bluuebunny/crossref_metadata_2025_split huggingface dataset:
G2 in G20: China, the United States and the World after the Global Financial Crisis
Authors: Garrett Geoffrey 
Published: January 2010

AbstractThe post‐global financial crisis world will be increasingly dominated by China and the United States. What the de facto G2 do, together, independently or in conflict, will increasingly define the global bounds of the possible. Both countries want to embed their bilateral diplomacy in the multilateralism of the G20. The problem for the emergent G2 in G20 global architecture is that economic relations between China and the US will be increasingly difficult to manage. The large economic imbalances between the two countries, in which China buys American debt and Americans buy Chinese goods, will endure. Before the crisis, the codependence these imbalances created was a source of stability in Sino–American relations. After the crisis, they will be a source of frustration and conflict, as the second half of 2009 showed. To manage economic relations between China and the US effectively, the G20 agenda will have to move from crisis management to strategic planning for the global economy. The G20 will also have to become more institutionalized, but in a way that resembles more a nonexecutive board of directors of a multinational firm than a management committee of C‐level executives.Policy Implications

The world will be characterized by a de facto China–US G2 after the financial crisis.
Despite new commitments from both countries, large‐scale China–US economic imbalances will persist.
Dueling protectionism and economic nationalism are the biggest potential medium‐term threats to China–US relations.
Nesting the de facto G2 in the de jure G20 is the best hope for managing China–US tensions.
The G20 should be institutionalized as the board of directors for overseeing the Bretton Woods system, not as a replacement for it.
Spatial characteristics of canopy disturbances in riparian old-growth hemlock – northern hardwood forests, Adirondack Mountains, New York, USA
Authors: Curzon Miranda T. , Keeton William S. 
Published: January 2010

Gap dynamics in temperate, late-successional forests influence important riparian functions, including organic matter recruitment and light environments over streams. However, controls on gap dynamics specific to riparian forests are poorly understood. We hypothesized that (i) gaps are larger and more frequent nearer streams, (ii) gaps cluster at within-stand scales, and (iii) tree damage type and gap fraction vary among riparian landforms. All gaps within four 6–9 ha plots in riparian old-growth eastern hemlock ( Tsuga canadensis (L.) Carrière) – northern hardwood forest in the Adirondack Mountains, New York, USA, were mapped and measured. We recorded species, damage type, and diameter at breast height for gapmakers and dominant perimeter trees. Spatial distribution was assessed with Ripley’s K. Spatial autocorrelation in gap area and tree damage type were assessed using Moran’s I. Linear regression analysis defined relationships between proximity to streams and gap area and frequency. Expanded gap fraction ranged from 28.3% to 47.6%. Gaps were randomly distributed at scales ≤25 m and clustered at scales of 63–122 m. Distribution patterns were not consistent at other scales. Convergent and divergent landforms significantly influenced gap fraction, tree damage type, and species distributions. Positive correlations between convergent topography and gap area suggest an interaction between low-order riparian landforms and gap formation dynamics in late-successional forests.
Effect of thinning, fertilization with biosolids, and weather on interannual ring specific gravity and carbon accumulation of a 55-year-old Douglas-fir stand in western Washington
Authors: Kantavichai Rapeepan , Briggs David G. , Turnblom Eric C. 
Published: January 2010

Marketing timber is shifting from logs, lumber, and veneer measured volumetrically to include carbon storage and energy that are based on dry mass. Conversion between volume and dry mass relies on accurate estimates of wood specific gravity (SG). We measured width and SG of growth rings and their earlywood and latewood components with X-ray densitometry on trees from controlled, thinned, biosolid fertilized, and combined treatments applied to a 55-year-old Douglas-fir ( Pseudotsuga menziesii (Mirb.) Franco) stand. We developed models to predict interannual SG from climate and treatment effects and compared 20 year changes in dry mass and carbon storage with estimates from biomass equations and from the Wood Handbook average SG. Thinning increased latewood width but did not affect ring SG. Biosolid fertilization increased earlywood and latewood width and decreased ring SG 8% by decreasing earlywood SG, latewood SG, and latewood percentage. SG decreased with increased July soil moisture deficit; alternatively, SG increased with increased July total precipitation. Warmer mean March–May or August–November temperatures also increased SG. Because of the effects on SG, dry mass and carbon storage changes differed from volume changes produced by the treatments. Dry mass estimates using the average Wood Handbook SG or those calculated from biomass equations were inconsistent between treatments, with errors up to 50%.
Stem form and compression wood formation in young Pinus radiata trees
Authors: Lachenbruch Barbara , Droppelmann Fernando , Balocchi Claudio , Peredo Miguel , Perez Erika 
Published: January 2010

