - 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronides (NNAL-Glucs) - have now emerged as leading biomarkers for the study of carcinogen exposure in non-smokers exposed to ETS. Subsequent work has consistently demonstrated elevated levels of NNAL plus NNAL-Glucs in the urine of people exposed to ETS in various field studies and throughout life. These studies strongly support the epidemiologic data demonstrating that ETS exposure causes lung cancer in non-smokers and have likely had an impact on tobacco control.
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PMID:A biomarker of exposure to environmental tobacco smoke (ETS) and Ernst Wynder's opinion about ETS and lung cancer. 1699 60

A 70-year-old man with a past history of lung resection for early stage lung cancer was admitted to our hospital because of worsening exertional dyspnea. Right heart catheterization revealed severe pulmonary arterial hypertension (PAH) with pulmonary vascular resistance of 1671.64 dyne.sec.cm(-5). The patient was treated with sildenafil added to an oral prostacyclin analog, beraprost, and long term oxygen therapy. His exertional dyspnea continued to improve until his sudden death following nasal bleeding. Autopsy revealed marked thickening of pulmonary arteriolar walls, but no recurrence of lung cancer, significant pulmonary embolism or pulmonary parenchymal disease. His PAH could not be explained by the mild airway obstruction or sleep apnea syndrome, and unrelated pulmonary vascular disease was suspected.
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PMID:[Unexplained pulmonary arterial hypertension in a patient with lung resection, treated with sildenafil and beraprost]. 1714 79

To evaluate the effect of DNA repair gene XRCC1 polymorphisms on the risk of lung cancer in a northeastern Chinese population, we studied five cSNPs in the XRCC1 gene, three that lead to non-synonymous changes: Arg194Trp, Arg280 His and Arg399Gln and two that lead to synonymous changes: Pro206Pro and Gln632Gln. A hospital-based case-control study consisted of 247 lung cancer cases and 253 cancer-free controls matched on age, gender and ethnicity. PCR-RFLP was used for genotyping. Carriers of the minor G-allele of Pro206Pro were at significantly increased risk of lung cancer (adjusted OR=1.96, 95% CI=1.26-3.06, P=0.003). Stratified analyses revealed a significantly decreased risk of lung cancer associated with the AG/AA genotype of Arg280His (AG+AA versus GG, OR=0.38, 95% CI=0.19-0.75, P=0.005) among never smokers, although there was no interaction between Arg280His and smoking. In a haplotype analysis, a haplotype defined by Arg194Trp(C)-Pro206Pro(G)-Arg280His(G)-Arg399Gln(G)-Gln632Gln(G) was associated with increased risk of lung cancer (OR=28.60, 95% CI=2.49-331.31, P=4.45x10(-5)). No associations were observed for the other polymorphisms or haplotypes. Our results suggest that the XRCC1 Pro206Pro polymorphism or the haplotype encompassing the minor allele may contribute to genetic susceptibility for lung cancer in this northeastern Chinese population. To our knowledge, this is first report that XRCC1 Pro206Pro influences cancer risk.
Lung Cancer 2007 May
PMID:The DNA repair gene XRCC1 and genetic susceptibility of lung cancer in a northeastern Chinese population. 1731 90

Cauda equina syndrome (CES) may be caused by tumor, herniated disc, trauma and spinal infections. However, CES due to occult lung cancer has not been reported in the literature. A 50-year-old man presented with a subacute CES caused by an intradural metastasis of an adenocarcinoma of the lung to the lumbosacral cauda fibers. His lumbosacral magnetic resonance imaging (MRI), showed a well-demarcated, intradural extramedullary mass lesion resembling a neurinoma at the L4/5 level. The patient underwent an L4-L5 laminectomy. The operative findings were also suggestive of neurinoma with involvement of three nerve roots, and a well-demarcated tumor without infiltration into the subarachnoid space. Although the findings of the operation were suggestive of neurinoma, final pathological diagnosis revealed metastatic carcinoma. Immunohistochemistry revealed clear cell adenocarcinoma metastasis. Chest X-ray and high resolution contrasted pulmonary computed tomography were normal. Positron emission tomography (PET) showed a lung mass, at the left apex. The patient was treated with chemotherapy and post-operative spinal radiotherapy was also performed. The CES resolved after the operation and the patient was followed up for 2 years with no recurrence. MRI of intradural cauda equina metastasis may be similar to that of intradural nerve sheath tumor. Surgery and postoperative radiotherapy may be effective for the treatment of CES due to lung carcinoma. Definitive diagnosis is by histopathological examination with immunohistochemistry. If the primary cancer cannot be detected by conventional radiological techniques, PET may be helpful.
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PMID:Spinal metastasis of occult lung carcinoma causing cauda equina syndrome. 1733 30

A 53-year-old black man was diagnosed with poorly differentiated adenocarcinoma of the lung and treated initially with 4 cycles of paclitaxel in combination with carboplatin and external-beam radiation therapy with a good clinicoradiologic response. The patient tolerated the chemotherapy well and did not develop any skin or nail changes during that period of time. His lung cancer recurred 10 months later, when he was found to have bone metastases. Second-line chemotherapy with pemetrexed 500 mg/m2 intravenously every 3 weeks was commenced. A week prior, the patient was started on folic acid 1 mg orally daily and given an injection of vitamin B12 1000 microg intramuscularly that was continued every 3 cycles thereafter. Dexamethasone 4 mg orally twice daily was given around the time of chemotherapy administration to prevent the dermatitis associated with the drug. The patient denied taking other drugs. Two months into his second-line chemotherapy, he developed multiple, concomitant, transverse and longitudinal black lines in all of his fingernails and toenails. After an interval of 3 months, he presented a complex pattern of nail hyperpigmentation, from combined dense horizontal and longitudinal streaks in some nails to diffuse black discoloration in others (Figure). Other associated changes included koilonychia, dystrophy, and friability of nail plates. Along with normal results of a hepatorenal panel and normal serum vitamin B12 and folate levels, no metabolic or endocrinologic alterations were present to explain the nail pigmentation and dystrophic changes. Results of his mycologic examination and cultures came back negative. When questioned, he denied taking any other drugs including other alternative medicine approaches or vitamin supplements, particularly retinoids, well known for causing severe nail dystrophy.
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PMID:A complex pattern of melanonychia and onycholysis after treatment with pemetrexed for lung cancer. 1736 81

A 79-year-old patient was admitted with fever and shortness of breath. His medical history included treatment for lung cancer 3 years previously. The patient's clinical and radiological status remained unchanged despite antibiotic treatment for pneumonia. No infectious pathogen could be identified. Treatment with systemic steroids for suspected cryptogenic organizing pneumonitis (COP) was started. Following steroid treatment the patient's shortness of breath ameliorated and C-reactive protein was normal. Three weeks after admission Mycobacterium avium complex (MAC) grew in sputa cultures and therefore a diagnosis of MAC pneumonia was made.
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PMID:[Mycobacterium avium pneumonia in an HIV negative patient]. 1739 31


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