The carbon impact of short-haul tourism: A case study of UK travel to Southern France using life cycle analysis

Tourism holds a significant share in the global carbon footprint. Transportation to the destination is recognized as the primary contributor, although its contribution can be less dominant in the context of short-haul travel. Previous studies do not provide a critical comparative analysis of how changes in travel behaviour, notably modal shift, affect the total carbon impacts from short-haul holidays; nor do they explore the relative contribution of the specific elements of the holiday product or account for global variations when measuring those contributions. This paper presents a carbon impact assessment case study of short-haul tourism to Southern France by British tourists. It applies an advanced, Life Cycle Assessment-based, method of evaluation, the hybrid DEFRA-LCA (Ecoinvent) approach, which is capable of appraising both the direct and the embodied 'indirect' greenhouse gas emissions. The principal finding supports the traditional view that transportation generates the largest carbon footprint and that the most significant carbon savings can be achieved by switching from air and car-based travel to train and coach. However, the study also indicates that if tourists stay at the destination longer, and travel to the destination by train or coach, the destination-based elements of the holiday can make a large carbon contribution and even outweigh the share of the transit element. The Life Cycle Assessment also shows that the 'indirect' greenhouse gas emissions from tourism in Southern France are significant, thus emphasizing the importance of their incorporation into future carbon impact appraisals. © 2013 Elsevier Ltd. All rights reserved

An isogenic experimental model identifies b-catenin as a molecular target in ovarian cancer metastasis

Session - Tumor Biology: no. 650This journal suppl. entitled: Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LAOvarian cancer metastasis is closely associated with unfavorable outcomes, yet the underlying mechanisms remain obscure. Here we establish an isogenic model that could mimic the spontaneous metastasis of human ovarian cancer. Given that tumor cells are heterogeneous in nature, an isogenic pair of highly metastatic (HM) and non-metastatic (NM) cell lines with opposite metastatic capabilities was derived using in vitro and in vivo selection. Incorporation of the luciferase gene into the cell pair allowed non-invasive monitoring of the metastatic events by bioluminescent imaging in vivo. Orthotopic implantation of HM into the ovarian bursa of NOD/SCID mice resulted in metastases within the peritoneum with ascites formation, thus representing the major dissemination pattern of human ovarian cancer cells. However, NM failed to form detectable metastases, although it was tumorigenic at the ovarian bursa. In comparison with NM, HM displayed higher spheroid-forming ability and had higher expression of stemness marker genes, which are characteristics of cancer stem-like population. By proteomic profiling and pathway analysis, HM is found to be enriched in the oncogenic β-catenin signaling, a pathway elevated in ovarian cancer metastases. Tumor initiation and metastasis of HM was dramatically impaired when β-catenin was specifically knocked down. We further demonstrated that β-catenin could down-regulate the expression of Dicer, a major component of the microRNA machinery. These results together suggest that this model could help to delineate the molecular mechanisms for ovarian cancer metastasis, and provide clinically relevant insights to target metastasizing ovarian cancer cells. ©2016 American Association for Cancer Research

Nur77: A potential therapeutic target in cancer

ReviewThe orphan nuclear receptor Nur77 (also known as NR4A1, NGFIB, TR3, TIS1, NAK-1, or N10) is a unique transcription factor encoded by an immediate early gene. Nur77 signaling is deregulated in many cancers and constitutes an important molecule for drug targeting. Areas covered: Nur77 as a versatile transcription factor that displays distinct dual roles in cell proliferation and apoptosis. In addition, several recent insights into Nur77's non-genomic signaling through its physical interactions with various signaling proteins and its phosphorylation-dependent regulation will be highlighted. The possible mechanisms by which Nur77 supports carcinogenesis and specific examples in different human cancers will be summarized. Different approaches to target Nur77 using mimetics, natural products, and synthetic compounds are also described. Expert opinion: These latest findings shed light on the novel roles of Nur77 as an exploitable target for new cancer therapeutics. Further work which focuses on a more complete understanding of the Nur77 interactome as well as how the different networks of Nur77 functional interactions are orchestrated in a stimulus or context-specific way will aid the development of more selective, non-toxic approaches for targeting Nur77 in future. © 2012 Informa UK, Ltd.link_to_subscribed_fulltex

GABPA inhibits invasion/metastasis in papillary thyroid carcinoma by regulating DICER1 expression

The ETS family transcription factor GABPA is suggested as an oncogenic element, which is further supported by the recent reporting of it as the sole ETS member to activate the mutant TERT promoter in thyroid carcinomas (TC). However, it remains unclear how GABPA contributes to TC pathogenesis. The present study is designed to address this issue. TERT expression was significantly diminished in TERT promoter-mutated TC cells upon GABPA inhibition. Surprisingly, GABPA depletion led to robustly increased cellular invasion independently of TERT promoter mutations and TERT expression. DICER1, a component of the microRNA machinery, was identified as a downstream effector of GABPA. GABPA facilitated Dicer1 transcription while its depletion reduced Dicer1 expression. The mutation of the GABPA binding site in the DICER1 promoter led to diminished basal levels of DICER1 promoter activity and abolishment of GABPA-stimulated promoter activity as well. The forced DICER1 expression abrogated the invasiveness of GABPA-depleted TC cells. Consistently, the analyses of 93 patients with papillary thyroid carcinoma (PTC) revealed a positive correlation between GABPA and DICER1 expression. GABPA expression was negatively associated with TERT expression and promoter mutations, in contrast to published observations in cancer cell lines. Lower GABPA expression was associated with distant metastasis and shorter overall/disease-free survival in PTC patients. Similar results were obtained for PTC cases in the TCGA dataset. In addition, a positive correlation between GABPA and DICER1 expression was seen in multiple types of malignancies. Taken together, despite its stimulatory effect on the mutant TERT promoter and telomerase activation, GABPA may itself act as a tumor suppressor rather than an oncogenic factor to inhibit invasion/metastasis in TCs and be a useful predictor for patient outcomes