Cell Lung Cancer Patients (cell + lung_cancer_patient)

Distribution by Scientific Domains
Medical Sciences66%

Kinds of Cell Lung Cancer Patients

  • non-small cell lung cancer patient
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    Selected Abstracts

    Intratumoural chemotherapy of lung cancer for diagnosis and treatment of draining lymph node metastasis

    JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 3 2010
    Firuz Celikoglu
    Abstract Objectives Reviewed here is the potential effectiveness of cytotoxic drugs delivered by intratumoural injection into endobronchial tumours through a bronchoscope for the treatment of non-small cell lung cancer and the diagnosis of occult or obvious cancer cell metastasis to mediastinal lymph nodes. Key findings Intratumoural lymphatic treatment may be achieved by injection of cisplatin or other cytotoxic drugs into the malignant tissue located in the lumen of the airways or in the peribronchial structures using a needle catheter through a flexible bronchoscope. This procedure is termed endobronchial intratumoural chemotherapy and its use before systemic chemotherapy and/or radiotherapy or surgery may provide a prophylactic or therapeutic treatment for eradication of micrometastases or occult metastases that migrate to the regional lymph nodes draining the tumour area. Conclusions To better elucidate the mode of action of direct injection of cytotoxic drugs into tumours, we review the physiology of lymphatic drainage and sentinel lymph node function. In this light, the potential efficacy of intratumoural chemotherapy for prophylaxis and locoregional therapy of cancer metastasis via the sentinel and regional lymph nodes is indicated. Randomized multicenter clinical studies are needed to evaluate this new and safe procedure designed to improve the condition of non-small cell lung cancer patients and prolong their survival. [source]

    Five years survival in metastatic non-small cell lung cancer patients treated with chemotherapy alone or chemotherapy and melatonin: a randomized trial

    JOURNAL OF PINEAL RESEARCH, Issue 1 2003
    P. Lissoni
    Abstract: Numerous experimental data have documented the oncostatic properties of melatonin. In addition to its potential direct antitumor activity, melatonin has proved to modulate the effects of cancer chemotherapy, by enhancing its therapeutic efficacy and reducing its toxicity. The increase in chemotherapeutic efficacy by melatonin may depend on two main mechanisms, namely prevention of chemotherapy-induced lymphocyte damage and its antioxidant effect, which has been proved to amplify cytotoxic actions of the chemotherapeutic agents against cancer cells. However, the clinical results available at present with melatonin and chemotherapy in the treatment of human neoplasms are generally limited to the evaluation of 1-year survival in patients with very advanced disease. Thus, the present study was performed to assess the 5-year survival results in metastatic non-small cell lung cancer patients obtained with a chemotherapeutic regimen consisting of cisplatin and etoposide, with or without the concomitant administration of melatonin (20 mg/day orally in the evening). The study included 100 consecutive patients who were randomized to receive chemotherapy alone or chemotherapy and melatonin. Both the overall tumor regression rate and the 5-year survival results were significantly higher in patients concomitantly treated with melatonin. In particular, no patient treated with chemotherapy alone was alive after 2 years, whereas a 5-year survival was achieved in three of 49 (6%) patients treated with chemotherapy and melatonin. Moreover, chemotherapy was better tolerated in patients treated with melatonin. This study confirms, in a considerable number of patients and for a long follow-up period, the possibility to improve the efficacy of chemotherapy in terms of both survival and quality of life by a concomitant administration of melatonin. This suggests a new biochemotherapeutic strategy in the treatment of human neoplasms. [source]

    Course of psychological distress and its predictors in advanced non-small cell lung cancer patients

    PSYCHO-ONCOLOGY, Issue 6 2006
    Tatsuo Akechi
    Abstract This study investigated longitudinal changes and predictive factors for psychological distress among 85 newly diagnosed advanced non-small cell lung cancer (NSCLC) patients. Whereas tension-anxiety after diagnosis (T1) was significantly reduced at two months (T2) and six months (T3) after diagnosis and depression-dejection at T1 was significantly reduced at T2, other forms of psychological distress, including anger,hostility, vigor, fatigue, and confusion, did not show significant changes. Total mood disturbance did not show significant change. Only a higher total mood disturbance at T1 was a significant predictor of total mood disturbance at T3. These findings demonstrate that most types of psychological distress experienced by advanced NSCLC patients is likely to persist during the subsequent clinical course. The findings also suggest that initial psychological distress itself after cancer diagnosis is the most important predictor for subsequent psychological distress and that early intervention beginning immediately after the disclosure of a diagnosis of cancer is one way to prevent and/or reduce subsequent psychological distress in advanced NSCLC patients. Copyright © 2005 John Wiley & Sons, Ltd. [source]