The crooked stems of some individuals of radiata pine ( Pinus radiata D. Don) can hinder volume recovery and wood quality. To infer causes of crookedness and to learn how lean angle affects compression wood (CW) formation we studied 5-year-old trees in southern Chile. Eight initially straight and eight initially crooked trees were tethered initially to angles of 15° or 30° or were left untethered for 131 days (48 trees total). There were no significant differences between straight and crooked trees in the extent of CW in pretreatment wood or in the relationship between stem angle and CW extent. Crooked trees, however, righted themselves more quickly than did straight trees at angles <15°, a result that supports the overcompensation hypothesis for the development of crooked stems. Stem angle had a complex effect on CW extent. In 2- to 3-year-old wood there was no meaningful effect of angle on CW extent. One-year-old wood produced less CW at stem angles <10° than at stem angles >10°, but above or below that threshold, there was no meaningful effect of angle on CW extent. The intertree differences in CW extent, as well as the correlation of leader CW extent with bole CW in the best individuals, suggests that CW assays could be used for early screening for wood quality.
Spatiotemporal variability in tree and stand mortality caused by spruce budworm outbreaks in eastern Quebec
Authors: Bouchard Mathieu , Pothier David 
Published: January 2010

We evaluated spruce budworm ( Choristoneura fumiferana (Clem.)) outbreak effects in nine study areas (60–86 ha each) located in the boreal forest of eastern Quebec (Canada). In each area, spruce budworm outbreak effects were measured from vegetation plots, dominant canopy and understory tree age structures, retrospective analysis of aerial photographs, defoliation records, and host tree growth reductions (dendrochronology). Large-scale synchronous outbreaks were detected across the region around the years 1880, 1915, 1950, and 1980. Overall, contrarily to what was expected for a region where host species (balsam fir ( Abies balsamea (L.) Mill.), Picea spp.) content is relatively high, these spruce budworm outbreaks seemed to have a relatively minor influence on stand dynamics, with the exception of the most recent outbreak (1980). This outbreak resulted in major stand mortality in the southern part of the region and favored the establishment of extensive tracts of young even-aged stands with few residual mature trees. This very abrupt increase in outbreak severity compared with earlier outbreaks, perhaps due to climatic or random factors, suggests that historical trends in successive outbreak severity should be extrapolated very cautiously and that the study of several outbreak cycles is needed to establish a range of natural variability that can be used to develop an ecosystem forest management strategy.
Novel Candidate Cancer Genes Identified by a Large-Scale Cross-Species Comparative Oncogenomics Approach
Authors: Mattison Jenny , Kool Jaap , Uren Anthony G. , de Ridder Jeroen , Wessels Lodewyk , Jonkers Jos , Bignell Graham R. , Butler Adam , Rust Alistair G. , Brosch Markus , Wilson Catherine H. , van der Weyden Louise , Largaespada David A. , Stratton Michael R. , Futreal P. Andy , van Lohuizen Maarten , Berns Anton , Collier Lara S. , Hubbard Tim , Adams David J. 
Published: January 2010

Abstract
Comparative genomic hybridization (CGH) can reveal important disease genes but the large regions identified could sometimes contain hundreds of genes. Here we combine high-resolution CGH analysis of 598 human cancer cell lines with insertion sites isolated from 1,005 mouse tumors induced with the murine leukemia virus (MuLV). This cross-species oncogenomic analysis revealed candidate tumor suppressor genes and oncogenes mutated in both human and mouse tumors, making them strong candidates for novel cancer genes. A significant number of these genes contained binding sites for the stem cell transcription factors Oct4 and Nanog. Notably, mice carrying tumors with insertions in or near stem cell module genes, which are thought to participate in cell self-renewal, died significantly faster than mice without these insertions. A comparison of the profile we identified to that induced with the Sleeping Beauty (SB) transposon system revealed significant differences in the profile of recurrently mutated genes. Collectively, this work provides a rich catalogue of new candidate cancer genes for functional analysis. Cancer Res; 70(3); 883–95
EWS/FLI1 Oncogene Activates Caspase 3 Transcription and Triggers Apoptosis In vivo
Authors: Sohn Eun Jung , Li Hongjie , Reidy Karen , Beers Lisa F. , Christensen Barbara L. , Lee Sean Bong 
Published: January 2010

