Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to describe disruptions in quality of life (QOL) in women suffering from lung cancer, the leading cause of cancer-related death in the United States. QOL was measured with the CARES-SF. Symptom distress was measured with the modified Symptom Distress Scale, and functional status was measured with the Karnofsky Performance Status Scale. Sixty-nine women with lung cancer participated in a one-time data collection. The typical subject was under 65 years of age, married, has had primary or recurrent non-small cell lung cancer for over 12 months, had limited disease, and was not currently receiving treatment. Subjects had greater disruptions in global QOL and its dimensions compared to a normative heterogeneous female cancer sample. The most prevalent serious disruptions were fatigue, difficulty with household chores, worry about ability to care for self, and worry about cancer progression. The global CARES-SF score was moderately correlated to functional status (r = 0.69, p = < 0.001), and to symptom distress (r = 0.72, p = < 0.001). Symptom distress was associated strongly with the physical subscale of QOL (r = 0.80, p = 0.001) and significantly but less strongly with all other dimensions of QOL. Significantly greater differences in disruptions of quality of life occurred in women younger than 65 years (p = 0.04), women with recurrent disease (p = 0.003), and women with low income (p = 0.008). In stepwise regression, symptom distress predicted 53% of the variance followed by functional status (59%) and recurrence (63%) when QOL was the outcome variable.
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PMID:Women with lung cancer: impact on quality of life. 838 54

It is well known that immunosuppression may contribute to the progression and chemotherapy-resistance of cancer. Recent studies have demonstrated that lymphocytes with the phenotype of CD4+CD25+ regulatory T cells (T-regs) contribute to immune dysfunction in cancer patients, and a relative increase in CD4+CD25+ regulatory T cells is related to immunosuppression and tumor progression in patients with some malignancies. In the present study, we evaluated the prevalence of T-regs in the peripheral blood of patients with breast cancer and non-small cell lung cancer. The phenotype of lymphocyte CD4+CD25+ cells was analyzed in peripheral blood of patients with breast cancer (n=22) and non-small cell lung cancer (NSCLC) (n=17). The population of CD4+CD25+ cells in CD3+ and CD4+ cells was evaluated by flow cytometric analysis with triple-color staining. Patients with breast cancer did not have a higher percentage of CD4+CD25+ cells in the total CD3+ and CD4+ cells in their peripheral blood than healthy volunteers. In contrast, patients with recurrent NSCLC had significantly higher percentages of CD4+CD25+ cells in CD3+ (47.6%) and CD4+ (71.0%) than healthy volunteers (n=10) who had CD4+CD25+ cells in CD3+ (33.7%, p=0.02) and CD4+ (52.2%, p<0.03). The population of CD4+CD25+ T-regs in the peripheral blood of patients with non-small cell lung cancer was significantly higher than that in healthy volunteers but not in breast cancer patients. These findings suggest that the use of T-reg-targeted immunomodulatory therapy may be a more effective strategy for patients with non-small cell lung cancer than for those with breast cancer.
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PMID:CD4+CD25+ regulatory T cells in the peripheral blood of patients with breast cancer and non-small cell lung cancer. 1621 Dec 95

Epithelial-to-mesenchymal transition (EMT) has profound impacts on cancer progression and also on drug resistance, including epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). Nowadays, there is still no predictive biomarker identified for the use of EGFR-TKIs in non-small cell lung cancer (NSCLC) patients with wild-type EGFR. To clarify the role of EMT phenotype as a predictive marker for EGFR-TKI, we performed a retrospective study in 202 stage IV or recurrent NSCLC patients receiving gefitinib or erlotinib therapy from June 2008 to September 2012 in our institute. Clinical data and EGFR mutational status were collected, while epithelial, epithelial to mesenchymal, not specified or mesenchymal phenotype were classified according to EMT markers such as E-cadherin, fibronectin, N-cadherin and vimentin by immunohistochemistry. Epithelial phenotype was more frequently found in patients with EGFR mutation (p = 0.044). Epithelial phenotype was associated with a significantly higher objective response rate (23.5 vs. 11.1 vs. 0.0 vs. 2.4%, p = 0.011), longer progression-free survival (4.4 vs. 1.9 vs. 1.7 vs. 1.0 months, p < 0.001) and longer overall survival (11.5 vs. 8.9 vs. 4.5 vs. 4.9 months, p < 0.001) compared to epithelial to mesenchymal, not specified and mesenchymal phenotype in the wild-type EGFR subgroup. In the subgroup with EGFR mutation, the trend remained but without a statistically significant difference. In conclusion, epithelial phenotype was more likely expressed in patients with EGFR mutation and was associated with a better outcome in advanced NSCLC patients with wild-type EGFR, which indicates that the EMT phenotype might be a potential marker to guide EGFR-TKI therapy in this population.
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PMID:Epithelial phenotype as a predictive marker for response to EGFR-TKIs in non-small cell lung cancer patients with wild-type EGFR. 2477 40