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Cancer Death Worldwide (cancer + death_worldwide)
Selected AbstractsModifiable Risk Factors Still Major Cause of Cancer Deaths WorldwideCA: A CANCER JOURNAL FOR CLINICIANS, Issue 2 2006Article first published online: 31 DEC 200 No abstract is available for this article. [source] A different pattern of cytotoxic T lymphocyte recognition against primary and metastatic tumor cells in a patient with nonsmall cell lung carcinomaCANCER, Issue 1 2005Tetsuya So M.D. Abstract BACKGROUND Lung carcinoma represents the most frequent cause of cancer death worldwide because of tumor metastases. The objective of the current study was to analyze the immunologic response during the progress of lung carcinoma metastasis. METHODS The authors established two tumor cell lines that were derived from primary and metastatic lesions in a patient with lung carcinoma (Patient G603). One cell line (G603L) was established from the primary lesion, and the other cell line (G603AD) was established from a metastatic lesion in the right adrenal gland 7 months after the patient underwent surgery for the primary lesion. Autologous regional lymph node lymphocytes were stimulated with CD80-transfected G603L cells, then cytotoxic T lymphocytes (CTLs) were induced against both lung carcinoma cell lines. RESULTS Both G603L cells and G603AD cells expressed Class I human leukocyte antigen, intracellular cell adhesion molecule 1, and lymphocyte-associated antigen type 3 (LFA-3), but not Fas or Fas ligand on their surfaces. By stimulation with CD80-transfected G603L cells, 2 CTL clones (H2/17 and H2/36) were established from the bulk CTLs. CTL clone H2/17 lysed G603L cells but not G603AD cells, suggesting that the antigen recognized by CTL clone H2/17 was abrogated during the process of metastasis. In contrast, CTL clone H2/36 lysed both G603L cells and G603AD cells, indicating that the antigen recognized by CTL clone H2/36 was maintained in the tumor cells throughout tumor progression. CONCLUSIONS The results demonstrated the possibility that some tumor-associated antigens may be abrogated during the process of metastasis, although others are maintained. The identification of these antigens will lead to a better understanding of their immunologic role during disease progression in patients with lung carcinoma. Cancer 2005. © 2004 American Cancer Society. [source] OCIA domain containing 2 is highly expressed in adenocarcinoma mixed subtype with bronchioloalveolar carcinoma component and is associated with better prognosisCANCER SCIENCE, Issue 1 2007Tadashi Ishiyama Although lung adenocarcinoma is a major cause of cancer death worldwide, details of its molecular carcinogenesis and stepwise progression are still unclear. To characterize the sequential progression from bronchioloalveolar adenocarcinoma of the lung (BAC, in situ carcinoma) to adenocarcinoma mixed subtype with BAC component, polymerase chain reaction-based cDNA suppression subtractive hybridization (SSH) was carried out using two representative cases of BAC (non-invasive tumors) and adenocarcinoma mixed subtype with BAC (invasive tumors). Through differential screening, virtual reverse northern hybridization and quantitative real-time reverse-transcription,polymerase chain reaction (qRT-PCR) we selected five genes (TncRNA, OCIAD2, ANXA2, TMED4 and LGALS4) that were expressed at significantly higher levels in invasive adenocarcinoma mixed subtype with BAC than in BAC. After in situ hybridization and qRT-PCR analyses, we confirmed that only the OCIAD2 gene showed significantly higher expression in the tumor cells of invasive adenocarcinoma mixed subtype with BAC than in BAC (P = 0.026). We then carried out in situ hybridization of OCIAD2 in 56 adenocarcinoma mixed subtype with BAC component and assessed the correlation between OCIAD2 expression and clinicopathological features. In contrast to our expectation, the patients with OCIAD2 expression showed a better clinical outcome than those without OCIAD2 expression, and OCIAD2 expression showed an inverse correlation with lymphatic invasion, blood vessel invasion and lymph node metastasis. These results suggest that OCIAD2 begins to express at the progression from in situ to invasive carcinoma, and is associated with the favorable prognosis of adenocarcinoma mixed subtype with BAC component. (Cancer Sci 2007; 98: 50,57) [source] Environmental exposure to carcinogens causing lung cancer: Epidemiological evidence from the medical literatureRESPIROLOGY, Issue 4 2003Melissa J. WHITROW Objective: In 2000 there were 1.1 million lung or bronchial cancer deaths worldwide, with relatively limited evidence of causation other than for smoking. We aimed to search and appraise the literature regarding evidence for a causal relationship between air pollution and lung cancer according to the 10 Bradford Hill criteria for causality. Methodology: A MEDLINE search was performed using the following key words: ,lung neoplasm', ,epidemiology', ,human', ,air pollution'and ,not molec*'. The criteria for inclusion was: cited original research that described the study population, measured environmental factors, was of case control or cohort design, and was undertaken after 1982. Results: Fourteen papers (10 case control, four cohort studies) fulfilled the search criteria, with a sample size ranging from 101 cases and 89 controls, to a cohort of 552 cases and 138 controls. Of the 14 papers that fulfilled the search criteria the number of papers addressing each of the Bradford Hill critera were as follows: Strength of association: eight studies demonstrated significant positive associations between environmental exposure and lung cancer with a relative risk range of 1.14,5.2. One study found a negative association with relative risk 0.28. Consistency: eight of 14 studies found significant positive associations and one of 14 a significant negative association. Specificity: tobacco smoking and occupational exposure were addressed in all studies (often crudely with misclassification). Temporality: exposure prior to diagnosis was demonstrated in nine studies. Dose,response relationship: evident in three studies. Coherence, analogy: not addressed in any study. Conclusion: Evidence for causality is modest, with intermediate consistency of findings, limited dose,response evidence and crude adjustment for important potential confounders. Large studies with comprehensive risk factor quantification are required to clarify the potentially small effect of air pollution given the relatively large effects of tobacco smoking and occupational carcinogen exposure. [source] | ||||||||||