Abstract
EWS/FLI1 is a fusion gene product generated by a chromosomal translocation t(11;22)(q24;q12) found in Ewing sarcoma. EWS/FLI1 encodes an aberrant transcription factor with oncogenic properties in vitro. Paradoxically, expression of EWS/FLI1 in nontransformed primary cells results in apoptosis, but the exact mechanism remains unclear. In primary mouse embryonic fibroblasts derived from conditional EWS/FLI1 knock-in embryos, expression of EWS/FLI1 resulted in apoptosis with concomitant increase in the endogenous Caspase 3 (Casp3) mRNA. EWS/FLI1 directly bound and activated the CASP3 promoter, whereas small interfering RNA–mediated knockdown of EWS/FLI1 led to a marked decrease in CASP3 transcripts in Ewing sarcoma cell lines. Ectopic expression of EWS/FLI1 resulted in an increased expression of CASP3 protein in heterologous cell lines. Importantly, expression of EWS/FLI1 in the mouse triggered an early onset of apoptosis in kidneys and acute lethality. These findings suggest that EWS/FLI1 induces apoptosis, at least partially, through the activation of CASP3 and show the cell context–dependent roles of EWS/FLI1 in apoptosis and tumorigenesis. Cancer Res; 70(3); 1154–63
Role of Cationic Channel TRPV2 in Promoting Prostate Cancer Migration and Progression to Androgen Resistance
Authors: Monet Michaël , Lehen'kyi V'yacheslav , Gackiere Florian , Firlej Virginie , Vandenberghe Matthieu , Roudbaraki Morad , Gkika Dimitra , Pourtier Albin , Bidaux Gabriel , Slomianny Christian , Delcourt Philippe , Rassendren François , Bergerat Jean-Pierre , Ceraline Jocelyn , Cabon Florence , Humez Sandrine , Prevarskaya Natalia 
Published: January 2010

Abstract
Castration resistance in prostate cancer (PCa) constitutes an advanced, aggressive disease with poor prognosis, associated with uncontrolled cell proliferation, resistance to apoptosis, and enhanced invasive potential. The molecular mechanisms involved in the transition of PCa to castration resistance are obscure. Here, we report that the nonselective cationic channel transient receptor potential vanilloid 2 (TRPV2) is a distinctive feature of castration-resistant PCa. TRPV2 transcript levels were higher in patients with metastatic cancer (stage M1) compared with primary solid tumors (stages T2a and T2b). Previous studies of the TRPV2 channel indicated that it is primarily involved in cancer cell migration and not in cell growth. Introducing TRPV2 into androgen-dependent LNCaP cells enhanced cell migration along with expression of invasion markers matrix metalloproteinase (MMP) 9 and cathepsin B. Consistent with the likelihood that TRPV2 may affect cancer cell aggressiveness by influencing basal intracellular calcium levels, small interfering RNA–mediated silencing of TRPV2 reduced the growth and invasive properties of PC3 prostate tumors established in nude mice xenografts, and diminished expression of invasive enzymes MMP2, MMP9, and cathepsin B. Our findings establish a role for TRPV2 in PCa progression to the aggressive castration-resistant stage, prompting evaluation of TRPV2 as a potential prognostic marker and therapeutic target in the setting of advanced PCa. Cancer Res; 70(3); 1225–35
FKBPL Regulates Estrogen Receptor Signaling and Determines Response to Endocrine Therapy
Authors: McKeen Hayley D. , Byrne Christopher , Jithesh Puthen V. , Donley Christopher , Valentine Andrea , Yakkundi Anita , O'Rourke Martin , Swanton Charles , McCarthy Helen O. , Hirst David G. , Robson Tracy 
Published: January 2010