    Prognostic model to predict outcomes in nonsmall cell lung cancer patients treated with gefitinib as a salvage treatment

    CANCER, Issue 7 2009
    Min Jae Park MD
    Abstract BACKGROUND: A prognostic model based on clinical parameters for nonsmall cell lung cancer (NSCLC) patients treated with gefitinib (250 mg/day) as a salvage therapy was devised. METHODS: Clinical data regarding a total of 316 metastatic or recurrent NSCLC patients who were treated with gefitinib were analyzed. RESULTS: Poor prognostic factors for overall survival (OS) by multivariate analysis were an Eastern Cooperative Oncology Group (ECOG) performance status of 2 to 3 (hazards ratio [HR] of 2.07; 95% confidence interval [CI], 1.57-2.73 [P < .001]), the presence of intra-abdominal metastasis (HR of 1.76; 95% CI, 1.33-2.34 [P < .001]), elevated serum alkaline phosphatase (HR of 1.50; 95% CI, 1.13-2.00 [P = .005]), time interval from diagnosis to gefitinib therapy of ,12 months (HR of 1.48; 95% CI, 1.12-1.95 [P = .005]), low serum albumin (HR of 1.45; 95% CI, 1.09-1.92 [P = .009]), progression-free interval for previous chemotherapy of ,12 weeks (HR of 1.40; 95% CI, 1.0-1.84 [P = .015]), white blood cell >10,000/,L (HR of 1.38; 95% CI, 1.02-1.85 [P = .032]), and ever-smoker (HR of 1.33; 95% CI, 1.02-1.75 [P = .033]). Of the 272 patients applicable to this prognostic model, 41 patients (15%) were categorized as a good prognosis group (0-1 risk factors), 100 patients (37%) as an intermediate prognosis group (2-3 risk factors), 81 patients (30%) as a poor prognosis group (4-5 risk factors), and 50 patients (16%) as a very poor prognosis group (,6 risk factors). The median OS from the time of gefitinib treatment for the good, intermediate, poor, and very poor prognosis groups were 18.0 months, 11.2 months, 4.0 months, and 1.3 months, respectively (P < .001). CONCLUSIONS: This prognostic model based on easily available clinical variables would be useful to identify patients who might derive more benefit from gefitinib treatment and to make decisions in clinical practice. Cancer 2009. © 2009 American Cancer Society. [source]

    GM3 synthase gene is a novel biomarker for histological classification and drug sensitivity against epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer

    CANCER SCIENCE, Issue 10 2007
    Mariko Noguchi
    Expression of gangliosides and alterations in their composition have been observed during cell proliferation and differentiation and in certain cell cycle phases, brain development and cancer malignancy. To investigate the characteristics of GM3 synthase, SAT-I mRNA and ganglioside GM3 expression levels in lung cancer, we examined the expression levels of SAT-I mRNA as well as GM3 in 40 tumor tissues surgically removed from non-small cell lung cancer patients. Adenocarcinoma tissues expressed SAT-I mRNA levels that were significantly higher than those of squamous and other carcinomas (P < 0.0001). Moreover, the SAT-I mRNA levels were high in the bronchioalveolar carcinoma subtype and low in the solid and mucin subtypes of adenocarcinomas (P = 0.049, 0.049 and 0.013, respectively). To clarify the relationship between SAT-I mRNA and epidermal growth factor receptor (EGFR)-tyrosine kinase (TK) inhibitor sensitivity, we carried out drug sensitivity tests for the EGFR-TK inhibitors gefitinib and AG1478 using eight adenocarcinoma cell lines expressing no EGFR mutations. The IC50 values for gefitinib and AG1478 decreased dramatically with increasing SAT-I mRNA levels (R2 = 0.81 and 0.59, respectively), representing a wide range of drug sensitivities among adenocarcinoma cell lines. To explore a possible mechanism of how GM3 could enhance the sensitivity to EGFR-TK inhibitors, the SAT-I gene was introduced stably into a GM3-negative clone of murine 3LL lung cancer cells to produce GM3-reconstituted clones. We found an increase in EGFR protein levels and gefitinib sensitivity in GM3-reconstituted cells, suggesting the involvement of GM3 in the turnover of EGFR protein. Therefore, it is highly expected that, by measuring the expression levels of SAT-I mRNA in lung biopsy samples from non-small cell lung cancer patients, enhanced pathological identification and individualized chemotherapeutic strategies can be established for the appropriate use of EGFR-TK inhibitors. (Cancer Sci 2007; 98: 1625,1632) [source]