AbstractThe HSP90 chaperone and immunophilin FKBPL is an estrogen-responsive gene that interacts with estogen receptor α (ERα) and regulates its levels. In this study, we explored the effects of FKBPL on breast cancer proliferation. Breast cancer cells stably overexpressing FKBPL became dependent on estrogen for their growth and were dramatically more sensitive to the antiestrogens tamoxifen and fulvestrant, whereas FKBPL knockdown reverses this phenotype. FKBPL knockdown also decreased the levels of the cell cycle inhibitor p21WAF1 and increased ERα phosphorylation on Ser118 in response to 17β-estradiol and tamoxifen. In support of the likelihood that these effects explained FKBPL-mediated cell growth inhibition and sensitivity to endocrine therapies, FKBPL expression was correlated with increased overall survival and distant metastasis-free survival in breast cancer patients. Our findings suggest that FKBPL may have prognostic value based on its impact on tumor proliferative capacity and sensitivity to endocrine therapies, which improve outcome. Cancer Res; 70(3); 1090–100
RBCK1 Drives Breast Cancer Cell Proliferation by Promoting Transcription of Estrogen Receptor α and Cyclin B1
Authors: Gustafsson Nina , Zhao Chunyan , Gustafsson Jan-Åke , Dahlman-Wright Karin 
Published: January 2010

Abstract
Cell cycle regulatory pathways in breast cancer are incompletely described. Here, we report an important role in estrogen receptor α (ERα)–positive breast cancer cells for the protein kinase C1 (PKC1)–interacting protein RBCK1 in supporting cell cycle progression by driving transcription of ERα and cyclin B1. RBCK1-depleted cells exhibited increased accumulation in G2-M phase of the cell cycle, decreased proliferation, and reduced mRNA levels for ERα and its target genes cyclin D1 and c-myc. Chromatin immunoprecipitation revealed that ERα transcription is associated with RBCK1 recruitment to the ERα promoter, suggesting that transcriptional regulation is one mechanism by which RBCK1 affects ERα mRNA levels. G2-M phase arrest was mediated independently from reduced ERα levels, instead associated with transcriptional inhibition of the key G2-M regulator cyclin B1. In breast tumor samples, there was a positive correlation between levels of RBCK1, ERα, and cyclin B1 mRNA levels. Our findings suggest that RBCK1 regulates cell cycle progression and proliferation of ERα-positive breast cancer cells by supporting transcription of ERα and cyclin B1. Cancer Res; 70(3); 1265–74
Identification of Breast Tumor Mutations in BRCA1 That Abolish Its Function in Homologous DNA Recombination
Authors: Ransburgh Derek J.R. , Chiba Natsuko , Ishioka Chikashi , Toland Amanda Ewart , Parvin Jeffrey D. 
Published: January 2010

Abstract
Effects of breast cancer–associated gene 1 (BRCA1) missense mutations on the function of BRCA1 protein in DNA recombination have been little studied. In this report, we adapted a homology-directed recombination (HDR) assay to analyze the effects of BRCA1 mutations on this function. Using a HeLa-derived cell line with a genomically integrated recombination substrate, we expressed an endonuclease creating a double-stranded break in the substrate that the HDR assay scores by generation of green fluorescent protein–positive cells. By combining RNA interference (RNAi) that targets cellular BRCA1 mRNA with expression of RNAi-resistant BRCA1 mutants, we could effectively substitute selected point mutants to test these in the cellular recombination assay. We found that ∼300 residues at both termini of the BRCA1 protein were essential for HDR. Whereas some mutations analyzed were neutral, mutations that altered any zinc-coordinating residue or generated M18T and T37R alterations were defective for recombination. This study established a robust assay system to analyze the function of BRCA1 in regulating homologous recombination, which is critical for its tumor suppressor function. Cancer Res; 70(3); 988–95
Caffeine-Mediated Inhibition of Calcium Release Channel Inositol 1,4,5-Trisphosphate Receptor Subtype 3 Blocks Glioblastoma Invasion and Extends Survival
Authors: Kang Sang Soo , Han Kyung-Seok , Ku Bo Mi , Lee Yeon Kyung , Hong Jinpyo , Shin Hye Young , Almonte Antoine G. , Woo Dong Ho , Brat Daniel J. , Hwang Eun Mi , Yoo Seung Hyun , Chung Chun Kee , Park Sung-Hye , Paek Sun Ha , Roh Eun Joo , Lee Sung joong , Park Jae-Yong , Traynelis Stephen F. , Lee C. Justin 
Published: January 2010

AbstractCalcium signaling is important in many signaling processes in cancer cell proliferation and motility including in deadly glioblastomas of the brain that aggressively invade neighboring tissue. We hypothesized that disturbing Ca2+ signaling pathways might decrease the invasive behavior of giloblastoma, extending survival. Evaluating a panel of small-molecule modulators of Ca2+ signaling, we identified caffeine as an inhibitor of glioblastoma cell motility. Caffeine, which is known to activate ryanodine receptors, paradoxically inhibits Ca2+ increase by inositol 1,4,5-trisphospate receptor subtype 3 (IP3R3), the expression of which is increased in glioblastoma cells. Consequently, by inhibiting IP3R3-mediated Ca2+ release, caffeine inhibited migration of glioblastoma cells in various in vitro assays. Consistent with these effects, caffeine greatly increased mean survival in a mouse xenograft model of glioblastoma. These findings suggest IP3R3 as a novel therapeutic target and identify caffeine as a possible adjunct therapy to slow invasive growth of glioblastoma. Cancer Res; 70(3); 1173–83
Inactivation of the Quinone Oxidoreductases NQO1 and NQO2 Strongly Elevates the Incidence and Multiplicity of Chemically Induced Skin Tumors
Authors: Shen Jun , Barrios Roberto J. , Jaiswal Anil K. 
Published: January 2010

Abstract
The cytosolic quinone oxidoreductases NQO1 and NQO2 protect cells against oxidative stress by detoxifying quinones and preventing redox cycling. In this study, we used double knockout (DKO) mice deficient for NQO1 and NQO2 to investigate the role of these antioxidative enzymes in a two-stage model of inflammatory skin carcinogenesis. In this model, tumors are caused by exposure to topical carcinogen dimethylbenz(a)anthracene or benzo(a)pyrene (BP) followed by twice weekly application of proinflammatory phorbol 12-myristate 13-acetate. On this classic chemical carcinogenesis protocol, DKO mice showed a significantly higher skin tumor frequency and multiplicity compared with control wild-type or single knockout mice. Analysis of skin from wild-type and DKO mice exposed to BP for 6, 12, or 24 hours revealed a relative delay in the activation of p53, p63, p19ARF, and apoptosis in DKO mice, consistent with a negative modifier role for NQO1/NQO2 in carcinogenesis. Our findings offer genetic evidence of the significance of quinone oxidoreductases NQO1 and NQO2 in limiting chemical skin carcinogenesis. Cancer Res; 70(3); 1006–14
Increased Expression of Annexin A3 Is a Mechanism of Platinum Resistance in Ovarian Cancer
Authors: Yan Xuedong , Yin Jie , Yao Huiyu , Mao Ning , Yang Yili , Pan Lingya 
Published: January 2010

Abstract
Resistance to platinum drugs has emerged as a major obstacle in the treatment of ovarian cancers. Through proteomic analysis, we have found that the expression of annexin A3, a member of the Ca2+ and phospholipid-binding annexin family, is significantly increased in platinum-resistant ovarian cell lines. Anti–annexin A3 immunostaining indicated that cancers from platinum-resistant patients also possess higher levels of annexin A3 than those from platinum-sensitive patients. Although expression of annexin A3 made susceptible ovarian cancer cells more resistant to platinum, expression of antisense annexin A3 downregulated its expression and rendered the resistant cells more sensitive to platinum. In athymic mice, the growth of tumors from inoculated SKOV3 cells was inhibited by the administration of platinum, whereas tumors from annexin A3–expressing SKOV3/Ann were resistant to platinum treatment. Interestingly, the intracellular platinum concentration and platinum-DNA binding are significantly lower in annexin A3–overexpressing cells than those in parental cells. The lower cisplatin concentration was also accompanied by reduced induction of p53, which could be restored by downregulation of annexin A3. These results indicate that increased expression of annexin A3 is a mechanism of platinum resistance in ovarian cancer. It seems to act by preventing uptake or accumulation of platinum in cells. Therefore, it is conceivable that annexin A3 could be a target for therapeutic intervention and may also serve as a biomarker for drug resistance in ovarian cancer patients. Cancer Res; 70(4); 1616–24